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Lomte DB et al. Int J Med Res Health Sci. 2013;2(4):719-723

International Journal of Medical Research

&

Health Sciences

www.ijmrhs.com Volume 2 Issue 4 Oct-Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886Received: 10

thJuly 2013 Revised: 8

thAug 2013 Accepted: 15

thAug 2013

Research article

COMPARATIVE STUDY ON EFFICACY & SAFETY OF INTRAVENOUS IRON SUCROSE

VERSUS INTRAMUSCULAR IRON SORBITOL THERAPY IN ANEMIA DURING

PREGNANCY

*Lomte DB1, Bhosale RS

2, Jambdade V

3, Gore PR

4

1

Asso. Prof, Dept. of Pharmacology, Dr. V.P.M.C. Nashik, Maharashtra, India2,4Civil Hospital Nashik,

3Head of Dept., OBGY, Civil Hospital Nashik, Maharashtra, India

*Corresponding author email: [email protected], [email protected]

ABSTRACT

Aims and Objectives: To compare the efficacy, safety, and rate of response of intravenous iron sucrose

and intramuscular iron Sorbitol therapy for anemia during pregnancy. Material and Methods: 100

antenatal cases of gestational age 16-32 weeks were included in this prospective study. Cases were

randomly divided into two groups. Group A, having 50 cases received intravenous iron sucrose, and

50cases in group B received intramuscular iron sorbitol. Response to therapy in both groups was studied

and compared. Results: The mean pretherapy hemoglobin in group A was 6.49 g/dl and in group B was

6.48 g/dl. The rise in hemoglobin after 4 weeks of starting therapy was 3.52 g/dl in group A and 2.33

g/dl in group B The difference was Statistically significant (P<0.01) The mean time taken to achieve

target hemoglobin (>11 g/dl) was 6.37 weeks in group A and 9.04 weeks in group B. In group A, 8%

(four) cases had grade I adverse effects. In group B, 24% (12) cases had grade I adverse effects. The

difference was statistically significant (P=0.027). In both the groups no case discontinued the therapy.

Conclusion: Intravenous iron sucrose is safe, convenient, more effective, and faster acting therapy than

intramuscular iron sorbitol therapy for treating moderate to severe anemia during pregnancy.

Keywords: Iron sucrose, Iron sorbitol, Pregnancy, Iron deficiency.

INTRODUCTION

Anemia is associated with higher perinatal

mortality and morbidity1. Anemia is the most

common hematologic abnormality diagnosed

during pregnancy. It is most often caused by iron

deficiency & occasionally by more complex

conditions involving deficient production of or

accelerated destruction of erythrocytes.1 In

developing countries nearly two third of the

pregnant women suffering from anemia out of

which 95% of cases are having iron deficiency

anemia.2

Over the past years, various routine methods like

oral iron therapy, intramuscular iron therapy, and

blood transfusion were used to treat anemia

during pregnancy3,4

. These methods are not

without deficiencies, and also there areconditions in which these conventional iron

therapies are not helpful, like inadequate

DOI: 10.5958/j.2319-5886.2.4.115



720


gastrointestinal absorption, late pregnancy, and

intolerance to required oral iron, requirement of

emergency supplement, and severe anemia with

contraindications to blood transfusion5. So, to

treat these conditions, we require a relatively

new mode of iron therapy with better efficacy,less side effects, fast action and better

compliance. Intravenous iron sucrose therapy

seems to be a safe convenient and more effective

treatment for anemia during pregnancy

MATERIALS AND METHODS

After the approval of Institutional Ethics

committee of Dr VPMC, Nashik, total 100

antenatal women between 16 and 32 weeks of gestation with hemoglobin level of 8 g/dl or less,

attending the outpatient department & antenatal

ward at Civil Hospital Nashik, were included in

the present study.

Inclusion Criteria: 1. Pregnant women aged

≥18, gestational week between 16 to 32, at

baseline with normal antenatal screening test

results, Pregnant women willing to give conform

consent form for the study 2. Iron deficiency

anemia defined as Hb concentration ≤ 8g/dl,

serum iron less than 60 micro g/dl, and total iron-

binding capacity more than 400 micro g/dl

Excusing Criteria: 1. The cases having

hemoglobin level >8 g/dl 2. Gestational age <16

or >32 weeks

3. History of allergic reaction to previous iron

therapy 4. Anemia due to causes other than iron

deficiency.

All the 100 cases enrolled in the study were

assigned into two groups. Group A: 50 cases

received intravenous iron sucrose, Group B: 50

cases received intramuscular iron sorbitol

therapy. Iron was given after proper sensitivity

testing in both the groups. All the selected cases

were subjected to a thorough history taking,

general, systemic and obstetrical examination.The dose of iron required in both the groups was

calculated by the formula

Total iron required =Body weight (kg) X Hb

deficit X 0.3 + (Body Wt.(kg) X10)

[Hb deficit=target Hb- patient s̀ Hb (Target

Hb=11g/dl)]

In group A iron sucrose was given as 150 mg (3

ampoules, each of 2.5ml) in 100 ml of 0.9%

normal saline infusion over 1 hr every third dayup to the total calculated dose. In group B, iron

sorbitol complex was given as a daily

intramuscular injection of 1.5 ml till the total

calculated dose, by means of ‘Z’ technique. All

the cases were monitored for adverse effects.

Adverse effects were graded as grade I and grade

II. Grade I reactions were mild to moderate and

settled with an antiallergic drug but not requiring

discontinuation of drug. Grade II reaction was

severe in nature threatening the life of patients

and requiring discontinuation of therapy.

Statistical analysis:

Statistical analysis was carried out by using

paired‘t’ test for comparing effects of

intravenous iron sucrose & intramuscular iron

sorbitol before and after therapy. For

comparisons between intravenous iron sucrose &

intramuscular iron sorbitol ‘unpaired t’ test was

applied.

RESULTS

Table 1: Demographic distribution of cases

Group A

(n=50)

Group B

(n=50)

Mean age (years) 26.46 26.62

Mean period of gestation 24.48 23.94

Parity >2 (% of cases) 68 56Socioeconomic status class

IV or lower (%of cases)

76 80



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Table 2: Hemoglobin level before starting therapy

Hemoglobin level

(g/dl)

Group A Group B

No. % No. %

<4 6 12 3 6

4.1-6 8 16 12 24

6.1-8 36 72 35 70

Mean 6.49 6.48

P value >0.05

Table 3: Hemoglobin level 2 and 4 weeks after starting therapy

Hemoglobin

level (g/dl)

After 2 weeks of therapy After 4 weeks of therapy

Group A Group B Group A Group B

No. % No. % No. % No. %

5-7 7 14 12 24 - - 5 107.1-9 16 32 33 66 9 18 21 42

9.1-11 27 52 5 10 39 78 24 48

>11 - - - - 2 4 - -

Mean 8.79 7.74 10.01 8.81

P value < 0.01 <0.01

Table 4: Time period taken to achieve target hemoglobin level (>11g/dl)

Time period

(weeks)

Group A Group B

No. % No. %

2-4 3 6 - -

>4-8 42 84 17 34

>8-12 5 10 28 56

>12 - - 5 10

Mean 6.37 9.4

P value <0.01

Table 5: Adverse effects in both the groups

Adverse effects (all grade I) Group A Group B

No. % No. %

Local phlebitis 2 4 - -

Shivering and weakness 1 2 - -

Moderate abdominal pain 1 2 - -

Local pain - - 6 12

Skin staining - - 6 12

Headache - - 1 2

Total 4 8 12 24



722


The mean pre therapy hemoglobin level in group

A was 6.49 g/dl and in group B was 6.48 g/dl

(Table 2). In group A, the mean hemoglobin

level after 2 weeks of staring therapy was 8.79

g/dl with a rise of 2.33 g/dl. In group B, the mean

hemoglobin level after 2 weeks of startingtherapy was 7.74 g/dl with a rise of 1.26

g/dl(Table 3) the difference was statistically

significant (P<0.01).

After 4 weeks of starting therapy, the mean

hemoglobin level in group A was 10.01 g/dl with

a rise of 3.52 g/dl and I group B mean

hemoglobin was 8.81 g/dl with a total rise of

2.23g/dl from the pre therapy level (Table 3).

The difference was statistically significant(P<0.01). In group A, 90% (45) cases achieved

target hemoglobin level after 8 weeks of starting

therapy, while in group B only 34% (17) cases

achieved target hemoglobin levels after 8 weeks

of therapy. The difference was statistically highly

significant (P< 0.001).

The mean time period taken to achieve target

hemoglobin level was 6.37 g/dl in group A and

9.04 weeks in group B (Table4). The difference

was found to be statistically significant (P<0.01).

In group A, 8% (four) cases had grade I adverse

effects: while in group B, 24% (12) cases had

grade I adverse effects (Table5). The adverse

effects were minimal and managed

symptomatically. On statistically analyzing the

results, the difference was found significant (P=

0.027).

In group A, 60% (30) cases were completely

relieved of their clinical symptoms at 4 weeksafter therapy: while in group B, only 20% (10)

cases were completely relieved of their

symptoms. The difference was statistically

highly significant.

DISCUSSION

The current study was undertaken to evaluate the

efficacy and safety of intravenous iron sucrose

therapy for treating anemia during pregnancy andcompare it with intramuscular iron sorbitol

therapy. The rise in hemoglobin level in cases,

which were given intravenous iron sucrose

therapy, was 2.3 g/dl after 2 weeks and 3.52 g/dl

after 4 weeks (table 3). It was significantly

higher when compared to rise after intramuscular

iron sorbitol therapy. The rise in hemoglobin

level was 2.6 g/dl in intravenous group and 1.2g/dl in intramuscular group after 3 weeks of

therapy in the study by Hashmi et al.5

In the

study conducted by wali et al.6

the rise in

hemoglobin level was 2.8 g/dl after 3 weeks of

intravenous iron sucrose therapy.

90% (45) cases achieved the target hemoglobin

level of >11g/dl after 8 weeks of intravenous iron

sucrose therapy, while only 34% (17) cases

achieved target hemoglobin level after 8 weeksof intramuscular iron sorbitol therapy. The

difference was statistically significant (p< 0.001).

In the study by Hashmi et al.6, 80% cases

achieved target hemoglobin in intravenous iron

group and only 20% cases achieved target

hemoglobin level in intramuscular iron group

after 6 weeks of therapy.

In our study, the mean time period taken to

achieve the target hemoglobin level was 6.37

weeks in intravenous iron sucrose group and 9.04

weeks in intramuscular iron sorbitol group

(Table 4) this difference was statistically

significant (P<0.01). In the study by Raja et al.8

the mean time period to achieve target

hemoglobin level was 5 weeks in the intravenous

iron sucrose group.

Only 8 % (four) cases had adverse effects which

were of grade I type with intravenous iron

sucrose therapy, while 24% (12)9-12

cases hadgrade I adverse effect with intramuscular iron

sorbitol therapy (Table 5). The difference was

statistically significant (P= 0.027). There were no

grade II adverse effects in either of the groups. In

the study conducted by Wali et al.7, 12% cases

had grade I adverse effects, with intravenous iron

sucrose therapy, while 50% cases had grade I

adverse effects with intramuscular iron sorbitol

therapy. In group A, 60% (30) cases werecompletely relieved of their symptoms: while in

group B, only 20% (10) cases were completely



723


relieved of their symptoms. The difference was

statistically significant (P<0.001). The results of

our study shown that the mean hemoglobin level

achieved in intravenous iron sucrose group was

significantly higher and the rate of increase in

hemoglobin level was also higher inintravenous group. The number of cases

achieving target hemoglobin was significantly

higher in intravenous group and also the target

hemoglobin was achieved in a shorter time

period in intravenous group. The incidence of

adverse effects was also significantly lower in

intravenous group.

CONCLUSION

Intravenous iron sucrose therapy is safe,

convenient, more effective, and faster acting than

intramuscular iron sorbitol therapy for the

treatment of moderate to severe anemia during

pregnancy.

REFERENCES

1. Fernando Arias, Shirish ND. Anemia in

pregnancy. Text book of Obstetrics. 2010,466-469

2. Allen LH. Pregnancy and iron deficiency:

Unresolved Issues. Nutr Rev. 1997; 55; 91-

101.

3. Bayoumeu F, Subiran-Buisset C, Baka NE.

Iron therapy in iron deficiency anemia in

pregnancy: intravenous route versus oral

route. Am J Obstet Gyneco. 2002; 186; 518-

22.

4. Kanani SJ, Poojara RH. Supplementation

with iron & folic acid enhances growth. Jr

Nutrition 2000; 130:452S-455S

5. Perewusny KG, Huck R, Huck A. Parenteral

iron-sucrose complex. Br. J Nutr. 2002;88;3-

10

6. Hashimi Z, Bashir G, Azzem P. Effectiveness

of intra-venous iron sucrose complex versus

intra-muscular iron sorbitol in iron deficiency

anemia. Ann Pak Inst Med Sci. 2006;2;188-

91.

7. Waili A, Mushtaq A. Comparative Study-

efficacy. Safety and compliance of

intravenous iron sucrose and intramuscular

iron sorbitol in iron deficiency anemia of pregnancy. J Pak Med Assoc. 2002; 52; 392-

95.

8. Raja KS, Janjua NB, Khokhar N. Intravenous

iron Sucrose complex therapy in iron

deficiency anemia in the pregnant women.

Rawal Med J. 2003; 28; 40-3.

9. Sharma JB, Vibha Fatedar. Iron deficiency

anemia in pregnancy. Obs & Gynae Today.

2006;9(3);147-148.10. Pollitt E, Soemangri AG, Yunis F, cognitive

effects of Iron deficiency anemia. Lancet

1985; 1:158.

11. Lazoff B, Jimenez E, Walf AW long term

developmental out come of infants with iron

deficiency. New Eng I J Med 1991;

325(10):687-95.

12. Abel R, Raja ratnamJ, Sapatkumar V.

Anemia in pregnancy impact of iron, IEC,

RUSHA Depatt Tamilnadu: CMC Vellore

1999.



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Shravya etal., Int J Med Res Helath Sci. 2013;2(4):724-729


&

Health Sciences




thAug 2013

Research article

IMMEDIATE EFFECT OF SURYANADI PRANAYAMA ON PULMONARY FUNCTION

(VENTILATORY VOLUMES AND CAPACITIES) IN HEALTHY VOLUNTEERS

Shravya Keerthi G1, Hari Krishna Bandi

2, Suresh M

3, *Mallikarjuna Reddy N

4

1Dept of Physiology, Narayana Medical College, Nellore Currently affiliated with JIPMER, Puducherry,

India.2Department of Physiology, JIPMER, Puducherry, India

3Dept of Physiology, Meenakshi Medical College Hospital & Research Institute, Kancheepuram,

Tamilnadu, India4Department of Physiology, Narayana Medical College, Nellore, Andhra Pradesh, India

*Corresponding author email: [email protected]

ABSTRACT

Objectives: we found only effects of at least a short term practice extended over a period of a few days

to weeks of pranayama (alternate nostril breathing) rather than acute effects of unilateral right nostrilbreathing (suryanadi pranayama). Keeping this in mind the present study was designed to test the

hypothesis that 10 min. of right nostril breathing have any immediate effect on ventilatory volumes and

capacities in healthy volunteers. Methodology: Forced vital capacity (FVC), Forced expiratory volume

in the first second (FEV1), Forced expiratory volume percent (FEV1 /FVC%), Peak expiratory flow rate

(PEFR), Forced expiratory flow25-75% (FEF25-75%), Maximum voluntary ventilation (MVV), Slow vital

capacity (SVC), Expiratory reserve volume (ERV), Inspiratory reserve volume (IRV) and Tidal volume

(TV) were recorded before and after Surya Nadi Pranayama. Results & Conclusion: There was a

significant increase in FVC (p<0.0001), FEV1 (p<0.0007), PEFR (p<0.0001), FEF25-75% (p<0.0001),

MVV (p<0.0001), SVC (p<0.0001), ERV (0.0006), IRV (p<0.0001) and TV (0.0055) after suryanadipranayama. The immediate effect of suryanadi pranayama practice showed alleviation of ventilatory

capacities and volumes. Any practice that increases PEFR and FEF25 – 75% is expected to retard the

development of COPD’s. The increase in PEFR, vital capacities and flow rates by suryanadi pranayama

practice obviously offers an increment in respiratory efficiency and it can be advocated to the patients of

early bronchitis and as a preventive measure for COPD.

Keywords: Pulmonary function, Suryanadi pranayama, immediate effect, ventilatory volumes and

capacities

INTRODUCTION

Yoga is the best lifestyle, which aims to attain

the unity of mind, body and spirit through asanas

(exercise), pranayama (breathing), and

meditation1.

Pranayama, the fourth step of astang

DOI: 10.5958/j.2319-5886.2.4.116



725


yoga is an important component of yoga

training2

. Pranayama and Asanas are considered

as important part which is prescribed by modern

medicine too. Many physicians now recommend

yoga to the patients at risk for heart diseases, as

well as those with back pain, arthritis, depressionand other chronic diseases

3.The beneficial effects

of Pranayama are well reported and have a sound

scientific basis. It was reported different types of

Pranayama produce different physiological

responses in healthy young volunteers2,4

.

Pranayama is a method of breathing and chest

expansion exercise which has been reported to

improve cardio respiratory function in health and

disease

5,6

. The practice of pranayama has beenknown to modulate cardiac autonomic status

with an improvement in Cardio respiratory

functions5, 7

. Autonomic nervous system consists

of two branches i.e; sympathetic nervous system

and parasympathetic nervous system. Although

individual asana and pranayama practices can

selectively affect sympathetic or parasympathetic

nervous system, the overall effect of yoga

practice is to bring a state of parasympathetic

dominance2,8,9. The practice of breathing exercise

increases parasympathetic activity and decreases

sympathetic activity, improves cardiorespiratory

functions by affecting oxygen consumption,

metabolism and skin resistance9-11

.

Humans breathe preferably through one nostril at

a time. Kayser defined nasal cycle as a

phenomenon of alternating congestion,

decongestion response of erectile tissues of nasal

turbinate and septum of two nostrils, whicheffectively altered the unilateral nasal resistance

and was existent on account of prevailing

sympathetic and parasympathetic tone12

.The

preferred nostril alternates in a simultaneous

congestion-decongestion cycle. The nostril

congestion-decongestion cycle is believed to

reflect the dynamic lateralization of the

autonomic nervous system10,13

. Prolonged

unilateral nostril breathing as a result of completeor partial nasal obstruction is correlated with a

number of chronic disorders such as unilateral

migraine, peptic ulcer, dysmenorrhoea, lack of

libido, cardiac symptoms, fever,

hyperthyroidism, asthma, inadequate oral intake

and electrolyte imbalance14

. It is believed that

there is an activation of the contra lateral cerebral

cortex with unilateral nostril breathing as evidentfrom the rise in EEG amplitude

10, 14. The right

hemisphere is believed to play a major role in

parasympathetic activity than the left

hemisphere13

. Left nostril breathing increases

intraocular pressure (IOP) by 4.5% while right

nostril breathing decreases IOP significantly13,14

.

Pranayama breathing through right nostril

increases sympathetic activity, left nostril

breathing reduces it.Breathing exercises have been recommended in

physiotherapy to improve respiratory and bowel

function, in occupational therapy to facilitate

spiritual emergence5,6,13

. It has been assumed

single nostril breathing can be used to

therapeutically influence autonomic function and

may significantly affect other hemisphere-

specific functions6,13

. Yoga practices can also be

used as psycho-physiological stimuli to increase

the secretion of melatonin which might be

responsible for perceived well-being and has a

calming effect on the mind, helps an individual

to de-stress. These yoga practices might be

interacting with various somatic and neuro-

endocrine mechanisms bringing about

therapeutic effects9,15

. This calming effect may

also exert profound physiological effects on

pulmonary, cardiovascular, and mental functions

of the brain7,11

.The literature search through PUBMED central

and other search engines, showed very scanty

data on immediate effects of suryanadi

pranayama on pulmonary functions. In our

literature search, we found only effects of at least

a short term practice extended over a period of a

few days to weeks of pranayama (alternate

nostril breathing) rather than acute effects of

unilateral right nostril breathing (suryanadipranayama). Keeping this in mind the present

study was designed to test the hypothesis that 10



726


min. of right nostril breathing have any

immediate effect on ventilatory volumes and

capacities in healthy volunteers.


Subject selection: This is a cross-sectional study

carried out in the Pulmonary Function Testing

Laboratory, Department of Physiology, Narayana

medical college (NMC), Nellore (A.P), India.

After obtaining approval of Institutional Ethics

Committee (IEC), pulmonary function tests were

conducted in 30 healthy volunteers in the age

group of 18 to 40 years; age, BMI matched

students and residents of NMC. The subjects of

both genders were included. Subjects with a pasthistory of smoking, hypertension, respiratory

diseases, chest wall injuries, congestive cardiac

failure, kyphoscoliosis and who are already

trained in yoga and exercise were excluded from

the study.

Study protocol: The volunteers were properly

explained about the objectives, methodology,

expected outcome and implications of the study

and written informed consents were obtained

from them. They were instructed to report to PFT

lab of Physiology department at about 9 A.M.

Their age, height, weight, was recorded and BMI

calculated. Volunteers are trained to right nostril

breathing (Suryanadi pranayama) by experienced

yoga teacher from Narayana Yoga and

Naturopathy College, and volunteers also get

familiarized with our research lab and procedure

of pulmonary function testing.

Methodology: Volunteers were asked to sit in a

calm, quiet airy place in an easy and steady

posture with the head, neck and trunk erect and

in a straight line in order to keep the body still.

Asked them to bring the right hand up to the

nose, fold the index and middle finger in a way

so that the right thumb closed the right nostril

and the ring finger closed the left nostril (Vishnu

Mudra)12

. The volunteer was asked to close the

left nostril by the ring finger and slowly breathein up to a maximum, through the right nostril by

counting 1to 6 over a period of 6 seconds and

then and exhale slowly up to maximum over a

period of 6 seconds. Recordings for pulmonary

function parameters were taken before and after

practicing suryanadi pranayama.

Pulmonary functions were assessed bycomputerized spirometer (Spirowin Version 2.0

of Genesis Medical systems pvt Ltd) which gives

ERS-93 predicted values at BTPS conditions.

After preliminary trials, a baseline reading was

taken. Volunteers followed the instructions given

by qualified and experienced yoga teacher for

Suryanadi pranayama of 6 cycles/min for 10

mins. After practicing Suryanadi pranayama (6

cycles/min) for 10 min, the test was performedthree times and the best reading was considered.

During the procedure, the subjects inhaled deeply

and then exhaled with maximum effort as much

as possible into the mouthpiece for FVC test. The

subjects inhaled deeply and exhaled slowly and

completely as much as possible, this was

repeated for 3-4 times followed by normal

respiration for SVC test. The following

parameters were recorded: Forced vital capacity

(FVC), Forced expiratory volume in the first

second (FEV1), Forced expiratory volume

percent (FEV1 /FVC%), Peak expiratory flow rate

(PEFR), Forced expiratory flow 25-75% (FEF25-

75%), Maximum voluntary ventilation (MVV),

Slow vital capacity (SVC), Expiratory reserve

volume (ERV), Inspiratory reserve volume (IRV)

and Tidal volume (TV).

RESULTS

The data were expressed as mean ± SD, were

analyzed using the GraphPad Instat Version3.0

for Windows, GraphPad Software, La Jolla

California USA, www.graphpad.com. The

Gaussian distribution of the data was determined.

Normally distributed data were tested by the

paired t-Test. Non-normally distributed data

were tested with the Wilcoxon signed rank test.

A value of P<0.05 was considered as significant.Table 1 shows the anthropometric parameters of

the subjects. Table 2 shows the respiratory



727


variables like ventilatory capacities, volumes and

flow rates before and after suryanadi pranayama.

There was significant increase in FVC

(p<0.0001), FEV1 (p<0.0007), PEFR (p<0.0001),

FEF25-75% (p<0.0001), MVV (p<0.0001), SVC

(p<0.0001), ERV (0.0006), IRV (p<0.0001) and

TV (0.0055) after suryanadi pranayama.

Table 1. Anthropometric parameters

Table 2. Comparison of respiratory variables before and after suryanadi pranayama

S.no Parameter Mean ± SD P value

Before After

1. FVC(L) 2.45 ± 0.49 2.75 ± 0.59 0.0001*

2. FEV1(L) 2.09 ± 0.49 2.30 ± 0.55 0.0007*

3. FEV1 /FVC% 83.82 ±10.59 84.29 ± 9.38 0.79

4. PEFR(L/S) 4.14 ± 1.32 4.32 ± 1.06 0.0001*

5. FEF25-75%(L/S) 2.62 ± 0.79 2.67 ± 0.62 0.0001*

6. SVC(L) 3.61 ± 1.93 4.47 ± 2.81 0.0001*

7. ERV(L) 1.22 ± 1.18 1.70 ± 1.54 0.0006*

8. IRV(L) 2.09 ± 1.85 2.87 ± 2.62 0.0001*

9. TV(L) 0.92 ± 0.49 1.07 ± 0.43 0.0055*

10. MVV(L) 69.39 ± 17.10 77.98 ± 19.65 0.0001*

FVC: Forced Vital capacity, FEV1: Forced Expiratory Volume in 1 sec, PEFR: Peak Expiratory Flow

rate, FEF25-75%: Forced Expiratory Volume, SVC: Slow vital capacity, ERV: Expiratory Reserve

Volume, IRV: Inspiratory Reserve Volume, TV: Tidal Volume and MVV: Maximal Voluntary

Ventilation. * signifies p< 0.001 which shows values are statistically significant.

DISCUSSION

Yoga is the ancient science which makes use of

voluntary regulation of breathing to make

respiration rhythmic, calm the mind to reach the

ultimate goal3,4

. A person practicing Pranayama

will try to keep his attention on the act of

breathing, leading to concentration which

removes his attention from day to day worries

and “de-stress” the individual3,4.

Each cycle of suryanadi pranayama is a complex

voluntary act, which includes two distinct

phases, Puraka, and Rechaka i.e., inspiration &

expiration. The technique of pranayama includes

specific rules regarding the method of breathing,

in terms of force of breathing, the duration of

each phase of breathing, the number of rounds of

pranayama and attention on breathing16

. The

various physiological changes occur duringdifferent phases of pranayama16

. During

pranayama, deep inhalation (puraka) stimulates

S.no Parameter Mean ± SD

1. Age (Yrs) 21.03 ±4.43

2. Weight (Kgs) 54.9±11.56

3. Height (m) 1.62 ± 0.09

4. BMI (kg/m ) 20.72 ± 3.28

5. BSA ( m ) 1.57 ± 0.18



728


the respiratory system and fills the lungs with

fresh air, retention of air (kumbhaka) raises the

internal temperature and increase the absorption

of oxygen, slow exhalation (rechaka) causes the

diaphragm to return to original position, air full

of toxins and impurities is forced out bycontractions of intercostals muscles

4,16. These are

the main components of pranayama which

massage the abdominal muscles and tone up the

working of respiratory organs of body4. This

deep inspiration, retention of air and slow

expiration increases the overall capacity of the

lungs and gradually improves the ventilatory

functioning of lungs4. Due to the proper working

of these organs, vital energy flows to maintainthe normal homeostasis of the body and thus it

helps in prevention, control and rehabilitation of

many respiratory diseases4, 16

. These results are

in line with the findings of Krogh and Lindhard,

which might be the result of impulses from

cerebral cortex influencing the respiratory

centre4.

From the results (table 2) it is evident that

immediate effect of suryanadi pranayama

showed significant improvement in FVC, FEV1,

PEFR, FEF25-75%, MVV, SVC, ERV, IRV and

TV. FEV1 is the volume of air that is exhaled in

the first second during FVC manoeuvre. It is

useful to detect generalized airway obstruction.

FEV1 /FVC% is the volume of air expired in the

first second, expressed as percentage of FVC. It

is a more sensitive indicator of airway

obstruction, than FVC or FEV1 alone. FEF25-75%

is the average flow rate during middle 50% of FVC. It indicates patency of the small airways.

FEF25-75% depends on non-bronchopulmonary

factors like, neuromuscular factors and

mechanical equipment factors of inertial

distortion of lungs. PEFR and FEF25 – 75% are the

first parameters to decline on many respiratory

diseases. Healthy persons expire 70 – 90% of FVC

in the first second of the test which means that

they take about 5 second to expire the last 10 – 30% of the FVC12

. Any practice that increases

PEFR and FEF25 – 75% is expected to retard the

development of COPD’s. Our results show the

positive impact of suryanadi pranayama on

PEFR and FEF25 – 75%.

These findings are similar to the study

conducted by Nidhi Jain et al., Baljinder Singh

Bal, Upadhyay et al. and Puja et al, showed a

significant increment in Peak expiratory flowrate (PEFR) and FEF 25-75%

12,14,15. The increased

PEFR might be a consequence of small airway

opening in lungs. The number of minute alveoli

in the lungs goes on increasing up to 8 yrs of age.

After this the alveoli increases only in size and

this is the ideal age to introduce pranayama16

.

The work of Yadav and Das attributed the

increase in PEFR by yogic exercise due to

following changes in respiratory dynamics i.e.,Increased respiratory muscle strength, cleansing

of airway secretions and efficient use of

diaphragmatic and abdominal muscles, thereby

emptying and filling the respiratory apparatus

more efficiently and completely3.

Previous studies also showed the effect of

Pranayama on alleviation of the respiratory

muscle efficiency and lung compliance by

reducing elastic and viscous resistance of lung

present during inspiration. Pranayama acts as

physiological stimuli for release of lung

surfactant and prostaglandins into alveolar spaces

which increase the lung compliances. Our

findings were consistent with the results of

sivapriya etal., immediate increase in PEFR and

increase in FVC, MVV, TV, Expiratory

capacities etc16

.

CONCLUSION

The immediate effect of suryanadi pranayama

practice showed alleviation of ventilatory

capacities and volumes. The increase in PEFR,

vital capacities and flow rates by suryanadi

pranayama practice obviously offers an

increment in respiratory efficiency and it can be

advocated to the patients of early bronchitis and

as a preventive measure for COPD.

Future Directions: Further research is requiredto determine whether forced nostril breathing has

greater effects than relaxed single nostril



729


breathing, and whether the effects are greater if

applied when a nostril is in its non-dominant

phase of the nasal cycle.

ACKNOWLEDGEMENT

We kindly acknowledge Mr. Sukumar BV,

Technical Supervisor, Pulmonary Function

Testing Laboratory, Naryana Medical College

(NMC) for his technical support, students and

residents of NMC, who have participated in the

study and led to complete the study successfully.

REFERENCES

1. Roopa BA, Anita Herur, Shailaja

Patil, Shashikala GV, Surekharani Chinagudi.Effect of Short-Term Pranayama and

Meditation on Cardiovascular Functions in

Healthy Individuals. Heart Views.

2011;12(2): 58 – 62.

2. Madanmohan. Effect of slow and fast

pranayamas on reaction time and

cardiorespiratory variables. Indian J Physiol

Pharmacol 2005; 49(3): 313-18.

3. Upadhyay Dhungel K, Malhotra V, Sarkar

D, Prajapati R. Effect of alternate nostrilbreathing exercise on cardiorespiratory

functions. Nepal Med Coll J 2008; 10(1): 25-

27.

4. Shivraj P. Manaspure, Ameet Fadia,

Damodara Gowda KM. Effect of selected

breathing techniques on respiratory rate and

breath holding time in healthy adults.

IJABPT.2011; 2(3): 225-29.

5. Sukhdev Singh. Effects of a 6-week nadi-shodhan pranayama training on

cardiopulmonary parameters. Journal of

Physical Education and Sports Management.

2011; 2(4): 44-47.

6. Chanavirut R. Yoga exercise increases chest

wall expansion and lung volumes in young

healthy thais. Thai journal of Physiological

sciences 2008; 19(1): 1-7.

7. Subbalakshmi NK, Saxena SK, Urmimala,

Urban JA, D’Souza. Immediate effect of

Nadi-Shodhana pranayama on some selected

parameters of cardiovascular, pulmonary, and

higher functions of brain. TJPS.

2005;18(2):10-16.

8. Madanmohan. Effect of six week yoga

training on weight loss following step test,

respiratory pressures, handgrip strength and

handgrip endurance in young healthysubjects. Indian J Physiol Pharmacol 2008;

52 (2): 164-70.

9. Pal GK, Velkumary S, Madanmohan. Effect

of short-term practice of breathing exercises

on autonomic functions in normal human

volunteers. Indian J Med Res.2004;120:115-

121.

10. Ravinder Jerath, John WE, Vernon AB,

Vandna Jerath. Physiology of longpranayamic breathing: Neural respiratory

elements may provide a mechanism that

explains how slow deep breathing shifts the

autonomic nervous system.Med Hypotheses.

2006;67(3):566-71.

11. Shankarappa V, Prasanth P, Nachal

Annamalai,Varunmalhotra. The short term

effect of pranayama on the lung parameters.

JCDR, 2012; 6(1):27-30.

12. Puja Dullo, Neeraj Vedi, Usha Gupta.

Improvement in respiratory functions after

alternate nostril breathing in healthy young

adults. Pak J Physiol 2008;4(2):15-16.

13. Venthan JM. Single-nostril breathing to

influence cognitive and autonomic Functions.

Indian Journal of Physiotherapy and

Occupational Therapy. 2008; 2(4):41-46.

14. Nidhi Jain, Srivastava RD, Anil Singhal. The

effects of right and left nostril breathing oncardiorespiratory and autonomic parameters.

IJPP 2005;49(4):469-74.

15. Baljinder Singh Bal. Effect of anulom vilom

and bhastrika pranayama on the vital capacity

and maximal ventilatory volume. J. Phys.

Educ. Sport Manag. 2010;1(1):11-15.

16. Sivapriya DV, Suba Malani S, Shyamala

Thirumeni. Effect of Nadi-Shodhana

pranayama on respiratory parameters in

school students”. Rec. Res. Sci. Tech.

2010;2: 32-39



730

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&

Health Scienceswww.ijmrhs.com Volume 2Issue3 July - Sep Coden: IJMRHS Copyright @2013 ISSN:2319-5886Received: 14th July 2013 Revised: 12th Aug 2013 Accepted: 18th Aug 2013

Research article

RELATIONSHIP BETWEEN THE RETINAL NERVE FIBRE LAYER (RNFL) PARAMETERS

AND VISUAL FIELD LOSS IN ESTABLISHED GLAUCOMA PATIENTS IN SOUTH INDIAN

POPULATION

*Elangovan Suma1, Puri K Sanjeev

2

1,2Assistant Professor of Ophthalmology, Meenakshi Medical College and Research Institute, Enathur,

Kanchipuram, Tamilnadu, India


ABSTRACT

Purpose: Optical coherence tomography (OCT) and Scanning LASER polarimetry (GDX-VCC) are

newer techniques to analyse retinal nerve fibre loss in glaucoma. This study aims to evaluate the

relationship between the Retinal Nerve Fibre Layer(RNFL) parameters measured using Stratus-OCT and

GDx-VCC and visual field loss by Octopus interzeag perimetry in established glaucoma patients in South

Indian Population. Materials and methods: Prospectively planned cross sectional study of 67 eyes of 34

established glaucoma patients on medical management. The mean age of patients was 46.911 years

(SD+13.531). A complete ophthalmic examination, automated perimetry with octopus interzeag 1-2-3

perimeter, retinal nerve fibre analysis with GDx VCC and Stratus OCT was done. The differences

between the mean RNFL parameters in the presence or absence of field defects were evaluated. Results:

The data analysed were mean deviation, loss variance, OCT total average nerve fibre thickness, GDX

VCC- TSNIT average and Nerve fibre indicator (NFI).The data were split into two subgroups on the basis

of presence or absence of visual field defect and analysed. The difference between the mean value of NFI

between the subgroups was highly significant with a p value < 0.01.The OCT parameter Total average

nerve fiber layer thickness differed significantly between the two subgroups (p value <0.05). The mean

GDx TSNIT average did not differ significantly between the two subgroups. Conclusion: The totalaverage nerve fibre thickness by OCT correlated better with visual field loss than the GDX TSNIT

average .Among the GDx parameters, the NFI was found to be a better indicator of visual field damage

than the average thickness.

Key words: Retinal nerve fibre analysis, OCT, GDX-VCC

INTRODUCTION

Glaucoma is a disease which is associated with

progressive damage to the optic nerve and retinalnerve fibre layer

1. Visual field loss in glaucoma

is due to structural damage and it is documented

by automated perimetry . However, the results of

perimetry are variable as the test is subjective2.

Up to 40 percent of the RNFL may be lost beforea defect is apparent on the visual fields

3,4.

DOI: 10.5958/j.2319-5886.2.4.117



731


Various studies have shown that structural

changes of the optic nerve head5-7

and nerve fibre

layer4,8-11

appear before the visual field changes.

The optic nerve head and RNFL changes over

time were studied by stereoscopic photographic

images. Though they provide objectiveinformation for comparisons, the interpretation of

photographs remains subjective, and variations in

assessment among even experienced observers are

well documented11-13

.

Furthermore, qualitative assessment of

photographs may not be sensitive to small

changes over time, and it is difficult to pick up

diffuse damage on these photographs. Newer

technologies such as confocal scanning laserophthalmoscopy (HRT), retinal thickness analyser

(RTA), scanning laser polarimetry with fixed and

variable corneal compensator (GDxVCC), optical

coherence tomography (OCT) have become

available that provide quantitative reproducible,

and objective measurements of RNFL thickness.

As visual field assessment has been considered as

the gold standard for glaucoma diagnosis, all

structure based investigatory modalities need to

compare with automated perimetry. The purpose

of this study is to evaluate the relationship

between structural changes evaluated by OCT and

GDX VCC and visual field defects in established

glaucomatous eyes.


This was a cross sectional study, prospectively

planned. 67 eyes of 34 glaucoma patients

attending glaucoma clinic were included in thisstudy after ethical committee clearance. Informed

consent was obtained from all the patients.

Inclusion criteria:

1. Established primary open angle glaucoma

patients (open angles>2 by Shaffer’s grading

on gonioscopy) on medical treatment and

routine follow up were chosen for the study.

The patients were diagnosed as glaucomatous

by the following criteria: at least three or more

occasions of elevated intra ocular pressure

>21 mm Hg now on medical control and

significant optic nerve head changes with or

without visual field defects.

2. Refractive errors : Hyperopia < +2.50D ,

Myopia < -3.00 D , Astigmatism<+2.00 D

3. Best corrected visual acuity 6/ 12 or better4. Pupil size 3.0-5.0 mm

5. Relative intelligence to understand the test and

patients co-operative for visual field analysis.

Exclusion criteria:

1. Closed angles /narrow angles by gonioscopy

2. All patients who had secondary glaucomas,

juvenile and congenital glaucomas, media

opacities, retinal and neurological pathologies.

3. Primary open angle glaucoma patients whoundergone surgical or laser therapy for

glaucoma

All subjects underwent a complete

ophthalmologic examination including

refraction, Slit lamp biomicroscopy for anterior

segment evaluation and fundus examination with

+90 D lens, gonioscopy, Intra ocular pressure

measurement using Goldmann applanation

tonometry and also direct ophthalmoscopy.

Glaucomatous appearance of the Optic disc was

defined as an increased C: D ratio, asymmetry of

the C: D ratio of >0.2 between the two eyes,

Neuro retinal rim thinning disc haemorrhage,

notching and excavation.

Visual field analysis was performed with Octopus

Interzeag1-2-3 perimeter. The tendency oriented

perimetry strategy was used An abnormal

visual field was defined as: Field plotting with

mean deviation > 4, Loss variance > 6 , a localdip in the Bebie‘s curve outside 2 SD normal

limits, Points of depressed sensitivity especially

in the arcuate areas, paracentral areas , nasal step

region or advanced tubular fields. All fields were

reliable with false positive and false negative

catch trials < 15%.

RNFL analysis was performed by OCT and GDX

VCC. All scans were performed by trained

technicians who were unaware of the patient’sdiagnosis.



732


RNFL analysis with Optical coherence

tomography: Retinal nerve fibre layer

measurements were obtained with Stratus OCT

(Zeiss) version 4.0.1. All scans were performed

by well trained technicians who were masked to

the patient diagnosis and characteristics. For eachpatient three 3.4 mm diameter circular scans were

obtained, judged to be of acceptable quality and

averaged by trained technicians to provide mean

measurements of RNFL thickness.

RNFL analysis with GDX VCC: The GDX

VCC (Version 5.2.3) is a scanning laser

polarimeter that measures RNFL thickness using

polarized light. The placement of the ellipse on

the disc margin for the scan was done by the sametechnician.

All scans were performed by the same well

trained technician. The disc margin on the image

was established with an ellipse whose parameters

were adjusted by the experienced technician who

was masked to the patient diagnosis and

characteristics. All these investigating modalities

were carried out within a period of 3 weeks to

obtain the best cross sectional comparison and to

nullify the effect of any temporal lag.

Statistical analysis: statistical analysis carried out

using SPSS™ software. Student’s t test was used

to derive the significance of the difference

between the means.

RESULTS

67 eyes of 34 established Primary open angle

glaucoma patients were analysed in this study.

The mean age of the patients in this study was

46.911 years (SD+13. 531) .The ages of these

patients ranged from 26 to 70 years. Out of the 34

patients, 10 patients were females accounting for

about 29.41%. The global visual field indices

obtained from octopus perimetry were mean

defect (MD) and loss variance (LV). The meanMD for our group of patients was 5.140±5.853

and the mean LV was 22.551± 20.79 . The

Retinal nerve fibre layer thickness was analysed

by Optical coherence tomography .The parameter

which was studied was the Total average nerve

fibre layer thickness (OCT T Avg). The GDX

VCC RNFL analysis parameters studied were the

TSNIT average (TSNIT Avg) and the nerve fibre

indicator (GDX NFI). (Table:1)

Table: 1. Analysis of the visual field indices obtained from octopus perimetry ( mean defect (MD) and loss

variance (LV)and OCT and GDX VCC parameters in the 67 study eyes:

ParameterPrimary open angle glaucoma (N=67)

MD

Mean± SD Min Max

5.140 ±5.85 -1.4 24.9

LV 22.551±20.79 1.8 88.4

OCT Total average thickness(microns) 87.74±22.21 20 129

GDX-VCC TSNIT average thickness

(microns)48.216± 9.02 24.160 64.710

GDX-VCC Nerve fibre indicator 32.463± 25.36 9 98



Suma etal.,

Table 2: Analysis of the RNFL par

Parameter Group

Normal

Mean ±MD -0.10±0.

LV 3.48±1.

OCTT Avg (microns) 96.92±1

GDXTSNIT(microns) 51.18±5

NFI 21.08±8

r = Pearsons correlation coefficie

** p< 0.01- significant at 1% lev

Fig 1: Bar chart showing the diffe

Analysis on the basis of presen

visual field loss: (Table:2, Fig

was split on the basis of presen

visual field loss and analysed. O

12 eyes did not show any field d

rest had a significant visual field l

Statistically significant differenc

to 0.05) – significant at 5% level)

the OCT Total average thick

±11.95 in the normal field gro

um±23.48 in the group with abno

When the GDX parameter, TS

analysed, no significant

appreciated between the t

(51.18+5.10 in the normal fiel

47.57±9.59 in the other subgroup( p > 0.05 – not significant at 5%

Int J Med Res Healt

ameters on the basis of presence or absence o

Significa

differenc

means (S

value

fields Abnormal fields

D Mean±SD.90 6.28±5.85 0.000

2 26.71± 20.73 0.000

1.95 85.75± 23.48 0.023*

.10 47.57±9.59 0.075***

.63 34.95±27.13 0.003

nt; p =p value , *p<0.05 (0.01 to 0.05) – sign

el, *** p> 0.05 – not significant at 5% level

ence between the mean values among the two

e or absence of

ure1): The data

e or absence of

t of the 67 eyes,

fect whereas the

oss.

(p <0.05 (0.01

was obtained for

ess (96.92 um

up and 85.75

rmal field)

IT average was

ifference was

wo subgroups

d subgroup and

; p value= 0.075 level ).

Significant differenc

between the two

parameter, NFI (21.0

subgroup and 34.95

field changes; the p v

DISCUSSION

This study was desi

determine the relatio

obtained by these tw

VCC) for quantitative

visual field defects

established glaucoma

population.

The primary strengt

instruments were com

The advantage of ex

733

Sci. 2013;2(4):730-736

visual field loss:

nce of

between the

tudents t Test ) P

ificant at 5% level

subgroups

was obtained (p< 0.01)

subgroups for the GDx

+8.63 in the normal field

27.13 in the subgroup with

lue obtained was 0.003).

ned with the objective to

nship between the results

methods( OCT and GDX

ly assessing the RNFL and

by autoperimetry in

tous eyes in south Indian

of this study is that the

pared in a single population.

mining the performance of



734


these instruments in a single population is that

population characteristic based variables are

eliminated, thus allowing direct comparison of the

results obtained with the different instruments.

Limitations of this study include a small number

of subjects. Another limitation, inherent in anycomparable study is that different diagnostic

techniques evaluated in this study are currently at

different stages of development. In general,

established technologies benefit from robust

normative databases and more sophisticated

analysis strategies. Also, different techniques may

identify different characteristics of glaucomatous

damage.

Various studies have demonstrated gooddiagnostic accuracy with different modalities of

imaging in glaucoma14-19

. Good comparability of

OCT and GDX has been demonstrated by many

studies in various stages of glaucoma20-24

The data were split into two subgroups on the

basis of presence or absence of visual field defect

and analysed (table: 4). A gross difference was

observed between the mean values of MD, LV,

OCT T Avg , TSNIT Avg, and NFI in the two

subgroups. The difference between the mean

values of M D and LV and NFI were highly

significant with a p value < 0.01- significant at

1% level. Also, the OCT parameter, Total average

nerve fiber layer thickness differed significantly

between the two subgroups (p value <0.05 –

significant at 5% level).

The mean GDx TSNIT average did not differ

significantly between the two subgroups. These

data could suggest that while using the GDx theNFI is a higher predictor of visual field damage,

than the GDX TSNIT average thickness. Also,

among the Total average nerve fibre layer

thickness measured by OCT and GDx (TSNIT

average), the OCT parameter seems to correlate

better with visual field damage than the GDx

parameter.

Studies by Kanamori et al have shown that visual

field defect has a strong correlation with OCTtotal average thickness25

.

Reus et al26

reported that GDx-VCC correlated

well with mild to moderate visual field loss in

glaucoma patients.

Our data demonstrated that patients with

advanced field defects have a greater RNFL loss.

Also, for a specific value of visual field indexthere was a large range of RNFL values. Two

explanations can be reasoned out for this: one is

the variability of the RNFL values among the

normal population and the other reason may be

the amount of RNFL damage required for the

field loss may vary among different patients. This

problem has been mentioned by other studies

also27

. The influence of variability among patients

can be overcome by conducting a longitudinalanalysis.

This is a Pilot study carried out in an attempt to

establish the relationship between the Visual field

indices and RNFL parameters in glaucoma

patients in our south Indian population. This study

brings out statistically significant correlations in

spite of the above limitations. This finding

validates both techniques as indicators of

glaucomatous damage. A similar study, if

undertaken, with a larger sample with inclusion of

the normal population as age matched controls

and carried out longitudinally would possibly

make the results much more specific. Also,

inclusion of glaucoma suspects, ocular

hypertensives and early glaucoma patients in

subsequent trials would serve to establish the

utility of these newer diagnostic technologies in

glaucoma management and research.

Outcomes of the study:

1. The total average nerve fibre thickness by

OCT correlated better with visual field loss

than The GDX TSNIT average.

2. Among the GDx parameters, the NFI was

found to be a better indicator of visual field

damage than the average thickness.

CONCLUSION

Though visual field testing is subjective, at

present it cannot be replaced by imaging



735


modalities. The new instruments are valuable

tools that have become available to provide

quantitative reproducible and objective

measurements of RNFL thickness.

Structural information provided by the OCT and

GDx and functional information provided by thefield analysis are both important and

complementary to each other

ACKNOWLEDGEMENT

The authors wish to express their gratitude to

Prof.V.Velayutham for his guidance and support

in carrying out this study.

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6. Pederson J. Anderson D. The mode of

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7. Quigley HA, Katz J. Derick RJ. An evaluation

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in monitoring progressive of early glaucoma

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8. Sommer A. Miller NR. Pollack I. The nerve

fiber layer in the diagnosis of glaucoma ArchOphthalmol 1977; 95 (12): 2149-56.

9. Summer A, Quigley HA, Robix AL.

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Arch Ophthalmol 1984; 102 (12): 1766-71.

10. Sommer A., Katz J, Quigley HA. Clinically

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onset of glaucomatous field loss. Arch

Ophthalmol 1991; 109 (1): 77-83.

11. Lichter PR. Variability of expert observes inevaluating the optic disc .Trans AM

ophthalmol Soc 1976, 74: 532-72.

12. Tielsch JM, Katz J, Quigley HA, Miller NR,

Sommer A. Intraobserver and inter observer

agreement in measurement of optic disc

characteristics. Ophthalmology 1988; 95: 350-

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13. Varma R, Steinmann WC, Scott IU. Expert

agreement in evaluating the optic disc for

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glaucoma. Arch Ophthalmol.2004;122:827---

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15. Bowd C, Weinreb RN, Wiliam JM. The

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with optical coherence tomography. Arch

Ophthalmol. 2000;118:22-26.

16. Zangwill LM, Bowd C, Berry CC.

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glaucomatous eyes using Heildelberg Retina

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methods to distinguish normaleyes from those

with glaucoma. Invest Ophthalmol Vis

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18. Chen HY, Huang ML. Discrimination

between normal and glaucomatouseyes using

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Am J Ophthalmol 2003; 135:4:521-29.

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Sahera etal., Int J Med Res Health Sci. 2013;2(4):737-744


&

Health Scienceswww.ijmrhs.com Volume 2 Issue 4 Oct-Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886Received: 14th July 2013 Revised: 12th Aug 2013 Accepted: 18th Aug 2013

Research article

GENDER DIFFERENCES IN AUTONOMIC FUNCTIONAL STATUS IN RESPONSE TO

STRESS

Sahera Shabnam S1, Gopathy Sridevi

2, *Prema Sembulingam3

1Student, final year,

2Lecturer in the Department of Physiology, Sathyabama University Dental College

and Hospital, Jeppiar Nagar, Rajiv Gandhi Salai, Chennai, Tamilnadu, India3

Professor of Physiology, Madha Medical College and Research Institute, Kuntrathur Main Road, Kovur,Thandalam near Porur, Chennai, Tamilnadu, India

* Corresponding author email: [email protected]

ABSTRACT

Introduction: Men and women are similar in their cognitive appraisal of a stress. But their behavior is

different when exposed to stress. As stress responses and cognitive abilities are closely associated with

autonomic nervous system, an attempt had been made to evaluate the behavioral pattern of autonomic

functional status in males and females under stressed conditions. Methodology: 30 normal young male

and female students (15 each) participated in this study. Systolic blood pressure (SBP), diastolic blood

pressure (DBP), heart rate (HR) and heart rate variation (HRV) were recorded before and after postural

change, Valsalva maneuver and cold exposure. Results: SBP and DBP decreased and HR increased

after standing from lying posture (p < 0.000) in both the genders. But the changes were less in males

than in females (SBP and HR – non significant, DBP p < 0.008,) 30:15 ratio was higher in males (p <

0.001) upon standing. After Valsalva maneuver, SBP decreased (p < 0.05) and DBP increased (p <

0.000) with a higher Valsalva ratio (p < 0.002) in females than in males. After exposure to cold, males

showed more decrease in SBP and DBP and less increase in HR (non-significant) than females.

Discussion: Results reveal more sympathetic activity in males than in females when exposed to stress.

This may be because of the altered baroreceptor mechanism, male-female type of fat distribution,difference in vascular bed resistance, influence of cortisol and hypothalamus-pituitary-adrenal axis.

Conclusion: The fact that females have less tolerance to stress may help us in understanding the sex

linked pathophysiology of cardiovascular diseases and developing a different approach in treating the

similar cardiovascular disease in men and women.

Key words: Blood pressure, Heart rate, Heart rate variation, Postural change, Valsalva

maneuver, Cold pressor test

INTRODUCTION

The World Health Organization (WHO) defines

health as “A state of physical, mental and social

wellbeing and not necessarily the absence of

disease and infirmity”. The conventional

definition of health normally fails to take care of

“tension” or “stress”, the two universally

DOI: 10.5958/j.2319-5886.2.4.118



738


recognized phenomena which are more

prevailing in the developed countries, but by no

means, absent elsewhere.

Stress of any kind induces physical and mental

disturbances in an individual mainly because of

its role in creating an imbalance between thedemands of an environment and the capability of

the individual to meet these demands. Sometimes

it may end up with an anxiety-like state with the

exaggerated response. The cognition of the stress

and the physiological responses associated with

stress are all believed to be integrated and

interpreted in the autonomic nervous system

(ANS)1. Among the two divisions of ANS, viz.,

Sympathetic division and the parasympatheticdivision, sympathetic division are concerned

with “flight and fight” reactions which help an

organism to cope up with emergency reactions

with the expenditure of unusual bodily sources

and parasympathetic division is concerned with

the conservation of bodily sources.

Normally, the reciprocal inhibition between these

two systems is responsible for the normal

behavioral homeostasis in an individual1

However, when exposed to a stressed situation,

depending upon the type and intensity of the

stress, a series of responses occur which are

expressed in a slightly exaggerated pattern both

physically and emotionally. It is generally

believed and noticed that in a similar stress

situation, the females react in a more pronounced

manner, creating an anxiety-like state than the

males.

Though But most of the studies weredisproportionately based more on the males than

on females. As a result, the processes involved in

stress responses in females are less well

understood. And, until the late 1990s, there was

no scientific proof to show the sex differences in

the autonomic functional status during stress.

However, in the last decade, an avalanche of

studies has come up to demonstrate such

differences.Leonard Sax had shown that exposure to stress

modulates the autonomic functions in both males

and females and parasympathetic nervous system

(PNS) played a major role in females and

sympathetic nervous system (SNS) played a

major role in males in controlling autonomic

responses2. According to Aimee Midei, females

were capable of confronting the stress in a betterway than males; he noticed that nonhuman

female primates showed more substantial female

preference under stress compared to males and

their coping style is more emotion-focused than

that of males3

due to more involvement of SNS.

Yet another report contradicted these statements

with the suggestion that men and women

responded identically to achievement-related

stressor

4

.As the reported evidences reflect a lot of

controversies, it is worthwhile to reinvade the

field and re-search for the gender differences in

autonomic functions in response to stress.

Objective: 1. To evaluate the autonomic

functional status in normal subjects by using the

cardiovascular parameters viz, BP, HR and HRV

2. To find out whether these parameters reflect

any gender differences under various stressed

situations


30 normal young healthy students of both

genders (15 in each gender) in the age group of

17 to 20 years participated in this study from

Sathyabama Dental College and Hospital,

Jeppiaar Nagar, Rajiv Gandhi Road, Chennai. All

participants were non-exercisers, non-athletics

and non-smokers. Those who were on

medication for some reason or other and obese

persons were excluded from this study. In

females, recording was done in their pre-

ovulatory period. The Institutional Ethical

Committee had cleared the project. Written

informed consent was obtained from all the

participants after explaining the experimental

procedure and making them fully aware of their

role in the project. Simple bedside tests of autonomic functions based on the cardiovascular

reflexes, postulated by Ewing and Clarke5

and



739


adapted by Prema Sembulingam et al6

were

chosen for the present study.

The cardiovascular parameters recorded in the

present study were blood pressure (BP) as

systolic blood pressure (SBP) and diastolic blood

pressure (DBP) to assess the sympathetic activityand heart rate (HR) and heart rate variation

(HRV) to assess the parasympathetic activity.

HRV was assessed in the form of 30:15 ratio and

Valsalva ratio. These parameters were recorded

under basal conditions and after various stressed

conditions namely lying to standing posture, cold

pressor test (CPT) and Valsalva maneuver (VM).

BP and HR were recorded by using fully

automated BP apparatus (OMRON). HRV wasassessed from Lead II Electrocardiogram (ECG)

recorded in three channels Student Physiograph

as 30:15 ratio in postural change and as a

Valsalva ratio (VR) in Valsalva maneuver.

Procedure

1. Postural change: The subject was made to lie

down in supine position. After five minutes of

mental and physical rest, the basal BP and HR

were recorded. Then, the subject was instructed

to get up briskly and stand erect without any

support and the three parameters were measured

immediately after standing. Simultaneously,

ECG was recorded continuously in lead II in the

lying posture (10 waves), while getting up and

after standing (60 waves). 30:15 ratios was

calculated from the ECG as the longest R-R

interval at around 30th

beat divided by the

shortest R-R interval at around 15th

beat after

standing.2. Valsalva maneuver: After measuring the

basal BP and HR in sitting posture, the subject

was instructed to blow into the

sphygmomanometer to raise the mercury column

to about 40 mmHg5, 6

and retain it at that level

for 15 Sec. BP and HR were recorded

immediately after 15 seconds’ strain and an ECG

was recorded continuously before (10 waves),

during and after the strain (60 waves).Valsalva ratio was calculated from the ECG as

the ratio of the longest R-R interval after the

maneuver to the shortest R-R interval during the

maneuver.

3. Cold pressor test: CPT was performed as

described by Hines and Brown7

with a slight

modification; ie., in the present study the test was

performed in sitting posture whereas in theprevious study, it was performed in supine posture.

After recording the basal BP and HR, the subject

was instructed to immerse the dominant hand up to

the wrist joint in cold water with the temperature

of 50

C for one minute. At the end of one minute,

BP and HR were recorded from the other hand.

Statistical analysis: The data were analyzed in

the computer by using Student‘t’ test in SPSS

Software (17

th

version). Values were expressedas mean ± SD and Significance was fixed at the

level of p < 0.05.

RESULTS

Anthropometric parameters: There was no

significant difference in the age and BMI

between the males and females. But expectedly,

the height and weight of the males were

significantly more than those of females (p <

0.002, 0.001) (Table 1)

Effect of postural change on BP and HR in

males and females: There was a highly

significant decrease in SBP upon standing from

lying posture (p < 0.000%) in both males and

females and the decrease was less in males (-

17.00 ± 11.15) than in females (-20.87 ± 11.29)

though it was not statistically significant (p <

0.168) (Table 2)

DBP also showed highly significant decrease

after standing from supine posture (p < 0.000) in

both the groups (Table 2). Between the groups,

the level of decrease was significantly less in

males than in females (p < 0.008) (Table 2)

HR increased significantly after standing from a

lying posture in both the groups (p < 0.000%)

and the increase was less in males (16.87 ± 8.95)

than in females (19.73 ± 8.21) but not

significantly (p < 0.354) (Table 2).



740


Effect of Valsalva maneuver on BP and HR in

males and females: SBP showed highly

significant decrease (p < 0.000) after VM in

males and females and the level of decrease was

less in males than in females (p = < 0.052) (Table

3)DBP showed different behaviour in both the

groups. In males DBP decreased significantly (p

< 0.000) and in females it increased significantly

(p < 0.000). Between the groups, the level of

increase in females was more than the level of

decrease in males (p < 0.002). HR increased

slightly in males without significance but in

females HR showed highly significant decrease

after VM (p < 0.002) (Table 3)

Effect of cold pressor test on BP and HR in

males and females: SBP, DBP and HR showed

highly significant decrease after CPT in both

males and females (p < 0.000, 0.007 and 0.000respectively) and there was no significant

difference in the level of decrease (Table 4)

30:15 ratios: 30:15 ratio was more in males than

in females and the difference was highly

significant (p < 0.001) (Table 5).

Valsalva ratio: VR was more in females than in

males and the difference was highly significant

(p < 0.002) (Table 5).

Table 1: Comparison of anthropometric parameters between males and females

Table 2: Effect and the difference in the effect of postural change on BP and HR in males and females

variables Gender Mean ± SD Mean difference P value

Age (years) Male 18.73 ± 0.70 0.40 ± 0.91 0.111

Female 18.33 ± 0.62

Height (cm) Male 176.00 ± 7.72 10.17 ± 10.12 0.002*

Female 165.83 ± 8.44

Weight (kg) Male 69.07 ± 8.44 11.33 ± 10.11 0.001*

Female 57.73 ± 5.15BMI Male 22.37 ± 3.09 1.39 ± 3.31 0.127

Female 20.98 ± 1.43

Posture

ParametersGender Lying Standing P value

Mean difference:

Lying to standingP Vlaue

SBP(mm HG)

Male 109.60 ±10.21 92.60 ± 7.60 0.000* - 17.00 ± 11.15 0.168Female 92.27 ±9.39 71.40 ±6.28 0.000* - 20.87 ± 11.29

DBP

(mm HG

Male 72.53 ±5.24 60.60 ± 5.15 0.000* - 10.27 ± 5.080.008*

Female 65.27 ±6.76 48.40 ±6.27 0.000* - 16.87 ± 7.09

HR

(beats/min)

Male 76.80 ±7.10 93.67 ± 6.16 0.000* 16.87 ± 8.950.354

Female 69.60 ±10.25 89.33 ±9.08 0.000* 19.73 ± 8.21



741


Table 3: Effect and the difference in the effect of Valsalva maneuver on BP and HR in males &

females

VM - Valsalva maneuver

Table 4: Effect and the differences in the effect of cold pressor test on BP and HR in males and females

CPT – Cold pressor test

Table 5: 30:15 ratio and Valsalva ratio in males and females

DISCUSSION

The results of the present study confirm the

existence of gender difference in the functional

status of ANS under basal conditions as well as

stressed conditions. Males were found to have

higher sympathetic activity than females which

was revealed by the behavioral pattern of SBP,

DBP, HR and 30:15 ratios in postural change and

Valsalva maneuver (Table 2, 3, 4, 5). All these

indicate that females have less tolerance to stress

than the males. This correlates with the results of

previous studies showing that women were

significantly less capable of meeting the

orthostatic challenges in maintaining BP than

males8, 9

.

Various mechanisms were postulated for this

gender difference in response to stress. Greater

orthostatic intolerance in women was associated

with less responsiveness of specific mechanisms

of blood pressure regulation. Normally, BP is

regulated by baroreflex mechanism and renin-

VM

ParametersGender Before VM After VM

p

value

Mean

differencep value

SBP(mm HG)

Male 109.53 ±8.65 91.40 ±7.89 0.000* - 18.13 ± 14.67 0.05*Female 103.00 ±14.41 71.93 ±8.81 0.000* - 31.07 ± 15.32

DBP

(mm HG

Male 69.47 ±7.11 51.07 ±8.01 0.000* - 10.27 ± 5.080.000*

Female 55.87 ±5.10 78.07 ±7.36 0.000* - 16.87 ± 7.09

HR

(beats/min)

Male 84.60 ± 10.43 87.47 ±9.24 0.319 3.40 ± 11.090.002*

Female 78.00 ± 8.41 63.27 ±5.54 0.000* 11.13 ± 14.28

CPT

Parameters Gender Before CPT After CPTp

value

Mean

difference

after CPT

p

value

SBP

(mm HG)

Male 110.13 ±10.21 82.80 ±8.82 0.000* - 27.33 ± 12.920.878

Female 96.53 ±8.54 69.80 ±6.38 0.000* - 26.73 ± 15.32

DBP

(mm HG

Male 64.87 ±6.63 50.53 ±5.36 0.000* - 14.33 ± 8.560.389

Female 61.87 ±8.24 51.33 ±7.06 0.007* - 10.53 ± 13.01

HR(beats/min)

Male 76.87 ±7.96 54.73 ±8.11 0.000* - 22.13 ± 10.630.640

Female 94.27 ±12.04 69.87 ±5.91 0.000* - 24.49 ±13.58

Parameter Male Female Sig

30:15 ratio 1.52 ±0.24 1.26 ±0.16 0.001*

Valsalva ratio 2.06 ±0.51 2.35 ±0.44 0.002*



742


angiotensin mechanism through sympathetic

nervous system (SNS)10-12

. Immediately after

standing from a lying position, blood pools in the

legs, decreasing the venous return and cardiac

output drastically. This leads to transient

decrease in BP and increase in HR. Thesechanges are attributed to cardiac vagal

withdrawal leading to increased sympathetic

activity13

. The present study also shows that

females demonstrated greater elevation in HR

(non-significant) than the males (Table 2) upon

standing from a lying position. Lack of statistical

significance may be attributed to less number of

subjects. Similar results were observed in other

studies also

14, 15

. Leading to the hypothesis thatvagal withdrawal may the more important

mechanism than sympathetic activity in the

regulation of BP in women16, 17

. The results of

the present study confirm those of previous

investigations18, 19

that women have significantly

lower capacity to regulate blood pressure and

maintain orthostatic function compared with

men.

The greater 30:15 ratio in males in the present

study also depicts a higher sympathetic activity

in males (Table 5). According to Convertio, in

males, the sympathetic discharge is more in

lower limbs whereas in females it is more in

upper limbs17

. This may be the reason for greater

30:15 ratio in males than in females. Another

school of thoughts postulates that these male-

female differences in sympathetic activity are

related to body fat distribution17, 19

. Elevated

sympathetic activity was found to be morecommon in ‘male’ type fat distribution than the

female type fat distribution11

. Frey and Hoffler

found that in most of the vascular beds, males

showed greater sympathetically mediated

vasoconstriction than the females16

.

There are controversial statements regarding the

effect of VM on BP and HR in the literature13- 15

.

Basically, VM initially creates a low intra-aortic

pressure which stimulates the sympatheticnervous system. Following the release of the

breath, a vagal response is triggered to decrease

the heart rate. In the present study females

showed highly significant decrease in DBP and

HR and less significant decrease in SBP

compared to that of males (Table 3) depicting a

reduced sensitivity to baroreceptors during a

VM16. This is further substantiated by theincreased VR in females in our study.

When exposed to cold stress, SBP and DBP

decreased both in males and females and the

decrease was more in males than in females in

the present study (non-significant) (Table 4).

This result correlates with the results of the other

studies20,21

. The response to cold may be due to

the stimulation of thermoreceptors leading to

increased sympathetic activity and this is morepronounced in males than in females

20, 21. The

lack of statistical significance in our present

study may be may be because of less number of

subjects.

Rick Nauert further confirms the gender

difference in the stress response. When exposed

to stress, men develop “fight and flight” attitude

through the hypothalamus-pituitary-adrenal

(HPA) axis with elevated cortisol level and

women adopts “tender and befriend” nature

through activation of the limbic system-the

higher center for emotions22

.

Vasan et al says that men and women differ in

the size of the heart and blood vessels - men

having larger size than the women of the same

age and race. It comes as a surprise to know that

men and women differ not only in the

physiological aspects of stress management but

also in their anatomical setup of organ sizes23

.Admittedly, a number of subjects are less in the

present study which may be the reason for lack

of significance in a few places. But our results

are substantiated by the previous documentations

in the literature which encourages us to develop

the study further in a different angle and prosper.

The results may help us in designing sex-based

diagnostic tools, understanding the sex linked

pathophysiology of cardiovascular diseases anddeveloping a different approach in treating the



743


similar cardiovascular disease in men and

women.

CONCLUSION

This study enlightens the growing evidence of

the gender differences in the response to stress

with the implication that females have less

tolerance to stress than males. Understanding the

differences in the physiological and emotional

reactions to stress between boys and girls may

help the parents and teachers to handle them

more carefully and help them to develop positive

coping strategies in life and challenge the

stressors psychologically and psychosomatically

and avoid unpleasant and unwanted incidents of suicides. Knowing the cause is the first step in

preventing the consequences.

ACKNOWLEDGEMENT

This project is the “Student’s research project”

scheme of ICMR in the Year 2011, Ref.No:

2011-02610. We are thankful to ICMR for

sponsoring our undergraduate project. Our

thanks are due to Sathyabama University DentalCollege for permitting us to apply for the scheme

and encouraging us to complete it successfully.

Our thanks are due to our lab technician, Ms.

Sunitha, for her valuable technical assistance.

REFERENCES

1. Martin B. Anxiety and neurotic disorders.

John Wiley and Sons, Inc. New York. 1971;

21-34

2. Leonard Sax. Six Degrees of Separation.

What Teachers Need to Know about the

Emerging Science of Sex Differences?

Educational Horizons Spring. 2006; 190-200

3. Aimee Midei. Gender Differences in

Behavioral Responses to Stress. Fight or

Flight vs Tend and Befriend. Molecular

Psychiatry 2003;310-206-9

4. Ptacek JT, Dodge KL. Gender differences in

coping with stress: when stressor and

appraisals do not differ. Pers Soc Psychol B.

1994; 20: 421 – 30.

5. Ewing DJ and Clarke BF; Diagnosis and

management of diabetic autonomic

neuropathy.Br Med Journal. 1982; 285: 916-

186. Prema Sembulingam, Sembulingam,

Namasivayam.. Evaluation of autonomic

status in generalized anxiety disorder

patients. Biomedicine 2000; 20(2):109-121

7. Hines EA and Brown GE. The cold pressor

test for measuring the reactibility of the blood

pressure; Deta concerning 571 normal and

hypertensive subjects. The American Heart

Journal. 1936; 11 (1): 1-98. Frey MAB, and GW Hoffler. Association of

sex and age with responses to lower-body

negative pressure. J. Appl. Physiol. 1988; 65:

1752 – 56

9. Frey MAB, Mathes KL, Hoffler GW.

Cardiovascular responses of women to lower

body negative pressure. Aviat. Space

Environ. Med. 1986;7: 531 – 38

10. Guyton and Hall. Text Book of Medical

Physiology 12th Ed. Saunders ELSEVIER.

Page 201

11. Ganong’s Review of Medical Physiology, a

LANGE medical book, 23rd

Ed. Tata

McGraw Hill Education Private Limited,

Page 558

12. Sembulingam K, Prema Sembulingam.

Essentials of Medical Physiology, 6th

Ed,

JAYPEE Brothers Medical Publishers (P)

LTD. 2013; Chapter 103, Page 607-60913. Ewing DJ, Hume I, Campbell I W, Murray

A, Neilson JMM and Clarke BF. Autonomic

mechanism in the initial heart response to

standing. J Appl Physiol. 1980. 49: 809-814

14. Montgomery LD, PJ Kirk, PA Payne, RL

Gerber, SD Newton, and BA Williams.

Cardiovascular responses of men and women

to lower body negative pressure. Aviat. Space

Environ. Med. 1977;48: 138 – 4515. White DD, Gotshall RW, and A Tucker.

Women have lower tolerance to lower body



744


negative pressure than men. J. Appl. Physiol.

1996;80: 1138 – 43

16. Frey MAB, Hoffler GW. Association of sex

and age with responses to lower-body

negative pressure. J. Appl. Physiol.

1988;65:1752 – 5617. Convertio VA. Gender differences in

autonomic functions associated with blood

pressure regulation. American Journal of

Physiology: 1909;20:8

18. Hogan TR, Cubitt M, Ecken MK, and Davis

JE. Effect of gender on orthostatic tolerance

(Abstract). Med. Sci. Sports Exerc. 1995;27:

S188

19. Jones PP, Snitker S, Skinner JS, Ravussin E.Gender differences in muscle sympathetic

nerve activity: effect of body fat distribution.

American Journal of Physiology.1996; 270 :

363-66.

20. Bartelink ML, de Wit A,Wollersheim

H,Theeuwes A and Thien T. Skin vascular

reactivity in healthy subjects: influence of

hormonal status. Journal of Applied

Physiology. 1993;74(2): 727-32

21. Bartelink ML, Wollersheim H, Leesmans E,

de Boo T, Thien TA standardized finger

cooling test for Reynaud’s phenomenon:

diagnostic value and sex differences.

European Heart Journal. 1993;14:614-62.

22. Rick Nauert. Response to stress is gender

specific. http://psychcentral.com/news/ 2007/

11/20/respose-tstressis gender specific/ 1559.

Source: University of Pennsylvania School of

Medicine23. Vasan RS, Larson MG, Levy D, Evans JC,

Benjamin EJ. Distribution and categorization

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sex-specific classification and its prospective

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745

Vanitha et al., Int J Med Res Health Sci. 2013;2(4):745-749


&


Research article

EFFECT OF TELMISARTAN ON SERUM LIPID PROFILE IN PATIENTS WITH

HYPERTENSION AND DYSLIPIDEMIA

*Vanitha M1, Vijayal K

2

1Department of Pharmacology, Osmania Medical College, Hyderabad

2Department of Pharmacology, Dr VRK Women’s Medical College & Research Institute, Hyderabad


ABSTRACT

Background and Objectives: Hypertension and dyslipidemia are two major risk factors for

cardiovascular disease and they commonly occur together. Management of dyslipidemia in a

hypertensive patient significantly reduces the total cardiovascular risk .Telmisartan is an Angiotensin

receptor blocker with a partial agonistic action on PPAR-. In the present study, the effect of

Telmisartan on serum Lipid Profile was evaluated in hypertensive patients who also have associated

Dyslipidemia and also the efficacy of Telmisartan in reducing systolic and diastolic BP was assessed in

these patients. Materials and Methods: A total of 50 outpatients from the medical outpatient

department of Gandhi Hospital, Secunderabad, were enrolled into the study. These patients had grade І

essential Hypertension and mild dyslipidemia. After the study period of 24 weeks, the efficacy of

Telmisartan in reducing serum lipid profile was evaluated apart from its effect on reducing systolic and

diastolic BP. Results: Telmisartan was very effective in reducing serum triglycerides (27 %↓, P<0.01),

VLDL-C (27 %↓, P<0.01), LDL-C (22%↓, P<0.01). It also decreased serum cholesterol by 16%

(P<0.01). HDL-C increased by 14% (P<0.05). Telmisartan in a dose of 40-80 mg/day, significantly

reduced both systolic BP by 18 %( P<0.01) and diastolic BP by 12 %( P<0.01) Conclusion: In our

study, Telmisartan proved to be effective not only in controlling BP, but had a favorable effect on lipid

profile also So, in conclusion, all the patients with uncomplicated Hypertension and mild dyslipidemiacan be effectively treated with Telmisartan.

Key words: Telmisartan, Hypertension, Dyslipidemia, Serum lipid profile

INTRODUCTION

Coronary heart disease continues to be the

leading cause of morbidity and mortality in the

world1. Several factors increase the risk of CHD

such as hypertension, advancing age,

dyslipidemia, type 2 diabetes mellitus, family

history of coronary artery disease, cigarette

smoking, obesity etc,. Hypertension and

dyslipidemia are the most common risk factors

for cardiovascular disease. It is found that

hypertensive patients have lower levels of HDL-

cholesterol and higher levels of triglycerides

compared to normal individuals. In patients with

DOI: 10.5958/j.2319-5886.2.4.119



746


hypertension, dyslipidemia substantially

increases the cardiovascular risk. So, there is a

need for disciplined diet plan and appropriate

pharmacological therapy in these patients. The

exact pathophysiology by which dyslipidemia

may be involved in the development of hypertension is not well established. Lipid

disorders cause endothelial dysfunction and this

may become manifest as hypertension

edication therapy for hypertension and

dyslipidemia is becoming more complicated, as

over two-thirds of patients require two or more

anti-hypertensive agents and at least one lipid

lowering agent. The mechanism of action of

majority of anti-hypertensive drugs in use todayis to primarily target the factors which contribute

to development of increased blood pressure.

They do not in any way modify the

pathophysiological mechanisms causing

dyslipidemia. Angiotensin II receptor blockers

(ARB) are efficient anti hypertensive agents that

act through inhibition of AT1 receptors. In

experimental models, as well as in some clinical

trials, ARBs have been found to significantly

affect lipid metabolism .More precisely; ARBs

improved the overproduction and accumulation

of TGL in the liver, in experimental models,

through mechanisms independent of their

hypotensive action2. Furthermore, there are

preclinical studies showing that telmisartan

exerts a favourable effect on lipid abnormalities,

due to its partial activation of peroxisome

proliferator-activated receptor-gamma (PPAR-).

The finding that Telmisartan acts as both anARB and a partial agonist of PPAR- has

important implications in the prevention of

atherosclerosis and cardiovascular disease.

Moreover, it has been shown that activation of

PPAR-, downregulates the expression of

angiotensin II type I receptor and modifies the

effects of angiotensin II on intracellular signaling

pathways3.Telmisartan is a potent,

insurmountable and highly selective antagonistof AT1 receptors, with a long terminal

elimination half-life, Telmisartan is capable of

activating the nuclear peroxisome proliferator-

activated receptor (PPAR) - also, in addition to

blocking the angiotensin II type I receptor.

PPAR- is a nuclear transcription factor that

exists in the form of a heterodimer complex with

the retinoid X receptor-4. Activation of PPAR-causes the receptor complex to affect the

expression of key target genes that mediate

beneficial effects on glucose and lipid

metabolism. Evidence for the importance of

PPAR- in regulating key features of the

metabolic syndrome comes from the studies of

individuals with mutated forms of the receptor.

Such individuals exhibit multiple features of the

metabolic syndrome, including severe insulinresistance, hypertriglyceridemia, elevated

concentrations of non esterified fatty acids, low

concentrations of HDL cholesterol and

hypertension. Infact PPAR- is an important

target for drugs used in the treatment of insulin

resistance, diabetes mellitus and the metabolic

syndrome4. Thiazolidinedione PPAR- activators,

pioglitazone and rosiglitazone are currently

available, and these agents have been shown toincrease the insulin sensitivity and decrease FA

and triglyceride concentrations in patients with

type 2 diabetes5.

In contrast to other ARBs, relatively low

concentrations of telmisartan were also found to

increase the expression of phosphoenol-pyruvate

carboxykinase (PEPCK) gene in human visceral

adipocytes. PEPCK is a key target gene that

contributes to the ability of PPAR- activators to

reduce the FA levels. Further evidence that

telmisartan activates PPAR- comes from the

findings that telmisartan induces adipocyte

differentiation in vitro and is more effective than

other ARBs in reducing serum concentrations of

glucose, insulin and triglyceride in rats

maintained on a diet rich in fats carbohydrates. In

contrast to glitazones, telmisartan is a selective

PPAR- modulator that activates only a subset of

genes targeted by the full PPAR- agonists and

that’s why it has fewer adverse effects compared



747


to full PPAR- agonists. Telmisartan is highly

lipophilic, and has a high mean volume of

distribution of 460-510 L. This high apparent

volume of distribution and the lipophilic nature

of telmisartan suggest that it may have greater

capacity to enter intracellular compartments and

gain better access to PPAR- than other ARBs


The present study was conducted in the

Departments of Pharmacology and Medicine,

Gandhi Medical College and Gandhi Hospital,

Secunderabad. 50 newly diagnosed cases of

essential hypertension, having dyslipidemia were

included in the study. The patients were enrolled

from the medical OPD and the study was

conducted in the period from October 2010 to

May 2011. After getting approval from the

Institutional Ethics Committee, newly diagnosed

cases of grade I essential hypertension were first

screened for dyslipidemia by doing serum lipid

profile after overnight fasting for about 10 hrs.

Those patients having both hypertension and

dyslipidemia were included in the study.Exclusion criteria: Patients with Diabetes

mellitus, secondary causes for hypertension,

Hepatic or renal insufficiency, coronary artery

disease or cerebrovascular diseases were

excluded from the study. The age of the patients

ranged from 38-65 years with a mean of 52 ± 1.2

years and consisted of 31 males (62%) and 19

females (38%). In each case after the informed

consent was obtained, a detailed clinical history

was taken. All the patients underwent complete

clinical examination including recording of

pulse, B.P, detailed clinical examination of

respiratory system, cardiovascular system and

central nervous system. The biochemical

investigations including Blood sugar, serum

creatinine and serum lipid profile were done.

LFT, TSH, X-ray chest and resting 12 leads

electrocardiogram were done in all the patients.

Serum lipid profile was repeated at the end of 24

weeks. All the patients were started on

Telmisartan 40 mg orally once daily. They were

followed up with BP recording once in 15 days

and the dose of telmisartan titrated according to

the response.

RESULTS

Initial lipid profile: The initial total serum

cholesterol in the patients ranged between 171-

281 mg/dl with a mean of 218.86 ± 3.91. The

initial serum triglycerides ranged between 93-

275 mg/dl with a mean of 170.8 ± 5.25. The

initial LDL-C, ranged between 107-197 mg/dl

with a mean of 144.08 ± 3.65. The initial HDL-

C, ranged between 32-58 mg/dl with a mean of

40.62 ± 0.76. The initial VLDL-C, rangedbetween 19-55 mg/dl with a mean of 34.16 ±

1.04. All the parameters including total

Cholesterol, LDL-C, Serum Triglycerides, HDL-

C and VLDL-C, were marginally higher in

female patients, when compared with male

patients.

Lipid profile after 24 weeks: (Table1): After

24 weeks of study period, the mean Total

Cholesterol decreased significantly from 218.86

mg/dl to 185.06 mg/dl (15%↓,P<0.01). The mean

Serum Triglycerides decreased significantly from

170.8 mg/dl to 123.86 mg/dl (27%↓, P<0.01).

The mean LDL-C decreased significantly from

144.08 mg/dl to 112.5 mg/dl (22%↓, P<0.01).

The mean HDL-C increased from 40.62 mg/dl to

47.5 mg/dl (14%↑, P<0.05). The mean VLDL-C

decreased from 34.16 mg/dl to 25.06 mg/dl

(27%↓, P<0.01).

Blood Pressure initial Vs after 24 weeks:

(Table2) The initial systolic BP ranged from 140-

160 mm Hg with a mean of 149.96 ± 1.0 mm Hg

and the initial diastolic BP ranged from 80-99

mm Hg with a mean of 92.88 ± 0.52 mm Hg.

After 24 weeks of treatment with Telmisartan,

the mean systolic BP in the patients decreased

significantly from 149.96 mm Hg to 122.72 mm

Hg (18%↓, P<0.01) Similarly, the mean DBP

also decreased from 92.88 mm Hg to 81.92 mmHg (12%↓, P<0.01).



748


Table.1: Lipid profile initial vs after 24 weeks

Lipid parameters (mean

values mg/dl)

Initial After 24 weeks % of P value

Total cholesterol

Serum TriglyceridesLDL – Cholesterol

HDL – Cholesterol

VLDL – Cholesterol

218.86± 3.91

170.8±5.25144.08± 3.65

40.62± 0.76

34.16± 1.04

185.06±5.29

123.86±0.52112.5±6.11

47.5±3.12

25.06±1.42

15%

27%22%

- 14%

27%

< 0.01

< 0.01< 0.01

< 0.05

< 0.01

Table.2: Blood pressure initial vs after 24 weeks

Parameters Initial After 24

weeks

% of P value

Mean Systolic BP (mm Hg)

Mean Diastolic BP (mm Hg)

149.96± 1.0

92.88 ± 0.52

122.72±3.4

81.92±2.33

18%

12%

< 0.01

< 0.01

DISCUSSION

Hypertension is not the only determinant of

cardiovascular damage and the propensity of a

subject to develop atherosclerotic vascular

disease is markedly affected by the presence of

other risk factors such as age, gender, obesity,

smoking, diabetes and dyslipidemia.

There is no doubt that the management of lipiddisorders in hypertensive patients ameliorates

their total cardiovascular risk. Clinical trials

suggest that some antihypertensive agents may

have a beneficial effect on lipid metabolism

through various possible mechanisms.

Telmisartan is an unique angiotensin receptor

blocker (ARB) with an additional PPAR-γ

modulating action6.

It is possible that the lipid lowering effect of

Telmisartan is due to numerous mechanisms. The

ARBs activate PPAR-γ which regulates lipid

metabolism; thereby reduce triglyceride and

LDL-C levels. Furthermore, there is

experimental evidence suggesting an interaction

between angiotensin system and lipid

metabolism. The ARBs reduce the AT-II

mediated endothelial injury and lipid

peroxidation by blocking the AT1 receptor7.

Telmisartan is commonly prescribed for grade Iessential hypertension in the medical outpatient

department. In the present study, the effect of

long term administration of Telmisartan on

serum lipid profile was evaluated. .The patients

who were enrolled into the study had both

hypertension and dyslipidemia. Also, the efficacy

of Telmisartan in reducing both systolic and

diastolic BP was evaluated in this study. In thepresent study, there was significant effect on

serum lipid profile in the patients, who were

given Telmisartan 40-80 mg/day, for 6 months.

The total serum cholesterol decreased by 16 %(

P<0.01), LDL-C by 22% (P<0.01), serum

triglycerides decreased by 27 %( P<0.01) and

VLDL-C decreased by 27 %( P<0.01). The

HDL-C increased by 14 %( P<0.05)

This favourable effect on serum lipid profile was

in addition to the proved effect of Telmisartan as

an antihypertensive drug. Telmisartan in a dose

of 40-80 mg/day, significantly reduced both

systolic BP by 18 %( P<0.01) and diastolic BP

by 12 %( P<0.01). In our study, Telmisartan was

well tolerated, except for some minor and

transient side effects like headache, dizziness and

fatigue in a few patients.

The significant effect of Telmisartan on serum

lipid profile in the present study is supported bypreclinical studies conducted on rabbits and also



749


by STAR trial, (Saga Telmisartan Aggressive

Research Study), a single arm, prospective,

multicentric clinical trial conducted in Japan on

197 patients with hypertension and dyslipidemia.

CONCLUSION

In our study, Telmisartan proved to be effective

not only in controlling BP, but had a favorable

effect on lipid profile also. Telmisartan treatment

results in amelioration of cardiovascular risk

factors, not only through arterial pressure

regulation but also through reduction of serum

lipid profile. So, in conclusion, all the patients

with uncomplicated hypertension and

dyslipidemia without other associated risk factorscan be effectively treated with Telmisartan.

ACKNOWLEDGEMENT

The authors are thankful to Management and

staff of Medical Out Patient Department ,Gandhi

Hospital, Secunderabad, Andhra Pradesh , for

providing necessary facilities to carryout the

research work .

REFERENCES

1. American Heart Association. Heart disease

and stroke statistics, 2007 update AHA,

Dallas, Texas,2007

2. Ran J, Hirano T, Adachi M. Angiotensin II

type I receptor blocker ameliorates

overproduction and accumulation of

triglycerides in the liver of Zucker fatty rats.

Am J physiol. Endocrinol. Metab. 2004; 2:227-32.

3. Takeda K, Ichiki T, Tokanar T. Peroxisome

proliferator-activated receptor gamma

activators down regulate angiotensin II type I

receptor in vascular smooth muscle cells

circulation 2000; 102: 1834-39

4. Pershad Singh HA. Peroxisome proliferator-

activated receptor –γ: therapeutic target for

diseases beyond diabetes. Expert opine investDrugs. 2004;13:215- 28

5. Diamant M Heine RJ. TZD in type 2

diabetes mellitus (Current clinical evidence).

Drugs.2003; 63:1373 – 05

6. Schupp M, Janke J, Clasen R. Angiotensin

type 1 receptor blockers induce peroxisome

proliferator – activated receptor activity.Circulation, 2004;109: 2054 – 57.

7. Keidar S, Kaplan M, Hoffman A.

Angiotensin II stimulates macrophage-

mediated oxidation of low density

lipoproteins. Atherosclerosis 1995; 115: 201-

15.



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Garg et al., Int J Med Res Health Sci. 2013;2(4):750-755


&

Health Sciences




thAug 2013

Research article

A STUDY OF AUTONOMIC FUNCTION TESTS IN OBESE PEOPLE

*Rinku Garg1, Varun Malhotra

2, Neera Goel

3, Usha Dhar

2, Yogesh Tripathi

2

1Assistant Professor,

2Professor,

3Assistant Professor, Department of Physiology, Santosh Medical

College, Ghaziabad, India


ABSTRACT

Background: Obesity is one of the common significant health hazards and is associated with autonomic

dysfunction. Aims and objectives: The present study was designed to assess the underlying autonomic

neuropathy in obese subjects and to compare it with age-matched controls. Material and Methods:

Thirty obese subjects in the age group of 21-40 years were recruited for the study. Six non-invasive

autonomic function tests were performed out of which four were based mainly on parasympathetic

control (Heart rate response to standing (30:15 ratio), The S:L (standing to lying) ratio, The Valsalva

ratio, Heart rate response to deep breathing ) and the other two were mainly sympathetic (IsometricHandgrip Exercise Test and Cold Pressor Test). Statistical Analysis: Results were analysed by ANOVA

with SPSS version 17.0 using unpaired‘t’ test. Results: Results showed that Heart rate response to

standing(30:15 ratio), The S:L (standing to lying) ratio, The Valsalva ratio, Heart rate response to deep

breathing, Isometric Handgrip Exercise Test and Cold Pressor Test were significantly lower (p <0.05)

in obese subjects as compared to control subjects. Conclusions: Latent autonomic neuropathy may be

present in otherwise healthy obese individuals. Early and regular screening of obese individuals is

necessary to prevent any future complications.

Keywords: Obesity, Autonomic nervous system, Cold pressor test

INTRODUCTION

Obesity is a condition in which excess body fat

accumulates to the extent that it may have an

adverse effect on health1. Obesity is a common

and significant health hazard2.

At an individual

level, an excess of energy intake and an

inadequacy of energy expenditure is thought to

explain most cases of obesity

3,4

. A complexinteraction among different factors like

endocrine, nervous, metabolic factors maintains

constant energy storage5. Obesity is considered

to be a risk factor for a variety of cardiovascular

conditions like hypertension, ischemic heart

disease and stroke3

and is characterized by

hemodynamic and metabolic alterations6.

Autonomic nervous system is a centre for the

coordination of different body system7. Since the

ANS is involved in energy metabolism and in theregulation of the cardiovascular system

8-10, it is

DOI: 10.5958/j.2319-5886.2.4.120



751


conceivable that one or more subgroups of

persons with idiopathic obesity have an alteration

in their autonomic nervous system that may

account for several clinical consequences of

obesity7. Laitinen et al

11showed that total body

fat and central body adiposity are associated withaltered autonomic activity.

MATERIAL & METHODS

The present study was a cross-sectional study,

conducted in Santosh Medical College;

Ghaziabad, and the study was approved by the

Institutional Ethics Committee.

Thirty obese subjects with BMI >30 were

selected for the study. The results were comparedwith thirty age-matched non-obese controls with

BMI between18.5-24.9.Informed consent was

taken from all the subjects. Subjects with age

above 40years, h/o any chronic illness, on any

medication, and smokers were excluded from the

study.

Height was measured using a standard

stadiometer with the subject standing in an erect

posture. The readings were taken to the nearest

0.1cm. Weight was recorded in kgs using a

calibrated weighing machine (Avery) scale with

a capacity of 120 kg and a sensitivity of 0.05 kg.

The BMI was calculated as the weight in

kilograms divided by the square of the height in

meters [weight (kg) /height (m2)]

12

Subjects were divided into 2 groups as per WHO

classification on BMI.

Group I-Control group with BMI 18.5-24.9kg/m2

Group II-Study group with BMI >30kg/m2

Table 1: WHO Classification of BMI13

BMI Category

<18.5 Underweight

18.5-24.9 Healthy

25-29.9 Overweight

30-39.9 Obese

>40 Morbid obese

The following autonomic function tests were

performed:

For Assessing Parasympathetic Activity

1. Resting heart rate was calculated from ECG

by using standard limb leads14

.

2. Heart rate response to standing (30:15

ratio) was calculated as the ratio between the

R-R interval at beats 30 and 15 of the ECGrecorded immediately upon standing.

15

3. The S:L (standing to lying) ratio was taken

as the ratio of the longest R-R interval during

the 5 beats before lying down to the shortest

R-R interval during the 10 beats in the ECG

after lying down16

.

4. The Valsalva ratio. Subjects were instructed

to exhale into a mouthpiece connected to a

mercury manometer and to maintain theexpiratory pressure of 40 mmHg for 15 Sec.

ECG was recorded during the manoeuvre and

45 sec after the manoeuvre. The ratio was

calculated between the maximum R-R

interval ( after release of strain) and the

minimum R-R interval (during strain)17

5. Heart rate response to deep breathing:

Heart rate was recorded first during normal.

Breathing (at rest), and then during deep

breathing (6/min). ECG 3rd & 6th respiration,

minimum R-R intervals and corresponding

heart rate were calculated18

.

For Assessing Sympathetic Activity:

Isometric Hand Grip Exercise Test: Before the

exercise, subjects were allowed to rest for 10

minutes in a quiet room to reduce the anxiety.

Resting blood pressure of all the subjects was

measured by the auscultatory method with the

help of a mercury sphygmomanometer

(DIAMOND). First Kortk off sound indicated

systolic blood pressure (SBP) and fifth Kortkoff

sound indicated diastolic blood pressure (DBP).

Isometric handgrip exercise test was done in both

the study group and control groups. After

recording basal blood pressure, subjects were

asked to perform isometric handgrip exercise.

Subjects were told to hold the handgrip spring

dynamometer in the right (or dominant hand) tohave a full grip on it. Handles of the



752


dynamometer were compressed by the subject

with maximum effort for few seconds. This

whole procedure was repeated thrice with rest in

between to prevent fatigue. Mean of the three

readings was referred as maximal isometric

tension (T max). Then, the subjects were askedto perform isometric handgrip exercise at 30% of

T max for 2 minutes. During the test, blood

pressure was recorded from the non-exercising

arm. Blood pressure was again recorded 5

minutes after completion of the exercise19

.

Cold Pressor Test: After recording basal blood

pressure, subjects were asked to dip left arm in

the cold water (temp at 2-40

C) for 2 minutes and

blood pressure was recorded from the right arm.

Blood pressure was once again recorded 5

minutes after hand was taken out from the coldwater

20.Statistical Analysis: Results were

analysed by ANOVA with SPSS version 17.0

using an unpaired‘t’ test

RESULTS

Table.2: Anthropometric variables

Variables Group I(Controls) Group II(Obese)

Age(yrs) 33.08±4.8 32.12±5.4

Height(mts) 1.62±0.42 1.51±0.56

Weight(kgs) 58.11±4.3 81.13±4.9

BMI(kg/m ) 22.11±1.04 35.13±2.08

Table 3: Parasympathetic function tests in Group I and Group II

Variables Group I

(BMI 18.5-24.9)

Group II

(BMI >30)

P value

Heart rate response to standing(30:15 ratio) 1.14± 0.11 1.06±0.02 <0.05

S:L (standing to lying)ratio 1.2±0.03 1.11±0.02 <0.05Valsalva ratio 1.65±0.28 1.45±0.11 <0.05

Heart rate response to deep breathing(HRDB) 23.46±4.31 16.46±2.11 <0.05

* p<0.05 versus group I

Table 4: Statistical analysis of sympathetic function tests in Group I and Group II

Variables Group I(BMI

18.5-24.9)

Group

II(BMI >30)

P

value

IHG SBP 12.2±1.2 8.3±1.3 <0.05

IHG DBP 12.1±1.4 8.1±1.2 <0.05CPT SBP 12.2±1.6 8.2±1.4 <0.05

CPT DBP 13.1±1.8 9.1±1.4 <0.05

Data presented in Table 3 shows that there was

significant decrease in the Heart rate response to

standing(30:15 ratio), Valsalva ratio & Heart rate

response to deep breathing (HRDB) in Group II

individuals as compared to Group I(p<0.05).S:L

ratio also decreased, and the decrease was

statistically significant(p<0.05).

Data presented in Table 4 shows that there was

significant decrease in the systolic and diastolic

blood pressure in obese subjects (group II) as

compared to controls (group I)during the

application of isometric handgrip exercise and

cold pressor tests (p<0.05) and the decrease was

statistically significant (p<0.05).



753


DISCUSSION

The results of the present study show that the

valsalva ratio, heart rate response to deep

breathing and heart rate response to standing

(30:15) in obese subjects were significantlylower as compared to the control group, it

indicates decrease in parasympathetic nerve

function and baroreflex sensitivity in obese

subjects. Baroreceptors resetting may occur in

obese individuals due to atherosclerosis that

hardens the carotid sinus walls. This decreases

compliance. Obese group is less responsive to

blood pressure changes to posture. Similar results

were shown by some other investigators21-,23

.

There was less increase of blood pressure

response to cold pressor test in the obese people

in contrast to the control group. The afferent

fibres for this response are the pain fibres which

are stimulated by placing the hand in cold water

and the efferent fibres are the sympathetic fibres.

A lesser increase in the blood pressure after the

cold water immersion points towards

sympathetic insufficiency in obese subjects20

.

Obesity impairs autonomic control of heart rateand blood pressure. Obese subjects exhibit lower

sympathetic response on exposure to cold. Our

study results were in accordance with reported

study of Monterio et al24

.There was also

decreased in blood pressure response to isometric

handgrip exercise test in the obese people in

contrast to the control group. It shows the

decreased activity of the sympathetic nervous

system25 or to a lower increase in peripheral

resistance to manoeuvres activating sympathetic

system26

. Baek et al27

stated that in normal

conditions sympathetic activity increases during

isometric handgrip exercise and cold pressor test.

This reduced sympathetic reactivity in

established obesity may be responsible for the

maintenance of obese state.

Valensi et al22

have demonstrated sympathetic

insufficiency in obese people. It was shown that

glucose induced inhibition of the lipid oxidation

rate in obese people is greater in the patients with

autonomic dysfunction which could be due to

decrease in parasympathetic activity.

Decrease in the sympathetic activity may result

in a disordered homeostatic mechanism thuspromoting excessive storage of energy as

suggested by Peterson9.

It has been shown that increased sympathetic

activity induced by cold water stress causes

norepinephrine release and elevation of blood

pressure more in obese subjects. This greater

increase in blood pressure might be contributed

by more release of endothelins, prostaglandins

and angiotensin II29, 30

in obese. Various

investigators have shown that parasympathetic

damage or decreased vagal tone may occur due

to hyperinsulinaemia or insulin resistance or

there may be decreased in baroreflex activity28

.

CONCLUSIONS

Obesity is associated with both sympathetic and

parasympathetic nervous system dysfunction

which may result in various cardiovascular

complications. So, if this dysfunction is

diagnosed early by doing various autonomic

function tests, it will be of great help in

identification of those which are prone to weight

gain and at risk of various cardiovascular

complications.

ACKNOWLEDGMENT

The authors are thankful to Dr. R K Arya,

Professor & HOD, Department of CommunityMedicine, for his help in statistics. We are also

thankful to subjects and all the technical staff for

their contribution in the completion of the

project.

Conflict of Interest: Nil

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Lambert G. Mechanism of sympathetic

activity in obesity-related hypertension.Hypertension.2006;48:787

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Hramaik IM, Sharma AM, Ur E.2006

Canadian clinical practice guidelines on the

management and prevention of obesity in

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Attali JR. Cardiac autonomic dysfunction inobese patients. Int J Obes Relat Metab Disord

1995;19(2): 113-18.

6. Colak R, Donder E, Karaoglu A, Ayhan O,

Yalniz A. Obesity and the activity of

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2000;30:173-76.

7. Bray GA. Autonomic and endocrine balance

in the regulation of energy balance. Fed Proc

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sympathoadrenal system in modulating

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autonomic and adrenal hypothesis. Clin

Endocrinol Metab 1984; 13: 521-46.

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Fell RD, McLeish KR, Pfeifer MA. Body fatand the activity of the autonomic nervous

system. N Engl J Med 1988; 28: 1077-83.

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dysfunction is associated with central obesity

in persons with impaired glucose tolerance.

Diabet Med 2011;28(6) 699-704.

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Principles of Internal Medicine. 17th

ed.

McGraw Hill;2008.P.462-67.

13. Hilsted J, Jenson SB. A simple test for

autonomic neuropathy in juvenile diabetes.

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14. WHO. Obesity: Preventing and managing the

global epidemic: Report of the WHO

consultation of obesity. Geneva:WorldHealth Organisation 1998.

15. Page MM, Watkins PJ. The heart in

diabetes:autonomic neuropathy and

cardiomyopathy. Clin Endocrinol Metabol

1977;6:377-88.

16. Rodrigues EA, Ewing DJ. Immediate heart

rate response to lying down: simple test for

cardiac parasympathetic damage in

diabetes.Br Med J 1983;800:287-9.17. Levin AB. A simple test of cardiac function

based upon the heart rate changes induced by

the valsalva maneuver.Am J Cardiol

1966;1:90-99.

18. Mathias CJ and Bannister R. Autonomic

failure. A Textbook of Clinical Disorders of

the Autonomic Nervous System.3rd

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Newyork: Oxford University Press;1992.

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JAW, Clarke RF, Cardiovascular response to

sustained handgrip in normal subjects and in

patients with diabetes mellitus: a test of

autonomic function. Clin Sci Mol Med

1974;46:295-306.

20. LeBlanc J, Dulac S, Cote J, Girard B.

Autonomic nervous system and adaption to

cold in man. J App Physiol 1975;39(2):181-

6.

21. Emdin M, Gastaldelli A, Muscelli E,Macerata A, Natali A, Camastra S and

Ferrannini E. Hyperinsulinemia and

autonomic nervous system dysfunction in

obesity: Effect of weight

loss.Circulation.2001;103:513-19.

22. Valensi P, Lormeau B, Dabbech M, Miossec

P, Paries J, Dauchy F. Glucose induced

thermogenesis, inhibition of lipid oxidation

rate and autonomic dysfunction in non-diabetic obese women. Int J

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23. Borne PVD, Hausberg M, Hoffman RP,

Mark AL and Anderson EA.

Hyperinsulinaemia produces cardiac vagal

withdrawl and nonuniform sympathetic

activation in normal subjects. Am J Physiol

Regul Integr Comp Physiol 1999;276:178-183.

24. Monteiro G, Chathoth V,K Kishan. Cardiac

autonomic response during a cold pressor test

in normal and overweight adults.

International Journal of Biomedical and

Advance Research 2012;3(6):514-516.

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RK. Assessment of respiratory and

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26. Valensi P, Bich Ngoc PT, Idriss S, Paries J,

Cazes P, Lormeauet B et al. Haemodynamic

response to an isometric exercise test in

obese patients. Influence of autonomic

dysfunction. Int J of Obesity 1999;23:543-49.

27. Baeks MA Van. The peripheral sympathetic

nervous system in human obesity. J

Endocrinol 2000;164:59-66.

28. Akhter S, Begum N, Ferdousi S, Khan SM.

Autonomoc neuropathy in obesity. J

Bangladesh Soc Physiol 2011;6(1):5-9.

29. Velasco M, Gomez J, Blanco M, Rodriguez I.

The cold pressor test: pharmacological and

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Srikanth et al., Int J Med Res Health Sci. 2013;2(4):756-761


&

Health Sciences


ndJuly 2013 Revised: 11


thAug 2013

Research article

PULMONARY FUNCTION TESTS IN TYPE II DIABETICS IN CORRELATION WITH

FASTING BLOOD GLUCOSE

* Srikanth Sajja1, Pragathi BH

2

1Professor, Department of Physiology, Dr PSIMS& RF, Chinnavutapalli, Andhrapradesh, India,

2

Tutor, Department of Physiology, St.Joseph Dental College, Eluru, Andhrapradesh, India.


ABSTRACT

Background & Objectives: Diabetes mellitus (DM) is a significant public health problem worldwide

which is associated with hormonal, metabolic and micro vascular abnormalities. The angiopathic

complications affect eyes, kidneys, nervous, cardiovascular and respiratory system, which are primarily

due to biochemical alterations in connective tissue. Materials & Methods: In this study, we included

100 subjects, 50 Diabetic (25 Male and 25 Female) and 50 (25 Male and 25 Female) healthy

individuals aged 30-55 years. The pulmonary function tests were performed by the computerizedspirometer in the Clinical Physiology Lab, Department of Physiology, Dr. PSIMS & RF,

Chinnavutapalli. Results: The results of our study showed a statistically significant reduction in

FEF50%, FEF75% & FEV1 /FVC ratio in diabetic male subjects when compared with control male

subjects (p< 0.0001) and diabetic female subjects showed a reduction in FEV1/FVC which is not

statistically significant (p = 0.0004) but we observed a statistically significant reduction in FEF50% &

FEF75% in diabetic female subjects when compared with control female subjects (p< 0.0001). On

spirometry, Diabetic subjects showed a significant reduction in FEV1/ FVC ratio, FEF 50%, FEF 75%

relative to non diabetic controls. Conclusion: We conclude from our study that diabetic subjects

showed impairment in lung function. We found a decrease in FEV1/FVC ratio, FEF50% and FEF75%in diabetic subjects as compared to control subjects.

Keywords: Diabetes, Forced Vital capacity, Forced expiratory Volume, Forced Expiratory Flow

INTRODUCTION

Diabetes is a systemic disease that produces

changes in the structure and function of several

tissues. The pathogenesis of diabetic

complications involves both microangiopathic

process and non-enzymatic glycosylation of

tissue proteins. This process results in

biochemical alterations in connective tissue

constituents leading to impaired collagen and

elastin cross-linked with a reduction in strength

and elasticity of connective tissue, also, due to a

non-enzymatic glycosylation of proteins 1.

Presence of an abundant connective tissue in the

DOI: 10.5958/j.2319-5886.2.4.121



757


lung and an extensive microvascular circulation

can be the possible cause of lung to be a ‘target

organ’ in diabetic patients2. Due to increase in

the incidence and prevalence of DM particularly

in Asian Indians, it is essential to study

pulmonary function in patients having type2 DMand examine their correlation with

microangiopathic complications. Several clinical

studies3, 4,5

have suggested a possible association

between pulmonary function abnormalities and

diabetic renal microangiopathy and retinopathy.

Changes in pulmonary diffusing capacity for

carbon monoxide (DLCO) as a manifestation of

pulmonary microangiopathy have been reported6.

Defective pulmonary function in asymptomaticdiabetic patients is more prevalent than generally

recognized involving 60% of adult cases.

Autopsy findings in human diabetic subjects and

experiments in rats with diabetes, have included

thickening of the alveolar epithelia, pulmonary

capillary basal lamina, centrilobular emphysema,

and pulmonary microangiopathy7.These

anatomical changes may be due to the

biochemical alteration of connective tissue

constituents caused by a non-enzymatic

glycosylation of proteins and peptides induced

by chronic high circulating glucose8.Tests of

lung mechanical function include measurement

of lung elasticity , airflow resistance, and forced

spirometric pulmonary function tests. Diabetes

has been inconsistently associated with

spirometric abnormalities in a number of small

retrospective cross-sectional studies, involving

even fewer than 50 subjects. Alterations such ashyperglycaemia, oxidative stress from auto-

oxidation of glucose, non-enzymatic protein

glycosylation, and alterations of nitric oxide

(NO) metabolism have been reported as

metabolic markers of the diabetic state. The

source of free radicals in diabetes is not fully

understood, but glycation of proteins can lead to

oxidative stress by direct release of O2 and H2O2

and activation of phagocytes through aspecialized receptor for advanced glycation end

products. Oxidants include reactive oxygen

species (ROS), reactive nitrogen species (RNS),

sulfur centered radicals and others. Phagocytic

cells generate large amounts of NO and other

ROS. Peroxynitrite (ONOO−) is formed when

NO reacts with superoxide (O−). This reaction

occurs rapidly and promotes the nitration of biomolecules including protein tyrosine residues.

Peroxynitrite anion and peroxynitrous acid

(ONOOH) can freely pass through lipid

membranes and can mediate oxidation, nitration,

or nitrosation reactions. Peroxynitrite is more

than two orders of magnitude more potent than

H2O2 in catalyzing lipid oxidation in vivo.

During diabetes, there are also disturbances in

antioxidant defense systems evidenced byalterations in antioxidant enzymes

9, impaired

glutathione metabolism10,11

and decreased

ascorbic acid levels11,12

.

The pathophysiologic connection between

diabetes and lung function was explained by a

possible pro-inflammatory stimulus of

hyperglycemia causing impaired lung function

through increased intrapulmonary inflammation

and apoptosis. Another possible cause of

impaired lung function could be increased

sclerosis of bronchial arteries as a consequence

of generalized arteriosclerosis in diabetes.

Diaphragm elevation with increased closing

volume and decreased FVC in absence of

detectable bronchial obstruction is another

possible cause of impaired lung function.

MATERIALS & METHODS

In this study, we included 100 subjects, 50

Diabetic (25 Male and 25 Female) and 50

healthy individuals (25 Male and 25 Female)

aged 30-55 years, after obtaining their consent.

An approval was obtained from Institutional

Ethical committee. Individuals were classified as

having diabetes (as per the criteria Adapted from

American Diabetes Association Criteria 1997), if

any of the following criteria were met: fasting

glucose level of at least 7.0mmol/lit (126mg/dl);non fasting blood glucose level at least 11.1



758


mmol/lit (200mg/dl); current use of anti diabetic

medication.

Inclusion criteria: The persons who had never

smoked and without any self reported respiratory

complaints or any history of respiratory diseases.

Exclusion criteria: Individuals with heavysmoking, Alcohol intake, Anemia, Malnutrition,

productive cough, Exertional dyspnoea, and

cardiovascular diseases, Individuals with chronic

lung diseases (like pulmonary TB, Bronchial

asthma, Chronic Bronchitis, etc), Individuals

who had undergone Abdominal & Chest surgery,

Kypho scoliosis, Pectus carinatum, Pectus

excavatum, Occupational diseases like

Pneumoconiosis.Procedure: The pulmonary function tests were

performed by Computerized Spirometer model

RMS Helios 401 in the Clinical Physiology Lab,

Department of Physiology, Dr. PSIMS& RF,

Chinnavutapalli. First FVC was recorded using

the Helios spirometer as per the instructions.

For SVC test same procedure is followed but the

subject is instructed to take a deep breath

followed by deep exhalation. Both inhalation and

exhalation should be performed to the maximumextent but slowly. After this patient was

instructed to take few gentle and normal breaths.

For MVV test patient was asked to breathe

deeply and quickly through the mouthpiece for

12-15 sec. The maneuver should imitate rapid

breathing during exercise. Fasting blood glucose

levels are estimated by using NIPRO Diagnosis

Blood Glucose Monitoring System.

Statistical analysis: The statistical analysis wasperformed using Graph Pad Prism – 5.0 Version.

As the analysis is done between the groups,

UNPAIRED T – TEST was used.

RESULTS

Table: 1. Comparison of Mean Values of FEV1/FVC, FEF50% and FEF75% in Male, female subjects

PARAMETERMale Fe male

CONTROL DIABETIC P-value CONTROL DIABETIC P-value

FEV1/ FVC 82.4± 1.63 79.5± 1.87 0.0001 80.4± 1.35 78.9± 1.40 0.0004

FEF50%

(L/sec)3.8± 0.31 3.0 ± 0.50

0.0001* 3.8± 1.24 2.6±0.33 0.0001*

FEF75%

(L/sec)1.26± 0.13 1.02± 0.20

0.0001* 1.2± 0.12 0.9± 0.11 0.0001*

When compared with Control male subjects, the

Diabetic male subjects showed a reduction of

mean FEV1/ FVC ratio by 3.51 % ( i.e.,2.9 ) , a

reduction of mean FEF50% by 21.05 % (i.e., 0.8

L/s) and a reduction in the mean FEF 75% by

19.04 % ( i.e., 0.24 L/s ). When compared with

Control female subjects , the Diabetic female

subjects showed a reduction of mean FEV1/

FVC ratio by 3.48 % ( i.e.,1.8 ) , a reduction of

mean FEF50% by 31.57% (i.e., 1.2 L/s) and a

reduction in the mean FEF 75 by 25% ( i.e., 0.3

L/s ).

On spirometry, the Diabetic subjects showed a

significant reduction in FEV1/ FVC ratio, FEF

50%, FEF 75% relative to non diabetic controls.

The results of our study showed a reduction in

FEV1 /FVC ratio in diabetic male subjects when

compared with control male subjects which is

statistically significant (p< 0.0001 ) and also,

diabetic female subjects showed a reduction in

FEV1/FVC which is not statistically significant

(p = 0.0004). The results of our study showed a

statistically significant reduction in FEF50% in

diabetic male subjects when compared with

control male subjects ( p< 0.0001 ) and also ,



759


diabetic female subjects showed a statistically

significant reduction in FEF50% ( p value <

0.0001 ). The results of our study showed a

statistically significant reduction in FEF75% in

diabetic male subjects when compared with

control male subjects (p< 0.0001) and thediabetic female subjects also showed a reduction

in FEF75% (p< 0.0001) which is statistically

significant.(Table-1)

DISCUSSION

A lot of studies dealing with the problem of lung

dysfunction in diabetes mellitus are cross-

sectional, with the inclusion of a small number of

patients suffering either from insulin-dependentdiabetes mellitus (type I) or type II diabetes

mellitus.

Diabetes mellitus has an impact on the

mechanical and microvascular function of the

lung and influences ventilatory control.

Numerous studies of lung function in diabetic

subjects have shown slightly decreased indices of

forced expiration and lung volumes in both type I

and type II diabetes mellitus. Lange P , Groth S,

Kastrup J et al.,13

conducted study to find the

relation between diabetes mellitus, forced vital

capacity and forced expiratory volume in one

second. They observed that diabetic subjects in

all age groups showed an impairment of lung

function. The forced vital capacity (FVC), forced

expiratory volume in one second (FEV1) and

forced mid-expiratory flow are reduced by 8 –

20% with a moderately restrictive defect without

airway obstruction 14,15,16. Other studies failed to

show significant differences between patients

with diabetes and normal controls in spirometric

lung function tests17, 18

. The Cardiovascular

Health Study19

in determining reference

standards for a healthy population, found

diabetes to be significantly associated with a

decreased FEV1. In the Framingham Heart

Study20

, diagnosis of DM was associated with a

greater reduction in FVC than FEV1, suggestinga restrictive pathology. On the contrary, when

those with diabetes on therapy were excluded,

higher levels of fasting blood glucose were

associated with larger reduction in FEV1 than

FVC. The resulting progressive decrement in

residual FEV1/ FVC ratio with increasing level

of blood sugar suggests that higher fasting bloodsugar was associated with more obstructive

physiology. In the Fremantle Diabetes Study21

reduced spirometric lung function was observed

in patients with type 2 diabetes.

Goya wannamethee S, Gerald Sharper A, Ann

Rumley et al22

prospectively studied the

relationship between lung function, risk of type-2

diabetes. They opined that inflammation may be

the cause for these associations. They concludedthat Restrictive rather than obstructive

impairment of lung function is associated with

incident type 2 diabetes. Ali M.O, Begum S,

Begum N et al.,23

conducted studies to observe

the relation between different lung function

parameters in type 2 diabetic patients. They

concluded that the ventilatory function of lung

may be reduced in type 2 diabetes which may be

related to the duration of the disease. Mohhamed

Irfan, Abdul jabbar, Ahmed Suleman Haque et al24

studied about the pulmonary function in

Diabetics. They observed impaired lung function,

independent of Smoking in diabetics. The results

of our study were in accordance with this study.

The decline of FEV1 and FVC in diabetic

individuals is similar to that observed in non-

diabetic subjects in certain longitudinal studies25

.

Few studies have been conducted for

investigating respiratory muscle function indiabetes mellitus.

DLCO was used to study pulmonary vascular

changes. Even though some studies showed no

defects in diabetes mellitus26

, the majority of

studies reported reduced diffusing capacity

among diabetic patients27

. Carmela Maiolo,

Ehab I Mohamed, Angela Andreoli28

conducted

studies to assess the relation between Body Fat

Distribution & reduced pulmonary function inobese Type 2 Diabetic adult women. They

concluded that the DLCO and respiratory muscle



760


function explain the relationship between

pulmonary dysfunction and body composition.

A potential mechanism that explains the finding

of decreased lung function was decreased muscle

strength in diabetic subjects because of defective

muscle metabolism 29 or it may be due toinflammatory origin.

CONCLUSION

The cause for the decline in lung function in

diabetes remains unclear. Taking into

consideration of increased prevalence of

lifestyle-related chronic diseases like diabetes,

the complications for patients with diabetes, with

overt pulmonary diseases claim special attention.To study the possible pathophysiological

mechanisms further research is needed. Our

study has several limitations. First, there were

less number of subjects. So we cannot generalize

the result in different groups i.e., diabetic and

control groups. Secondly, we did not measure

DLCO in our subjects. Several studies showed a

reduction in DLCO in diabetic subjects, also in

subjects with normal spirometric values. Lung

function should be monitored regularly to know

the degree of impairment in diabetic or pre -

diabetic subjects.

ACKNOWLEDGEMENT

We acknowledge the subjects who participated in

the study.

Conflicts of Interest: None

Source of Funding: Nil

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9. Strain JJ. Disturbances of micronutrient and

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Fisher E, Yue DK et al. Changes in hepatic

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11. Gumieniczek A, Hopkala H, Wojtowicz Z,

Wysocka M. Changes in antioxidant status of

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92.14. Engstrom GM, Janzon L. Risk of developing

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insulin-dependent diabetes. Diabetes 1987;

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17. Mori H, Okubo M, Okamura M, Yamane K,

Kado S, Egusa G et al. Abnormalities of

pulmonary function in patients with non-

insulin- dependent diabetes mellitus. Intern

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Lebzelter J, Blum I, Fink G. Pulmonary

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19. Enright P, Kronmal R, Higgins M, Schenker

M, Haponik E. Spirometry reference values

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GT, Gottlieb DJ. Association between

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Davis WA. Reduced pulmonary function and

its associations in type 2 diabetes: the

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22. Wannamethee SG, Gerald shaper A, Rumley

A. Lung functions and risk of Type 2Diabetes and fatal and nonfatal major

coronary heart disease events: possible

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Care. 2010;33:1990 – 96

23. Ali MO, Begum S, Begum N, Ali T, Ferdousi

S, Begum A: FVC, FEV1 and FEV1/FVC%

in Type 2 Diabetes and Their Relationships

with Duration of the Disease. J BangladeshSoc Physiol. 2009;4(2): 81-87

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Safia Awan: Pulmonary functions in patients

with diabetes mellitus. Lung India.

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25. Lange P, Parner J, Schnohr P, Jensen G.

Copenhagen City Heart Study; longitudinal

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Ludwig H. Lung elasticity in juvenile-onset

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28. Maiolo C, Mohamed EI, Andreoli A,

Candeloro N, Rossi P, De Lorenzo A. Is

altered body fat distribution responsible for

reduced pulmonary function in obese type 2

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Raveendra et al., Int J Med Res Health Sci. 2013;2(4): 762-767


&

Health Sciences




ndAug 2013

Research article

EVALUATION OF ANTIULCER ACTIVITY OF ETHANOLIC EXTRACT OF MOMORDICA

DIOICA ON PYLORUS LIGATURE INDUCED AND IBUPROFEN INDUCED ULCER IN

ALBINO RATS

Raveendra Kumar N1, Siva Kumar N2, Yakaiah Vangoori3

1Associate Professor, 2Assistant Professor of Pharmacology, Alluri Sitaramaraju Academy of Medical

Sciences (ASRAM), Eluru, Andhra Pradesh, India3Assistant Professor of Pharmacology, Santhiram Medical College, Nandyal, Andhra Pradesh, India


ABSTRACT

Objective: The aim of the present study is to evaluate the anti-ulcer activity of Ethanolic extract of

Momordica Dioica in pylorus ligation and ibuprofen induced gastric ulcers in rats. Methods: Gastric

ulcer was induced by giving ibuprofen (200mg/Kg) and by pylorus ligation method. The animals used

for the experiment were divided into 4 groups for each model, 6 rats in each group. In pylorus ligationmodel, all groups of rats were pre-treated with test drugs, Group-I (control) received 2%gum acacia-

2ml/100g, Group-II (standard) received Ranitidine (60mg/kg.) and group-III, IV were treated with

Ethanolic extracts 150mg/kg, 300mg/kg. respectively orally 30mins prior to pylorus ligation. The

Antiulcer activity of Momordica Dioica was assessed by determining and comparing gastric volume,

free acidity, total acidity, pH, percentage of ulcer protection, ulcer index. In ibuprofen induced ulcer

model, all groups of rats were treated with test drugs for 7 days prior to ibuprofen induced ulcer.

Animals were divided into 4 groups and treated with drugs as in above model. After 7 days of treatment,

animals were fasted for 24 hrs. Ulcers were produced by giving ibuprofen (200mg/Kg) on the day of

sacrifice. The animals were sacrificed 4 hours later and stomachs were open along the greater curvatureand ulcers were graded. Percentage of ulcer protection, ulcer index were observed and calculated.

Results: The extract of Momordica Dioica in pylorus ligation model, it decreased the ulcer index (1.66)

and there was a decrease in total gastric acid and free acid (p<0.0001), and increases the pH value

(p<0.0001) and also reduces the total gastric volume (p<0.0003), increases the percentage of ulcer

protection (61.66%). In ibuprofen induced ulcer model, it decreases the ulcer index (10.66) and

increases the ulcer protection (72.09%). Conclusion: The Ethanolic extract of Momordica Dioica was

clearly shows a protective effect against total acid, free acid, gastric volume and ulcer index and also

increases pH and percentage of protection against ulcers in both models.

Key words: Momordica Dioica, Gastric protection, Ibuprofen, Ulcer Index

DOI: 10.5958/j.2319-5886.2.4.122



763


INTRODUCTION

Peptic ulcer remains a prevalent condition

affecting up to 10% of the population and is

responsible for considerable morbidity and loss

of work time

.1

the high incidence and chronicityof the suffering and decreased ability to work

associated with it, has made peptic ulcer an

important health problem. An ulcer is thought to

develop when the equilibrium is disturbed either

by enhanced aggressiveness or by lessened

mucosal resistance2 Drugs that affect acid and

enhance defensive mechanisms are available. Of

late, the concept is now changing from chemical

pH to microbial Hp (pH= acidity, Hp= H.pylori)3

Flood gates of research on Helicobacter pylori

actually opened up when Marshall and Warren in

1984 demonstrated the association between this

organism with active chronic gastritis and peptic

ulcer4Long term use of NSAIDs can also cause

gastric ulcer. Treatment cost is estimated more

than 2-4$ billion per year, so most of the ulcers

heal by using synthetic drugs. After 6-8 weeks

there is a problem of recurrence of side effects.

Therefore people prefer natural product drugs fordisease treatment. Over 3 quarters of the world

population relieved by plants and plant extracts

for health care. More than 30% of the entire plant

species at one time or other has been used for

medicinal purpose 5 Momordica Dioica is an

important medicinal plant with potent anti-

inflammatory activity. It contains the various

chemical classes such as alkaloids, tannins,

flavonoids, carbohydrates. Momordica Dioica

commonly known as teasel gourd and used as

vegetable.15 Momordica dioica Roxb belongs to

the family Cucurbitaceae6 and under the genus

Momordica, a genus of annual or perennial

climbers that contains about 80 species.

Momordica dioica climber plant commonly

known as Teasle Gourd, Kakrol, Kankro, Kartoli,

Kantoli, Kantola, Kantroli, Ban karola or Small

bitter-gourd is a relatively small oval to ovoid

vegetable. It is also called as janglee karela. It isoften cultivated for its fruits, which are used as

vegetable. The Fruits are reported to show anti-

inflammatory, anti-ulcer, anti-oxidant, and

hepatoprotective6. Traditionally this fruit was

used in ulcer but scientifically not proved. Hencethe present study was aimed to investigate the

anti ulcer effect of Momordica Dioca in

experimental animal models


Experimental animals: Swiss albino rats

weighing 150-200g of either sex were used for

this experiment, supplied by authentic animal

suppliers Sainath Agencies, Hyderabad, AP, and

India. They were randomly distributed into

groups and housed in cages (6/cage) and kept

under standard conditions at 26±2° C and relative

humidity 44-56% and 10 hours light: 14 hrs dark

cycles each day for 1 week before and during the

experiments. All animals were fed the standard

rodent pellet diet and ad libitum. This study was

cleared by the institutional animal ethics

committee according to CPCSEA guidelines.

Plant material: Fresh green fruits of Momordica

Dioica popularly known as spine gourd were

obtained in sufficient quantity from local forest

in Eluru, A.P in March 2013.They were carefully

washed to remove dust particles and other

foreign materials and cut into small pieces dried

in shaded areas. The dried pieces of fruit make a

fine powder with grinder.

Preparation of alcohol extract: The dried fine

powder of the Momordica Dioica powder wasweighed on balance 30g. and taken into the sac

like cloth material and placed in the Soxhlet

basket. 300 ml of ethyl alcohol was taken as

solvent into the Soxhlet flask. Cold tap water

must flow through the inlet and outlet of the

condenser. The Soxhlet apparatus kept running

for 24hours for proper extraction. The extract

laden solvent falling from the Soxhlet basket is

dark in color and it becomes clearer, that

indicates the extraction process is finished. At

the end of the extraction process the solvent is



764


then evaporated7, total yields was 5gm,

percentage yield was16.6% as mg per gm dried

powder. The extract 600mg was suspended in

2ml of 2% Gum acacia and administered

according to dose mentioned as bellow by oral

route.Experimental design: The animals used for the

experiment were divided into 4 groups for each

model, 6 rats in each group.

In Pylorus ligation model: All groups of rats

were pre-treated with test drugs, Group-I

(control) received 2% gum acacia-2ml/100g,

Group-II (standard) received Ranitidine

(60mg/kg) 8 and group-III, IV were treated with

Ethanolic extracts 150mg/kg, 300mg/kgrespectively orally 30mins prior to pylorus

ligation. After giving drugs all groups of animals

were anesthetized with ether and lower

abdominal wall was opened and pyloric end was

ligated. Then abdominal wall was closed with

interrupted sutures. During this procedure strict

aseptic conditions were maintained to prevent

infections. After 4 hours of pylorus ligation,

animals were sacrificed and stomach was opened

along with the greater curvature and total gastric

contents were collected and centrifuged. The

Antiulcer activity of Momordica Dioica was

assessed by determining and comparing gastric

volume, free acidity, total acidity, pH, percentage

of ulcer protection, ulcer index.

In the Ibuprofen induced ulcer model, all

groups of rats were treated with test drugs for 7

days prior to ibuprofen induced ulcer. Animals

were divided into 4 groups and treated withdrugs as in above model. After 7 days of

treatment, animals were fasted for 24 hrs. Ulcers

were produced by administration of ibuprofen

(200mg/Kg)9. The animals were sacrificed after 4

hours administration of ibuprofen and stomachs

were open along the greater curvature and ulcers

were graded. Percentage of ulcer protection ulcer

index were observed and calculated.10

Gastric juice collection: gastric juice wascollected and filtered through glass wool in a

measuring cylinder. The gastric contents were

centrifuged at 3000rpm for 5 min, and the

supernatant was used for the estimation of total

acidity (pH). The volume of gastric juice was

expressed as ml/100g of body weight.11

Estimation of total acidity: 1 ml of supernatantwas diluted to 10 ml of distilled water. The

solution was titrated against the 0.05 ml/L NaOH

using phenolphthalein as an indicator. Titration

was continued until the color changed to light

pink. The volume of NaOH required was noted

and was taken as corresponding to the total acidity.

Acidity was expressed as Total acidity = (volume

of NaOH × Normality × 100)/ 0.1(mEq/L).12

The ulcer score was determined by using a 10 ×magnifying hand lens. The scoring of severity of

ulceration was as follows: 1 mm (pin point)= 1;

1-2 mm=2; >2 mm=3; >3 mm=4. The mean ulcer

score was determined by dividing the total ulcer

indices in a group by the total number of animals

in that group. Ulcer score = total ulcer index (UI)

in a group/ total number of animals in that group.

The curative ratio of an ulcer was determined by

subtracting the test ulcer score from the control

ulcer score divided by the control ulcer score.

The result was multiplied by 100.13

Statistical analysis: The results obtained were

expressed as Mean±SEM and were analyzed by

the application of One-way Analysis of Variance

(ANOVA)

RESULTS

Pylorus ligation method: Extract of Momordica

Dioica (150mg/Kg, 300mg/Kg) treated animals

has shown significant reduction in Ulcer Index,

Volume of Gastric juice (p<0.001), total acid and

free acid (p<0.001) and also it increases the pH

(p<0.001), percentage protection (61.66%) when

compared with the control group. Standard drug

treatment with ranitidine (60mg/Kg) also showed

significant reduction in Ulcer Index, Volume of

Gastric juice, total acid and free acid and also

increases in pH and percentage of protection(92.37%).



765


Table 1: Effect of Momordica Dioica on pylorus ligation ulcer model (n=6, Mean±SEM)

Grou

p

Treatment Dose Gastric contents (Mean±S.E.M) Ulcer

index

% of ulcer

protectionVol. of

gastric juice

Total acid Free acid pH

1 Control-2%

GA

2ml/100g 4.70±0.34 94.33±3.59 32.33±1.56 2.03±0.12 4.33 0%

2 Standard-

Ranitidine

60mg/kg 2.98±0.15**

*

53.33±4.07**

19±1.36* 4.79±0.14**

0.33 92.37%

3 Test-T1-

extract

150mg/kg 4.15±0.27* 79.83±4.14*

27.83±0.98*

*

3.46±0.26*

2.8 35.33

4 Test-T2-

extract

300mg/kg 3.18±0.21** 63±2.54** 25.50±1.89* 3.98±0.13**

1.66 61.66

*P<0.05, **P<0.01, ***P<0.001 compared to Control.

Ibuprofen induced ulcer model: Extract of

Momordica Dioica (150mg/Kg, 300mg/Kg)

treated animals has showed significant reduction

in Ulcer Grades (p<0.001), Ulcer Index (10.66)

with high dose (300mg/Kg) and increase in

percentage of protection (72.09%) when

compared to control group. Standard drug

treatment with ranitidine (60mg/Kg) also showed

significant reduction in Ulcer Index and increase

in percentage of protection (95.65%).

Table: 2. Effect of Momordica Dioica in Ibuprofen induced ulcer model

*P<0.05, **P<0.01, ***P<0.001 compared to Control.

DISCUSSION

In spite of tremendous development in the field

of synthetic drugs during recent era, they are

found to have some or other side effects, whereasplant products or homeo drugs still hold their

own unique place by the way of having no side

effects. Peptic ulcer disease is a chronic

inflammatory disease characterized by ulceration

in the upper GI.14 The pathophysiology of ulcers

is due to an imbalance between aggressive

factors (acid, pepsin, H.pylori and NSAIDs) and

local mucosal defensive factors (mucous,

bicarbonate, blood flow and prostaglandins). The

integrity of gastro duodenal mucosa is

maintained through a hemostatic balance

between these aggressive and defensive factors.

The major cause of gastric ulcer is the chronicuse of NSAIDs. Therapeutic& adverse effects of

NSAIDs have been attributed to the ability of

these drugs to inhibit the action of

cyclooxygenase (COX). COX is responsible for

the synthesis of prostaglandins that normally

inhibit acid secretion, as well as having a

protective effect on gastric mucosa. Infection of

the stomach mucosa with H.pylori – a gram

negative spiral shaped bacterium is now

generally considered as the major cause of gastro

Groups Treatment Dose Ulcer grade

(Mean±SEM)

Ulcer index % of ulcer

protection

1 Control-2% GA 2ml/100g 33.33±3.33 38.2 0

2 Standard-ranitidine 60mg/kg 1.66±1.66 1.66 95.65

3 Test-T1-extract 150mg/kg 26.66±2.10* 27.99 26.72

4 Test-T2-extract 300mg/kg 10±4.47* 10.66 72.09



766


intestinal ulcers. Treatment includes H2-receptor

antagonists (Cimetidine), proton pump inhibitors

(Omeprazole) and cytoprotectives (Misoprostol).

Antacids like Aluminium hydroxide &

magnesium hydroxide are used often to

neutralize excess gastric acidity in the stomach.Due to problems associated with recurrence after

treatment, there is a need to seek an alternative

drug against gastrointestinal ulcers. 15 The

present investigation demonstrated the efficacy

Momordica Dioica of plant extract against

gastric ulceration induced by two experimental

models viz. Pylorus ligation induced gastric

ulceration and Ibuprofen induced ulceration.

In pylorus ligation model, the plant extract of Momordica Dioica produces a decrease in the

ulcer number, total gastric volume, total acid,

and free acid and increases the pH and

percentage of ulcer protection (61.66%) and in

standard drug (Ranitidine) treated animals the

percentage of ulcer protection (92.37%) when

compared with control group (0%). High dose of

extract (300mg/Kg) more active than low dose

(150mg/Kg) but less active than standard drug

(Ranitidine).

In Ibuprofen induced ulcer model, the plant

extract of Momordica Dioica produces a

decrease in the ulcer number and increase in

percentage of ulcer protection (72.09%) and with

standard drug the percentage of ulcer protection

(95.65%) when compared to control group (0%).

High dose of extract (300mg/Kg) more active

than low dose (150mg/Kg) but less active than

standard drug (Ranitidine).The anti ulcer property of Momordica Dioica in

both the experimental models explained above, is

due to presence of flavonoids, terpenoids,

tannins, and triterpenes. The triterpenes are

known as an anti-ulcer agent and their action has

been mentioned to be due to activation of cellular

proteins, reduction of mucosal prostaglandin

metabolism, cytoprotective actions and reduction

of gastric vascular permeability and remainingcompounds have been shown to scavenger free

radicals.16-18 The results in the present study

seem to provide support for the use of

Momordica Dioica as an anti-ulcer drug in folk

medicine. Therefore, also in view of its large use

in India further investigations are needed to

know about its anti-ulcer activity in humanbeings.

CONCLUSION

The present study indicates that the plant

Momordica Dioica has potential anti-ulcer

activity against pylorus ligation and Ibuprofen

induced ulcers in experimental animals. So this

activity of plant probably due to the compounds

present such as Flavonoids and triterpenes. Sothe plant Momordica Dioica uses for both

Ayurvedic and Modern drug development areas

because of its phyto-medicinal uses but it needs

further clinical trials before complete trust and

usage.

ACKNOWLEDGEMENT

The author Dr. Raveendra Kumar expresses

extreme pleasure and thanks to management of ASRAM, Eluru for giving the opportunity to do

this research work. And also thanks to co-authors

and technicians for their support throughout this

work.

REFERENCES

1. Colin W. Howden and Richard H Hunt,

James H. Lewis: Peptic Ulcer Disease. A

Pharmacological approach to gastrointestinaldisorders.1994; 1st ed.:3-21

2. Lawrence and Bennett: Clinical

Pharmacology. 8th ed. ELBS Publication;

Churchill Livingston; Edinburgh, 1997; 567.

3. Aggarwal KK, Chopra K.L: Peptic ulcer

disease: Changing concepts from pH to HP.

Speciality issue of Ind. J. of Clinical Practice

on Gastroenterology. 1995;9-10.

4. Marshal BJ, Warren JR. Unidentified curvedBacilli in the stomach of patients with



767


gastritis and peptic ulcer Lancet

1984:1(8390):1311-1315.

5. Kumar A, Nirmala V. Gastric anti ulcer

activity of the leaves of Caesalpinia

pulcherrima. Indian J. Pharm.1992;(4)67-68

6. Shreedhara CS, Vaidya VP. Screening of Momordica dioica for hepatoprotective, anti-

inflammatory, anti oxidant activities. Natural

product science. 2006; 12(3):157-61

7. Asli Semiz, Alaattin SEN. Antioxidant and

chemoprotective properties of Momordica

charantia L. (bitter melon) fruit extract.

African Journal of Biotechnology. 2007;

6(3): 273-277.

8. Ramesh L Londonkar. Studies on activity onvarious extracts of Mentha arvensis Linn.

Against drug induced gastric ulcer in

mammals, World J gastrointestinal

Oncology. 2009; 1(1): 82-88.

9. Hegde DA, Khosa RL, Goel RK. Antiulcer

and cytoprotective action of Wedelia

calendulace Less. Ancient Sci. Life. 1994;

14:77 – 81.

10. Sastri BN. The wealth of India-raw materials.

CSIR, New Delhi.1962;.2:408.

11. Nwinyl FC, Binda L, Ajoku GA. Evaluation

of aqueous extract of Boswollia dalzielii stem

bark for anti microbial activities and

gastrointestinal effects. African J of

Biotechnol.2004;3;284-88

12. Antonial J, Sertie A. Anti ulcer activity of

ethanol extract of Sesbania grandiflora.

Brazilian J Pharm Sci. 2007;37:20-26.

13. Khayaei M, Salehi H, Protective effect of falcaria vulgaris extract on ethanol induced

gastric ulcer in rats. Iranian J Pharmacol Ther

2006;5:43-46.

14. Cola- Miranda M. Anti-ulcerogenic activity

Indigo for a truxillensis kunth. Biota

neotropico 2006; 6 available from URL:

http:// www.biotaneotropica.org.br

15. Enaganti S. Peptic ulcer disease. Hospital

Pharmacist 2006; 3:16-18.

16. Ashok P, Rajani GP, Sinnathambi A, Hulkoti

B, Desai B, Rajendran R. Studies on corneal

permeation and oculo-hypotensive effect of

benazepril in chronic and acute models of glaucoma. Iranian J Pharmacol Ther. 2006;

5:141-44.

17. Rajkapoor B, Anandan R, Tayakar B. Anti-

ulcer effect of Nigella sativa Linn. against

gastric ulcers in rats. Cur Sci 2002;(77)82:25

18. Rajkapoor B, Tayakar B, Anandan R,

Murugesh N. Anti-ulcer effect of dried fruits

of Carrica papaya Linn. in rats. Ind. J.

Pharmaceutical Sci. 2003; 52: 122-25.



768

Aniket et al., Int J Med Res Health Sci. 2013;2(4): 768- 772


&


Research article

STUDY AMONG BETEL QUID CHEWERS FROM INDIAN POPULATION

*Adhikari Aniket1, De Auley

1, Podder Gargi

1, De Madhusnata

2

1Research Scholar,

2Professor, Department of Genetics, Ramakrishna Mission Seva Pratishthan,

Vivekananda Institute of Medical Sciences, 99 Sarat Bose Road, Kolkata - 700026


ABSTRACT

Background: Oral cancer is most common in males and also in females. Betel quid (BQ) is the main

causative agent of oral cancer. Areca catechu, a major component of BQ, contains certain alkaloids that

give rise to nitrosamines. Mitotic index (MI) and Micronuclei (MN) were studied among the studied

population. Methods: In this present study subjects were screened from Department of E.N.T. &

Department of Oral and Facio maxillary of RKMSP hospital, and different areas of Eastern and North

Eastern states of India. For mitotic index (MI) blood leukocyte cultures were analyzed and for

micronuclei (MN) buccal mucosa were examined. Results: Some of them had more than one addiction.

Micronuclei percentage and mitotic index both higher than normal. Conclusion: Betel quid play a role

in changing the oral pathology and thus causes oral cancer.

Keywords: Oral cancer, betel quid, micronuclei, mitotic index

INTRODUCTION

Oral premalignancies are very common in betel

quid chewers and is the most common cancer

worldwide. 45% and 60% mortality depend upon

the patient group and the disease frequentlyassociated with tobacco smoking, chewing. Lip,

tongue, palate, gum and cheek these parts of the

oral cavity are effected from tobacco chewing .

Malignancies of the oral cavity arise from the

precancerous lesion such as leukoplakia,

erythroplakia and pre cancerous condition such

as oral submucous fibrosis. Oral squamous cell

carcinoma and the most common oral

premalignancies such as leukoplakia and oral

submucous fibrosis appear to be related to the

habit of betel quid (BQ) chewing in South East

Asia, whereas in Western countries cigarette

smoking and heavy alcohol consumption are the

main causative agents. Areca nut (Areca

catechu), a major component of BQ. Areca nutcontains certain alkaloids that give rise to

nitrosamines, some of which such as N -

nitrosoguvacoline, 3-(methylnitrosamino)

propionitrile, 3-methylnitrosamino

propionaldehyde and N -nitrosoguvacine, are

shown to be carcinogenic.1These BQ-specific

nitrosamines may act as an adjunct to tobacco-

specific nitrosamines that are strongly implicated

as an etiologic factor for leukoplakia and oral

submucous fibrosis. Metabolic activation of

several nitrosamines was reported to be catalyzed

DOI: 10.5958/j.2319-5886.2.4.123



769


by cytochrome P450 enzymes (CYPs), large

multi-gene family enzymes important in phase I

metabolic activation reactions. Furthermore,

reactive oxygen species are generated in the oral

cavity during BQ chewing due to the addition of

slaked lime [Ca(OH)2] into BQ.2Among

xenobiotic metabolizing enzymes, the CYP2A

family is characteristic of its catalytic properties

to nitrosamines.3

Several workers have

investigated the chemopreventive action of tea

against cancer.4,5,6

Consumption of black tea has

been shown to exert a protective effect against

oral precancerous lesions.7

Epigallocatechin-3-

gallate (ECG), is one of the major component of

green tea which inhibit cell growth and alsoreduce tumor incidence. Since the formation of

micronuclei in the eukaryote cells is an end point

of chromosomal damage or segregation errors.8

The presence of micronuclei reflects a genotoxic

or carcinogenic exposure. Association with

chromosomal aberrations, micronuclei acts as a

good indicator of genotoxic exposure. The assay

is reliable and technically easy to perform. The

present study was carried out by the Department

of Genetic Toxicology, in collaboration with the

Departments of ENT and Oral Maxillofacial

surgery, of the Ramakrishna Mission Seva

Pratishthan (RKMSP) Hospital, Kolkata.

The purpose of this study is to see whether

percentage and chromosomal damage are more

in oral cancer.

PATIENTS AND METHODS

After the Institutional Ethics committeeapproval, study was conducted in ENT and Oral

Maxillofacial department of RKMSP Hospital.

Inclusion criteria: Screening of subjects was

carried out in 3 settings:-

I) Camp in Eastern India: 220 subjects were

screened at a camp held in Bankura, Purba

Midnapur, North West Bengal. Out of them, 133

were betel quid chewers were included in the

study

II). North East camp: 56 subjects were screened

at a camp held in Karimganj, Assam. Out of

them, 33 were betel quid chewers.

III) RKMSP Hospital: 35 subjects were screened

out of them 24 cases were betel quid chewers.

Out of 24, 7 subjects had pre cancerous lesion, 6subjects had squamous cell carcinoma, 11

subjects had pre cancerous condition.

Total 311 subjects were screened from different

areas of Eastern India, North East India and

E.N.T and Oral Maxillofacial OPD of RKMSP

hospital. Among them total 190 subjects included

for study who were betel quid chewers, from

each person conform consent was taken.

Exclusion criteria: The subjects who had nobetel quid chewing habit. The subjects who had

betel quid chewing habit and any type of

precancerous lesion, precancerous condition

related with betel quid was included in this study.

Screening of subjects was carried out by

administering questionnaires.

Methods: Detailed history was taken from all

cases by filling up questionnaire.

Parameters studied: Leukocyte culture,

Micronuclei (MN) study

Leukocyte culture: - Peripheral blood was

collected from all subjects. Human leucocyte

culture was carried out by the method of

Moorhead PS et al9

modified by the method of

Sharma and Talukder.10

A total of 4 ml of

peripheral venous blood was collected from each

patient under aseptic condition with the help of a

sterile disposable needle and transferred to a

heparinized vial. Leucocyte rich plasma (0.5 ml)was added to a 5 ml of culture media (RPMI

1640, Sigma, St. Louis, USA) supplemented with

20 % foetal bovine serum (Sigma) and

Phytohaemagglutinin M (0.04 ml / ml of culture

media, GIBCO BRL). The cultures were

incubated at 37o

C. After 70 hours incubation,

colchicines (0.2 ml of 0.04% / ml) was added.

Two hours later, cells were centrifuged at 1000

rpm for 5 min, treated with prewarmed KCL(0.075M) for 15 min, centrifuged at 1000 rpm for

5 min, and fixed in methanol: acetic acid (3:1).



770


Fixed cell suspension was taken on clean grease

free glass slide and air dried. The preparation

was stained with aqueous Giemsa. All slides

were coded and 1000 blast cells were scored to

determine mitotic index per individual.

Micronuclei (MN) study: - For Micronucleistudy Premoistened wooden spatula was used to

sample cells from the oral mucosa. The spatula

was applied to a precleaned microscope slide.

After air dried the smear fixation was done by

methanol. Slides were stained by the Giemsa

solution and the MN frequency was scored using

the criteria described by Sarto et al.11

The same

person scored 1000 cells blindly in each case todetermine the MN Percentage.

RESULTS

Table 1: Detailed history of subjects of different areas

PLACE NO

AGE GROUP

( in years)

Addiction

N o B Q

A d d i c t i o n

T e a D r i n k e r

N o n

T e a D

r i n k e r

B e l o w 3 0

3 1 - 4 0

4 1 - 5 0

5 1 - 6 0

6 1 - 7 0

A b o v e 7 0

S m o k i n g

A l c o h o l

B e t e l Q u i d

North East camp

(Assam, Karimganj)

56 1 2 12 24 11 6 9 6 33 23 40 16

Eastern India camp

Bankura,Dhulai 34 5 20 8 1 0 0 16 14 19 15 34 0

East Midnapur,

Bibhisanpur

46 22 13 3 6 2 0 28 29 36 10 40 6

North, Atghara 89 28 18 21 15 6 1 27 3 56 33 73 16

Narrah, Bankura 51 8 13 12 8 6 4 14 5 22 29 49 2

RKMSP hospital 35 2 7 8 11 7 0 20 8 24 11 29 6

TOTAL 311 66 73 64 65 32 11 114 65 190 121 265 46

Table 2: Micronuclei and Mitotic Index of betel quell chewers.

PLACE Micronuclei (%)

(Mean ± SE)

Mitotic Index

(Mean ± SE)

Dhulai, Bankura 26.29 ± 1.95 3.94 ± 0.23

Bibisanpur, East Midnapore 12. 31 ± 2.75 8.66 ± 0.67

Atghara 4.76 ± 1.26 5.07 ± 0.60

RKMSP Hospital ----- * 4.54 ± 0.33

Narrah, Bankura 4.61 ± 2.82 4.28 ± 0.62

(Normal values of MI are < 4% and MN is < 1%)

*Study of micronuclei of oral cancer cases was not possible due to severe ulceration and bleeding and

cases were unable to open their mouth. Mean value of mitotic index of all cases having betel quid

chewing habit was 5.29 ± 0.49 and mean percentage of micronuclei were 12 ± 2.19



771


Total 311 subjects studied (Table 1), out of

which 56 subjects from North East camp

(Karimganj, Assam), 220 subjects from East

India and 35 subjects from RKMSP hospital. Out

of 56 subjects from North East 58.92% were

betel quid chewers and 71.42% were tea drinker.They took betel quid more than once. Out of 33

betel quid chewers, 6 cases took betel quid

occasionally, rest of them took BQ 3-4

times/day. Out of 34 subjects from Dhulai,

Bankura, 55.88% were betel quid chewers and all

of them were tea drinker. Out of 19 betel quid

chewers, 13 cases took betel quid occasionally,

rest of them took BQ 2-5 times/day. Out of 46

subjects from East Midnapore 78.26% were betelquid chewers and 86.95% were tea drinker. Out

of 36 betel quid chewers, 5 cases took betel quid

occasionally, rest of them took BQ 7-16

times/day. Out of 89 subjects from North 24 Pgs

62.92% were betel quid chewers and 82.02%

were tea drinker. Out of 56 betel quid chewers,

19 cases took betel quid occasionally, rest of

them took BQ 6 -10 times/day. Out of 35

subjects from RKMSP hospitals 68.57% were

betel quid chewers and 82.85%were tea drinker.

Out of 24 betel quid chewers, 12 subjects took

betel quid occasionally, rest of them took BQ 4-9

times/ day.

90% subjects were coming from rural areas at

Karimganj. All subjects were from Dhulai,

Bibhisanpur, Narrah, Atghara under rural areas.

10% subjects were coming from rural areas of

RKMSP Hospital and rests on them were from

urban areas.Mean value of mitotic index (MI) of all cases

having betel quid chewing habit was 5.29 ± 0.49

and mean percentage of micronuclei (MN) were

12 ± 2.19 (Table 2)

DISCUSSION

According to World Health Organisation (WHO)

data, the standardized mortality rate for 2002 was

2.2 deaths per 100,000 populations. Oral canceris one of the leading cancers in most Asian

countries.12

In another study the prevalence of

head and neck cancers was found to be

significantly high at 54.48% in the population of

North Eastern India. Gurkha and pan masala has

been shown to be carcinogenic in experimental

animals, causing tumors in various organs. Noeffective techniques have yet been developed for

making direct chromosome preparation from

epithelial tissues. They concluded that the

gradual increase in Clinical chemoprevention

trials on oral pre-malignancies have used MN in

oral mucosa as a surrogate endpoint of cancer

.13

These findings clearly suggest a causal link

between MN and cancer.Micronuclei are the

small extra nuclei cells which is formed inmetaphase and anaphase stage. The presence of

micronuclei reflects a genotoxic and

carcinogenic exposure since it is associated with

chromosome aberrations.14

Micronuclei have

been used as an important marker. In our study

we have seen that mitotic index of all subjects

having betel quid chewing habit and mean

percentage of micronuclei were higher than

normal. Normal values of MI are < 4% and MN

is < 1%.

M. Sulkowska,15

observed that mitotic index

count was high in oral squamous cell carcinoma

cases. Mitotic activity has proven to be an

efficient prognostic indicator of squamous cell

carcinoma of various sites.

CONCLUSION

Betel quid has an immense role in changing the

oral pathology and developing oral cancer. In

this present study it has been found that the

micronuclei percentage can be used as a

biomarker. The Micronuclei percentage and

mitotic were higher than normal.

ACKNOWLEDGEMENTS

The authors are thankful to the Secretary,

Ramakrishna Mission Seva Pratishthan, for kind

permission to use the laboratory for this work.The authors are also thankful to the National Tea



772


Research Foundation, India for financial support

of this work.

REFERENCES

1. Hoffmann D, Brunnemann KD, Prokopczyk

B, Djordjevic MV. Tobacco-specific N-nitrosamines and Areca-derived N-

nitrosamines: chemistry, biochemistry,

carcinogenicity, and relevance to humans. J.

Toxicol Environ Health .1994; 41:1-52.

2. Nair U J, Nair J, Mathew B , Bartsch H.

Glutathione S-transferase M1 and T1 null

genotypes as risk factors for oral leukoplakia

in ethnic Indian betel quid/tobacco chewers.

Carcinogenesis .1999; 20:743 –

48.

3. Fujita K, Kamataki T. Role of human

cytochrome P450 (CYP) in the metabolic

activation of N-alkylnitrosamines:

Application of genetically engineered

Salmonella typhimurium YG7108 expressing

each form of CYP together with human

NADPH-cytochrome P450 reductase. Mutat

Res. 2001; 483:35 – 41.

4. Lambert JD, Yang CS .Cancer

chemopreventive activity and bioavailability

of tea and tea polyphenols. Mutat Res. 2003;

523-524: 201-8.

5. Talukder G, Sharma A .Tea as a protectant in

human cancer. National Tea Research

Foundation. Special Issue. 2004.

6. Mukherjee P, Podder S, Talukder G, Sharma

A .Protection of black tea extract against

chromosome damage induced by two heavy

metals in mice. Pharmaceutical biology.1999; 37: 243- 7.

7. Halder A, Roychowdhury R, Ghosh AK, De

M. Black Tea (Camellia sinensis) as a

Chemo preventive agent in oral precancerous

lesions. Journal of Environmental Pathology,

Toxicology and Oncology, USA. 2005;

24(2):103- 6.

8. Geard CR, Chen CY. Micronuclei and

clonogenecity following low and high dose

rate -irradiation of normal human fibroblasts.

Radiat Res .1990; 124: 856-61.

9. Moorhead PS, Nowell PC, Mellman WJ,

Battips DM, Hungerford DA. Chromosome

preparation of leucocyte culture from human

peripheral blood. Exper Cell Res.1960; 20:613 -6.

10. Sharma A, Talukder G. Chromosome

methodology .Lab Procedures Hum Genet.

1974; 61- 75.

11. Sarto F, Tomanin R, Giacomelli L, Canova

A, Raimondi F, Guiotto C, Fiorentino MV.

Evaluation of chromosomal aberrations in

lymphocytes and micronuclei in

lymphocytes, oral mucosa and hair root cellsof patients. Mutat Res.1990; 228: 157-69.

12. Lin Sc, Chen YJ, Kao SY, Hsu MT, Lin CH,

Yang SC, et al. Chromosomal changes in

betel associated oral squamous cell

carcinoma and their relationship to clinical

parameters . Oral Oncol. 2002; 38: 266 -73.

13. Fenech M. Nutritional treatment of genome

instability: a paradigm shift in disease

prevention and in the setting of

recommended dietary allowances. Nutrition

Res Rev.2003; 16:109 – 22.

14. Roberts DM .Comparative cytology of the

oral cavities of Snuff users. Acta Cytol.

1997; 41:1008 -014.

15. Mariola Sulkowska, Waldemar Famulski,

Stanislaw Sulkowski, Joanna Reszed,

Maruisz Koda, Marek Baltaziak, et al .

Correlation between Bcl -2 protein

expression and some clinico pathologicalfeatures of oral squamous cell carcinoma.Pol

J Pathol. 2003; 54(1):49 -52.



773

Rudragouda et al., Int J Med Res Health Sci. 2013;2(4): 773-779


&

Health Sciences




thAug 2013

Research article

STUDY OF PALMAR DERMATOGLYPHICS IN PATIENTS WITH ESSENTIAL

HYPERTENSION BETWEEN THE AGE GROUP OF 20-50 YEARS

Rudragouda S Bulagouda1, Purnima J Patil

2, *Gavishiddppa A Hadimani

3, Balappa M Bannur

4, Patil

BG5, Nagaraj S. Mallashetty

6, Ishwar B Bagoji

3

1Asso. Prof Dept,

2Undergraduate Student,

3Lecturer,

4Professor & HOD,

5Professor,

6Post Graduate

Student, Dept. of Anatomy, Shri B M Patil Medical College Hospital and Research Centre BLDE

University Bijapur, Karnataka India


ABSTRACT

Background: In present study, we tried to determine significant palmar dermatoglyphic parameters in

case of essential hypertensive’s in age group between 20-50 years and whether the parameters can be

used for screening purpose i.e., early detection of hypertension. Method: With the use of modified

Purvis Smith method, Black duplicating ink (Kores, Bombay) was smeared on both hands one by oneand prints will be taken by rolling the hands from wrist creases to finger tips on the roller covered

with bond paper. While crystal bond paper, applied firmly over a wooden pad, was used for recording

the inked epidermal ridge patterns. Rolled finger prints were recorded after applying uniform

pressure on white bond paper from ulnar to radial side. Complete palm impression, including the

hollow or the palm was obtained over paper. Thus one set of finger prints and palm prints was

obtained. The prints obtained were immediately examined with hand-lens. Result: Right hand and left

hand of the both male and female study group showed more number of arches than controls. Right

hand and left hand of the both male and female study group showed more number of Radial loops than

controls. The right hand and left hand of both male and female control group showed more number of ulnar loops than study group. The right hand and left hand of the male control group showed more

number of Whorls than study, while in females, the right hand study group showed more number of

whorls than control group and the left hand study group showed less number of Whorls as

compared to control group. Conclusion: The present study indicates that there are some genetic factors

which are involved in the causation of essential hypertension and it is possible to certain extent to

predict from dermatoglyphics individual’s chance of acquiring essential hypertension. Like clinical

history, examination and investigations, the dermatoglyphics will play an important role revealing the

genetic susceptibility to essential hypertension.

Keywords: Palmar Dermatoglyphics, Essential Hypertension, Arches, Loops, Whorls

DOI: 10.5958/j.2319-5886.2.4.124



774


INTRODUCTION

The term Dermatoglyphics [from the Greek,

Derma = skin, glyphic = carvings] is the

scientific term coined by Prof. Harold

Cummins. The analysis of dermal ridges andtheir configurations by studying prints of them

is called Dermatoglyphics1. The term is also

used as a collective name for all the features of

ridged skin. The skin patterns are studied from

prints or impressions2. In ancient India,

palmistry, an art of fortune telling by reading

the pattern of friction ridges and palmar lines,

dates from about 2000 B.C.3.

Dermatoglyphics has been studied extensively

in chromosomal disorders, single gene disorders

and those disorders whose genetic basis is not

clear.

Amidst oceans of causes of human suffering,

hypertension “the silent killer of mankind” is a

public health problem. If untreated, it produces

a lot of complications like heart attack, heart

failure, stroke and kidney diseases. The

prevalence of hypertension is 59.9 and 69.9 per

1000 in males and females blood pressure inhypertensive’s even by 2mm can reduce the

overall mortality by 3%4.Twin studies have

shown that genetic factors play an important

role in the pathogenesis of essential

hypertension5. By analyzing various parameters

of dermatoglyphics in the palms and fingers, it

is aimed to prevent the ill effects of the disease

by modifying the risk factors. Dermatoglyphics

helps in the early detection of cases of

essential hypertension6. There is a steady

increase in hypertension prevalence over the

last 50 years, more in urban than in rural areas.

It is well recognized that hypertension is now a

major health problem in India7. The relevance

of dermatoglyphics is not to diagnose, but to

prevent by predicting a disease; not for defining

an existing disease, but to identify people with

the genetic predisposition to develop certain

diseases.

MATERIALS & METHODS

The study was carried for a period of 3

months from July 2011 to September 2011,

with diagnosed Essential hypertensive patients

attending out-patient and in-patient, medicine

department, BLDE University’s, Shri B. M.

Patil medical college, Hospital and Research

Centre, Bijapur were selected. 100 patients [50

Males and 50 Females] between the age group

of 20-50 years were taken up for the study

and 100 healthy people of same age group

included both sexes as control. Informed

consent was taken from individual persons and

the study was approved by Institutional Ethics

Committee of Shri B M Patil Medical College.

Inclusion criteria: Clinically diagnosed cases of

essential hypertension

Exclusion criteria:

1. Any deformities of fingers and palm and

Infected hand

2. Diseases causing secondary hypertension

3. Chromosomal abnormalities like

Klinefelter’s syndrome, Turner’s

syndrome etc.

4. Deep burns of fingers and palms leadingto scars.

Material used: wooden table of suitable

height, ‘kores’ duplicating ink, roller, white

crystal bond paper, magnifying lens, soap,

needle, scale, water and towel.

Method: The modified Purvis Smith method

was applied. Patients were asked to wash both

their hands with soap and water so as to

remove any oil or dirt. Black duplicating ink

(Kores, Bombay) was smeared on both handsone by one and prints will be taken by rolling

the hands from wrist creases to finger tips on the

roller covered with bond paper8,9

.

Fingerprints: The distal phalanges of person’s

right hand were inked over the tile by firm

pressure on the dorsum, starting from little

finger. The distal phalanges of left hand were

similarly inked10.

While crystal bond paper, applied firmly over awooden pad, was used for recording the inked

epidermal ridge patterns. Rolled finger prints



775


were recorded after applying uniform pressure

on white bond paper from ulnar to radial side.

Palm Print: Palm prints of both hands were

obtained after inking them with help of rubber

roller. A white crystal bond paper was wrapped

around a wooden rod placed on the table. Thehand was horizontally placed against it and the

rod was gradually rolled on the table. Complete

palm impression, including the hollow or the

palm was obtained over paper. Thus one set of

finger prints and palm prints was obtained. The

prints obtained were immediately examined with

hand-lens and care was taken to include all

essential details. Dermatoglyphics of sole and

toes were not recorded (fig 1).The study included both qualitative and

quantitative tests. Qualitative study includes

finger print patterns (whorls, radial loop, arches,

and ulnar loop) and in the palm includes simian

line and Sydney line. Quantitative study

includes Total Finger Ridge Count, Absolute

Finger Ridge Count and atd angle. To analyze

finger pattern frequency, the fingertip pattern

configurations were classified as arches (A),

loops (L), whorls W). The arches were

further recorded as simple (A), or tented (At)

arches depending upon the presence or absence

of a triradius. For statistical purpose, both were

grouped together as arches only. Statistical

calculations were done by arithmetic mean andstandard deviation, Z test and Chi-square test

applied wherever necessary.

OBSERVATION

Development of dermatoglyphic pattern is

under genetic control. Hence qualitative and

quantitative study of dermatoglyphic traits may

give us a clue to the susceptibility of essential

hypertension.The Quantitative Analysis includes: The

Total Finger Ridge Count (TFRC), Absolute

Finger Ridge Count (AFRC) and ‘atd’ Angle

(fig 2)

The Qualitative Analysis includes: Analysis

fingertip patterns of Right hand and left hand

separately, right hand and left hand combined

and abnormal palmar creases Sydney line (Sy

line) and simian line(Sm line).

Fig.1: Procedure of finger and Palm prints Fig.2: Atd angle measurement



776


Table 1: Digit wise frequency of pattern

Male Female

Study Group Control Group Study Group Control Group

Right

Hand

Left

Hand

Right

Hand

Left

Hand

Right

Hand

Left

Hand

Right

Hand

Left

Hand

Arch 25 18 04 07 22 19 0 4LoopRadial 26 30 11 21 31 32 23 21

Loop Ulnar 115 116 131 120 100 113 129 118

Whorl 84 86 104 102 97 86 88 112

Simian Line absent in right and left hands of both male & female hypertensive individuals

Table 2: Presence of Sydney Line in Right Hand

Male Female

Study Group Control Study Group Control

Right Hand Present 14 0 22 0Absent 36 50 28 50

Left Hand

Present 15 0 14 0

Absent 35 50 36 50

Table 3: Total finger ridge count (Mean±SEM)

Study Group (Hypertensive) Control (Normal) Inference

Male 80.3 ± 1.4 84.3 ± 1.4 Significant

Female 84.7 ± 1.6 83.8 ± 1.2 Not significant*P<0.05 compared to control group

Table 4: Absolute finger ridge count (Mean ± S.D)

Study Group Control t testP value Inference

Male 103.9 ± 14 109.9 ± 18 1.85 0.067 not significant

Female 112.6 ± 18.4 110 ± 14.6 0.77 0.443 not significant

Table 5: atd Angle (Mean ± S.D)

Study Group Control t p Inference

Male

Ri ht Hand 40.76 ± 5.77 39.45 ± 7.18 1.00 0.32 not si nificant

Left Hand 41.87 ± 5.54 41.91 ± 6.38 0.03 0.977 not significant

Female

Right Hand 41.03 ± 8.59 42.84 ± 4.92 1.10 0.275 not significant

Left Hand 39.31 ±6.52 39.34 ± 6.5 0.03 0.979 not significant

On statistical analysis atd angle was not significant in both the hands of male and female study and

control group.

DISCUSSION

Hypertension “the silent killer of mankind” is a

public health problem. If untreated, it produces a

lot of complications like heart attack, heartfailure, stroke and kidney diseases. The

prevalence of hypertension is 59.9 and 69.9 per

1000 in males and females blood pressure in

hypertensive’s even by 2mm can reduce the

overall mortality by 3%4. The relevance of

dermatoglyphics is not to diagnose, but to

prevent by predicting a disease; not for definingan existing disease, but to identify people with

genetic predisposition to develop certain



777


diseases. There are various studies mentioned

about the dermatoglyphic pattern in various

diseases like pulmonary tuberculosis, Diabetes

Mellitus Type II Essential Hypertension,

Eczema, psoriasis and alopecia areata and even

in healthy Indian children11-14

. Present study is

compared with a study by K M Godfrey15.

In present study, we tried to determine

significant palmar dermatoglyphic parameters in

case of essential hypertensive’s in age group

between 20-50 years and whether the

parameters can be used for screening purpose

i.e., early detection of hypertension.

Qualitative Analysis

Arches: Right hand and left hand of the both

male and female study group showed morenumber of arches than controls. K M Godfrey

studied dermatoglyphics of hypertensive

patients and found that arches were least

common in the study group15

.

Radial loops: Right hand and left hand of the

both male and female study group showed more

number of Radial loops than controls. K M

Godfrey studied dermatoglyphics of

hypertensive patients and found that loops in

general i.e., both radial and ulnar loops were

most common in the study group15

.

Ulnar loops: The right hand and left hand of

both male and female control group showed

more number of ulnar loops than study group. K

M Godfrey studied dermatoglyphics of

hypertensive patients and found that loops in

general i.e., both radial and ulnar loops were

most common in the study group15

.

Whorls: The right hand and left hand of themale control group showed more number of

Whorls than study, while in females, the right

hand study group showed more number of

whorls than control group and the left hand

study group showed less number of Whorls as

compared to control group. On study of K M

Godfrey on dermatoglyphics of hypertensive

patients found that whorls were second most

common in the study group.Sydney Line: 14 cases had Sydney line in male

and 22 in female study group. All the cases in

control had sydney line. There is no study of

sydney line in the available literature.

Simian Line: No cases in study as well as

control group had simian line. There is no study

of simian line in the available literature.

II) Quantitative Analysis:Mean The Total Finger Ridge Count (TFRC):

The Mean the Total Finger Ridge Count

(TFRC) in Male patients was lesser 80.3 with

S.D. of 10.1 as compared to male control group

which had TFRC 84.3 with S.D. of 10.0 This

difference was statistically significant (P=.05).

The Mean Total Finger Ridge Count (TFRC) in

female patients was higher 84.70 with S.D. of

11.6 as compared to female control group whichhad TFRC 83.38 with S.D. of 8.64. This

difference was statistically not significant

(P=0.515).

Mean Absolute Finger Ridge Count (AFRC):

The Mean Absolute Finger Ridge Count (AFRC)

in Male patients was lesser 103.9 with S.D. of 14

as compared to male control group which had

AFRC 109.9 with S.D. of 18. This difference

was statistically not significant (P=0.067). The

Mean Absolute Finger Ridge Count (AFRC) in

female patients was higher 112.6 with S.D. of

18.4 as compared to female control group which

had AFRC 110 with S.D of 14.6. This difference

was statistically not significant (P=0.443).

Mean ‘atd’ Angle: The Mean ‘atd’ angle in

right hand of male patients (40.76°) was more

than that of controls (39.45°). It was less in left

hand of patients (41. 87°) than that of controls

(41.97°). This difference was not statisticallysignificant. The Mean ‘atd’ angle in right hand

of female patients (41.3°) was lesser than that of

controls (42.84°). Similarly it was less in left

hand of patients (39.31°) than that of controls

(39.34°). This difference was statistically not

significant. K M Godfrey studied

dermatoglyphics of hypertensive patients and

found that the mean palmar atd angle was 41.7

(5.5) degrees6.



778


CONCLUSION

In present study, we tried to determine

significance of palmar dermatoglyphic

parameters in case of essential hypertension in

age group between 20-50 years and whetherthese parameters can be used for screening

purpose i.e. to identify people with genetic

predisposition to develop to essential

hypertension. The analysis revealed the

following findings:

Significant findings in qualitative and

quantitative analysis of both sexes of essential

hypertension in age group between 20-50 years

were: the Mean Total Finger Ridge Count

(AFRC) in study group of males was lesser when

compared to control group.

The present study indicates that there are some

genetic factors which are involved in the

causation of essential hypertension and it is

possible to certain extent to predict from

dermatoglyphics individual’s chance of acquiring

essential hypertension. Like clinical history,

examination and investigations, the

dermatoglyphics will play an important rolerevealing the genetic susceptibility to essential

hypertension.

At present there are very few studies on

palmar dermatoglyphics in essential

hypertension. The findings of previous studies

are many ways similar to our present study. But

still the number of studies is limited. Since this is

an interesting subject, more number of studies is

expected. This was a small study consisting of

100 patients. Hence its findings can’t be

generalized. So further large case controls are

needed to establish the exact relation between

essential hypertension and dermatoglyphics and

utility of dermatoglyphics in prediction of

susceptibility to essential hypertension.

ACKNOWLEDGEMENT

Authors are thankful to ICMR for selecting

this project for short term studentship (ICMR-

STS-2011 Reg. no. 201102292) project and for

funding. Authors are also thankful to Principal

and Anatomy department staff of Shri B M Patil

Medical College Hospital and Research centre

BLDE University for kind support.

REFERENCES

1. Bannister LH, Berry MM, Collins P,

Dyson M, Dussek JE, Ferguson MWJ.

Gray's Anatomy. Integumental system.38th

ed. NewYork: Churchill Livingstone;

2000.p.380.

2. Holt SB. Significance of dermatoglyphics

in medicine. Clinical pediatrics

1973;12(8):471-83.

3. Saha KC. Dermatoglyphics. Indian MedAssoci 1970; 54: 428.

4. Park K. Hypertensive. Park’s Textbook of

Preventive and Social Medicine. 18th

Ed.

Banarsidas Bhanot; 2005; 295.

5. Chobanian VA, Bakris GL, Black HR,

Cushman WC, Green LA, Izzo JL.

Hypertension. American Heart Association

2003; 42; 1206.

6. Godfrey KM, Barker DJP, Peace J, Cloke J,Osmond C. Relation of fingerprints and

shape of the palm to fetal growth and adult

blood pressure. British Medical Journal

1993; 307: 405-09.

7. History of dermatologlyphics. Available from

url: http//www.handanalysis.net/library/

derm_ history. htm accessed on 2005 June

28.

8. Schaumann B, Alter M. Dermatoglyphics in

medical disorders. New York: Springer

Verlag; 1976.p.1-129.

9. William JB. Embryonic development of

epidermal ridges and their Configurations-

Birth defects: Original Article Series 1991;

27:95-112.

10. Schaumann B, Alter M. Dermatoglyphics in

medical disorders. New York:Springer

Verlag;1976.p.1-129.

11. Desai SD, Hadimani GA. Dermatoglyphics

and Health Anatomica Karnataka; 2013: 7(1),



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01-09

12. Kumar S, Kumar N, Mangal BD.

Dermatoglyphics in healthy Indian children:

An analysis of finger prints, palm prints,

axial triradii, and ‘atd’ angle, sole and toe

prints. Indian J Pediatric 1974; 41:249-56.13. Babu SS, Powar BP, Khare ON, Palmar

Dermatoglyphics in Pulmonary Tuberculosis.

J. Anat Soc.India 2005; 54:64-6.

14. Pour Jafari H, Farhed DD, Yazdani A, Hashe

Mzadeh CM. Dermatoglyphics in patients

with eczema, psoriasis and alopecia areata.

Skin Res Technol 2003; 9:240-44.

15. Oladipo GS, Osogba IG, Bobmanuel I,

Ugboma HAA, Sapira MK, Ekeke ON.Palmar Dermatoglyphics in Essential

Hypertension Amongst Rivers Indigenes.

Australian J of Basic and Applied Sci.

2010;4(12): 6300-05



780

Manisha et al., Int J Med Res Health Sci. 2013;2(4): 780-785


&

Health Sciences


stAug 2013 Revised: 20


stSep 2013

Research article

A STUDY OF MORPHOLOGY OF VERMIFROM APPENDIX IN 200 CASES

Chaudhari Manisha L1, Kapadia Divyesh M

2, *Kanani Sanjay D

3, Patel Jitendra P

4, Shah Ritesh K

5,

Nirvan Ashok B6

1Assistant Professor, Department of Anatomy, Gujarat Adani Institute of Medical Sciences, Bhuj, Gujarat2Assistant Professor,

4Associate Professor, Department of Anatomy, Smt.N.H.L.Municipal Medical College,

Ellisbridge, Ahmedabad, Gujarat, India3Tutor, Department of Anatomy, GCS Medical College, Naroda road, Ahmedabad, Gujarat, India

5Assistant Professor, Department of Anatomy, GCS Medical College, Naroda road, Ahmedabad, Gujarat6Associate Professor, Department of Anatomy, B.J.Medical College, Asarwa, Ahmedabad, Gujarat


ABSTRACT

Aims: To study the various positions of vermiform appendix, and its relation to various diseases of the

vermiform appendix, and average length and external diameter of the vermiform appendix.

Materials & Methods: This study was conducted on 200 cases – 100 cadavers from the dissection

laboratory with an age range of 50 – 90 years. The dissection was performed in the dissection hall of Smt.

N.H.L. Municipal Medical College, Ahmedabad, B. J. Medical College, Ahmedabad, A.M.C.M.E.T.

Medical College, Ahmedabad, and 100 cases from postmortum room of V. S. Hospital from August 2009 to

December 2012. Result and Observation: classic coeliac trunk with emission of the left gastric, splenic and

hepatic arteries was found in 76(76 %) cadavers. Haller's tripod, in which the three arteries originated at the

same level and in the terminal portion of the coeliac trunk was observed in 18(18%) cadavers. In 16 cadavers

inferior phrenic arteries originated from coeliac trunk was observed. In 8 cadaver’s variations regarding

disposition of the left gastric, splenic and hepatic arteries also regarding the number of emitted arteries

observed. Conclusion: Appendix is only organ in our body which has not constant anatomical position.From various positions of vermiform appendix we can understand the possible outcome of the appendicitis

specifically location of site of pain.

Key words: Appendix, Position, Length, Diameter

INTRODUCTION

The Appendix is a narrow worm like structure

present in the right iliac fossa, arising from the

posteromedial wall of the caecum about 2 cms

below the ileo-caecal junction and has no

constant anatomical position. The length of

appendix varies from 2 to 20 cms with an

average 2 of 9 cms. A variation in the position of

the appendix, along with the degree of

DOI: 10.5958/j.2319-5886.2.4.125



781


inflammation makes the Clinical presentation of

appendicitis notoriously inconsistent.

Misdiagnosis in different age groups is from 10

to 33%1. The attachment of the base of appendix

remains fairly constant, but the tip can be found

anywhere in Retrocaecal, Pelvic, Subcaecal, Paracaecal, Post ileal and Preilea positions.

Appendicitis in different positions may mimic

other diseases in retrocolic – colitis, Post ileal –

ureteric colic, Pelvic inflammatory disease2,

Torsion of ovarian cyst & Ruptured tubal

gestation, Sub hepatic – hepatitis, biliary colic3.

The only invariable feature is its origin from the

caecum at the site of coalescence of all three

taenia coli

4

. Though considered by most to be avestigial organ, its importance in surgery is

mainly due to its propensity for inflammation

that results in the clinical syndrome known as

acute appendicitis, and is the most common

cause of “acute abdomen” in young adolescents3.

MATERIALS AND METHOD

Material: This study was conducted on total 200

cases, 100 cases taken from dissection laboratory

of the anatomy department, Smt. N.H.L.

Municipal Medical College, Ahmedabad, B. J.

Medical College, Ahmedabad, and

A.M.C.M.E.T. Medical College, Ahmedabad

with an age range of 50-90 years of both sexes.

The cadavers were embalmed through the carotid

and femoral arterial perfusion of formaldehyde

solution, spirit, water and glycerine and

preserved in a weak formalin solution before

dissection, and remaining 100 cases are taken

from postmortem room of Sheth V. S. Hospital

from August 2009 to December 2012.

Method: Length of vermiform appendix was

measured by nylon thread from root to tip of

appendix. Thread’s length was measured by

vernier caliper. External diameter was measuredby vernier caliper at a maximum external

diameter of the appendix. Dissection done

according to cunningham’s manual of practical

anatomy.

RESULTS

Keeping in view the aim of the study mentioned

earlier, following observations were recorded: In

the present study the total number of cases was200 (136 Males and 64 Females). Table.1 shows

the position of vermiform appendix in present

study (Figure.1 Retrocoecal position, Figure.2

Pelvic position, Figure.3 Post ileal position,

Figure.4 – Subcoecal position, Figure.5 –

Paracoecal position, Figure.6 – Subhepatic

position). In present study most common position

in male and female was retrocaecal founded in

75 cases (55.14%) and 36 cases (56.25%)

respectively; and least common position in male

was subhepatic founded in 01 case (0.007 %) and

in female was paracaecal founded in 03 cases

(0.04%). No case of preileal and promontory

position was found.

Table.2 shows the calculation of external

diameter and length of vermiform appendix in

present study. In present study the average length

of vermiform appendix was 5.436 cm in 200

cases and average external diameter was7.0450cm in 200 cases.

Table 1: Position of vermiform appendix

Serial number Position Male Female Total Percentage

1 Retrocaecal 75 36 111 55.5 %

2 Pelvic 32 15 047 23.5 %

3 Postileal 14 04 018 9 %

4 Subcaecal 07 06 013 6.5 %

5 Paracaecal 07 03 010 5 %

6 Subhepatic 01 00 001 0.5 %Total 136 64 200 100 %



782


Table 2: Calculation of external diameter and length of vermiform appendix

MALE FEMALE

External

Diameter (mm)

Length

(Cm)

External

Diameter (mm)

Length

(Cm)

Maximum 15 9 14 7Minimum 3 2 4 2.4

Mean 7.3014 5.5647 6.5000 5.1625

Median 7 5.6 6 5.4

SD 2.8029 1.3348 2.2253 1.1086

Table 3: Comparison of different positions of the vermiform appendix of present study with other studies

Author No.of

specimen

Retro-

caecal

Pelvic Postileal Preileal Sub-

caecal

Para-

caecal

Sub-

hepatic

Solanke TF 125 38.4% 31.2% 12% 4% 11.2% 2.4% -

Varshney S et

al.9

600 19% 53% 1% 2% 7% 18% -

Golalipour MJ2

117 32.4% 33.3% 2.6% 18.8% 12.8% - -

Cecil P G 10,000 65.28% 31.1% 0.40% 1.00% 2.26% 0.5%

Clegg Lamptey

JNAet al11

1358 67.3% 21.6% 3.8% 4.9% - 2.4% -

Shah& Shah 591 62% 31% 0.4% 11% 2% - -

Bailey Love - 74% 21% 0.5% 1% 1.5% 2% -

In Present Study 200 55.5% 23.5% 9% - 6.5% 5.0% 0.5%

Table 4: Comparison of length of the vermiform appendix of present study with other studies

Year Author Shortest

Centimeters

Longest

Centimeters

Mean

Length (cm)

Mean External

Diameter (mm)

1891 Ferguson 2.2 - 10.13 8

1895 Berry 3.1 13.3 8.3 -

1913 Deaver 1.0 23 8-9 3-5

1918 Lewis 2.0 20 8.3

1923 Arthur

Robinson18

1.8 23 9.2 6

1927 Royster 2.5 29.4 7.5 -

1932 Donald C.

Collins20

- 24.5 8.2 2

2012 Present

Study

2 9 5.436 7.035



783


Fig 1: Retrocaecal Position of Appendix (1-

appendix, 2-caecum, 3-ileum)

Fig 2: Pelvic position of appendix (1-appendix, 2-

caecum, 3-ileum)

Fig 3: Post-ileal position of appendix (1-appendix,

2-ileum, 3-caecum)

Fig 4: Subcaecal position of appendix (1-caecum,

2-appendix)

Fig 5: Paracaecal position of appendix (1-caecum,

2-appendix)

Fig 6: Subhepatic position of appendix (1-liver, 2-

bile, 3-appendix, 4-caecum )

DISCUSSION

The ultimate position of the appendix is

profoundly influenced by the changes in the

position and shape which the caecum undergoes

during development and growth. The

primordium of cecum and vermiform appendix

i.e. caecal diverticulum appears in the 6th week

as a swelling on the antimesentric border of the

caudal limb of the midgut loop. After the

completion of the gut rotation, the caecal

diverticulum occupies a position on the right side

of the abdominal cavity5.

Table.3 shows the comparison of different

positions of the vermiform appendix of present

study with other studies



784


Retrocaecal and retrocolic positions of the

appendix were by far the commonest6

(58%).

Incidence of postileal position was also fairly

common (10%)6. Probably the common position

of the appendix (retrocaecal) is its resting

position. It might rest in this position if there isno infection in the abdomen. A surgeon or an

anatomist can see the position of the appendix

only during the surgery or dissection. There are

no studies on various positions of the appendix in

the same individual on different

days/weeks/months/years. Studies of the

positions of appendix every month in an

individual using a scanner might confirm the

hypothesis that vermiform appendix keepschanging its position according to the presence of

infection7.

Table.4 shows the comparison of length of the

vermiform appendix of present study with other

studies.

CONCLUSION

Appendix is the only organ in our body which

has not constant anatomical position. Various

positions of vermiform appendix are useful to

understand the location of site of occurrence of

pain during appendicitis. Retrocaecal appendix

has symptoms of upper urinary tract infection,

due to irritation of the adjacent ureter. In pelvic

position pain may be felt when the thigh is flexed

and medially rotated, because the obturator

internus is stretched. Pelvic appendix may irritate

the bladder or rectum causing suprapubic pain,

pain with urination, or feeling the need to

defecate. Postileal position in some males, can

irritate the ureter and cause testicular pain. In

sub-hepatic position, the patient have pain in the

right hypochondriac region. From various

positions of vermiform appendix we can

understand the possible outcome of the

appendicitis specifically location of site of pain.

Appendix is supplied by end artery which is one

of cause of occurrence of appendicitis.Appendicular artery which is branch of inferior

division of iliocolic artery goes through appendix

along mesoappendix.

ACKNOWLEDGEMENTS

We sincerely thankful to our Professor and Head

of the Department of Anatomy, Smt.N.H.L.

Municipal Medical College, B.J.Medical College

and AMC MET Medical College, Ahmedabad,

Professor and Head of the Department of

Forensic Medicine, Smt.N.H.L. Municipal

Medical College who not only acted as guide but

also as a mentor for successfully completing this

research.

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Tumkur Anatomica. A Study of Variations in

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Karnataka. 2011; 5(2):17-23.



785


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13. Baily & Love Practice of Surgery, 24edition,

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14. Ferguson, John. Some Important Points

Regarding the Appendix Vermiformis. Am.

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1913

17. Lewis WH. Anatomy of the Human Body,

Twentieth Edition. Philadelphia: Lea and

Febiger; 1918.

18. Arthur Robinson. Cunningham's Textbook of

Anatomy, Fifth Edition. Edinburgh: WilliamWood and Co; 1923.

19. Royster HA. Appendicitis. New York:

Appleton and Co.; 1927.

20. Donald C. Collins. The Length and position

of the vermiform appendix - A Study of

4,680 Specimens. Ann Surg. 1932; 96(6):

1044 – 48.



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Shaji et al., Int J Med res Health Sci. 2013;2(4): 786-792


&

Health Scienceswww.ijmrhs.com Volume 2 Issue 4 Oct - Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886

Received: 3rd Aug 2013 Revised: 22nd Aug 2013 Accepted: 3rd Sep 2013Research article

A COMPARITIVE STUDY ON CRYO, PULSED ULTRASOUND AND ITS COMBINATION

THERAPIES ON DELAYED ONSET OF MUSCLE SORENESS

*Shaji J. Kachanathu1, Manoj Kumar

2, Pavas Jaiswal

3, Shibili Nuhmani

4, Sajith Vellappally

5

1,5College of Applied Medical Sciences, King Saud University, KSA

2,3Faculty of Applied Medical Sciences, Manav Rachna International University, India

4Department of Physiotherapy, Jamia Hamdard, New Delhi, India

*Corresponding author e-mail: [email protected]

ABSTRACT

Objectives: Individuals engage in strenuous physical activity to which they are unaccustomed usually

land up in a phenomenon called Delayed Onset of Muscle Soreness (DOMS) and results in pain, muscle

stiffness and swelling. The current study was aimed to see the effect of cryo, ultrasound and its

combination therapies on the reduction of symptoms of DOMS. Materials and Methods: A total of 30

subjects with the mean age of 22.1 ± 5.9 years participated in the study. Subjects were randomly

allocated to three groups A, B and C (n=10) and induced DOMS by a standard exercise protocol. Each

group received different treatment application i.e. ultrasound (US), cryotherapy (CT) and combination

(C) of both. Study outcomes were measured by Perceived Muscle Soreness (PMS), Relaxed-Elbow

flexion angle (rEFA), Plasma Creatine Kinase (CK) level at 0 hours (pre-exercise), 24hrs, 48hrs, 72hrs

and at 92hrs. Results: All three groups showed improvement with respect to their interventions, whereas

the C group, after 96 hours of post-exercise the rEFA return to its near normal range as compared to the

other two groups. Although there was a rise in the plasma CK level in all three groups, however the C

group was effective in minimizing the rising level of CK and also in the reduction of muscle soreness at

successive time intervals and reaches to baseline after 96 hours of post-exercise. Conclusion: The

combined application of cryotherapy and pulsed ultrasound immediately after exercise induced muscledamage is a better choice of treatment, It is also observed that cryotherapy was more effective than

pulsed ultrasound alone treatment in reduction of symptoms.

Key words: Muscle soreness, Cryotherapy, Ultrasound, Range of motion, Creatine Kinase

INTRODUCTION

Delayed onset muscle soreness (DOMS) refers to

the skeletal muscle pain that follows novel

eccentric exercise.1,2

The intensity of soreness

increases during the first 24 hrs, peaks at 24 – 48

hrs, and subsides within five to seven days of

postexercise.1

The sore muscles are described as

feeling stiff, tender, and aching especially after

palpitation or movement but these common

DOI: 10.5958/j.2319-5886.2.4.126



787


symptoms rarely require medical attention.1,3

DOMS is typically experienced by all individuals

regardless of fitness level, and is a normal

physiological response to increased exertion, and

the introduction of unfamiliar physical activities.

It can occur any number of times throughoutone’s life

4. Researchers hypothesis that DOMS is

related to muscle structural damage that is

followed by ion imbalance, inflammation, and

pain1,2,3

. Muscle damage includes disrupted

sarcolemma, T-tubules, myofibrils, cytoskeletal

protein, and sarcoplasmic reticulum (SR)3,5,6

.

Immediate soreness may be due to bio-

mechanical end products of metabolism affecting

nerve endings or temporary hypoxia due tomuscle ischemia. Severity of the soreness

depends upon the complexity of the exercise7.

Due to the sensation of pain and discomfort,

DOMS can impair physical fitness and

performance, so prevention and treatment of

DOMS is of great concern to coaches, trainers,

and therapists8.

Some strategies proposed to alleviate DOMS

include pre and post-exercise stretching, light

exercise, ultrasound, topical analgesics, and it is

also common for the clinician to recommend

NSAIDs to decrease the magnitude of these

characteristics. None of these treatments,

however, completely attenuate DOMS7,9,10

.

Studies also reported that sports massage reduces

DOMS and CK when administered 2 hours after

the termination of eccentric exercise11

.

Present clinical practice, cryotherapy and

ultrasound therapy are used as the focal point forthe immediate management of musculoskeletal

injuries. The objectives of the current study were

to track the efficacy of ultrasound, cryotherapy

and its combination on CK levels, PMS, and

rEFA during DOMS.


The current study approved by the Institutional

Ethics Committee, a total thirty healthy subjectsof 15 males and 15 females with a basic

characteristic of 22.1 ± 5.9 years of age, 169.5 ±

10.3 cm of height, and weight of 62.8 ± 19.5 kg.

None of the subjects had performed upper body

weight training within the last 6 months,

experiencing any musculoskeletal injury and

pain, under any medication and phases of themenstrual cycle. The present study was obtained

ethical committee clearance from the parent

organization. Each subject was clearly explained

about the DOMS-inducing exercise protocol and

informed written consent was also collected from

all the subjects prior to the study. Subjects were

randomly allocated into three groups A, B and C

(n=10) with equal gender distribution. Each

group received different treatment application i.eultrasound (US), cryotherapy (CT) and

combination (C) of both with respective to their

group. After completing the pre-exercise

evaluation by the investigator and self arm

stretching by each subject then asked to perform

an exercise of elbow flexors to induce DOMS by

eccentric exercises in non-dominant arm.

Subjects began with a 13.5-kg (30-lb) dumbbell.

Beginning in full elbow flexion, subjects were

instructed to lower the dumbbell to full extension

over 3 seconds. Upon reaching full extension, the

investigator assisted the subjects in returning the

weight to the starting position. Subjects

performed continuous repetitions until they could

no longer control the weight during the 3-second

period. At this point, the weight was reduced by

2.25 kg (5 lb), and the protocol was repeated. As

subjects continued to fatigue, the weight was

sequentially lowered in 2.25-kg (5-lb) incrementsuntil a total weight of 2.25 kg (5 lb) was reached.

At this weight, subjects were asked to perform

repetitions either to fatigue or until 10 repetitions

completed. Treatment was applied (respective to

their groups). On successive 24 hours interval

treatment was repeated. Cryotherapy was given

by ice bag (crushed ice) method. Ice crushed and

filled in the polythene bag. One layer of towel

wrapped around the ice bag to avoid directcontact of skin to the bag. Cryotherapy was



788


applied for 20 minutes continuously. Pulsed

ultrasound treatment with frequency of 1 MHz,

duty cycle of 20%, ratio 1:4, intensity of 0 .8

w/cm2, was given on the muscle belly for 7

minutes. Treatment head of 3cm diameter is used

for the treatment. Ultrasonic gel is used to astransmission medium. In combination therapy,

cryotherapy was given for 10 minutes, and then

pulsed US applied for 4 minutes with five

minutes of interval after cryotherapy. Study

outcomes were measured by Perceived Muscle

Soreness (PMS), Relaxed-Elbow flexion angle

(rEFA), Plasma Creatine Kinase (CK) level at 0

hours (pre-exercise), 24hrs, 48hrs, 72hrs and at

92hrs.

RESULTS

Data analysis of outcome variables was done

with the help of one-way ANOVA, post hoc test,

and Chi-square test for all three groups named as

Group A – U. S, Group B – Cryo, and Group C –

Cryo +US (Table:4 and 5). After 96 hours of

post exercise statistical analysis using one-way

ANOVA indicated significant differences (p=.

001) between all three treatment groups, with

maximum recovery in C Group. Results showed

a rise in the plasma CK level at successive level

in the three different treatment groups, althoughthe minimal rise in the C Group (Table:1;

Figure:1.). After 96 hours of post-exercise

analysis showed significant difference (p=.000)

between the plasma CK levels of three different

groups. PMS value was higher in the Group-A

and this value was peak during the 24-48 hours

of post-exercise, although there was least

increased in the value in the Group-C and it

reached toward near normal level at 96 hours of post exercise in C group (Table:2; Figure:2.).

rEFA value was again higher in the Group-A

and this value was peak during the 24-48 hours

of post-exercise in A group, although there was

least increased in the Group- B and C and it

reached toward near normal level at 96 hours of

post exercise in C group (Table:3; Figure:3.).

Table.1: Plasma CK level (IU/L) in groups at different time interval

Groups 0Hrs. 24 Hrs. 48Hrs. 72Hrs. 96Hrs.G-A 149.0±10.9 880.6±90.7 1520.6±72.0 1784.2±94.8 2010.6±88.7

G-B 150.1±10.5 805.6±96.5 1487.8±76.6 1684.4±88.5 1796.2±90.0

G-C 145.0±15.6 685.8±67.9 1276.4±65.9 1467.0±92.2 1547.0±96.4

Table: 2. PMS (cm) level in groups at different time interval

Groups 0Hrs. 24 Hrs. 48Hrs. 72Hrs. 96Hrs.

G-A 0.0±0.0 3.4±0.52 3.4±0.52 2.6±0.51 1.6±0.69

G-B 0.0±0.0 2.6±0.69 2.3±0.48 1.4±0.48 0.5±0.52

G-C 0.0±0.0 2.5±0.50 2.1±0.31 1.1±0.31 0.3±0.48

Table: 3. rEFA (degrees) in groups at different time interval

Groups 0Hrs. 24 Hrs. 48Hrs. 72Hrs. 96Hrs.

G-A 14.1 ±1.4 20.0±1.9 20.1±2.0 18.4±1.5 16.4±1.5

G-B 14.0±1.6 18.1±1.1 7.6± 0.8 16.2±1.0 15.2±1.2

G-C 13.4±1.5 17.0±1.4 7.6± 0.8 14.8±1.1 13.9±1.1



789


Table: 4. rEFA and Plasma CK level within and between groups

One-way ANOVA

Post 96 hrs.

Sum of

Squares

df Mean

Square

F Sig.

rEFA Between Groups 31.27 2 15.63 9.00 .001

Within Groups 46.90 27 1.74

Total 78.17 29

Between Groups 1076643.20 2 538321.60 51.63 .000

CK Within Groups 281526.00 27 10426.89

Total 1358169.20 29

Table: 5. PMS analysis in groups

Chi-Square Tests Value df Asymp.Sig (2-sided)

Pearson Chi-Square 19.000(a) 4 .001

Likelihood Ratio 23.755 4 .000

Linear-by-Linear Association 14.586 1 .000N of Valid Cases 30

A 9 cells (100.0%)have expected count less than 5. the minimum expected

count is 2.00

Fig:1. Plasma CK level in groups at different Fig:2. PMS level in groups at different time interval

time interval

Fig:3. rEFA in groups at different time interval

0

500

1000

1500

2000

2500

0Hrs. 24 Hrs. 48Hrs. 72Hrs. 96Hrs.

Plasma CK

G-A

G-B

G-C

0

0.5

1

1.5

2

2.5

3

3.5

4

A x i s T

i t l e

Perceived Muscle Soreness

G-A

G-B

G-C

0

5

10

15

20

25

0Hrs. 24 Hrs. 48Hrs. 72Hrs. 96Hrs.

rEFA

G-A

G-B

G-C



790


DISCUSSION

The objectives of the present study was to track

the efficacy of ultrasound, cryotherapy and its

combination on CK levels, PMS, and rEFA

during DOMS. The treatment of cryotherapy andpulsed ultrasound therapy immediately after

exercise induced muscle damage is effective in

reducing stiffness as relaxed arm angle, and

reduction in muscle soreness level, and lower

value of plasma CK activity. In the current study

all three groups’ results showed improvement

with respect to their interventions, whereas the C

group, after 96 hours of exercise the rEFA return

to its near normal range as compared to the other

two groups. Although there was a rise in the

plasma CK level in all three groups, however the

C group was effective in minimizing the rising

level of CK at 96 hours of post-exercise and the

muscle soreness was reduced significantly in

both B and C groups and reached almost to

baseline after 96 hours of post-exercise.

The present study used pulsed US as an

intervention and its positive effects on the results

were supported by the mechanical effects, stablecavitations, and micro streaming are believed to

aid tissue regeneration and healing8. Acoustic

micro streaming and cavitation increase the

diffusion of ions and metabolites across the cell

membranes and enhance the reparative process12

.

Changes in calcium permeability are associated

with enhanced tissue healing12

. Increased sodium

permeability may reduce pain and spasm by

altering neural activity12

. In the current study

these factors might have improved the muscle

soreness.

Until little researches have been performed on

rEFA and its role with pulsed US, Cryo

therapies. Continues US with its thermal effect

was normally used to increase range of

motions13

. In the previous studies also observed

that any reduction of significant evidence of

perceived soreness and relaxed elbow angle

indicates healing and treatment effect. Our

finding also supports with the data from US

alone treatment for an acute inflammation

response is effective for DOMS8. Elbow range of

motion was actually a function of subjectivesoreness in this study. Subjects were asked to

actively extend the elbow to physiological

limitation or to pain tolerance. Because no

subject recovered full extension (relative to

pretest values) by 96 hrs, pain undoubtedly

played a role in rEFA. Joint stiffness and

decreased mobility are common following

muscle injury, and movement may be more

discouraged by the stiffness than by pain, but the

subjects were extending the elbow to the point

that any further extension would be too painful;

thus, rEFA was an indicator of how much pain

subjects were experiencing.

Studies indicated the positive results of

cryotherapy with pulsed ultrasound in the

treatment of acute muscle injuries and pulse

ultrasound therapy helped in regeneration of

muscle fibers, which ultimately reduce the

healing time8,13,14

. In case of muscle sorenesscombined therapy almost improved the muscular

function by means of near normal relaxed arm

angle and with minimal muscle pain. However in

the case of plasma CK level, there was minimal

raised in the value of combined group as

compared to the other two groups, but failed

completely to decrease in the value at successive

time interval.

CK levels depend on age, gender, race, muscle

mass, physical activity and climatic condition15

.

High levels of CK in apparently healthy subjects

may be correlated with physical training status,

as they depend on sarcomic damage; strenuous

exercise that damage skeletal muscle cells results

in increased CK total CK activity is markedly

elevated for 24 hours after the exercise bout16

.

Although previous researches indicated that it

was not a good indicator of DOMS because it

varies with many possibilities and sometimes it



791


did not relate to other symptoms of DOMS.

Pulsed ultrasound therapy helps in the

regeneration of skeletal myofibers after DOMS.

By reducing the symptoms of DOMS this study

indicated that if deep temperature at tissue level

was reduced and pulse ultrasound used withoutheating effect it can facilitate the recovery of

muscle soreness and regeneration of muscle

fibers17

. A study suggested that sports massage

will reduce DOMS and CK when administered 2

hours after the termination of eccentric exercise.

This may be due to a reduced emigration of

neutrophils and/or higher levels of serum

cortisol11,

the micro massage effect of US also

contributed to the positive result.Gulick et al. (1996) was reported that there was

decreased in the muscle soreness level in the

cryotherapy group after treatment and on the next

day and stated that was because of numbing

effect of cold modality depress the excitability of

the free nerve ending and peripheral nerves

which increases the threshold and decreased

pain. This was proved in previous studies as they

measure local pain thresholds after treatment

with ice give varying results, with the effects

lasting from 30 minutes to 12 hours. Cold also

slows the conduction velocity of peripheral

nerves18

.

In our study observed the effect of pulsed

ultrasound therapy and cryotherapy individually

and in its combination form by reducing the

symptoms of DOMS. It is also observed It is also

observed that cryotherapy was more effective

than pulsed ultrasound alone treatment inreduction of symptoms. Studies also proved

immediate application of cryotherapy reduced

the tissue temperature as well as the demand of

oxygen at injured cell. This helps in the

minimizing secondary damage to muscle due to

hypoxia and increased in temperature. And if

there is less damage to muscle and less edema

formation at the cellular level, recovery will be

easy as compared to high temperature at tissuelevel. This effect of cryotherapy was supported

in the past studies as they provide evidence for

secondary injury in tissue due to exercise

induced muscle soreness and effective way of

treatment19,20

.

CONCLUSION

The combined application of cryotherapy and

pulsed US immediately after exercise induced

muscle damage, was effective to reduce the

symptoms of DOMS and it facilitated the tissue

healing. It is also observed that cryotherapy was

more effective than pulsed ultrasound alone

treatment in reduction of symptoms. This showed

through the reduction in the presence of

symptoms and their severity. Only plasma CKlevel showed persistent increased in all groups at

successive intervals. Although that was least

raise in the cryotherapy with a pulse ultrasound

group, but this group also unable to completely

decrease the persistent increase in CK level. It

helps in maintaining the plasma CK level at

minimal value compared to other two groups. So

if cryotherapy with pulse ultrasound used in

appropriate methods it will show positive results

in the reduction of symptoms of DOMS.

REFERENCES

1. Armstrong RB. Mechanisms of exercise-

induced delayed onset muscular soreness: a

brief review. Med Sci Sports

Exerc.1984;16:529-38.

2. MacIntyre DL, Reid WD, McKenzie DC.

Delayed onset muscle soreness: the

inflammatory response to muscle injury and

its clinical implications. Sports

Med.1995;20:24-40.

3. Clarkson PM, Sayers SP. Etiology of

exercise induced muscle damage. Can J Appl

Physiol.1999;24:234-48.

4. Kolt GS. Physicaltherapies in sports and

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5. Child RB, Saxton JM, Donnelly AE.

Comparison of eccentric knee extensors

muscle actions at two muscle lengths on

indices of damage and angle specific force

production in humans. J Sports

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Muscle fatigue and pain after eccentric

contractions at long and short muscle

lengths.Clin Sci.1988;74:553-7.

7. Grossman JM, Arnold BA, Perrin DH,

Kahler DM. Effect of ibuprofen on pain,

decreased range of motion, and decreased

strength associated with delayed onset

muscle soreness of the elbow flexors. Journalof Sport Rehabilitation.1995;4:253-263.

8. Stay JC, Richard MD, Draper DO, EdD,

Schulthies SS, Durrant E. Pulsed Ultrasound

Fails To Diminish Delayed-Onset Muscle

Soreness Symptoms. J Athl Train.

1998;33(4): 341 – 346.

9. Bougie JD. Management of delayed onset

muscle soreness: a review of literature.

Sports Chiropractic and

Rehabilitation.1997;11:1 – 10.

10. Gulick DT, Kimura IF, Sitler M, et al.

Various treatment techniques on signs and

symptoms of delayed onset muscle soreness.

Journal of Athletic Training.1996;31:145-52.

11. Smith LL, Keating MN, Holbert D. The

effects of athletic massage on delayed onset

muscle soreness, creatine kinase, and

neutrophil count: a preliminary report. J

Orthop Sports Phys Ther. 1994;19:93-99.12. Dyson M. Mechanisms involved in

therapeutic ultrasound. Physiotherapy.

1987;73:116-120.

13. Rose S, Draper DO, , Schulthies SS, Durrant

E. The Stretching Window Part Two: Rate of

Thermal Decay in Deep Muscle Following 1-

MHz Ultrasound. J Athl Train. 1996; 31(2):

139-43.

14. Mickey CA, Bemier JN, Perrin DH. Ice and

ice with nonthermal ultrasound effects on

delayed-on set muscle soreness.

JAthlTrain.1996;31(1):19.

15. Brancaccio P, Limongelli F, Maffulli N.

Monitoring of serum enzymes in sport,British journal of sports medicine.

2006;40(2):96-97.

16. Brancaccio P, Limongelli F, Maffulli N.

Creatine kinase monitoring in sports

medicine, British Medical Bulletin. 2007;81-

82:209-230.

17. Stauber WT .Delayed-onset muscle soreness

and muscle pain. In Zachazewski J, Magee D

and Quillen W (Eds): Athletic Injuries andRehabilitation. Sydney: WB Saunders

Company, 1996;pp.92-97.

18. Gulick DT, Kimura IF, Sitler M, Paolone M,

Paolone A, Kelly JD. Various treatment

techniques on signs and symptoms of delayed

onset muscle soreness. J Athletic Training.

1996;31:145-152.

19. Olson JE, Stravino VD: A review of

cryotherapy. Phys Ther. 1972;52:840-853.

20. Oliveira NML, Rainero EP, Salvini TF.

Three intermittent sessions of cryotherapy

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793

Vasudha et al., Int J Med Res Health Sci. 2013;2(4): 793-798


&

Health Sciences


thAug 2013 Revised: 25


thSep 2013

Research article

MORPHOLOGICAL STUDY ON SUPRASCAPULAR NOTCH AND SUPERIOR

TRANSVERSE SCAPULAR LIGAMENTS IN HUMAN SCAPULAE

*Vasudha TK1, Ashwija Shetty

1, Sadashivana Gowd

1, Rajasekhar SSSN

2

1Department of Anatomy, Subbaiah Institute of Medical Sciences & Research Centre, Shimoga,

Karnataka, India2Department of Anatomy, Melmaruvathur Adiparasakthi Institute of Medical Sciences and Research,

TamilNadu, India


ABSTRACT

Background: The scapula is a flat triangular bone situated on the posteroleteral aspect of thoracic wall

between second and seventh rib. The coracoid process of scapula projects upward and, medial to the

base of coracoid process is the Suprascapular Notch (SSN). Morphology of SSN is considered to be a

risk factor for Suprascapular Nerve (SN) entrapment in combination with an anomalous SuperiorTransverse Scapular Ligament (STSL). Aim: To review and document the morphology of suprascapular

notch, degree of ossification of superior transverse scapular ligament and its clinical correlation.

Materials and Methods: The study was carried out by visual observation on 115 dried human scapulae.

Result: It was observed that 115 scapulae showed different shapes with symmetrical ‘U’, the most

common type (34.78%). There was a unique variation in one left scapula, where SSN was replaced by a

narrow groove (0.86%). Conclusion: This study will help to correlate suprascapular nerve entrapment

with a specific type of SSN.

Keywords: Suprascapular notch, Superior transverse scapular ligament, suprascapular nerve

entrapment.

INTRODUCTION

Suprascapular notch is situated at anterolateral

end of the superior border of scapula, separating

the root of coracoid process from superior border

of scapula. The notch is bridged by the STSL,

which is attached laterally to root of coracoid

process and medially to the limit of the notch.

This ligament converting the notch into the

foramen, transmits suprascapular nerve to

supraspinous fossa, whereas the suprascapular

vessels pass backwards above the ligament1.The

morphology of the suprascapular notch is

considered to be a risk factor for suprascapular

nerve entrapment either in combination with an

anomalous STSL or as a narrowed notch2.

Accordingly this notch is an important landmark

of the suprascapular nerve during arthroscopic

DOI: 10.5958/j.2319-5886.2.4.127



794


shoulder operation3. Previously SSN has been

classified by many researchers based on complex

geometrical calculations. Studies reveals, 6

different types of anatomical variations of the

suprascapular notch, including complete absence

of notch have been reported in Nigerianpopulation

4,5. Koepell and Thompson (1959)

were the first to describe the SN entrapment

syndrome6

.They reported that abduction or

horizontal adduction of the shoulder exerted

traction on the SN, which led to its compression

against the STSL. The anatomical variation of

the SSN includes the variation in shape,

complete or partial ossification of STSL.

Rengachary et al observed 6 basic types of SSNin 2011 scapulae

7. The purpose of this study was

to document the incidence, morphology and

clinical significance of SSN and the existence of

ossified STSL.


The study was conducted on 115 dried human

scapulae (54 right and 61 left) obtained from

bone library, Department of Anatomy, Subbaiah

Institute of Medical Sciences and Research

Centre, after obtaining clearance from the

Institutional Ethics Committee. This is an

observational study, conducted from January

2012 to February 2013. Scapulae were analyzed

for morphology of SSN and degree of

ossification of STSL, irrespective of age, sex andrace. Scapulae with damaged SSN were excluded

from the study. The results were documented by

photographs.

RESULTS

In the present study different shapes of SSN and

degree of ossification of STSL were documented

in Table 1 and Table 2. Table 1 shows different

types of SSN. Among different typessymmetrical ‘U’ shape is most common followed

by ‘J’ shaped notch. In one of 115 dry human

scapulae, SSN was replaced by a narrow groove,

which extended from lateral end of superior

border to the spinoglenoidal notch. Table 2

shows different degrees of ossification of STSL,

which includes both complete and partial

ossification. In one left scapulae out of 115, there

was notch with foramen.

Table.1: Different types Suprascapular Notch

Shape of SSN No. of Scapulae

[Right & Left]

Percentage (%)

Symmetrical U shaped 39 [22 & 07] 34.78

Shallow U 07 [03 & 04] 6.08

J shape 22 [10 & 12] 19.13

Wide notch 08 [04 & 04] 6.95

Indented 09 [04 & 05] 7.82Hockey stick 06 [04 & 02] 5.21

Deep U 07 [04 & 03] 6.08

Absence 07 [05 & 02] 6.08

Groove 01 [00 & 01] 0.88

Table.2: Types of different degrees of ossification

Degree of Ossification No. of Scapulae

[Right & left]

Percentage (%)

Complete 05 [ 02 & 03 ] 4.34

Partial 02 [ 01 & 01 ] 1.73

Notch with foramen 01 [ 00 & 01 ] 0.86



Vasudha et al.,

Table.3: Comparison of different

present study.

Shapes of

SSN

Previous studies

Sinkeet et al

2010

Symmetrical 29

Shallow U 21

J shape -

Wide notch -

Indented -

Hockey stick 22

Deep U -

Absence 2.12

Groove -V shape 5.18

SSN: Suprascapular Notch, STS:

Fig 1: Different Shapes of SSN.

c) One edge of SSN was longer,

SSN was absent, g) slight notch

the width.

Int J Med Res Health Sci.

shapes of SSN and degree of ossification of S

(%)

Polguj et al

2010

Iqbal et al

2010/11

Soni et

20122.3 14/13.2 58

- - -

- 00/22 27

57.7 - -

- 00/27.5 03

- - -

24.4 - -

- 10/23 02

- - - - 68/20 07

Superior Transverse Scapular Ligament.

a) Width and breadth of SSN equal, b) Wi

d) Width is more wider, e) Almost like a

as present, h) a groove replacing SSN,

795

2013;2(4): 793-798

S of previous studies with

Present study

(%)

al

34.78

6.08

19.13

6.95

7.82

5.21

6.08

6.08

0.88 -

th is greater than breadth,

shape of hockey stick, f)

i) breadth is greater than



Vasudha et al.,

a) Complete

Fig 2: Different degrees of ossifi

STSL c) Ossified band of STSL d

DISCUSSION

Study on morphology of SSN

ossification of STSL, is d

researchers. Joe De Beer, in his sthe shape of the notch and calc

been shown to be associated wit

of SN entrapment, resulting in

wasting of supraspinatus an

muscles8. Dunkelgrun et al stated

notches had a larger area than

notches, leading to the assump

shaped notch is more likely to be

nerve entrapment9.

A study by Sinkeet et al (20

population)10

classified 6 types

description, which also includes

ossification. According to their

represent wide ‘U’, Type II repr

Type III, which has explained ha

represents symmetrical, Type IV

shape, Type V&VI are related t

ossification of STSL, to the prese

Polguj et al (2010)11

found that,scapulae the maximal depth(M

more than superior transv

(STD),which represents deep

study. Two scapulae (2.3%) had

STD, represents symmetrical of

(57.7%) scapulae the STD was l

represents wide ‘U’ of present.

In a study by Iqbal et al12, 13

2011

population, in their two differentthat 4 types of notches, with 10

(type 1), 14% symmetrical ( ty

Int J Med Res Health Sci.

b) Partial c)

ation of STSL a) STSL was completely calc

ividing the SSN into foramen below and not

and degree of

ne by many

tudy stated that, ified STSL has

h increased risk

weakness and

infraspinatus

that ‘U’ shaped

the ‘V’ shaped

ion that a ‘V’

connected with

10, in Kenyan

of SSN with

degree of STSL

study Type I

sents ‘J’ shape,

most common,

represents ‘V’

o the degree of

nt study.

in 21 (24.4%) D) of notch is

erse diameter

‘U’ of present

equal MD and

present, in 47

onger than MD,

-12 in Pakistani

studies showed without notch

e 2), 68% ‘V’

shape ( type 3) and 8

which is having a g

length as compared toet al (2012) reported

common ty pe, with ‘V’

Regarding degree o

ossification of STSL

7%, and 3% by Silva

201010

, polguj et al 2

201214

, respectively.

reported by Sinkeet et

11%.

Notch with foramen is

as bony bridge, which

divide it into a bony

notch superiorly16

.

variation in 2 scapul

(0.98%).

In the present study w

shapes of notch depen

also different degrees

illustrated in Table 1awith previous studies

shapes are thought

predisposition for SN

a small notch gives

impingement than a lar

Our study also showe

in one left scapulae

extending from lateral

its spinoglenoidal notcAssuming this groov

ligament, converting

796

2013;2(4): 793-798

Notch with foramen

ified, b) partially calcified

h above

% inverted ‘V’ ( type 4)

reater inferior maximum

superior length. Soni Garg that, symmetrical is most

shape least common14

.

f ossification, complete

as reported, 30.76%, 3%,

et al 200715

, Sinkeet et al

1011

, and Soni Garg et al

artially ossified STSL is

al 18% and G. Soni et al

described by Natsis et al

limit the area of SSN and

foramen inferiorly and a

e found such type of

ae out of 204 scapulae

e have explained different

ing on size and shape and

of ossification which are

d Table 2, and compared in Table 3. These various

to play a part in the

ntrapment, assuming that

larger chance of nerve

ge notch.

a unique variation found

that, presence of groove

end of superior border to

h, where SSN was absent. e in living bridged by

groove into osseofibrous



797


tunnel which may cause increased risk of SN

entrapment.

CONCLUSION

The shape of SSN and ossified STSL has been

shown to be associated with increased risk of SN

entrapment, resulting in weakness and wasting of

supraspinatous and infraspinatous muscles. A

reduction in the height of the SSN substantially

narrows the suprascapular foramen, should be

considered as a possible etiologic factor in SN

entrapment. Anatomical knowledge of such

variations should be kept in mind by a

radiologist, Orthopaedicians and neurosurgeons

as these variations may alter the technique of surgery.

ACKNOWLEDGEMENT

We sincerely thank the management and staff of

the Dept. of Anatomy of Subbaiah Institute of

Medical Sciences and Research Centre, Shimoga,

Karnataka in India.

Declarations: Funding: None

Competing interests: None declared

REFERENCES

1. Standring S, Gray’s, The Anatomical Basis

of Clinical Practice 40th edition.2008, 794-

95.

2. Bayramoglu A, Demiryurek D, Tuccar E,

Erbil M, Aldur MM, Testik O, Doral MN.

Variations in anatomy at the suprascapular

notch possibly causing suprascapular nerveentrapment: an anatomical study. Knee Surg

Sports Traumatol Arthroscopy, 2003; 11:393-

98.

3. Bigliani LU, Dalsey RM, McCann PD, April

EW. An anatomical study of the

suprascapular nerve. Arthroscopy. 1990;

6:301-05.

4. Natsis K, Totlis T, Tsikaras P, Appell H G

Skandalakis P, Koebke J. Proposal for

classification of SSN: a study on 423 dried

scapulae. Clin Anat 2007; 20:135-39.

5. Ofusori DA, Ude RA, Okwuonu Cu,

Adesanya OA. Complete absence of SSN in a

Nigerian scapule: a possible cause of

suprascapular nerve entrapment. Int. J

Shoulder Surg. 2008; 2:85-86.

6. Kopell HP, Thompson WA. Pain and frozenshoulder. Surg Gynecol Obstet 1959; 109:92-

96.

7. Rengachary SS, Neff JP, Singer PA, Brackett

CF. Suprascapular nerve entrapment

neuropathy: A clinical, anatomical and

comparative study. Part 1: Clinical study.

Neurosurg. 1979; 5:441-46.

8. Joe De Beer and associates. Current trends in

management of suprascapular nerveentrapment Cape Shoulder Institute, South

Africa.

9. Dunkelgrun M, Lesaka K, Park SS, Kummer

FJ, Zuckker-man JD. Interobserver reliability

and intraobserver reproducibility in

suprascapular notch typing. Bull Hosp Joint

Dis.2003; 61: 118-22.

10. Sinkeet SR. The suprascapular notch: its

morphology and distance from the glenoid

cavity in a Kenyan population; Folia

Morphol, 2010; 69:241-45.

11. Polguj M. Correlation between Morphometro

of the SSN and anthropometric

measurements of the scapula. Folia Morphol,

2011; 70,109-15.

12. Khadija Iqbal and Rameez Iqbal.

Classification of Suprascapular Notch

According to Anatomical Measurements in

Human Scapulae; J of the college of physicians and surgeons Pakistan 2011, 21

(3): 169-70.

13. Iqbal K, Iqbal R, Khan SG. Anatomical

variations in shape of suprascapular notch of

scapula; J Morphol.Sci. 2010,27(1): 1-2.

14. Soni G, Malik VS, Shukla L, Chabbra S,

Gaur N. Morphometric Analysis of the

Suprascapular Notch. The Internet Journal of

Biological Anthropology. 2012; 5(1): DOI:10.5580/2b19 -



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15. Silva JG. High Incidence of Complete

Ossification of the Superior Transverse

Scapular Ligament in Brazilians and its

Clinical Implications. Int. J. Morphol., 2007;

25(4):855-59.

16. Natsis K. A bony bridge within thesuprascapular notch. Anatomic study and

clinical relevance – Case report. Aristotle

University Medical Journal, 2008; 35(1):29-

33.



799

Iqbal et al., Int J Med Res Health Sci. 2013;2(4): 799-808


&

Health Sciences




thSep 2013

Research article

VERTEBROBASILAR VARIANTS AND THEIR BASIC CLINICAL IMPLICATIONS

*Iqbal S.

Professor, Department of Anatomy, Amala Institute of Medical Sciences, Amala Nagar, Thrissur,

Kerala, India.


ABSTRACT

Objectives: Cerebrovascular diseases are the leading illness affecting the modern world with a high

mortality rate. The posterior circulation of the brain consists of vertebrobasilar system, shows a high

incidence of anomalies in the form of hypoplasia, fenestrations and asymmetry of the vessels, which

precipitate the development of vertebrobasilar insufficiency and posterior circulation stroke. A detailed

knowledge of the vertebrobasilar variants is essential in the diagnosis, treatment as well as in educating

the patients suffered from posterior circulation stroke. The present study is aimed to analyze the size,

asymmetry and anomalies of the vertebrobasilar system and their implications in posterior circulation

infarcts. Materials and methods: Fifty adult brains were studied during routine dissection of the

cadavers. The base of the brain with intact vertebral, basilar and posterior cerebral arteries were

dissected, preserved in 10% formalin and analyzed for the variations in the size, length and asymmetry

in the configuration. The dimensions of the vessels were measured using graduated calipers. Results:

Anomalies of the basilar artery were found in 14% of the brains, in the form of hypoplasia, fenestration

and terminal expansion at its bifurcation. The vertebral arteries showed asymmetry with right vertebral

were hypoplastic in majority of the brains. Conclusions: The variations of the vertebrobasilar system

increase the risk of vertebrobasilar insufficiency and posterior circulation stroke. Anomalies of the

vertebrobasilar arteries were also found to be associated with aneurysms. The right vertebral artery hasbeen frequently hypoplastic and there was no consistent correlation between the left vertebral

dominance and right handedness of the person. Hypoplastic vessels were frequently associated with

vertebrobasilar territory ischemic stroke.

Keywords: Hypoplasia, Fenestration, Dolichoectasia, Asymmetry, Dimensions, Infarction.

INTRODUCTION

Cerebrovascular disorders are one of the leading

ailments affecting the modern mankind with high

incidence of mortality rate; with high levels of

disabilities among those who survive

cerebrovascular accidents1. Vertebrobasilar

system constitutes the posterior circulation of the

brain, supplies brainstem, cerebellum and

occipital lobes of the cerebrum, shows a high

incidence of anomalies. Anomalies of the

vertebrobasilar system may precipitate the

DOI:10.5958/j.2319-5886.2.4.128



800


development of cerebrovascular diseases viz.,

stroke and aneurysms. Variations in the form of

hypoplasia and duplications are often prevalent.

Asymmetry of vertebral arteries is quite

common, but the amount of blood reaches the

basilar artery remains constant due to the contralateral large vertebral artery

2. Vertebral artery

hypoplasia or asymmetry is frequently associated

with posterior circulation stroke (PCS)3, 4

. The

basic knowledge of vertebrobasilar variants is

essential in diagnosis, treatment as well as in

educating and training the patients suffered from

posterior circulation stroke. In the cases of

occlusion of an internal carotid artery, the

principal source of blood supply is through thevertebrobasilar system, but the size and patency

of these arteries are quite variable. The vertebral

asymmetry can cause insufficiency in the

posterior circulation, which results in

vertebrobasilar ischemia. Asymmetrical vertebral

arteries are also considered to be one of the risk

factors for pontine infarction. Various types of

anomalies exist in different populations, but the

anomalies of the vertebrobasilar complex in

Indian population have been reported only by

few authors previously, based on cadaveric

analysis. So the objective of the present study is

to analyze the size, asymmetry and anomalies of

the vertebrobasilar system and their implications

in posterior circulation infarcts. The surgical

importance lies in its application during the

exposure of the vertebrobasilar territory and a

thorough knowledge of the vascular variants will

increase the success of the procedure. Theinference obtained from this work is also useful

for the sonologists in improving their diagnostic

skills and for anatomists in enhancing their

knowledge in teaching.


Fifty adult brains were studied from the regular

dissection hall cadavers over a period of Jan

2008-2013. The cadavers were obtained byfollowing the procedures in accordance with the

ethical standards of experimentation. The bases

of the brain including the brain stem with intact

vertebral, basilar and posterior cerebral arteries

were fixed in 10% formalin for 10 days. The

intra cerebral portion of the vertebral, basilar and

the proximal posterior cerebral arteries were

dissected carefully under water, dried andpainted with fevicryl red colour. The sub-

arachnoid portions of the vertebral and basilar

arteries were then analyzed for the variations in

the size, length and any asymmetry in the

configuration. The dimensions of the component

vessels were measured using graduated calipers

(sensitivity: 0.1 mm). We focused on the basilar

artery and the upper segment of the vertebral

artery. The results obtained were recorded andtabulated.

OBSERVATIONS

Basilar artery: The basilar artery was normal in

43 circles (86%). Anomalies were found in 7

cases (14%). Progressive narrowing of the basilar

artery was seen in two circles (4%) [Fig-1.A]. A

cobra-hood like terminal expansion at its

bifurcation was found in 4 circles (8%) [Fig-

1.B]. Partial duplication of the basilar artery in

the form of fenestration, in its proximal part was

found in one circle (2%) [Fig-1.C]. In this circle

the proximal segment of the basilar artery

duplicated immediately into two unequal

divisions. The larger division (thickness 2.8 mm)

occupied the basilar sulcus, while the smaller one

(thickness 1.6mm) deviated slightly to the right

and ran forwards for a short distance, and then

joined the main division 6mm away from itsorigin. The rest of the basilar artery showed

progressive narrowing. The vertebral arteries in

this case were unequal in size. The origin of

basilar artery was at the ponto-medullary

junction in 35 circles (70%). In 13 circles it was

1 cm below ponto-medullary junction (upper

medulla) and in 2 circles it was 1cm above the

ponto-medullary junction. The basilar artery

terminated opposite to the ponto-mesencephalic junction in 32 circles (64%). It bifurcated at the

upper pons in 16 circles and in 2 circles at the



Iqbal et al.,

level of mammillary bodies.

diameter of the basilar artery was

1

Vertebral artery: Bilateral

vertebral arteries were encounter

in this series (56%). Asymmetry22 circles (44%). The left vessel

Table: 1. Average dimension of ve

Name of the ves

Basilar artery

Vertebral artery

Table: 2. Average dimensions of b

Name of the

author

Length of t

Range

(mm)

Pai et al22

24 - 35

Idowu et al19

20 - 40

Present study 18 - 37

Fig.1: A-Progressive narrowing

the basilar artery at its bifurcat

proximal portion, D-Hypoplastic

Int J Med Res Health Sc

he length and

given in Table-

symmetrical

ed in 28 circles

was observed in was larger than

the right in 14 circles a

left in 8 circles. Hyp

were seen in 5 brains

artery was hypoplastic

and the right one was

[Fig-1.E]. The averageartery was given in Ta

tebral and basilar arteries

selLength (mm) Diameter (

Range Average Range

18-37 30 2.8-5.1 3

- - 1.6-3.9 2

silar and vertebral arteries as reported in lite

e basilar artery Diameter of basilar artery

Average

(mm)

Range

(mm)

Average

(mm)

24.9 3 - 7 4.3

31.42 2.5 - 5.5 3.82

30 2.8 - 5.1 3.9

f (hypoplastic) basilar artery, B-Cobra-hood

ion, C-Partial duplication (Fenestration) o

left vertebral artery & E-Hypoplastic right v

801

i. 2013;2(4): 799-808

nd the right larger than the

oplastic vertebral arteries

(10%). The left vertebral

in 2 brains (4%) [Fig-1.D]

narrow in 3 brains (6%)

diameter of the vertebral le-1.

m)

verage

.9

.1

rature

Diameter of vertebral

artery

Range

(mm)

Average

(mm)

3.4 (L) &

2.9 (R)3.15

- 2.98

1.6 - 3.9 2.1

like terminal expansion of

f the basilar artery at its

rtebral artery.



802


DISCUSSION

In the present study 86% of the brains displayed

a normal basilar artery with a uniform diameter

throughout its length. Anomalies of the basilar

artery were rare and include duplication orfenestration, rarely hypoplasia, segmental aplasia

and plexiform channels5.

An unusual anomaly in

the form of a fenestration in the proximal part of

basilar artery was noted in 2% of the brains. The

proximal portion of the vessel was divided into

two unequal divisions. The larger division

(2.8mm) lies in the basilar sulcus and the narrow

smaller division (1.6mm) deviates slightly to

right and then fuses with main division with a

fenestration window of about 6mm. There was

no associated aneurismal dilatation in these

cases. The occurrence of this anomaly can be

explained on the basis of embryological

development. During the development of the

intracranial arteries, two bilateral, longitudinal

vascular channels differentiate along the ventral

surface of the hind brain from a plexus fed by

intersegmental and transitory pre-segmental

branches of the dorsal aorta and its forwardcontinuation. These longitudinal channels are

later connected cranially with the terminal

branches of the internal carotid arteries and

caudally with the vertebral arteries through the

first cervical intersegmental arteries. Fusion of

these two longitudinal channels results in the

formation of the basilar artery. The incomplete

fusion of two longitudinal vascular channels in

its proximal portion may result in the formation

of this anomaly. This type of anomaly seemed to

be reported rarely in the literature reviewed.

Dodevski et al6

reported two cases of

fenestrations of the basilar artery out of the 50

patients analyzed under computed tomography

angiography (CTA), an incidence of 4%. The

fenestration windows in these cases were 3.68

mm and 8 mm. There were no associated

aneurysms in these cases. Sanders et al7

in their

retrospective review of 5190 cerebral

angiograms, reported 37 patients with 38

fenestrated arteries viz., 16 basilar, 10 vertebral,

9 middle cerebral and 3 anterior cerebral arteries.

The angiographic incidence of basilar artery

fenestration was 0.3%. In 5 cases the fenestration

was at the proximal basilar artery, in 7 cases in

the mid basilar artery and in 4 cases in the distal

part of the basilar artery.Fenestration is the partial/complete duplication

of a part of a vessel with or without a common

adventitial layer. It appears in different forms,

with a small mass of vascular tissue separating

the two lumens to the actual duplication of a part

of the affected vessel7. Fenestration of the basilar

artery was most frequent, followed by vertebral

and middle cerebral artery duplications8. The

reported incidence of basilar artery fenestrationsrange from 0.02% to 0.6% in angiographic

series, 2.0% on magnetic resonance angiography

and from 1.3% up to 6.0% in autopsy studies.

The reason for the wide range in the incidences

can be explained by the fact that in some cases

the duplication is not complete and in others it is

not angiographically evident. The commonest

site of basilar fenestration was in its proximal

part close to the junction of the vertebral arteries.

Basilar fenestration was commonly found

associated with aneurysms. There were local

defects in the medial walls of the duplicated

segment at proximal end of the fenestration. The

tunica media was deficient with discontinuity of

the elastic fibers. These structural changes in the

proximal end of the fenestration are similar to

those seen in arterial bifurcations and were

consistent with the causes of intracranial

aneurysms6

.Sanders et al

7found a 7% incidence of aneurysm

in basilar fenestration. In all intracranial

fenestrations, the overall incidence of aneurysms

at the fenestration site was 3%. A majority of

aneurysms arises at the proximal junction of the

fenestration. So in patients with vertebrobasilar

aneurysms, the associated fenestrations should

always be looked for. The basilar artery

fenestrations may sometimes misinterpreted fordissecting aneurysms or thrombosis in patients

with stroke leading to incorrect diagnosis and

mismanagement8. Vertebrobasilar artery



803


fenestrations may also found to be associated

with brain stem ischemia or infarctions.

Collateral branches may arise from the limbs of

the fenestrated vessels. These findings should be

analyzed in detail and the fenestrations should be

differentiated from aneurysm before surgery inorder to prevent inadvertent clipping of a limb of

the fenestration including these branches6.

The cause of the basilar hypoplasia is still not

known as other arterial abnormalities.

Embryologically, the posterior circulation begins

as two paired plexiform longitudinal neural

arteries and they start to fuse to form the basilar

artery at 5 weeks of gestation, while the

trigeminal artery begins to involute

9.

The size of an artery depends on the area that ultimately

irrigates and an artery becomes unnecessary

during development if the area undergoes

regression. Therefore basilar artery hypoplasia is

believed to be the consequence of the persistent

primitive trigeminal artery (PPTA)10

. It has also

been suggested that large posterior

communicating artery, which was commonly

seen in these cases, may show the persistent flow

from carotid to vertebrobasilar circulation and

this may cause vertebrobasilar hypoplasia. In

addition, malformations, injuries that effect

acting either in the perinatal period (such as basal

meningitis, arteritis and arterial occlusion) or in

the early childhood trauma, may impede the

normal reproduction of the smooth muscle cells

in the media from maintaining the capacity of the

artery to grow with the brain, have been

suggested in development of hypoplasticarteries

11. When associated with persistent

primitive trigeminal artery, basilar artery

hypoplasia occurs commonly at proximal part of

the vessel and usually associated with vertebral

artery hypoplasia12.

Previous studies of stroke in young adults have

not so far included hypoplastic cerebral vessels

among the potential causes of cerebral ischemia.

Chaturvedi et al

13

had suggested that hypoplasticbasilar artery might be a predisposing factor for

ischemic stroke and the mean age of all cases

was 49.8 out of 4000 cases he has examined.

Szdzuy and Lehmann14

described angiographic

findings of incomplete fusion of the distal part of

the basilar artery associated with vertebral artery

hypoplasia in two cases presented with

symptoms of brain stem ischemia and termed this

condition as distal hypoplasia. It was speculatedthat poor retrograde flow due to hypoplastic

distal basilar artery might make easy occurrence

of infarction. Demonstration of these hypoplastic

narrowing is also of importance since

atherosclerotic disease may also appear at an

earlier age if the native vessel is hypoplastic and

would become stenosed sooner than a large

vessel15.

Moreover, embolic occlusions tend to

involve the distal basilar segment and usuallyresult in fatal consequences. It has been recently

concluded that magnetic resonance angiography

(MRA) can demonstrate entire/partial hypoplasia

of the basilar system. Moreover, the

demonstration of these hypoplastic vessels may

be clinically important, since it has been

suggested that hypoplastic vertebrobasilar

vessels should be considered among the potential

causes of cerebral ischemia in young adults13.

In

reviewing the literature, symptomatic entire

basilar artery hypoplasia has been described only

in 13 cases by three previous reports11, 13, 14.

Hypoplastic basilar arteries were encountered in

4% of circles in this series. We conclude that

hypoplastic basilar arteries as a predisposing

factor should always be investigated in posterior

circulation stroke patients, and MRA as a non-

invasive tool, should be considered in diagnosis

of these basilar abnormalities.Dolichoectasia is the dilated, elongated and

tortuous vessels affecting vertebrobasilar

systems. It is also known by other names such as

megadolichoectasia, fusiform aneurysms or

tortuous vertebrobasilar system. It may compress

the cranial nerves, causes ischemia, subarachnoid

hemorrhage (SAH) and sometimes obstructive

hydrocephalus. On reviewing literature, the

incidence of VBD was to be 4.4%, and it usuallyaffects women. The basilar trunk was commonly

involved (40%), followed by vertebral arteries.

VBD is caused by either a congenital



804


vasculopathy of the tunica intima or hypertensive

stress on the vessel wall deranging the collagen

and elastin meshwork of the media and

downgrades the vessel. Neurological symptoms

manifest in 10% of the patients, in the form of

ischemic stroke, temporary/permanent motordeficits, hydrocephalus, cerebellar dysfunction

and brain stem compression, which may be mild

to severe. The most frequent clinical picture is

due to cranial nerve compression or brain stem

ischemia or intracranial bleeding16,17

. Tomoyuki

Nishizaki et al18

reviewed 23 patients with VBD

and found seven cases (30%) of intracranial

aneurysms. It was in the form of fusiform as well

as multiple and giant aneurysms. Rupture of thedolichoectatic basilar artery is considered

unlikely and rarely presented with cerebellar

hemorrhage. In our studies we have found a

cobra-hood like terminal expansion of the basilar

artery at its bifurcation in 8% of the circles.

Idowu et al19

also observed that the diameter of

the basilar artery was relatively constant

throughout its course except for the widening at

its terminal bifurcation. These terminal

widenings/expansions were probably in the form

of minor variants of the above mentioned

dolichoectasia. And we are not sure about the

antemortem history of these patients with regard

to hypertension or any other congenital

malformations of the vasculature to explain the

above anomalies, since our specimens were

randomly collected from the dissection hall

cadavers.

The basilar artery terminates at the ponto-mesencephalic junction in 64% of the cases. In

32% of the brains the vessel bifurcated at the

upper pons and in the remaining 4% of the cases,

opposite to the mammillary bodies. Stopford20

found that the basilar artery had bifurcated at the

upper border of pons in 97.5% of the specimens

and below this level, ie, at the upper pons in the

remaining 2.5% of the cases. Sacki and Rhoton21

have reported that the vessels had bifurcatedopposite to the interpeduncular fossa in 88% of

the specimens, at the upper pons in 10% of the

brains and in the remaining 2% of the cases, the

bifurcation has indented the mammillary bodies.

Idowu et al19

stated that the basilar artery extends

from the lower to the upper border of the cisterna

pontis in 98% of the brains; and early bifurcation

at the mid pontine region in 2% of the cases. It

terminates at the ponto-mesencephalic junctionby running a straight course in 60% of the cases,

convex to the right in 18% and convex to the left

in 18% of the cases and forming a loop in 4% of

the cases. The dimensions of the basilar artery

were compared with that of other workers in

Table-2. Our measurements were more or less

coincides with that of other workers.

Asymmetrical vertebral arteries were commonly

encountered and were found in 44% of the brainsin this series. The left vertebral artery was larger

in diameter than the right in 28% of the cases and

the right vessel was larger in 16% of the brains.

Cloud and Markus23

concluded that the left VA

was dominant in approximately 50%; the right in

25% and only in the remaining quarter of cases

was the two vertebral arteries of similar caliber.

Seydel24

found that the vertebral arteries were

asymmetrical in 39.79% of the specimens and

further reported that the left vessels was larger

than the right in 26.53% and the right vessels

was larger in 13.26% of the cases. Stopford20

gave the ratio of left to right vertebral arteries

was 51:41 for diameter predominance and stated

that it was equal on both sides in only 8% of the

cases, out of the total 150 specimens they have

examined. Gillilan25

also stated without giving

any figures, that the cranial vertebral arteries

were frequently unequal in size, the right beingmore often smaller. Kirgis et al

26have reported a

case of congenitally small vertebral artery and a

relatively large contra lateral vertebral artery and

further added that the discrepancy in the caliber

of the vertebral arteries was not uncommon and

there was no consistent correlation between the

asymmetry of these arteries and the asymmetry

of the circle of Willis. So from the present

observation as well as from the findings of others, it is inferred that the cranial vertebral

arteries are usually unequal in size, the left vessel

is generally larger than the right. There was no



805


clear cut reason for the existence of this

asymmetry. But the development of this

asymmetry was related to vascular requirements

of the brain. Numerous authors had investigated

the correlation between the dominance of the left

vertebral artery and right handedness and viceversa. But there is no definite evidence to

correlate the vertebral dominance and

handedness. So based on the findings of the

present study and also from others’ observations,

it is inferred that there seems to be a possibility

of a greater flow on the left side in the cranial

vertebral arteries and there is no consistent

relation between the asymmetry of these arteries

and the asymmetry of the circle of Willis.Hypoplasia of vertebral artery (HVA) is not rare

in normal population, but is more frequent in

patients with posterior circulation stroke (PCS).

Congenital variations in the size of the vertebral

arteries were frequently encountered ranging

from asymmetry to severe hypoplasia of one

vertebral artery. In reviewing the literature most

of the workers agreed, that the external diameter

of 2mm or less was considered to be

hypoplastic15. Other workers with the help of the

colour duplex ultrasonography defined the HVA

with flow volume less than 30-40 ml/min in the

vertebral artery. The absence of uniform

description of HVA is due to the lack of studies

on the healthy individuals, smaller size of sample

groups and inadequate sonographic findings to

support HVAs. In the more recent observations

using colour coded ultrasonographic studies, a

diameter of less than 2.2mm was consideredhypoplastic, which was mainly based on

hemodynamic changes and supported by

ipsilateral flow resistance, contralateral diameter

and flow volume27.

In our study we fixed that the

external diameter of less than 2mm was

considered hypoplastic. On reviewing the

literature, we found that about 1.9% to 35.2% of

the brains have unilateral HVA and makes little

contribution to basilar artery flow. It is alsoworthwhile to mention that in all the above

works the right vertebral artery was more

hypoplastic than the left vessel. Hypoplastic

vertebral artery was found in 10% of the total 50

brains analyzed in our study. Hypoplasia was

commonly observed on the right side (6%),

which was consistent with findings of other

workers.

Chaturvedi et al13 suggested that a hypoplasticvertebrobasilar system was considered to be a

predisposing factor in the posterior circulation

ischemia. Ipsilateral hypoplasia of vertebral

artery was more frequent in patients with lateral

medullary syndrome and concluded that HVA

conferred an increased probability of ischemic

stroke3.

In the studies conducted by other

workers, HVA was significantly more frequent in

posterior territory ischemic stroke compared withhealthy subjects or patients with anterior

circulation stroke3, 4, 28

. Chuang et al28

examined

191 acute ischemic stroke patients in the age

group 55.8 ± 14.0 years, with the help of the

magnetic resonance angiogram (MRA) and

duplex ultrasonography and confirmed the

overall increase in the incidence of a unilateral

congenital HVA in the cases of brainstem /

cerebellar infarction. They also postulate that

hypoplastic VA might cause a decrease in the net

flow volume which conditions the development

of ischemic stroke in posterior cerebral

circulation. In addition, HVA with additional risk

factors such as hypertension, hyperlipidemia,

diabetes and smoking was also reported to

contribute to ischemic brainstem stroke, even in

young patients29.

Watanabe et al30

correlated asymmetry of

vertebral artery and pontine infarction inJapanese population and concluded that patients

with small diametric VA of the right side

significantly had infarctions in the same side of

the pons and suggest that VA asymmetry is

considered to be one of the risk factors of pontine

infarction and that MRA can be useful in the

examination of the cerebral artery as a valuable

and non-invasive screening method. The average

diameters of the vertebral artery were comparedwith the values of other authors in Table 2.

The end results of the anomalies of the

vertebrobasilar system in this study was not a



806


true reflection of the general population in the

frequency of the vertebrobasilar anomalies,

because our data were limited to only 50 adult

cadaveric brains without any neurological

diseases. In addition our sample group was so

small and Indian origin, it may also limitgeneralizations of these anomalies based on our

study results. The inference of this study will

inform neurosurgeons, sonologists and patients

about the potentially vulnerable vertebrobasilar

circulation and further autopsy, angiographic,

and magnetic resonance imaging analysis were

needed to augment these clinical implications.

CONCLUSION

Cerebrovascular diseases are one of the leading

problems in modern medicine with high

incidence of mortality rate. The vertebrobasilar

system which supplies one fourth of the brain

shows a high incidence of variations in the form

of hypoplasia, fenestrations and asymmetrical

configuration. These variations increase the risk

of vertebrobasilar ischemia and posterior

circulation stroke. Our study was conducted to

analyze the size, asymmetry and anomalies of the

vertebrobasilar system, using fifty adult

cadaveric brains. The common variations

encountered were hypoplasia of vertebrobasilar

arteries, fenestrations of basilar artery and

asymmetrical vertebral arteries. The role of these

anomalies was discussed in causing the posterior

circulation stroke. The left vertebral artery was

significantly larger in diameter than the right and

there seems to be more blood flow on the left

side than on the right half of the brain and there

was no consistent correlation between the

vertebral dominance and handedness.

Hypoplastic vertebral artery was frequently

common in the normal population and there was

a high incidence of its association with

vertebrobasilar territory ischemic stroke.

ACKNOWLEDGEMENTS

We acknowledge Prof. Mini Kariappa, Professor

and HOD of Anatomy, Dr. Ajith. TA Professor

of Biochemistry, Mr. Remith RP Assistant

Professor of Anatomy, Dr. Sugathan KR, Tutor

in Anatomy, Smt. Sindu CD, Smt. Lissy CD and

Mr. Mathews PP of Amala Institute of Medical

Sciences, Thrissur, Kerala for their valuable help

and assistance to make this work a reality.

ABBREVATIONS

CT: Computerized tomography, CTA: Computed

tomography angiography, MRA: Magnetic

resonance angiography, PPTA: Persistent

primitive trigeminal artery, MRI: Magnetic

resonance imaging, VBD: Vertebrobasilar

dolichoectasia, VA: Vertebral artery, HVA:

Hypoplasia of vertebral artery, SAH:Subarachnoid hemorrhage

Conflict of Interest: Nil

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9. Padget DH. The development of the cranial

arteries in the human embryo. Contrib

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11. Hegedus K. Hypoplasia of the basilar artery.

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12. Boyko OB, Curnes JT, Blatter DD, Parker

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Gorelick PB. Ischemia in the territory of a

hypoplastic vertebrobasilar system.

Neurology. 1999; 52: 980-983.

14. Szdzuy D, Lehmann R. Hypoplastic distal

part of the basilar artery. Neuroradiology.

1972; 4: 118-20.

15. Fischer CM, Gore I, Okabe N, White PD.

Atherosclerosis of the carotid and vertebral

arteries extracranial and intracranial. JNeuropathol Exp Neurol. 1965; 24: 455-

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16. Ubogu EE, Zaidat OO. Vertebrobasilar

dolichoectasia diagnosed by magnetic

resonance angiography and risk of stroke

and death: A cohort study. J Neurol

Neurosurg Psychiatry.2004; 75: 22-26.

17. Ritesh Kansal, Amit Mahore, Nitin Dange,

Sanjay Kukreja. Dolichoectasia of vertebrobasilar arteries as a cause of

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18. Tomoyuki Nishizaki, Norihiko Tamaki,

Naoya Takeda, Takayuki Shirakuni, Takeshi

Kondoh,Satoshi Matsumoto. Dolichoectatic

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809

Anjum et al., Int J Med Res Health Sci. 2013;2(4): 809-815


&

Health Sciences



ndSep 2013 Accepted: 12

thSep 2013

Research article

LIGHT EXPOSURE AT NIGHT AND ROTATING NIGHT SHIFT ASSOCIATED WITH

CIRCADIAN DISRUPTION OF 6-SULFATOXY MELATONIN

Anjum B1, Verma NS

2, Tiwari S

3, Singh R

1, Fatima G

1, Singh P

2, Mishra S

2, Mahdi AA

1

1Departments of Biochemistry,

2Departments of Physiology,

3Departments of Surgery, King George’s

Medical University, India


ABSTRACT

Background: Alterations in the sleep-wake cycle leads to decreased melatonin secretion and it may be

associated with sleep disorders and cancer risk. Exposure of light at night and rotating night shift

decrease the melatonin production due to acute suppression of pineal melatonin secretion during night

work has been suggested to increases cancer risks. Aims & Objectives: The objectives of the present

study were to investigate the effect of light exposure at night on circadian pattern of 6-Sulfatoxymelatonin levels in night shift nursing professionals. Material and Methods: 62 healthy nursing

professionals of both genders performing day and night shifts (continuous 9 days night shift with

alternate day shifts) were recruited. Urine samples were collected at around 8 hour intervals (afternoon

sample: between 13:00 to 15:00, night samples between 22:00 to 01:00 and morning samples between

05:00 to 08:00) while they were performing night duties and repeated when they were assigned day

duties. Night melatonin level was decreased as compared to morning melatonin. Results: Night

melatonin level was found declined as compared to morning level and this pattern was significant when

compared night melatonin between night (16.71 ± 11.98) vs day shift (22.71 ± 13.25) and morning

melatonin level between night (20.07 ± 14.13) vs day shifts (28.26 ± 14.14) (p<0.001). Conclusion:

Light exposure at night disrupts the circadian rhythm of melatonin secretion during night shift leads to

internal desynchronization.

Key words: Rotating night shift; Light at Night; Circadian rhythm; 6-Sulfatoxy melatonin.

INTRODUCTION

Rotating night shift disrupts the circadian

rhythms and has been associated with fatigue,

stress and sleep disturbances. Alterations in the

sleep pattern leads to decreased melatonin whichmight be associated with sleep disorders, anxiety,

depression, and stress and cancer risk. Those

who work in night shift may attempt to sleep

when their body clock is adjusted for the

awakening phase.1

This attempt disturbs the body

clock resulting in a contradictory relationshipbetween sleep time and circadian schedule. It is

possible that the circadian sleep propensity

DOI:10.5958/j.2319-5886.2.4.129



810


rhythm and hormonal rhythm are under influence

of circadian pacemaker as well as sleep habit.2

Majority of the circadian rhythms in our body

have both an endogenous component regulated

by an internal clock, viz. the suprachiasmatic

nuclei (SCN), and it synchronized with anexogenous component composed of a light-dark

cycle.3,4

Melatonin is a hormone (N-acetyl 5 methoxy-

tryptamine) synthesized and secreted principally

by the pineal gland at night under normal

environmental conditions. The pineal gland

decides whether or not to secrete melatonin and

the amount of melatonin secretion based on

information directly sent from the retina of theeye. The Retina of the eye contains a unique

subset of cells other than rods and cones, this

unique subset of cells produce a pigment called

melanopsin. Melanopsin allows a cell to detect

light and dark. Information collected by the

unique subset of cells is sent along the

retinohypothalamic tract (RHT), a sort of

information highway that extend from the retina

to the hypothalamus. In hypothalamus, this

information is transmitted to a cell called the

suprachiasmatic nuclei (SCN). The SCN of the

hypothalamus have melatonin receptors and

melatonin may have a direct action on SCN to

influence “circadian rhythm”.5

Melatonin secretion is enhanced in darkness and

decreased by light exposure. Exposure to

artificial light at night and disruption of the

endogenous circadian rhythm with suppression

of the melatonin synthesis has been suggestedmechanisms.

6Melatonin gives a measure of day

length, it can reset the clock by acting as

chemical zeitgeber. Melatonin is metabolized to

6-hydroxy-mel in the liver and the main

metabolite excreted in urine is 6-Sulphatoxy-

melatonin are more stable than 6-hydroxy

melatonin in serum. The concentration of 6-

Sulfatoxy melatonin or 6- hydroxyl melatonin

sulphate in urine correlates with the total level of melatonin in the blood during the collection

period. Melatonin levels in individuals with

normal sleeping patterns begin to increase during

the evening (~ 9:00 p.m.). Melatonin levels peak

at around 2:00 a.m. and return to baseline around

sunrise (~ 6:00 a.m.).7

Irregular sleeping patterns

can lead to circadian disruption and shift the

amplitude and timing of peak melatonin levels.The hypothalamic-pituitary adrenal axis (HPA),

has been identified as a potential mechanism of

neuroendocrine system that influenced by night

shift work through which circadian desynchrony

may lead to stress and ill-health.8

The present

study was planned to investigate the effect on

light exposure at night and rotating night on

circadian pattern of 6-sulfatoxy melatonin in

night shift nursing professionals.

MATERIAL & METHODS

The study was approved by the institutional ethic

committee (Ref. code: XXXIV ECM/B-P3), a

detailed proforma was explained to all

volunteers; written informed consent was

obtained from all the subjects. The study

volunteers willing to participate in the study were

recruited from Trauma Centre, GM andAssociated Hospitals, KGMU, Lucknow, UP,

India. Sixty two healthy night shift nursing

professionals, aged 20-40 year, performing

rotating night shift duties (continuous 9 days

night shift with alternate day shifts) from past 5-

6 years, the duration and pattern of shift work

were same among all the subjects. Inclusion

criteria: Subjects were working in continuous 9

days light at night exposure in each month. We

recruited nurses of both genders, age between

20-40 yrs from different wards and units viz.

Intensive care unit (ICU), surgical emergency,

Neurosurgery, Neurotrauma, Orthopaedics

emergency and Medicine emergency, who

worked in rotating night shift.

Exclusion criteria: Subjects with any

acute/chronic illness, known patients of diabetes

mellitus, other endocrinal disorders,

hypertension, coronary artery disease, subjects

taking oral contraceptive pills and chronic renal



811


diseases were excluded from this study.

Study design: The present prospective

observational study was planned to investigate

the effect of light exposure at night and rotating

night shift on circadian pattern of 6-sulfatoxy

melatonin in night shift nursing professionals andwhether they are reversible in due course of time.

Collection of Urine samples: Urine samples

were collected at around 8 hours interval in their

night shift and day shift schedules (afternoon

sample: between 13:00 to 15:00, night samples

between 22:00 to 01:00 and morning samples

between 05:00 to 08:00). The volunteers

themselves collected the samples in different

colour vials. For collection of urine samples, anotebook was provided to each subject with all

details regarding the timing and procedure for

sampling and their sleep-awake timing. Samples

were analyzed for 6-Sulfatoxy Melatonin by the

ELISA method.

RESULTS

There were total 62 (32 male and 30 females)

night shift nursing professionals recruited in the

present study. The effect of light at night

exposure on rotating night shift was investigatedby analyzing urinary 6-sulfatoxy melatonin

levels. All the data were summarized as Mean+

SD & baseline characteristics of male and female

night shift workers are given in Table 1. Groups

were compared by applying paired t test. A two

tailed (α=2), p<0.05 was considered significant,

p<0.01 moderate/very significant and p<0.001

highly significant. P value elucidate that if it is <

0.05, < 0.01, < 0.001 then the null hypothesis

would be rejected at 5 %, 1 % or 0.1 %

respectively. Statistical analysis was carried out

by using INSTAT 3.0 (Graph pad prism

software; San Diego, CA). Association of

variable between different shifts was done by

Pearson correlation analysis.

Table 1: Baseline characteristics of night shift workers.

Baseline Characteristics Night Shift Workers ( n = 62)

Age (years) 24.74 ± 3.81

Weight (kg) 53.21 ± 8.85

Height (cm) 160.44 ± 8.16

Body mass index (BMI) 20.59 ± 2.40

Marital Status

Married 16 (25.80%)

Unmarried 46 (74.19%)

Diet

Vegetarian 23 (37.10%)

Non-Vegetarian 39 (62.90%)

Data are presented as means ± SD.

Table 2: Correlation of Urinary Melatonin between Nights versus Day shift

Measured Variables Night Shift (NS) versus Day Shift (DS) ( n=62 )

6-Sulfatoxy Melatonin Afternoon Melatonin: NS vs DS r =0.13ns

Night Melatonin: NS vs DS r =0.51***

Morning Melatonin:NS vs DS r =0.18ns

ns= Non significant, ***p<0.001 highly significant



812


Fig 1: Mean Afternoon, Night and Morning melatonin during night and day shift

(AML: Afternoon Melatonin level; NML: Night Melatonin level; MML: Morning Melatonin level),

(*p<0.05, ***p<0.001; By paired t test; - Bar of the standard deviation).

Melatonin hormone also shows diurnal variation,

its level increases from midnight to early

morning and decreases in the late morning and in

day hours. This pattern was found altered inrotating night shift workers during night shift.

Melatonin synthesis directly depends upon

transport of signal of light in the day time and

conversion of serotonin into melatonin depends

upon signals of darkness received at night.

However, its level may differ from individual to

individual. Normal range of melatonin is 0.8-40

ng/ml, its levels increases at midnight and

declines in day time. Night 6-sulfatoxymelatonin

level was found declined as compared to

morning level and this pattern was significant

when compared night 6-sulfatoxymelatonin

between night (16.71 ± 11.98) vs day shift (22.71

± 13.25) and morning melatonin level between

night (20.07 ± 14.13) vs day shifts (28.26 ±

14.14) (p<0.001) (Figure 1). 6-sulfatoxy

melatonin level of evening and morning time

during night shift was positively associated with

that of during day shift. Since the pattern of melatonin secretion was altered in early morning

time during night shift hence this positive

association did not reach at significant level

(p>0.05);(Table 2). 6-sulfatoxy melatonin level

of night time during night shift was positivelyassociated with that of during day shift and this

association was highly significant (p<0.0005).

The result show that light exposure at night

effect on melatonin production during night shift.

Altered 6-sulfatoxymelatonin levels were found

at night and in the morning samples during night

shift.

DISCUSSION

Previous studies have reported that subjects

exposed to light and who remain awake at night

have lower levels of melatonin at night , as

melatonin synthesis always occurs at night,

particularly in the darkness. On the basis of the

finding of the previous studies, it has been

hypothesized that exposure of light at night

(LAN) is one of potential mechanisms of breast

carcinogenesis in the night shift workers through

decreased melatonin synthesis.6 Findings of the

recent study indicates that two nights of rotating



813


shift work may not change the timing of

melatonin production to the day among those

working at night.9

While the results of the

present and other studies indicate that working

six to eight or more night shifts per month may

disrupt the synthesis of melatonin.6 Finding of our study in agreement with previous study

indicate that night shift workers have

substantially lower level of 6-sulfatoxymelatonin

at night work and daytime sleep during night

shift, and levels remain low when night shift

workers sleep at night during day shift. Long

term chronic reduction in melatonin among night

shift workers may be an important carcinogenic

mechanism, which could affect the cancerrisk.

10,11Other studies have also reported higher

incidence of poorer sleep and its complications in

night shift workers.12-14

These findings reinforce

previous studies which reported elevated

exposure to cortisol on early shifts, relative to

‘normal’ later working days and rest days, might

promote pathogenic processes including insulin

resistance.15

and help to elucidate the increased

risks of cardiovascular diseases in rotating night

shift workers.16 In other study, the related

neurotransmitters like Urinary norepinephrine

and Epinephrine were higher during work than

non-work in the day, but in evening shift and

night shift workers, the difference was lesser and

in opposite direction. Working evening or night

shift are independent predictors of Non – dipper

status.17

During night shift the hormones are

more sensitive to endogenous components like

catecholamine, prolactin, and growth hormoneswhich showed an immune response to the shifted

sleep/activity cycle, evidencing a “masking

effect” due to the work activity. In another study,

hormones having stronger endogenous

components, such as cortisol and Melatonin,

showed a more stable pattern, with a slight

tendency for partial adjustment of cortisol during

the second night.18

The onset of sleep was

consistently followed by a decrease inconcentration of cortisol. While both sleep-wake

and light-dark transitions were consistently

associated with cortisol secretary pulses.19

It is

also reported that the sleep factor (time of onset

and/or period) seemed to be more potent in

modifying the circadian rhythm of serum

cortisol, especially with the night shift.20

Sleep

was initiated (on average) about three hours priorto the onset of melatonin production in night

shift workers while in day-active subjects

initiated sleep (on average) about three hours

after their melatonin onset. Thus, the sleep times

availed for night shift workers may not be well-

synchronized to their melatonin secretion

rhythm, assumed to mark the phase of their

underlying circadian pacemaker.21

The change in the Acrophase of 6-sulfatoxy-melatonin was associated with different shifts.

22

The overall advance of Melatonin profile was

primarily achieved during the initial exposure to

an 8h period of darkness. The present data

suggested that exposure to dark affects human

circadian phase.23

In the present study, subjects

with rotating shifts of 12 hrs night works had

complained of difficulty in sleep, decreased

calculative tasks, impaired cognitive functions,

decreased alertness, constipation, stress and

mental fatigue which is in accordance with the

other studies.24, 25

Quality and quantity of sleep

are also affected by rotating night shift. Duration

of sleep was shorter during day time at night shift

(3-4 hours less as compare to night time sleep

during day shift). Night shift nurses have

experience changes in aMT6s levels after six to

eight nights in a month and the findings might be

related to the increased cancer risk reported innight-shift workers and suggest that a short nap

during night-shifts may exert a positive effect to

night shift workers.26

The long term higher

intensity of light exposure during night work

may have decreased total melatonin production,

possibly by initiating re-entrainment and leads to

internal desynchronization that could be the

mediator between night shiftwork and cancer

risks.

27

In brief, it is possible that rotating nightshift appears to have adverse effects on body’s



814


physiological rhythm leads to hormone related

disorders and cancer risk.

CONCLUSION

In present study, we concluded that rotating night

shift disrupt the circadian pattern of melatonin

particularly at night and in the morning time

during night shift due to desynchronization.

However, recovery was found when subjects

went back to the day shift. Prolonged exposure of

light at night leads to decreased melatonin level

may be one factor contributing to an increased

risk of cancer and other endocrinal disorders in

rotating night shift workers.

ACKNOWLEDGEMENT

The authors gratefully acknowledge the

invaluable contributions of the nursing staff to

various aspects of the study. We would also like

to thank the Council of Science & Technology,

UP for financial support for this study.

Conflicts of interest: The authors declare that

there is no conflict of interest.

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and Netter P. Changes in cortisol secretion

during shift work :implication for tolerance

to shift work. Ergonomics.1998; 41(5):610-

21.

13. Akerstedt T. Sleepiness as a consequence of shift work. Sleep.1988;11:17-34.



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14. Rutenfranz J, Colquhoun WP, Knauth P,

Ghata JN. Biomedical and physiological

aspects of shift work. Scand J Work Environ

Health. 1977; 3:165-82.

15. Sack RL, Blood ML, Lewy AJ. Melatonin

rhythm in night shift workers. Sleep.1992;15(5):434-41.

16. Anagnostis P, Athyros VG, Tziomalos K,

Karagiannis A, Mikhailidis DP. Clinical

review: The pathogenetic role of cortisol in

the metabolic syndrome: A hypothesis. J Clin

Endocrinol Metab 2009;94(8): 2692-01.

17. Fujino Y, Iso H, Tamakoshi A, Inaba Y,

Koizumi A, Kubo T,et al. A prospective

cohort study of shift work and risk of ischemic heart disease in Japanese male

workers. Am. J. Epidemiol. 2006;164(2):

128-35.

18. Yamasaki,F., Schwartz,J.E., Gerber,L.M.,

Warren,K., and Pickering,T.G. Impact of

shift work and race/ethnicity on diurnal

rhythm of blood pressure and

catecholamines. Hypertension:1998; 32(3):

417-23.

19. Costa G, Bertoldi A, Kavocic M, Ghirlanda

G, Minors DS, Waterhouse JM. Hormonal

secretion of nurses Engaged in fast rotating

shift system. Int J Occup Environ

Health.1997; (Supll 2):S35-S39.

20. Coufrei Z, Moreno-Reyes R, Leproult R,

Vertongen F, VanCauter E, Copinshi G.

Immediate effects of an 8-hours advance shift

of the rest – activity cycle on 24h profile of

cortisol. Am.J.physiol Enocrinol Metab.2002;282(5):E1147-53.

21. Fujiwara S, Shinkai S, Kurokawa Y,

Watanable T. The acute effects of

experimental short-term evening and night

shifts on human circadian rhythm: the oral

temperature, heart rate, serum cortisol and

urinary catecholamines levels. Int.Arch

Occup Environ Health.1992;63(6):409-18.

22. Quera Salva MA, Guilleminault C, ClaustratB, Defrance R, Gajdos P, McCann CC. et al.

Rapid shift in peak melatonin secretion

associated with improved performance in

short shift work schedule. Sleep.1997;

20(12):1145-50.

23. Yan Cauter E, Moreno-Reves R, Akseki EL,

Hermite – Baleriaux M, Hirchfeld U, Leproult

R. et al. Rapid phase advance of the 24 – hmelatonin profiles in response to afternoon

dark exposure. Am J Physiol:1998;275 (1

pt1):E48-54.

24. Takahashi M, Fukuda H, Milki K, Haratani

T, Kurabayashi L, Hisanga N. et al. Shift

work related problems in 16h night shift

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Mahdi AA, Singh RK, et al. Association of

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Staffolani S, Strafella E, Nocchi L, et al.

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816

Ismail et al., Int J Med Res Health Sci. 2013;2(4): 816-822


&

Health Sciences



thSep 2013 Accepted: 15

thSep 2013

Research article

SEROPREVALENCEOF HBV, HCV AND HIV INFECTIVITY AMONG BLOOD DONORS IN

IBN SINA TEACHING HOSPITAL IN SIRT REGION OF LIBYA

Ismail Mahmud Ali1, *Amirthalingam R

2

1Hospital Director, Head, Assistant Professor, Department of Surgery,

2Specialist, Department of

Molecular biology, Ibn Sina Teaching Hospital, Sirt University, Libya. P.O.Box 705.

*Corresponding author email:[email protected]

ABSTRACT

Background &Aim:Numerous infectious diseases are spread by blood transfusion, particularly viral

infections. The hepatitis B virus (HBV), hepatitis C virus (HCV), and human immunodeficiency virus

(HIV) and other pathogenic organisms are transmitted through inappropriate screening of blood product.

These infected blood products are causing fatal, persistent and life frightening disorders. The

predominance of these viruses differs by ethnic group and geography. Scheme of the current study was

to statistical estimation of the incidence of HBV, HCV and HIV along with blood donors. Materials &Methods: The existing review was approved in Ibn Sina Teaching Hospital, Sirt Region of Libya. A

total of 16,929donors were analyzed by enzyme immune assay (EIA) kits from TaytecInc, Canada, for

the predominance of human immunodeficiency virus, hepatitis B and C virus, over a period of 17

months from January2012 to May 2013.Results: Among the blood donors, 81.40% were unpaid donors

and 18.60% were alternative donors. The total incidence in blood donors was 3.18%. The

seroprevalence of hepatitis B was uppermost (1.98%) followed by hepatitis C (1.20%) and

seroprevalence of HIV was nil among unpaid and surrogate donors. Conclusion: Present study was

emphasized the prevalence rates of HBV and HCV between charitable and alternative blood donors and

the HIVwas not detected in the current study.The prevalence rate was more in male among the blooddonors.

Keywords: Human immunodeficiency virus, Hepatitis B&C virus, Seroprevalence, Blood donors

INTRODUCTION

Blood transfusion is the transfer of blood and its

components such as red blood cells, platelets,

and plasma from donor to recipient. Donation of

the blood saves the life of millions of people

universally, and it is essential to the helpfulness

of the health system by supporting current

medicine as its key role in patient contribution1-

2.Today, the medical and surgical procedure like

organ transplantations, heart surgery, trauma,

cancer and hematologic condition such as severe

anemia, leukemia, sickle cell disease, and others

health emergency depends extremely on blood

DOI:10.5958/j.2319-5886.2.4.130



817


transfusions worldwide. Hence, in developing

countries, blood transfusion-transmitted

infections (TTIs) frequently terrorize the defense

of patients demanding blood transfusion, and

healthcare facility supplier faces serious

challenges with blood availability and protectionbecause of an improper facility. It is estimated

about 45% of 80 million blood donations through

the world are collected every year in rising

nation that included almost 80% of the world’s

population3-4.

In universal healthcare service provider, the

blood safety studies have integrated procedure

for clinical laboratory screening of HIV1&2;

human T-lymphotropic virus 1&2(HTLV);hepatitis B&C virus; West Nile virus,

cytomegalovirus; human herpes virus 8,

parvovirus B19, malaria; Creutzfeldt-Jakob

disease, influenza, chikungunya; dengue,

trypanosomacruzi and other viruses.

Furthermore, the very important subject that

making difficulties of transfusion because of

bacterial contamination of platelets in blood

products5.This screening protocol might be

differing from country to country and depend on

epidemiological condition. In addition to

infectious diseases threat, clinicians should also

supervise other risk, such as post blood

transfusion reactions. These include transfusion-

related lung injury (TRALI); transfusion

associated circulatory overload (TACO), and

transfusion-related immune modulation (TRIM),

post transfusion iron overload and graft versus

host diseases (GVHD)6

.The blood transfusion department contains

clinical methods and guidelines for screening of

blood before transfusion. If the screening

procedure and other regulation are not followed

well there is possibility to carry the risk of

spreading blood transfusion contagious

pathogens like HIV, HBV, HCV, Bacteria

(syphilis) and others7. Also, there is a 1% of

chance of transfusion related infection in eachunit of blood even if the procedure followed

well8.Therefore, the risk of blood transfusion-

transmitted infection today is minimized than

constantly, the delivery of safe blood products

stays behind inquiry to infection with accepted

and until now to be predictable human

pathogens9.

To supply of safety blood product fortransfusion, it's compulsory to introduce an

advanced technology like a nucleic acid test

(NAT) because of an excellent clinical sensitivity

and good specificity to detect infected blood

components as it identified pathogens prior in the

'window period' than enzymes immune assay10

.

Even though, it has some margin in blood

components with lesser range of viremia, which

can even free quantifiable by NAT

11

. Even withthis margin, the grouping of both enzymes

immune assay and NAT has notably condensed

the hazard of pathogen spread during transfusion12-13

.Also many scientific research data showed

that the comparison between p24 antigen

detection or conventional serological testing, it is

estimated that the use of NAT reduces the

detection time from 22 to 11 days for HIV; from

70 to 10 days for HCV and from 60 to 30 days

for HBV infection. Final outcome of this, the

prevalence risk for HIV is between 0.14-1.1 and

for HCV between 0.10-2.33 per million units’

transfused13-14.

The greater risk of HBV spread

through blood transfusion differ between the

countries. The HBV infection through blood

transfusion differs among 0.75 per million blood

donations in Australia, 3.6-8.5 in the USA and

Canada.0.91-8.7, also from North region 7.5-13.9

in the Southern region of Europe; up to 200 permillion blood contributions in Hong Kong,

mostly reflecting the universal epidemiology15

.

The objective of this study is to statistical

estimations of those pathogenic viruses such as

HBV, HCV and HIV in well blood contributor.

Hence, it needs to authenticate how well we are

responsibility in clinical laboratory and

proficiently in work with medical ethics. This

statistic may possibly assist in creating the statehealth plan to advance improve the background

and method to instruct the public concerning the



Ismail et al.,

subject matter of these burde

reduce the incidence of illness a

by these viral pathogens

transfusion.


Study Population: In the pres

incorporated 16,929 blood donors

All the donors have been screen

consultant before donation, w

voluntary and replacement in bl

department at Ibn Sina Teachi

tertiary care hospital Sirt region

the period of January 2012 to

ethics committee and an internalof the organization approved

Informed consent obtained f

patients.

Sample Collection: Five milli

venous blood was collected fro

using plain vacationer tubes afte

and clinical examination. All

allowed to clot and centrifuged

10 minutes. All serum samples

into sterile 2ml cryovial containe

-20°C until ready for use.

Serology:All donors samples w

enzyme immune assay (EI

TaytecInc, Canada, for HIV-1 an

antigen; HBsAg and Anti-HCV

EIA was authenticated by the a

instructed by the manufacturer

density of reagent blank and

mean value of positive and n

given with the test protocol. The

off) was considered as per compa

reporting positive and negat

Confirmed positive and negativ

used subjectively as an outsid

screening for our laboratory

donated blood was discarded if th

was found positive for any i

statistical analysis was done uware office excel 2007.

Int J Med Res Health Sci

s therefore to

d death formed

through blood

ent study were

(99% of male).

d with medical

o attended as

ood transfusion

ng Hospital, a

of Libya during

May 2013.The

appraisal panel the procedure.

om individual

liters (5ml) of

m each patient

r taking history

samples were

t 3000 rpm for

were separated

rs and stored at

re screened by

) kits from

igen and HIV-2

antibodies. The

proval standard

for the optimal

optimal density

gative controls

least value (cut

ny guideline for

ive outcomes.

samples were

e run in each

intention. The

e serum sample

nfectivity. The

sing Microsoft

RESULTS

A total 16,929 donor

study. Of these, 3152 (

and 13777 (81.40%)

of the samples were c

department not from

requirement of blood

donors’more than fe

donations while only

females. Among these

from 18 to 40 years.

donors, 535 were tes

healthy blood samples

were alternative d

predominance of HIVpositivity in blood sc

1.2% and 3.18%,in a

prevalence of HBsAg

(333 cases). Substitute

high incidence with lo

compared to the volu

The seropositivity of

1.20% (202 cases).

cases) had a low incidepatients as compared

(185 cases). Zero pre

among all blood dono

male blood is higher t

The agreeing rates for

for HBsAg infection f

in descending orde

transfusion transmitte

not been studied amon

Fig.1: Distribution of

96.82%

1.98% 1.20%

818

i. 2013;2(4): 816-822

s were integrated in the

18.60%) were replacement

ere voluntary donors.All

llected within transfusion

any other branch of

donation. Males blood

ale with16, 862(99.6%)

67(0.4%) donors were

, most of the donors aged

Out of the 16,929 blood

ted positive for donated

(3.18%).Out of these, 61

nors. In general, the

, HBsAg,HCV and total reening was 0%, 1.98%,

senting order (fig-1).The

in total donors was 1.98%

donors (44 cases) had a

frequency of patients as

ntary donors (289 cases).

HCV in total donors was

Replacement donors (17

nce with low frequency of to the voluntary donors

valence of HIVwas zero

rs. The infectivity rate of

han female blood donors.

seropositivity were peak

llowed by HCV infection

. The co-infection of

infectious diseases has

blood donors.

eroprevalence

Negative

HBsAg Positive

HCV Positive



819


DISCUSSION

Blood transfusion is a branch of medicine in the

healthcare sector. An incorporated strategy for

blood safety is required for elimination of

transfusion transmitted infections and forprovision of safe and adequate blood. The

infectious agents such as HIV, HBV and HCV

are important blood born and transfusion

transmitted infections throughout the world

including Libya. The previous research statistical

data has been established that prevalence rate of

HBsAg, anti-HCV and anti-HIV among blood

donors or the general population varied from

country to country16

.

In the present study, the prevalence of HBsAg

and anti-HCV antibodies was 1.98% and 1.20%

respectively. These prevalence rates can be

compared with other provincial studies from

Central Hospital (Tripoli), and from Libyan

National Center for Infectious diseases were

2.2%, 1.2%17

and others studies 22.7% was

reported with HCV infection through blood

transfusion18

.Also, these rates can be compared

with other studies from Egypt, from the EasternMediterranean region and elsewhere, the anti-

HCV in Egyptian blood donor’s studies found

13.6% were anti HCV antibodies detected as

infection18

.In Saudi Arabia the prevalence of

anti-HCV and HBsAg infection in blood donors

was 0.4% and 4%19

.

In current study none of the donors had a

confirmed positive result for HIV infections. The

comparisons of the prevalence of transfusionviruses among different sex blood donors may

not be valid because of high percentage of male

donors; this is due to low hemoglobulin in

females and the fact that women are less willing

to donate blood. The most of the donors (99%)

were male, which is similar to the preceding

report20, 21.

The differences in the incidence

between current and past studies may be credited

to differences in the sensitivities of the assay

used, and the criteria of positivity in the degree

to which individuals with risk factors for blood-

born viral infections may have been excluded.

In general, the prevalence rates of hepatitis B and

C were lower among young donors than older

donors. This confirms the results reported earlier

by other investigators22.In contrast, most of theblood donors in Libya are young men (18-

40years of age). It is recognized that this age

group is generally arrogant group example of

misusing of drug, insecure sex, and other

misbehavior habits for the transmission of the

virus. This may be explained on the essential of

increased exposure with age and on the fact that

a high awareness of blood born viral infections

has developed and a comprehensive vaccinationprogram against hepatitis B has been

implemented in Libya. It should be noted that the

carrier rate of HBV was higher than the carrier

rate of HCV in this study and in other studies23

.

These data suggested that the mode of

transmission and the efficiency of transmission

of HBV may be different from that of HCV.

The predominance of HBV and HCV between

blood donors was lower than it is in other

countries. The prevalence of hepatitis B among

blood donors was 3.8% in Syria23

, 9.8% in

Yemen24

, 2.1% in Egypt25

, >5.0% in Sudan26

,

10.7%in Cameroon27

, 8.8% in Tanzania28

and

(Africa 5-15%). Similarly, the prevalence of

HCV was 2% in Yemen24

, 4.8% in Cameron27

,

1.5% in Tanzania28

, and high in Egypt 13.6%25

.

This was probably due to the compulsory

screening of all emigrants prior to granting

residency in Libya. The other infectious agent of blood transfusion is HIV causes major health

problem in sub Saharan Africa where the

prevalence of HIV among blood donors ranges

between 2-20% in Kenya29

, and 5.9% in

Ethiopia30

.However, our results showed no

confirmed HIV in the analyzed blood donors.

Hence, the previous blood donors study in Libya

reported the prevalence rates of HIV was 0.4

%

31

.The frequency of HBsAg is more comparedto the anti-HCV.There is no way to ignore that

blood donation which is collected in the



820


“window” period of infectious might be

transmittable even though a negative antibody

test. Therefore, the introduction of screening

procedures for hepatitis B core antigen and

performance of NAT are advised in the blood

transfusion division in this locality.In feature direction, the implementation of new

technology like MALTI-TOF32

MS(Matrix-

Assisted Laser desorption/Ionization, Time of

Flight Mass Spectrometry) for the genomic

detection of the 101 blood groups antigen;DNA

microarray33

for complete blood groups typing;

and integrated microchip arrays or

nanotechnology34

are being developed to

enhance rapid screening of donated blood for anynumbers of infectious diseases to get paramount

donors for blood transfusion and get free from all

kinds of risk including viruses, bacteria and

blood typing. Further, taming public, generating

notice, consoling unpaid blood donation, high-

quality blood bank practice and employing a

meticulous donor range condition according to

blood transfusion by National Infectious

Diseases control Organization is an important

factor.

CONCLUSION

In 17 months period, 16929 units of blood

werecollected. A total positivity of blood;

HBsAg, anti-HCV and anti HIV were 3.18%,

1.98%, 1.20 % and 0% respectively. The

seroprevalence rate was tall in unpaid donors as

compared to surrogate donors because of most of

them charitable donors.The major limitation of

this study is the fact that there is no previous

study and or data available in this region for

comparison.

ACKNOWLEDGEMENT

We acknowledge the support provided by

technical staff from Blood Bank and Serology

division of Ibn Sina Teaching Hospital, Sirt

Region of Libya.

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823

Shelke et al., Int J Med Res Health Sci. 2013; 2(4): 823-827


&

Health Sciences




thSep 2013

Research article

A STUDY ON HEARING THRESHOLD PROFILE IN TRAFFIC POLICE PERSONNEL

*Shelke BN1, Aundhkar VG

2, Adgaonkar BD

3, Somwanshi SD

4, Gavkare AM

1, Ghuge SH

1


3Professor and Head,

4Associate Professor, Dept of Physiology, MIMSR Medical

College, Latur, Maharashtra, India2

Professor and Head of Dept, Dept of Physiology, Govt. Medical college, Miraj, Maharashtra, India

* Corresponding author email: [email protected], [email protected]

ABSTRACT

Introduction: Noise is one of the causes of preventable sensori-neural loss. The traffic police

personnel(TPP) busy in controlling traffic at heavy traffic junctions suffer from the ill effects of noise

and air pollution. Aim and objectives: The objective of this study was to assess the hearing threshold at

various frequencies of the traffic police persons exposed to the vehicular noise and comparison with

controls not exposed to noise. Material and methods: Thirty TPP and thirty controls were evaluated by

clinical methods and subjected to the Pure Tone Audiometry (PTA) in ENT department. Audiogramrecorded by using conventional techniques in both ears. RESULTS: There was a significant difference

in the hearing thresholds at frequency 2000 Hz, 4000 Hz and 8000 Hz of right and left ear between the

two groups. Conclusion: This study concludes an increased risk of noise induced hearing loss (NIHL)

for the environmental noise exposed subjects.

Keywords: Traffic police personnel, TPP, Hearing threshold, NIHL

INTRODUCTION

Automobile vehicles are the major sources of noise in the city, which originates from engines,

air turbulence and frictional contact of the

vehicle's tiresto the ground. Noise is one of the

causes of preventable sensori-neural loss. The

attention has to be given towards the problem as

no cure is available for noise induced hearing

loss because of irreversible damage to the hair

cells.1-4

Studies carried out by various workers

showed an average traffic sound in the city is

about 60-102 dB.5,6The traffic police personnel

busy in controlling traffic at heavy traffic

junctions suffer from ill effects of noise and airpollution. Irritation of upper respiratory tract

provokes them to use a mask to prevent the ill

effects of air pollution. However, the insidious

nature of the noise induced hearing loss keep the

majority of them unaware of the effects of noise

pollution.7,8

With this background, this study was carried out

to evaluate hearing threshold profile of traffic

police personnel serving at busy parts of streets

in the city.

DOI:10.5958/j.2319-5886.2.4.131



824


MATERIAL AND METHODS

After the approval from Secretary of ethical

committee this study was conducted in Miraj,

city of Maharashtra (India), between July to

December 2010 in 30 traffic police personnel

(TPP) and 30 normal healthy individuals as acontrol from the same city and residing in the

College campus. Written informed consents were

obtained from all the subjects.

Inclusion criteria: Age between 25 to 45 years.

Five years of exposure to traffic pollution, with

spending average 8 hours in busy traffic areas.

The thirty normal healthy individuals (control

group) were of the same age and sex. The

study and control group belonged to thesame ethnic group. All the subjects were males.

Exclusion criteria: A primary screening was

done in the medicine and ENT outpatient

department by personal history and otoscopic

examination. By taking detailed personal

history subjects having smoking habits,

diabetes mellitus and hypertension were

excluded from the study. Subjects having

conditions that may affect the hearing like ear

drum perforation, acute or chronic suppurative

otitis media, wax and suffering from ear diseases

were excluded from the study.

Thirty traffic police personnel and thirty controls

underwent a pure tone audiometry (PTA).

Audiometer used was Elkon EDA-3N3 Giga 3.

Audiometric testing was conducted in a

dedicated room that met the audiometer

manufacturer’s specifications, in ENT

department. Test was conducted in the morninghours before joining the duty hours to minimize

the effect of temporary threshold shift (TTS). Air

conduction was assessed by placing ear phones

on the ears. Each ear was evaluated separately

and the results were reported on the graph known

as an audiogram. Audiogram recorded by using

conventional techniques in both ears. The test

begun at 1000 Hz and then other frequencies

were tested in the following order 2000-

4000Hz repeated again followed by 500Hz

and 250 Hz. The examiner first familiarizes thesubject with the tone by delivering the sound at

an arbitrarily presumed supra-threshold level

oftesting frequency. When the subject hears

the tone, the tone is reduced by 10 dB till

subject stops hearing or fails to give a

response. Once this stage is reached the tone

raised by 5 dB. If the subject hears this tone, the

sound is again decreased by 10 dB. If he does not

hear it, the tone was again raised by 5 dB. Inthis way by several threshold crossings

(between 10-110 dB), the exact hearing

threshold was obtained when one gets at

least 3 out of five responses correct.

RESULTS

The age, height, body weight and BMI were

compared between the control and study group

using two tailed unpaired Student’s t test in

Microsoft Excel 2007. It was found that there

was no significant difference between two

groups for age in years , height in

centimeters, weight in kg BMI in kg/m2

(Table1).

The audiometry data was calculated in an excel

spreadsheet which was then exported R 3.0.1

version for analysis. The collected audiometry

data was analyzed by using two tailed un-

paired Student's t-test and the values were

expressed as mean ± SD of observed value.A

P-value of less than 0.05 was taken as significant

(Table II).

Table.1: Anthropometric parameters of control and study groups

Control group (n=30) Study group (n=30) ( p Value)

Age (years) 34.57±7.47 35.03±8.13 > 0.05

Height (cm) 171.9±5.55 172.63±4.71 > 0.05Weight (kg) 71.6±8.66 75.53±7.96 > 0.05

BMI (kg/m2) 24.24± 2.88 25.1± 2.67 > 0.05



825


Table II - Average hearing threshold at different frequencies in study and control groups

Hearing Thresholds Frequencies in Hertz Study group(n=30) Control group(n=30) p value

250 R 23.83±5.52 25.5±7.11 >0.05

L 25.83±5.26 24.83±6.08 >0.05

500 R 23.5±5.11 23.16±6.88 >0.05

L 24.33±4.49 25±5.41 >0.051000 R 21.66±5.14 21.66±5.62 >0.05

L 23.5±4.38 24.16±5.09 >0.05

2000 R 17.83±4.29 21±4.43 <0.05*

L 17.16±3.86 21.33±5.07 <0.05*

4000 R 17.33±4.86 33.83±15.57 <0.05*

L 17.50±4.50 33.83±17.89 <0.05*

8000 R 15.5±5.62 23.33±10.61 <0.05*

L 14.5±8.02 22.16±12.77 <0.05*

* Significant R- right ear L- left ear

Fig.1: Study group subject’s audiogram (Right & Left)

DISCUSSION

In the present study tested for the hearing

threshold audiometrically in right and left ear

separately. Mean hearing level at each tested

frequency was compared between noise exposed

TPP and non exposed groups using un-paired

Student t tests. There was a significant differencein the hearing threshold at frequency 2000 Hz,

4000 Hz and 8000 Hz of right and left ear

between the two groups.This is in agreement

with the finding of Jayesh et al who showed an

increased hearing threshold mainly affected

higher frequencies concentrated at 4000Hz in

textile workers exposed to industrial noise in

Gujrat9. Frequency specific analysis by McBride

et al10

andFrancois-Xavier Lesage et al11

showed

notches at 4 kHz in electrical transmission

workers and France Motorcycle police officers

respectively who had the expected associations

with exposure to noise. Similar raised hearing

thresholds at higher frequency were recorded in

Liquefied Petroleum Gas (LPG) Cylinder

Infusion Workers exposed to noise in Taiwan12

.

Our study confirmed the presence of 4000Hz

notch5 which is the classic sign of NIHL. Since

most significantly affected frequency was 4000

Hz for both right and left ears, paired t test was

conducted to evaluate whether there was any

significant difference for hearing loss between

right and left ears of study subjects. This showed

no significant difference of hearing loss between

right and left ears of study subjects. This finding

was similar with studies conducted on workers of

chromite mines13

. In the early stages of NIHL,the speech frequencies are less affected and the

patients have a very few symptoms and hence



826


they are usually unaware of the deleterious

effects of sound. Frequency area 4000-6000 Hz

is usually affected first with maximum at 4000

Hz. Any level of NIHL may muffle high-

frequency sounds such as whistles or buzzers and

may result in difficulty discriminating speechconsonant sounds such as those in the words fish

and fist, particularly in noisy environments with

background noise, many voices, or room

reverberation6,9

. The observed hearing

impairment was most probably related to the

prolonged exposure to road traffic noise. Daily

noise exposure, over long period affects the

hearing ability. The mechanism involved in noise

inducing hearing loss includes mechanicaldamage to cochlear structure and metabolic

overload due to excessive stimulation. The

severity of hair cell damage depends on sound

intensity. Exposure to noise at sub-traumatic

level exhibit a temporary threshold shift in

hearing, reversible with time away from the

hazardous exposure. Higher level of sound leads

to collapse of stereocilia and eventual permanent

damage to hair cell. Non-functioning of outer

hair cells raise the threshold sensitivity of inner

hair cell and greater stimulation is required to

initiate an impulse; which perceived as a

hearing loss5,13

.

Limitations: Some technical limitations could

not be avoided in this study. First, the timing of

the audiometry assessment in relation to when

subjects were last exposed to noise could not be

controlled. The French norm recommends

testing hearing 3 days after the last noiseexposure, but it was not possible to achieve

this in this study. Therefore, it is possible that

the effect of temporary threshold shift has led to

an overestimate of the real risk of NIHL.

The second limitation of the present study was

the small sample size of subjects, which was not

ideal for cross-sectional analysis and thus the

statistical significance of the results should

be interpreted with caution. We wereconstrained by the inability to find adequate

number of subjects as per criteria of study by

excluding smokers, females and exposure < 5

years within limited number of TPP in the study

area. So, it is important to replicate and extend

our observations to large population. We also

fail to quantify the noise level at the traffic

junctions.

CONCLUSION

This study concludes traffic police personnel

working on busy traffic junctions are at risk of

noise induced hearing loss. They have to make

aware of the ill effects of noise and motivate to

use personal protective devices like ear plugs and

ear muffs.

REFERENCES

1. Thomas A, Nor Mariah A, Fuad S, Kuljit R

Philip. Noise Exposure and Noise Induced

Hearing Loss Among Kuala Lumpur Traffic

Point Duty Personnel. Med J

Malaysia.2007;62(2):152-55.

2. Omidvari M., Nouri, J. Effects of noise

pollution on traffic policemen. Int. J.

Environ. 2009; 3(4):645-52.3. Abdel-Aziz Kamal M, SamiaEldamati E,

Ricky Paris. Hearing threshold of Cairo

traffic policemen. International Archives of

Occupational And Environmental Health

2004; 62:543 – 45

4. Itrat Jawed, AyubMusani, RaanaMahmood,

Wadood, YousufKhambaty, MohamadAsim.

The effect of traffic noise on the hearing

level of people on Karachi streets. J Pak Med

Assoc. 2010; 60(10): 813-816.

5. Nandi SS, Dhatrak SV. Occupational noise

induced hearing loss in India. Indian journal

of occupational and environmental medicine.

2008.12(2):53-56

6. Shrestha I, Shrestha BL, Pokharel M, Amatya

RCM, Karki DR. Prevalnace of Noise

Induced Hearing Loss among Traffic Police

Personnel of Kathmandu Metropolitan City.

Kathmandu Univ Med J. 2011;36(4):274-78



827


7. Tripathi SR, Tiwari RR. Self-reported

hearing quality of traffic policemen: a

questionnaire-based study. Indian journal of

occupational and environmental Medicine.

August 2006; 10(2): 82-84.

8. Kavana G, Venkatappa, Vinutha ShankarMS, NachalAnnamalai. Assessment of

knowledge, attitude and practices of traffic

policemen regarding the auditory effects of

noise. Indian J PhysiolPharmacol

2012;56(1):69 – 73

9. Solanki JD, Mehta HB, Shah CJ, Gokhale

PA. Occupational noise induced hearing loss

and Hearing threshold profile at high

frequencies. Indian journal of Otology.2012;18(3):125-28.

10. D I McBride, S Williams. Audiometric notch

as a sign of noise induced hearing loss.

Occup Environ Med 2001; 58: 46 – 51

11. Francois-Xavier Lesage, Nicolas Jovenin,

Frederic Deschamps, Samuel Vincent. Noise-

induced hearing loss in French police

officers. Occupational Medicine 2009;

59:483 – 486.

12. Shu-Ju Chang, Chin-Kuo Chang. Prevalence

and Risk Factors of Noise-induced Hearing

Loss among Liquefied Petroleum Gas (LPG)

Cylinder Infusion Workers in Taiwan.

Industrial Health 2009; 47: 603 – 610

13. SunamaniKarketta,

RajendraGartia,SomanathBagh. Occupational

hearing loss of the workmen of an open cast

chromite mines. Indian journal of

occupational and environmental medicine.2012;16(1) :18-21



828

Revathi et al., Int J Med Res Health Sci. 2013;2(4): 828-832


&

Health Scienceswww.ijmrhs.com Volume 2 Issue 4 Oct-Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886Received: 16th Aug 2013 Revised: 10th Sep 2013 Accepted: 21st Sep 2013

Research article

A COMPARATIVE STUDY ON LIFESTYLE AND METABOLIC PROFILE IN NORMAL

AND OBESE INDIVIDUALS

* Revathi R1, Swetha S

2, MeghalathaTS

1,Arunakumari R

3

1Lecturer,

2Assistant professor ,

3Professor and Head , Department of Biochemistry, Karpaga Vinayaga

Institute of Medical Sciences, Chinna Kolambakkam, Palayanoor, Madhuranthakam, Tamil Nadu


ABSTRACT

Background/Aim: The aim of the present study was to evaluate the lifestyle and metabolic profiles in

normal and obese. Material and Methods: A cross sectional study design was employed. Information

on body weight, height, body fat, food choices, diet and physical activity behavior were collected by a

questionnaire among 100 obese adults aged 18-35 years and compared with healthy individuals as

controls. Blood samples were collected to analyze blood glucose, heamoglobin and total cholesterol.

Result: Mean BMI for obese were 36.2±5 About 50% reported consuming no fruits or vegetables,

while 80% preferred fried food over other forms of cooked food. The majority (60%) engaged in <40

min of physical activity a day. Significant number of adults had Hb>13mg/dl. Blood glucose levels

(>100) & total cholesterol levels (>200) significantly higher (p<0.05) in obese individuals compared to

control. Conclusions: Dietary and physical activity behaviour of the participants were generally poor.

High blood glucose and cholesterol levels found among obese compared to normal. Innovative ways to

improve consumption of fruits and vegetables and increase physical activity among the obese are

needed.

Keywords: BMI, Waist circumference, Obesity

INTRODUCTION

Obesity has reached epidemic proportions in

India in the 21st

century with morbid obesity

affecting 5% of the country’s population1. India

is following a trend of other developing countries

that are steadily becoming more obese. The rate

of growth alarming considering that overweight

and obesity is a major health problem among

adults, but weight and dietary problems usually

start when people are children or adolescents.

There has been a steady increase in the

prevalence of overweight since the mid 1960’s

and the drastic increase is particularly notable in

recent years.2

If obesity extends into adulthood, it

puts individuals at risk for serious health

consequences, including type 2 diabetes,

osteoporosis and some cancers3-6

.

There are several eating patterns developed

during childhood and adolescence that can have

an immediate impact on overall health as well as

the noted long term consequences, such as type2

DOI:10.5958/j.2319-5886.2.4.132



829


diabetes. A high consumption of soft drinks and

juices may contribute to an imbalance between

intake and expenditure due to reduced effect on

satiety as compared to solid foods. Other dietary

patterns, which may be associated with increased

risk of obesity in adolescents, include skippingbreakfast and a low intake of fruits and

vegetables. Moreover, research indicates that

unhealthy dietary patterns (eg. dieting, high fat

diet, fast food, limited fruits and vegetables and

skipping breakfast) are linked to other high-risk

activities such as tobacco and drug use.7,8

This study therefore sought to assess lifestyle and

metabolic profile overweight/obesity as well as

their nutritional status.


The study was conducted in the department of

biochemistry in Karpaga Vinayaga Institute of

Medical Sciences, after the permission of the

Institutional Ethics Committee, Karpaga

Vinayaga Institute of Medical Sciences and

further sample processing has been done after

getting approval from the patient.Study design: A cross sectional study

Study population: 100 overweight/obese

individuals aged 18-35yrs were randomly

selected from sub rural hospital. Normal healthy

individuals with age matched controls were

taken.

Exclusion criteria: Hypertension, aneamia,

diabetes mellitus and other endocrine disorders.

A semi-structured questionnaire was

administered to solicit information on socio-

demographic variables like age and gender of

individuals, educational and occupational status

of parents as well as on food choices, diet and

physical activity.

To assess overweight and obesity in different age

groups, including adolescents, weight for height

is considered statistically valid measure9. The

preferred measure of weight for height is body

mass index (BMI).

BMI is accepted internationally as a standard for

the assessment of overweight and obesity in

adults because it correlates very highly with bodyfat

10, and it is especially well suited for

adolescents9

and adults. Waist circumference was

measured midway between the lowest rib and the

superior border of the iliac crest with a flexible

tape.

Dietary habits: To evaluate dietary habits, a

semi structured questionnaire was used to solicit

information on frequency of meal (breakfast,

lunch, supper and snacks) consumption.Physical activity (PA) behavior: To estimate

the PA habits, individuals were asked about the

number of minutes spent watching television,

walking, running, skipping, bicycle riding,

dancing or any indoor games.

Collection and preparation of samples:

Blood samples were collected after a twelve hour

fasting period (Overnight fasting) under aseptic

conditions, the obtained blood sample was

centrifuged and plasma was separated.

The plasma was analysed for the metabolic

parameters that includes, Glucose estimated by

GOD-POD method11

, Lipid profile analysis12

,

Haemoglobin by Acid Haematin

method13(SAHLI’S Haemoglobinometer).


All the data was analyzed by using SPSS

(version 16 for windows).continues variables are

presented as mean values and their standarddeviations (SD) and categorical variables as

frequencies, percentages or proportions. For all

comparisons-values<0.05 was considered

statistically significant.



830


RESULT

Table 1: Physical profile of the participants

Variables Normal (n=100) Obese (n=100) P- value

Age (years) 29.8 ±10.3 29.5 ± 9.8 0.04

BMI (kg/m²) 21.5 ± 2.0 36.2 ± 5.00.010

Waist circumference (cm) 35.5 ± 2.0 120.2 ± 9.0

0.010Hip (cm) 45.2 ± 0.72 130.0 ± 8.0

Waist/hip ratio 0.77 ± 0.05 0.92 ± 0.03

Table 1 shows increased BMI & waist/ratio compared to controls (p<0.05).The levels of BMI,

Waist/Hip ratio was significantly higher (p<0.05) in obese compared to normal subjects.

Table.2: Biochemical profile of the participants

Biochemical profileNormal

(n=100)Obese (n=100) p-value

Hb (g/dl) 13.2 ± 1.2 14.7 ± 0.9 0.05

Blood glucose (mg/dl) 87.5 ± 13.3 172.6 ± 19.2 0.02

Total Cholesterol (mg/dl) 179.6 ± 22.5 213.4 ± 30.3 0.02

Triglycerides (mg/dl) 120 ± 12.5 170 ± 20.5 0.03

HDL (mg/dl) 60 ± 25.8 35 ± 15.6 0.04

LDL (mg/dl) 95 ± 33.2 145 ± 20.2 0.02

Table 2 shows increased levels of Heamoglobin in obese compared to normal. Blood glucose and lipid

profile. The levels of Blood glucose and lipid profile was significantly higher (p<0.05) in obese

individuals compared to normal subjects.

DISCUSSION

Evidence in recent years suggests that obesity is

growing rapidly across the globe. Obesity is one

of the most important health related problemsfacing humans today. Obesity is associated with

increased mortality and morbidity through its

association with cardiovascular disease14

and a

variety of related conditions such as type 2

Diabetes Mellitus, musculoskeletal problems,

various malignancies and polycystic ovary

syndrome15

.The increasing prevalence of obesity

is a global phenomenon that is showing no signs

of abatin16.

Therefore, the public health

implications of obesity and its pathological

sequelea are set to become even more of a

priority for future governments and health-care

providers.

In our study, although we observed a regulareating pattern for most of the participants, food

choices were generally poor as these participants

preferred high calorie foods to diet rich in fruits

and vegetables. We observed that this age group

often remembered and purchased foods like

French fries, sweet and salty snacks, soft drinks

and fast foods. In a personal communication with

some participants, they revealed that they do not

consume fruits and vegetables daily because they

don’t find them in colleges/home.



831


Among various indices, the BMI was selected as

an indicator for total obesity. Furthermore, in this

particular population the BMI is significant and

highly correlated with other indices used for

estimation of total body fatness17

.The WC, the

waist hip ratio was selected as an indicator of obesity since WC is easy to measure and the

measurement error is low due to large

circumference.

In our findings we found significantly higher

hemoglobin levels among obese compared to

non-obese. The mechanism underlying the

relationship between obesity and hemoglobin

level is not well established. It has been

suggested that obese individuals have higherfood consumption and therefore, ingest more

iron18

.

In our study we also found that blood glucose

and total cholesterol was significantly higher in

obese compared to control. However, obesity is

known to be more common among individuals of

poor socioeconomic status of whom their diet is

usually characterized by higher carbohydrate

intake19

and high saturated fat in their diet

increases chances of having weight problems20.

Several studies have confirmed that overweight

and obese are at a risk of nutrient deficiencies as

a consequence of inadequate dietary intake

related to poor education or social factors, eating

disorders, unbalanced weight- reducing diets or

comorbidities21

.

CONCLUSION

Our findings show that overweight and obese

individuals have inadequate dietary and physical

activity behaviors. These behaviors may have

resulted in the poor nutritional status observed ie.

The prevalence of averagely high BMI, High

percentage body fat and high levels of

heamoglobin. This suggests that obesity control

to be achieved, concerned efforts of stakeholders

like the family, school, community, media,

government and food industry is crucial to createan environment that encourages healthy eating

behaviors among the obese. Innovative ways to

improve consumption of fruits and vegetables

and increase physical activity among obese

individuals are urgently needed.

REFERENCES

1. India facing obesity epidemic: experts.

http://hindu.com/2007/10/12stories/20071012

60940600. htm).

2. Lobstein T, Baur L and UauyR. Obesity in

children and young people: A crisis in public

health. Obes. Rev. 2004;5(1): 4-10.

3. Reilly JJ, Methven, McDowell ZC, Hacking

B, Alexander D. Health consequences of

obesity. Arch. Dis. Child. 2003,88: 748-524. Viana V, Sinde S and Saxton JC .Children's

eating behavior questionnaire: Associations

with BMI in Portuguese children. Brit. J.

Nutr., 2008.100:445-450.

5. Freedman DS, Khan LK, Dietz WH,

Srinivasan SR, Berenson GS. Relationship of

childhood obesity to coronary heart disease

risk factors in adulthood: The bogalusa heart

study. Pediatrics, 1997; 108: 712-18.

6. Must A, Jacques PF,Dalal CE, Bajema CJ,

Dietz WH. Long- termmorbidity and

mortalityo f overweighta dolescentsN. Eng J

Med. 1992 ;327:1350 – 55.

7. Heald F. Fast food and snack food: beneficial

or deleterious. J Adol Health. I 992:l 3:380-

383.

8. LytleL A, Roski J, Un healthy eat in agndo

their risk- takin behavior: are they related?

Annals New York Academy of Sciences.

1997 : Bl7 496.

9. Himes JH, Dietz WH. Cuidel inesfor over

weight in adolescent preventive services:

Recommendat ions from an expert commrttee

Am J Clin Nutr. l994; 5 9 : 3 0 7 – 3.

10. Guillaume M . Def in obesity in childhood:

current practice. Am J Clin Nutr. 1999;70

(l2):6l -13 0

11. Carl A.Burtis, Edward R.Ashwood,Estimation of glucose by glucose oxidase



832


method.Tietz., Text book of clinical

chemistry.1994,chapter 24:778-780.

12. Carl A.Burtis, Edward R. Ashwood,

Measurement of lipids, lipoproteins and

apolipoproteins Tietz.,Text book of clinical

chemistry 3rd edition.1994,chapter 25:837-845.

13. G.K. & Pal, Pravati, Sahli’s acid heamatin

method.Text book of practical physiology 2nd

edition.2006:13.

14. Hubert HB, Feinleib M, McNamara PM,

Castelli WP. Obesity as an independent risk

factor for cardiovascular disease: a 26-year

follow-up of participants in the Framingham

Heart Study. Circulation

1983, 67:968-77.15. TM Barber, MI McCarthy, JA Wass, S

Franks: Obesity and polycystic ovary

syndrome. Clin Endocrinol (Oxf) 2006,

65:137-45.

16. Bessesen DH. Update on obesity. J Clin

Endocrinol Metab 2008, 93:2027-34.

17. Khalid MEM, Mahmoud MSW, Elbagir

MahmadK. Fat indices in high and low

altitude populations in south western soudi

Arabia. Ann Saudi Med 1997;17:312-15

18. Camitta BM, Nathan DG. Anemia in

adolescence. Postgrand Med J 1975;57:151-

155

19. Theodore B.health implications of

overweight and obesity in the unitedstates.

Ann intern Med 1985;103:983-88

20. Katherine M, Flegal et al. Journal of

American medical association prevalence and

trends in obesity among U.S adults 1999-2008; January 20,2010.

21. Allard J. Should nutritional status be

routinely assessed and corrected before

bariatric surgery? Nat Clin Pract

Gastroenterol Hepatol. 2007;4:130 – 31



833

Tushar et al., Int J Med Res Health Sci. 2013;2(4): 833-839


&

Health Sciences

www.ijmrhs.com Volume 2 Issue 4 Oct - Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886

Received: 18th

Aug 2013 Revised: 11th

Sep 2013 Accepted: 22nd

Sep 2013

Research article

HAEMODYNAMIC RESPONSE TO NASOTRACHEAL INTUBATION UNDER GENERAL

ANAESTHESIA: COMPARISON BETWEEN FIBEROPTIC BRONCHOSCOPY AND DIRECT

LARYNGOSCOPY

*Tushar Bhavar1, Punia TS

2, JPS Bhupal

3, Harpreet Babrah

4, Banreet Bagri

5, Abhishek Singla

6

1

Assistant Professor,

6

Resident, Dept. of Anaesthesia & Intensive Care, Rural Medical College, PIMSLoni, Maharashtra, India2Professor & Head,

3Professor,

4Resident,

5Resident, Dept. of Anaesthesia & Intensive Care GMC,

Rajindra Hospital, Patiala.


ABSTRACT

Study Objective: To compare haemodynamic response in nasotracheal intubation under general

anaesthesia between FOB and DLS as one accomplished with a FOB is thought to attenuate the

circulatory responses to intubation as stimulation of the oropharyngeal structures may be avoided.Design: Randomized, prospective study. Patients: 50 ASA grade I and II patients of both sexes in the

age group of 18 - 60 years scheduled for an elective surgery under general anesthesia. Interventions:

Patients were randomly allocated to nasotracheal intubation facilitated with either the FOB [Group I] or

the DLS [Group II]. A uniform protocol of anesthesia was used. Measurements: Heart Rate [HR],

Systolic Blood Pressure [SBP], Diastolic Blood Pressure [DBP] & Mean Arterial Pressure [MAP] in

the two groups were compared at their baseline, post-induction values, at the time of insertion of the

scope, immediately after intubation & at 3, 5 and 10 minutes after intubation. Results: Haemodynamic

response in the form tachycardia, increase in SBP, DBP & MAP occurred in nasotracheal intubations

with both the fiberoptic bronchoscope and with direct laryngoscope. Tachycardia of similar magnitude

was noted in both the groups following insertion of scope and after intubation whereas SBP, DBP &

MAP were significantly high in Group II [p<0.01] at the time of intubation & SBP immediately after

intubation was significantly high in Group I[p<0.05] Conclusions: Fiberoptic bronchoscopy provides no

advantage over conventional laryngoscopy, in terms of decreasing the hemodynamic response to

nasotracheal intubation under general anaesthesia.

Keywords: Nasotracheal intubation, General Anaesthesia, Hemodynamic Responses, Fibreoptic

Bronchoscope, Macintosh Direct Laryngoscope, Difficult Intubation.

INTRODUCTION

Alfred Kirstein [1863 – 1922] first described

direct visualization of the vocal cords on 23

April 1895 and fiberoptic assisted tracheal

intubation was introduced into anaesthetic

DOI:10.5958/j.2319-5886.2.4.133



834


practice by Murphy in 1967 and Taylor & Towey

in 19721-3

. The popularity of fiberoptic intubation

has increased since the introduction of delicate

flexible fiberoptic laryngoscopes. However, it

remains a skill possessed by a minority of

anaesthetists in this country, the principalobstacles to dissemination of competence being

the relatively fragile nature of a costly instrument

and the difficulties of training. Fiberoptic

nasotracheal intubation can avoid the mechanical

stimulus to oropharyngolaryngeal structures

thereby it is likely to attenuate haemodynamic

response.4


After the Institutional Ethics Committee

approval, the study was conducted in Rajindra

Hospital Patiala in 50 patients of either sex, aged

18 to 60 yrs of ASA grade I and II scheduled to

undergone elective surgery under general

anaesthesia requiring intubation. A written

informed consent was obtained from each

patient. The patients were divided in two groups

randomly of 25 patients each.

Exclusion criteria: Patient’s refusing; those with

anticipated difficult airway, obesity,

cardiovascular and endocrine diseases, bleeding

disorders, history of nasal surgery or trauma,

nasal polyp or on drugs known to produce

changes in heart rate and blood pressure like beta

blockers, digitalis, calcium channel blockers, oral

contraceptives were excluded from study.

After a proper pre-anaesthetic checkup and

assessing fasting status patients were pre-

medicated with inj Glycopyrolate [0.2mg] I.M,

inj Midazolam [2mg] + Promethazine [25mg] IM

30 min before the elective surgery. Fifteen

minutes before shifting the patient to the OT

table, 0.1% Oxymetazoline nasal drops where

instilled in both the nasal passages. All patients

received tab. Alprazolam 0.25 mg before sleep

and 6 am on the day of surgery. After the patient

is brought to operation table baselinemeasurements of heart rate, blood pressure and

Spo2 were taken. Fentanyl in a dose of 1.5μg/kg

was administered intravenously 5 minutes before

induction. Patients were pre oxygenated with

100% O2 for 3 minutes.

General anaesthesia was induced with an

intravenous injection of Propofol, 2mg/kg and

intubation was facilitated with the use of Rocuronium 0.9 mg/kg intravenously. Then

patient were ventilated with 100 % oxygen.

Intubation was commenced exactly after 90

seconds of giving inj. Rocuronium.

In group I, nasotracheal intubation was carried

out with the aid of fiberoptic bronchoscope and

in group II with the aid of laryngoscope. A 7.00

mm internal diameter, cuffed endotracheal tube

[ETT] was used for female patients and 7.5 mminternal diameter cuffed ETT for male patients.

In group I the ETT lubricated with lignocaine

jelly was threaded over the fiberoptic

bronchoscope. The fiberoptic bronchoscope was

then introduced in the more patent nasal passage

and once in nasopharynx, glottis identified and

scope then advanced 5 to 7 cm beyond the

laryngeal inlet till carina is visible. The ETT was

then advanced into the trachea over the scope

and fiberoptic bronchoscope removed gently

through the endotracheal tube looking for

position of ETT.

Similarly in group II, ETT was introduced

through the more patent nasal passage. Direct

laryngoscopy was performed to visualize the

glottis and the endotracheal tube advanced into

trachea with the help of Magill's forceps. In both

the groups, after introduction of ETT,

anaesthesia was maintained with O2:N2O:40:60along with 1% isoflurane. The following

parameters were observed: heart rate [HR],

systolic blood pressure [SBP], diastolic blood

pressure [DBP] and mean arterial blood pressure

[MAP]. These parameters were recorded at

following time intervals: baseline value, after

induction, at the time of insertion of

laryngoscope/fiberoptic bronchoscope,

immediately after intubation and thereafter at 3,5 and 10 minutes. ECG and SPO2 were

monitored continuously as per the intervals



835


mentioned above. The study was terminated at

the end of 10 minutes after intubation. However

vitals were monitored throughout the surgery.

Time of intubation from cessation of mask

ventilation to connection of breathing circuit to

ETT was noted. And postextubation epistaxis if any noted.

Statistical analysis: Data was analyzed with

Graph Pad Prism 6.01 statistical softwares. The

male/female distribution & epistaxis between the

two groups were compared using fishers exact

stastical test. Demographic data, blood pressure,

heart rate, time of intubation & Spo2 were

compared between the two groups usingunpaired Students t-test.

RESULT

Table.1: Comparison demography, time of intubation, epistaxis & Spo2

Variables Group I Group II P value

Age [yrs] 36.84 ± 22.28 37.04 ± 21.06 0.9483

Sex [M:F] 9:16 3:22 0.0955

Weight [Kg] 60.2 ± 9.66 59.08 ±13.9 0.5112

Time req for intub. 69.52±37.18 18.2 ± 7.12 <0.0001*

Epistaxis 3[12%] 1[4%] 0.6092

Spo2 98.72±6.1 99.96±0.4 0.048*

Table.2: Comparison of haemodynamics FOB vs DLS Group.

Group I Group II P value

HR (bpm) Baseline 83.16±14.7 82.72±16.83 0.84

Aft. Induct. 77.76±13.7 76.12±13.88 0.40

At Insertion 88.96±15.85 88.56±21.99 0.88

Imm. Aft intub. 86.08±15 85.8±20.39 0.91

3min 83.04±14.58 82.28±13.4 0.705 min 81±14.44 80.52±12.65 0.80

10 min 79.84±14 79.4±12.62 0.81

SBP (mmHg) Baseline 122.48±14.24 122.04±14.67 0.83

Aft. Induct. 108.6±12.87 107.92±19.06 0.76

At Insertion 127.96±15.05 140±28.67 0.0005*

Imm. Aft intub. 141.4±16.4 133.16±31.23 0.02*

3min 121.36±14.54 116.64±21.3 0.07

5 min 118.8±13.61 114.12±22.8 0.08

10 min 116.52±13.81 114.36±22.71 0.42

DBP (mmHg) Baseline 79±13.65 79.6±18.77 0.79

Aft. Induct. 67.96±11.41 68.16±19.61 0.93

At Insertion 82.56±14.46 91.96±26.28 0.002*

Imm. Aft intub. 91.24±16 87.24±24.25 0.17

3min 78.64±14 75.24±21.8 0.19

5 min 76.72±13 74.44±19.73 0.33

10 min 76.6±13.53 75.4±24.8 0.67

MAP(mmHg) Baseline 93.5±13.5 93.75±15.68 0.90

Aft. Induct. 81.5±11.5 81.4±16.93 0.96

At Insertion 97.7±14.28 107.97±24.56 0.0007*

Imm. Aft intub. 107.96±15.72 102.55±24.69 0.07

3min 92.88±13.81 89.04±20.53 0.12

5 min 90.75±12.85 87.67±18.1 0.17

10 min 89.91±13.3 88.39±22.8 0.56

*Significant (P<0.05), values=Mean±SD



836


Mean age, weight & M:F were statistically

insignificant and so both groups were

comparable demographically. Epistaxis was seen

in both groups and was statistically insignificant.

It depends on proper preparation of patients.

Spo2 was continuously monitored duringintubation using either technique and it was

found that patients maintained 100% saturation

during induction, at the time of insertion of

FOB/DLS, at 3min, 5min and 10 min in both

Groups. In Group I, 4 patients and in group II, 1

patient had lower reading immediately after

intubation. Difference was statistically analysed

and found to be significant [p<0.05]. Mean time

for intubation in Group I using FOB was highcomparing that with DLS Group II. Difference in

intubation time was found to be statistically

significant [p<0.0001]. There was significant fall

of all parameters after induction comparing with

baseline [p<0.0001] in both groups. Comparing

both groups there was no significant difference.

At the time of insertion of FOB/DLS there was

significant rise of HR, SBP, DBP & MAP.

There was no statistically significant difference

of HR between two groups whereas SBP, DBP &

MAP were significantly high in Group II

[p<0.01]. HR remained high even after

intubation and returned to baseline value at 3min

in both groups. SBP, DBP & MAP further

increased after intubation and returned to

baseline value at 3min in FOB group while HR,

SBP, DBP & MAP remained high after

intubation but didn’t increase and returned to

baseline value at 3min in DLS group. Similarlymaximum mean HR was noted at the time of

insertion of FOB while maximum mean SBP,

DBP & MAP were seen immediately after

intubation using FOB in Group I. whereas

maximum readings of all parameters were noted

at the time of insertion of DLS in Group II.

Comparing both groups SBP immediately after

intubation was significantly high in Group I

[p<0.05]. In both groups HR, SBP, DBP andMAP were at baseline level at 3min and there

was no statistically significant difference

between two groups. In both groups HR, SBP,

DBP and MAP was below baseline at 5min and

10min.

DISCUSSION

Flexible fiberoptic intubation of the trachea is

now the method of choice when direct

laryngoscopy is expected to be difficult. The

cardiovascular response to tracheal intubation,

although transient, may be harmful to some

patients, mainly those with myocardial or

cerebrovascular disease. So we have conducted a

study to find out whether FOB has some

beneficial effect attenuating this hemodynamic

effect of intubation. Spo2 immediately afterintubation was low in group I and is due to

longer intubation time required for FOB.

Difference in intubation time was found to be

statistically significant [p<0.0001]. Our findings

were consistent with most of the studies

conducted.5-11

This difference is because FOB is

more technical, requires hand eye coordination

and one has to reach till carina using FOB and

then guide ETT over it and then withdraw FOB

looking for tube position whereas in DLS we

have direct vision of vocal cords, and also in

FOB the field of view is restricted.5

At the time

of insertion of FOB/DLS there was significant

rise of HR, SBP, DBP & MAP. This increase is

due to stress response to

laryngoscopy/bronchoscopy.9

There was no

statistically significant difference of HR between

two groups whereas SBP, DBP & MAP were

significantly high in Group II [p<0.01]. This

finding is not in acceptance with study by Michal

Barak, et al. which shows no significant

differences this may be due to different route of

intubation as they had used oral route for

intubating.9

Our results are consistent with study

conducted by J. E. Smith, et al. These differences

may arise because of the combined effects of

differences in airway stimulation and differences

in the duration of laryngoscopy between the twotechniques. The fibrescope may produce less

mechanical pressure on the tissues of the anterior



837


pharynx, which may therefore induce less reflex

sympathetic activity.6

SBP, DBP & MAP further

increased after intubation and returned to

baseline value at 3min in FOB group while HR,

SBP, DBP & MAP remained high after

intubation but didn’t increase and returned tobaseline value at 3min in DLS group. Comparing

both groups SBP immediately after intubation

was significantly high in Group I [p<0.05]. This

findings are consistent with study conducted by

J. E. Smith which shows that the increase in

systolic pressure was sustained for a longer

period in the fiberoptic group and concluded that

the cardiovascular responses associated with

fiberoptic intubation under general anaesthesiaappear to be more severe.

5This findings are also

consistent with study conducted by J. E. Smith,

et al. which shows that highest mean systolic

pressure in the fiberoptic group was delayed until

the second minute.6

This findings are also

consistent with most other studies.12,13

This may

be due to following reasons:

1. It has been shown that the longer the

intubation time the more likely is it to

develop hypercapnia, which can result in

hypertention and tachycardia.4

Longer time

may tend to produce more sympathetic

activity6

2. FOB necessitates the lifting of the jaw

upward to make a clear passage for the FOB

and for the tracheal tube to enter the glottis.

Lifting of the jaw upwards itself is sufficient

to cause a cardiovascular response similar to

those observed in the laryngoscopicintubation.

4,13

3. The advancement of the tracheal tube over

the FOB is often impeded when the

Murphy’s tip catches on the downward

sagging epiglottis, arytenoid cartilage, vocal

cords and anterior tracheal wall. On such

occasions, the successful intubation often

requires some specific maneuvers e.g.

rotating the tracheal tube, further lifting jawupward and adjusting the patient’s head-neck

position.4,13

4. During the fiberoptic intubation, the insertion

cord of the FOB must be placed into the

trachea for guidance followed by advancing

the tracheal tube over the insertion cord into

the trachea and then the FOB is removed.

This can cause repeated friction and irritationto the trachea.

4

5. The traction on the tongue which is necessary

to clear the airway which itself is a potent

stimulus as the Macintosh blade.5

6. Tracheal tube insertion itself is most invasive

stimuli.14

7. Longer intubation time may also cause

weaning of anaesthetic effect of inhaled

anaesthetic agent, hypoxia & hypercarbia inFOB group and minimal or negligible

interruption of inhaled anaesthetic agent in

DLS group this drawback was eliminated by

using a mask adapter by Makoto Imai, et al.

and found that FOB resulted in milder

hemodynamic changes compared to

conventional laryngoscopy, as they were able

to maintain anaesthesia during intubation.15

Even though there was significant high

haemodynamic response to laryngoscopy

compared to bronchoscopy at the time of

intubation which may be due to sudden severe

stress response to DLS compared to FOB during

intubation and also in DLS oropharyngeal

structures alongwith nasopharyngeal ones are

stimulated, there is no advantage of FOB in

attenuating haemodynamic response as there was

significant high SBP after intubation and SBP,

DBP and MAP remained high for longer time.This has been shown by most of the studies.

4-9,

12,13, 16-19

CONCLUSION

Fiberoptic bronchoscopy provides no advantage

over conventional laryngoscopy, in terms of

decreasing the hemodynamic response to

nasotracheal intubation under general

anaesthesia.



838


ACKNOWLEDGEMENT

It gives me pleasure to render my thanks to my

parents, and esteemed teachers Dr.T.S.Punia,

Dr.JPS Bhupal, Dr. Parmod Kumar & Dr. Rahul

Kunkulol. I thank my friends Dr.Subhash,Dr.Vishal, Dr.Nidhi, Dr.Jeevraj, Dr.Pavan,

Dr.Ruhi, Dr.Divya and all my department staff

for their support and help. Lastly, I thank all the

patients undergoing treatment who volunteered

to participate in this study and without which this

work would have not been possible.

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along the path of laryngoscopy. Acta Chir

Iugosl. 2009; 56(1): 61-66.

2. Murphpy P. A fibre-optic endoscope used for

nasal intubation. Anaesthesia 1967; 22: 489-

91.

3. Taylor PA, Towey RM. The broncho-

fiberscope as an aid to endotracheal

intubation. British journal of anaesthesia.

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4. Zhang Guo-hua, Xue Fu-shan, LI Ping, SUN

Hai-yan, LIU Kun-peng, XU Ya-chao. Effect

of fibreoptic bronchoscope compared with

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responses to orotracheal intubation. Chin

Med J 2007; 120(4): 336-38.

5. Smith JE. Heart rate and arterial pressure

changes during fibreoptic tracheal intubation

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6. Smith JE, Mackenzte AA, Sanghera SS,

Scott-knight. Cardiovascular effects of

fibrescope-guided nasotracheal intubation.

Anaesthesia 1989;44: 907-10.

7. Finfer SR, MacKenzie SI, Saddler JM,

Watkins TG. Cardiovascular responses to

tracheal intubation: a comparison of direct

laryngoscopy and fibreoptic intubation.Anaesth.Intens.care 1989: 17: 44-48.

8. Schaefer HG, Marsch SCU. Comparison of

orthodox with fibreoptic orotracheal

intubation under total i.v. anaesthesia. British

Journal of Anaesthesia 1991; 66(5): 608-10.

9. Michal Barak, Avishai Ziser, Avital

Greenberg, Sophie Lischinsky, BenoRosenberg. Haemodynamic and

Catecholamine Response to Tracheal

Intubation: Direct Laryngoscopy Compared

with Fibreoptic Intubation. Journal of

Clinical Anesthesia 2003; 15: 132 – 36.

10. Jakusenko, Kopeika, Mihelsons, Nagobade,

Vija Putniña, Pavars. Comparison of stress

response performing endotracheal intubation

by direct laryngoscopy, fibreoptic intubationand intubation by the glidescope

laryngoscope. 2008;62(4):176-81.

11. Aghdaii N, Azarfarin R, Yazdanian F, Faritus

SZ. Cardiovascular responses to orotracheal

intubation in patients undergoing coronary

artery bypass grafting surgery. Comparing

fiberoptic bronchoscopy with direct

laryngoscopy. Middle East J Anesthesiol.

2010;20(6):833-38.

12. Xue FS, Zhang GH, Sun HT, Li CW, Li P,

Liu KP et al. A comparative study of

haemodynamic responses to orotracheal

intubation with fibreoptic bronchoscope and

laryngoscope in children. Pediatric

Anesthesia 2006; 16: 743 – 47.

13. Ranju Singh, Pramod Kohli, Sunil Kumar.

Haemodynamic Response to Nasotracheal

Intubation under General Anaesthesia – A

Comparison between FibreopticBronchoscopy and Direct Laryngoscopy. J

Anaesth Clin Pharmacol 2010; 26(3): 335-39

14. Kapil Gupta, Kiran Kumar Girdhar, Raktima

Anand, Sumanth Mallikarjuna Majgi,

Surinder Pal Gupta, Payal Bansal Gupta.

Comparison of haemodynamic responses to

intubation: Flexible fibreoptic bronchoscope

versus bonfils rigid intubation endoscope.

Clinical Investigation. 2012;56(4):353-58.15. Makoto Imai, Chihoko Matsumura, Yukari

Hanaoka, Osamu Kemmotsu. Comparison of



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Watanabe, Yoshitaka Uchihashi, Hideyuki

Higuchi, Tetsuo Satoh. Evaluation of the

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Sun HT, et al. Blood pressure and heart rate

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direct laryngoscopy and a fibreoptic method.

Anaesthesia May 2006; 61(5): 444-48.

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Mohammad Ali Sahmeddini Kazem Samadi.

Comparison of the haemodynamic changes

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840

Amit et al., Int J Med Res Health Sci. 2013;2(4): 840-847


&

Health Sciences




thSep 2013

Research article

MUPIROCIN RESISTANCE IN CLINICAL ISOLATES OF STAPHYLOCOCCUS AUREUS IN

A TERTIARY CARE HOSPITAL SET UP IN NORTH INDIA

*Singh Amit K, Venkatesh Vimala, Singh Mastan

Postgraduate Department of Microbiology, King George Medical University, Lucknow, U.P, India


ABSTRACT

Background: Mupirocin is a topical antibiotic used for nasal decolonisation of methicillin resistant

Staphylococcus aureus (MRSA). While resistance to mupirocin has been described it is usually not

tested for in most clinical laboratories. Aim: The present study was carried out to detect the occurrence

of mupirocin resistance in clinical isolates of Staphylococcus aureus in a tertiary care hospital set up in

northern India. Materials and Methods: Staphylococcus aureus isolates obtained from clinical samples

received in the microbiology laboratory over a period of one year were included in this study. Mupirocin

resistance was detected by three phenotypic methods; disk diffusion method using 5µg and 200µgmupirocin disk to determine low-level and high-level resistance, broth microdilution method and an agar

dilution method for determining minimum inhibitory concentrations. Methicillin sensitivity was also

determined in the study isolates. Results: Of 250 non-duplicate Staphylococcus aureus isolates

obtained, 5 (2%) were found resistant to mupirocin. All mupirocin resistance isolates were shown to

have high-level resistance (minimum inhibitory concentration > 512µg/ml). All mupirocin resistant

isolates were also resistant to methicillin. Results obtained by all three phenotypic methods showed

good correlation. Conclusion: High-level mupirocin resistance is present in the northern Indian

population which may be of major concern to prevent the spread of MRSA in hospitals and community.

Keywords: Mupirocin resistance, MuH, MRSA

INTRODUCTION

Methicillin-resistant Staphylococcus aureus

(MRSA) is one of the major nosocomial

pathogen in healthcare institutions and

increasingly reported from hospitals and the

community worldwide.1, 2

Carriage of MRSA in

nose, axilla, perineum and hands of patients and

health care personnel is an important risk factor

for MRSA acquisition and spread.3

Decolonisation from the site of carriage is one of

the modalities for prevention of MRSA

infections in healthcare settings.4

Mupirocin

(pseudomonic acid A) derived

from Pseudomonas fluorescens is an important

topical antibiotic ointment for the nasal

decolonisation of MRSA in carriers.5-8 It acts by

binding specifically to the bacterial isoleucyl-

DOI:10.5958/j.2319-5886.2.4.134



841


tRNA synthetase (IRS) enzyme and inhibits its

protein synthesis.9

Along with its use as a

decolonising agent in health care personnel and

patients, it has also been used for treatment of

staphylococcal skin and soft tissue infections.10,11

Resistance to mupirocin is being increasinglyfound due to its irrational use, which leads to

improper decolonisation of MRSA from the site

of carriage and spread of infection.12,13

Although there is no such guidelines published

for mupirocin susceptibility testing, traditionally

susceptible strains have minimum inhibitory

concentration (MIC) ≤2 μg/ml while those

having a MIC of ≥4 μg/ml were designated as

resistant, and by disk diffusion method thosewith zone diameter of ≥14 mm with a 5μg disk

were taken as susceptible while zones of ≤14 mm

were considered resistant14

. However, recently

mupirocin-resistant strains have been grouped

into two distinct phenotypes: low-level resistance

(MuL) with MICs of 8-256 μg/ml, and high-level

resistance (MuH) with MICs ≥512 μg/ml. An

isolate with MIC ≤4 μg/ml is considered as

mupirocin-sensitive. With the previously used 5

μg mupirocin disk, MuL and MuH strains cannot

be differentiated. However it can be performed

by concomitant use of 5 μg and 200 μg

mupirocin disks.15

MuH strains have been found to be associated

with failure of mupirocin as a decolonising agent

as well as for treatment of skin and soft tissue

infections.16

Plasmid-mediated mupA encoding a

novel isoleucyl RNA synthetase is a major

genetic mechanism seen in high-level mupirocinresistance isolates.

17,18Whereas base pair

changes in native isoleucyl RNA synthetase gene

is seen in low-level mupirocin resistance

isolates18

. Various studies suggest that during

mupirocin prophylaxis transfer of mupA gene

from normal commensal flora of skin such as

Staphylococcus epidermidis to MRSA is

responsible for emergence of mupirocin

resistance.

19

Thus, this study was carried out to determine the

rates of high-level and low-level mupirocin

resistance in Staphylococcus aureus by disk

diffusion and MIC methods and to evaluate its

association with methicillin-resistant isolates.


Staphylococcus aureus isolates recovered from

clinical specimens comprising pus, blood,

various swabs and sterile body fluids received in

the Postgraduate Department of Microbiology,

King George Medical University, Lucknow,

during a one year period from August 2011 to

July 2012 from patients who attended the

outpatient department (OPD) or were admitted to

various inpatient departments (IPD) of Gandhi

Memorial & Associated Hospitals were includedin the study. Isolates from urine were not

included.

Clinical specimens were processed and isolates

were identified as Staphylococcus aureus by

routine microbiological procedures. Non-

duplicate Staphylococcus aureus isolates were

tested for mupirocin resistance by disc diffusion

method, broth microdilution method and agar

dilution method.

In the disk diffusion method, mupirocin disks of

5μg (SD748, Himedia Labs, India) and 200μg

(CT0523B, Oxoid, India) concentration were

used. Zone diameter of > 14 mm for both disks

was taken as susceptible for mupirocin. Whereas,

isolates that showed zone diameters < 14 mm in

the 5 μg disk but > to 14 mm in the 200 μg disk

were considered to be low-level mupirocin

resistant strains.15

All isolates with zone

diameters < 14 mm for both 5μg and 200μg disks

were considered to be high-level mupirocin

resistant strains15

(Fig. 1).

The broth microdilution method was done for

determination of Minimum Inhibitory

Concentration (MIC) on Mueller-Hinton broth

(MHB) with a final mupirocin concentration

ranged from 0.25 μg/ml to 512 μg /ml (Fig. 2).

Similarly agar dilution method was done for

determination of MIC on Mueller-Hinton agar(MHA) with same concentration. Mupirocin

MIC of < 4µg/ml was taken as susceptible, that



Amit et al.,

of 8µg/ml to 256µg/ml as low-

and > 512 µg/ml as high level res

Detection of methicillin

Staphylococcus aureus isolates

as per Clinical Laboratory Sta

(CLSI) 2012 guidelines by usingdisk

20. Antimicrobial susceptibil

Fig.1: Demonstration of high-lev

diffusion method

Fig.2: Broth microdilution meth

isolates

Fig.3: Agar dilution method for de

Int J Med Res Healt

level resistance

istance (Fig. 3).

resistance in

ere performed

ndards Institute

cefoxitin (30μg) ity testing was

done as per CLSI guid

diffusion method for

ampicillin (10 µg),

clindamycin (2 µg),

linezolid (30 µg), tetr

(1.25/23.75 µg), vanctest of significance app

el mupirocin resistance and mupirocin sen

d for determination of MIC of mupirocin

termination of MIC of mupirocin in Staphyloc

842

h Sci. 2013;2(4): 840-847

lines by Kirby-Bauer disk

the following antibiotics:

ciprofloxacin (5 µg),

erythromycin (15 µg),

acycline (30 µg), septran

mycin (30 µg). Statistical lied z-test.

sitive phenotypes by disk

in Staphylococcus aureus

occus aureus isolates



843


RESULTS

Among the 250 non-duplicate Staphylococcus aureus isolates included in study, 133 (53.2%) were

MRSA. Of these, 5 i.e., 3.76% of MRSA were mupirocin resistant Staphylococcus aureus (MupRSA).

Mupirocin resistance was not detected in methicillin sensitive Staphylococcus aureus (MSSA) isolates.

Table.1: MupRSA and MRSH strains among total Staphylococcus aureus isolates in different samples

Table.2: Distribution of S. aureus, MRSA and MupRSA in different clinical wards

Table.3: Antimicrobial sensitivity pattern of MRSA and MupRSA isolates

Samples S. aureus MRSA (%) MuH (%) MuL (%) 95% CI P-value

Pus 142 78 (54.93) 2 (1.4) - 0.9-6.06 <0.0001*

Blood 48 27 (56.25) 3 (6.25) - 0.7-22.96 <0.0001*

Genitourinary

specimens

11 1 (9.09) - -

Respiratory

specimens

39 23 (58.97) - - - -

Miscellaneous 10 4 (40.0) - - - -

TOTAL 250 133 (53.2) 5 (2.0) 0.53-6.99 <0.0001*

MRSA= Methicillin resistant Staphylococcus aureus, MuH= High-level mupirocin resistance,

MuL= Low-level mupirocin resistance, CI= Confidence Interval, * = Significant

WARDS S. aureus MRSA (%) MupRSA

(%)

95% CI P-value

Surgical 115 69 (60) 2 (1.73) 1.06-6.86 <0.0001*

• General

surgery

54 23(42.59) 0 - -

• Orthopaedics 29 21(72.41) 1(3.44) 4.35-13.87 <0.0001*

• Neurosurgical 32 20 (62.5) 1(3.12) 4.55-14.55 <0.0001*

Gynaecology 11 5 (45.45) 0 - -Paediatrics 67 30 (44.77) 3 (4.47) 0.74-20.74 <0.0001*

Medicine 20 11 (55) 0 - -

OPD 37 23 (62.16) 0 - -

Total 250 133 (53.2) 5 (2.0) 0.53-6.99 <0.0001*

MRSA= Methicillin resistant Staphylococcus aureus, MupRSA=Mupirocin resistance

Staphylococcus aureus, CI= Confidence Interval, * = Significant

Antibiotics Sensitive (%) Intermediate (%) Resistant (%)MRSA MupRSA MRSA MupRSA MRSA MupRSA

Ampicillin 7 (5.26) - 7 (5.26) - 119(89.47) 5 (100)

Ciprofloxacin 36 (27.06) - 10(7.52) - 87 (65.41) 5 (100)

Clindamycin 46 (34.58) 1 (20) 9 (6.77) 1 (20) 78 (58.65) 3 (60)

Erythromycin 44 (33.08) 1 (20) 6 (4.51) 1 (20) 83 (62.41) 3 (60)

Linezolid 133 (100) 5 (100) - - - -

Septran 44 (33.08) 3 (60) 12(9.02) 1 (20) 77 (57.89) 1 (20)

Tetracycline 68 (51.13) 3 (60) 9 (6.77) 1 (20) 56 (42.11) 1 (20)

Vancomycin 133 (100) 5 (100) - - - -MRSA= Methicillin resistance Staphylococcus aureus,

MupRSA= Mupirocin resistance Staphylococcus aureus



844


Amongst the mupirocin resistant isolates, all the

5 isolates were high-level mupirocin resistant.

Percentage of methicillin resistant and mupirocin

resistant Staphylococcus aureus isolates among

different samples is documented in the Table 1.

Distribution of samples according to the wardsfrom where they were received is documented in

Table 2. Amongst other antibiotics, percentage

resistance is documented in Table 3, with a

maximum resistance seen for ampicillin.

Vancomycin and linezolid were found to be the

most sensitive drugs across all staphylococcal

species.

DISCUSSION

Staphylococcus aureus is one of the most

frequently isolated pathogen from both

nosocomial and community associated infections

causing a wide range of infections from

abscesses, impetigo and cellulitis to deep seated

pyogenic lesions, pneumonias, meningitis and

septicaemias.1

Increasing number of infections

caused by MRSA strains has led to poorer

treatment outcome.

2

Mupirocin is an importanttopical antibiotic widely used for treatment of

skin and soft tissue infections caused by

Staphylococcus aureus.11

In healthcare institute it

is used for nasal decolonisation of health care

personnel to prevent the spread of MRSA among

co-workers and the patients.10

Emergence of

resistance to mupirocin is likely to worsen the

problem. Studies suggest mupA gene which

encodes mupirocin resistance is transferred from

commensal flora of skin to MRSA during

mupirocin therapy.19

This could be a threat to

irrational use of mupirocin as it may lead to the

development and spread of mupirocin resistance.

In this study, out of total 250 Staphylococcus

aureus isolates, 5 i.e. 2% showed mupirocin

resistance by disk diffusion method. All the

mupirocin resistant Staphylococcus aureus

isolates are high-level resistant strains as

determined by disk diffusion method and two

different MIC methods: broth microdilution

method and agar dilution method.

The percentage rate of high-level mupirocin

resistance in this study is consistent with other

studies conducted in different regions of India.2,21

Low-level resistance is not found in this setupwhich is in agreement with the study conducted

in Chennai by Oommen et al., but in contrast

Krishnan, et al., and Gadepalli, et al., has shown

1.5% and 1% low-level resistance,

respectively.2,21,22

In this study, none of MSSA

isolates showed resistance to mupirocin (either

high-level or low-level), and it is seen only in

MRSA isolates. Also, there was no significant

association seen between mupirocin resistancewith resistance to other antibiotics in this study,

which is in contrast to studies conducted by

MCDougal etal and Cadilla etal.23,24

Efficacious nasal clearance of MRSA for a

significant duration in carriers is shown in

mupirocin sensitive isolates. Emergence of high-

level mupirocin resistance has shown to be

associated with the failure of decolonisation

therapy among carriers and patients and offers

fewer topical treatment options16. However,

studies has suggested that low-level mupirocin

resistance strains can still be controlled with

normal dosage schedule of mupirocin ointment,

as it contains a higher concentration of mupirocin

(2000 μg/ml) than the MICs of low-level

mupirocin resistance strains.25

CONCLUSION

The present study has demonstrated the presenceof high-level mupirocin resistance in a major

tertiary care setup of northern India which is a

concern to prevent the spread of MRSA in

hospitals and community. This may be attributed

to irrational use of antibiotics as well as over the

counter sale of drugs. Nasal decolonisation of

MRSA in healthcare personnel is performed by

using 2% mupirocin ointment along with absence

from duty till culture reports are documentednegative and since low-level mupirocin

resistance can be treated with the normal dosage



845


of mupirocin ointment, thus detection of high-

level mupirocin resistance seems to be

mandatory. Hence, it would be advisable to

detect mupirocin resistance by using both 5 μg

and 200 μg mupirocin disks from carriers before

starting mupirocin decolonisation therapy so thatalternatives may be used.

ACKNOWLEDGEMENTS

Our thanks to Ms. Shubhra Mishra, Msc, PhD for

technical help during the study

REFERENCES

1. Grunden N. MRSA, a short history of a

monster microbe. Pittsburgh Regional

Healthcare Initiative. Reprinted from PRHI

Executive Summary, December 2003.

Available: http://www.prhi.org/docs

/MRSAa%20short%20history%20of%20a%2

0monster%20microbe12-1-2003.pdf

2. Gadepalli R, Dhawan B, Kapil A, Sreenivas

V, Jais M, Gaind R, Chaudhry R, Samantaray

JC, Udo EE. Clinical and molecularcharacteristics of nosocomial meticillin-

resistant Staphylococcus aureus skin and soft

tissue isolates from three Indian hospitals. J

Hosp Infect. 2009;73(3):253-63.

3. Hill RLR, Casewell MW. Local treatment of

MRSA carriage and colonization. In:

Cafferkey MT, ed. Methicillin-resistant

Staphylococcus aureus. New York: Marcel

Dekker, 1992:149 – 70

4. Hingst V, Vergetis W, Bommer J, Borneff M.

Prospective randomised placebo-controlled

study concerning the elimination of

Staphylococcus aureus by means of

mupirocin in patients undergoing

hemodialysis (poster). International Congress

on Management of Infection. Amsterdam. 5-

9 April 1992; Abstract p2: 110

5. Ellis MW, Grif fith ME, Dooley DP, et al.

Targeted intranasal mupirocin to prevent

colonization and infection by community-

associated methicillin-resistant

Staphylococcus aureus strains in soldiers: a

cluster randomized controlled trial.

Antimicrob Agents Chemother. 2007;

51:3591 – 8

6. Lally RT, Lanz E, Schrock CG. Rapid

control of an outbreak of Staphylococcus

aureus on a neonatal intensive care

department using standard infection control

practices and nasal mupirocin. Am J Infect

Control. 2004; 32:44 – 477. Paule SM, Robicsek A, Thomson RB Jr,

Kaul KL, Peterson LR. Three years of

universal surveillance and decolonization: the

effect on mupirocin resistance [abstract C2-

1069]. In: Program and abstracts of the 48th

Annual ICAAC/IDSA 46th Annual Meeting

2008 (Washington, DC):171

8. Doebbeling B, Breneman D, Marsh R,

Reagen D, Wenzel R. Multicentre study of

elimination of Staphylococcus aureus nasal

carriage with calcium mupirocin ointment in

healthy subjects. Proceedings of the 32nd

Interscience Conference on Antimicrobial

Agents and Chemotherapy. Oct 1992; 11-14

9. Yanagisawa T, Lee JT, Wu HC, Kawakami

M. Relationship of protein structure of

isoleucyl-tRNA synthetase with pseudomonic

acid resistance of Escherichia coli. A

proposed mode of action of pseudomonic

acid as an inhibitor of isoleucyl-tRNA

synthetase. Journal of Biological Chemistry.

1994; 269, 24304 – 9

10. West SK, Plantenga MS, Strausbaugh LJ.

Use of decolonization to prevent

staphylococcal infections in various

healthcare settings: results of an Emerging



846


Infections Network survey. Infect Control

Hosp Epidemiol. 2007; 28:1111 – 3

11. Chase McNeil J, Kristina G. Hulten, Sheldon

L. Kaplan and Edward O. Mason. Mupirocin

Resistance in Staphylococcus aureus Causing

Recurrent Skin and Soft Tissue Infections in

Children. Antimicrob. Agents Chemother.

2011;55(5):2431-33

12. Elaine S. Walker, Foster Levy, Mahmoud

Shorman, Gerard David, Jehad

Abdalla and Felix A. Sarubbi. A Decline in

Mupirocin Resistance in Methicillin-

Resistant Staphylococcus aureus

Accompanied Administrative Control of Prescriptions. J. Clin.

Microbiol. 2004;42(6):2792-95

13. Jacob S. Hogue, Patricia Buttke, LoRanee E.

Braun, and Mary P. Fairchok. Mupirocin

Resistance Related to Increasing Mupirocin

Use in Clinical Isolates of Methicillin-

Resistant Staphylococcus aureus in a

Pediatric Population. J. Clin. Microbiol.

2010;48(7):2599 – 00

14. Creagh S, Lucey B. Interpretive criteria for

mupirocin susceptibility testing of

Staphylococcus spp. using CLSI guidelines.

Br J Biomed Sci. 2007; 64:1 – 5.

15. de Oliveira NE, Cardozo AP, Marques De A,

dos Santos KR, Giambiagi-deMarval M.

Interpretive criteria to differentiate low- and

high-level mupirocin resistance in

Staphylococcus aureus. J of Medical

Microbiol. 2007;56:937-39

16. Perez-Roth E, Lopez-Aguilar C, Alcoba-

Florez J, Mendez-Alvarez S. High-level

mupirocin resistance within methicillin-

resistant Staphylococcus aureus pandemic

lineages. Antimicrob Agents Chemother.

2006; 50: 3207 – 11

17. Hodgson JE, Curnock SP, Dyke KG, MorrisR, Sylvester DR, Gross MS. Molecular

characterization of the gene encoding high-

level mupirocin resistance in Staphylococcus

aureus J2870. Antimicrob Agents

Chemother. 1994; 38:1205 – 08.

18. Udo EE, Jacob LE, Mathew B. Genetic

analysis of methicillin-resistant

Staphylococcus aureus expressing high- and

low-level mupirocin resistance. J Med

Microbiol. 2001;50:909 – 15

19. Hurdle JG, O Neill AJ, Mody L, Chopra I,

Bradley SF. In vivo transfer of high-level

mupirocin resistance from Staphylococcus

epidermidis to methicillin-resistant

Staphylococcus aureus associated withfailure of mupirocin prophylaxis. J

Antimicrob Chemother. 2005;56:1166-68.

20. Clinical Laboratory Standard Institute.

Performance Standards for Antimicrobial

Susceptibility Testing; Twenty-Second

Informational Supplement. 2012;32(1):70-71

21. Oommen SK, Appalaraju B, Jinsha K.

Mupirocin resistance in clinical isolates of

staphylococci in a tertiary care centre in

south India. Indian J Med Microbiol.

2010;28(4):372-5.

22. Krishnan PU, Miles K, Shetty N. Detection

of methicillin and mupirocin resistance in

Staphylococcus aureus isolates using

conventional and molecular methods: a

descriptive study from a burns unit with high

prevalence of MRSA. J Clin Pathol. Oct.

2002;55(10):745-8

23. Adriana Cadilla, Michael Z. David, Robert S.

Daum, and Susan Boyle-Vavra: Association

of High-Level Mupirocin Resistance and

Multidrug-Resistant Methicillin-Resistant

Staphylococcus aureus at an Academic

Center in the Midwestern United States. J.

Clin. Microbiol. 2010; 50: 95 – 100

24. McDougal LK, Fosheim G, Patel JB; TeamABCs. Emergence of resistance among USA



847


300 MRSA isolates causing invasive disease

in the US [abstract C1-166]. In: Program and

abstracts of the 48th Annual ICAAC/IDSA

46th Annual Meeting (Washington, DC,

2008):103.

25. Hudson IR. The ef ficacy of intranasal

mupirocin in the prevention of

staphylococcal infections: a review of recent

experience. J. Hosp Infect. 1994; 27, 81 – 98



848

Rupanjali et al., Int J Med Res Health Sci. 2013;2(4): 848-851


&

Health Scienceswww.ijmrhs.com Volume 2 Issue 4 Oct-Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886Received: 21st Aug 2013 Revised: 14th Sep 2013 Accepted: 27th Sep 2013

Research article

A STUDY TO ANALYZE THE PREVALENCE OF MARTIN GRUBER ANASTOMOSES

AMONG MEDICAL STUDENTS

*Rupanjali B1, Vijayalakshmi B

2, Chandrasekhar M

3

1Student,

2Professor,

3Dean and Head, Department of Physiology, Meenakshi Medical College and

Research Institute, Kanchipuram, Tamilnadu, India


ABSTRACT

The most frequently occurring anomaly in the upper extremities has been the Martin Gruber

Anastomoses (MGA) which occurs due to the crossover of nerve fibers from the median nerve to ulnar

nerve. This study was performed to investigate the prevalence of MGA in 100 healthy medical students

as it acts as an etiology to carpal tunnel syndrome and other hand injuries. A nerve conduction study for

median and ulnar nerve was performed by placing the surface electrodes on the Thenar, Hypothenar and

first dorsal interosseus muscle with their Compound Muscle Action Potential (CAMP) and their

amplitudes being evaluated. MGA was found in 23 out of 100 volunteers. This relatively high incidence

demonstrates the necessity for healthcare specialists to factor the MGA into their diagnosis.

Keywords: Martin Gruber Anastomoses, Nerve Conduction study, Compound Muscle Action Potential

INTRODUCTION

The Martin Gruber anastomoses is a

communicating nerve branch between the

median nerve and the ulnar nerve in the forearm.

It is one of the most commonanastomotic anomalies that occur between these

two nerves. This connection carries motor nerve

fibers. In case of nerve lesions of the median or

the ulnar nerves, the Martin Gruber anastomoses

can serve as a channel for alternative

innervations of portions of the forearm and hand.

This inconstant pattern of connection can serve

as an explanation for challenging differential

diagnosis1.

Median-ulnar nerve anastomosis in the forearm

is the most common form of anomalous

innervations which was first described by

Swedish anatomist R.Martin in 1763 and later by

Gruber in 1870 and thus referred to as Martin-

Gruber anastomoses. These anastomoses involveaxons leaving either the main trunk of the

median nerve or the anterior interosseous nerve,

crossing through the forearm to join the main

trunk of the ulnar nerve and ultimately

innervating the intrinsic hand muscles2-4

. It is to

be noted that not all the axons of the median

nerve will be involved in this anomalous route.

In the type I anastomosis the cross over fibers

terminate in the Hypothenar muscles, in the type

II anastomosis the cross over fibers terminate in

the first dorsal interosseous, in the type III

DOI:10.5958/j.2319-5886.2.4.135



849


anastomosis the cross over fibers terminate in the

Thenar muscles5.

The main purpose of this study is to draw

attention of clinicians or surgeons from

neurophysiology field to this anastomosis and to

avoid misinterpretations of different studies of needle electromyography and other nerve

conduction studies. Therefore for the assessment

of traumatic and entrapment lesions of median

and ulnar nerve and for surgical landmarks the

knowledge of this anastomosis is important.


100 healthy medical student volunteers of age

group 17-22 years were selected for this study.Among them 40 students were male and 60

students were females. An informed consent was

taken from the students to whom the study was

performed. Subjects with peripheral neuropathies

and patients having diabetes mellitus, neuropathy

was not included.

The procedure followed to test for MGA is

outlined below:6

Surface electrodes were placed on the right handThenar, Hypothenar and on the First Dorsal

Introsseous (FDI) muscles and were left in the

same position during the whole of the

electrophysiological testing. The median and the

ulnar nerves were stimulated supramaxilly at the

wrist and the elbow and the compound muscle

action potential (CMAP) were recorded with

their amplitudes being evaluated.

The electrodes were placed in standard

recording, reference and stimulation points.

Rectangular pulses of 0.2 m Sec duration were

used and the stimulus strength was

supramaximal.

The compound muscle action potentials (CMAP)

were recorded and the amplitude of each CMAP

was measured from the negative to the positive

peak of the response (peak to peak amplitude).

CMAP from the FDI, Thenar and Hypothenar

muscles larger (at least 1 mv) upon median nerve

stimulation at the elbow then at the wrist and

CMAP from one or more of these sites larger (at

least 1mv) upon stimulation of ulnar nerve at the

wrist than at the elbow were accepted as

indicators of presence of MGA.MGA criteria

2

A person is said to have Martin Gruber

Anastomoses based on the following:

If, on median nerve stimulation on the three

muscles-first dorsal interossei, hypothenar and

thenar, the amplitude at the wrist is greater than

the amplitude at the elbow, or If, on ulnar nerve

stimulation on the three muscles-first dorsal

interossei,hypothenar and thenar, the amplitudeat the elbow is greater than the amplitude at the

wrist.

Classification of Martin Gruber Anastomoses

In Type I anastomoses the crossover nerve fibers

terminate in Hypothenar muscles.

In Type II anastomoses the crossover nerve

fibers terminate in first dorsal interossei muscles.

In Type III anastomoses the crossover nerve

fibers terminate in thenar muscles5.

RESULTS

MGAs were found in 23 out of 100 subjects

tested: Out of these, 5 students were found to be

having type I (nerve fibers terminate in

Hypothenar muscles), 17 students were found to

be having type II (nerve fibers terminate in first

dorsal interossei muscle), and 1 student was

found to be having type III (nerve fibers

terminate in thenar muscles). In the group of 60

women 11 (18.3%) were found to have MGA. In

the group of 40 men, 12 (30%) were found to

have MGA. There are no significant racial or

gender differences in the prevalence of this

communication.



850


Fig 1: Prevalence of different types of MGA

DISCUSSION

MGA has been causing confusion in the

assessment of nerve injuries, carpel tunnel

syndrome and leprosy neuropathy. Because of its

high prevalence and different electro diagnostic

considerations, it can thus be concluded thatMGA is frequently encountered and it should be

kept in mind that abnormal innervations models

might influence the electrophysiological findings

and ultimately gives rise to faulty interpretations,

particularly in case of median and ulnar nerve

lesions. Mannerfelt was the first to use electro

diagnostic techniques to detect MGA and

reported a 15% incidence in a study of 41%7.

Crutchfeild and Gutmann found an incidence of

28% in the general population and 62% in 29

relatives of 5 subjects with MGA8. Gutmann

studied 13 extremities with MGA and reported

that anomalous innervations were present in all

of Hypothenar and FDI muscles and in 6% of

Thenar muscles9. Several other authors, using

electro diagnostic techniques have reported

incidences of MGA ranging from 8% to 26% in

patients with carpal tunnel syndrome (CTS)10, 11

.

CONCLUSION

Martin Gruber Anastomoses might lead to the

misdiagnoses of many syndromes that affect the

nerve supply of the upper limb especially the

intrinsic muscles of hand. There were absolutely

no noticeable racial or gender differences in the

prevalence of this communication. It is important

to understand the existence of this

communication and its location for correct

patience assistance. In our study the incidence of

type II MGA was relatively high. Fortunately,

this does not present any difficulty in routine

ulnar nerve conduction studies because the

recording electrodes are not placed on thismuscle. A potential difficulty arises in cases of

suspected lesions in the deep palmar branch of

the ulnar nerve, because the recording electrodes

should be placed on the dorsal interosseous

muscle10

.

REFERENCES

1. Unver Dogan, Nadire. The communications

between the ulnar and median nerves in

upper limb. Neuroanatomy 2009; 8:15-19.

2

8

1

11

3

9

0

12

5

17

1

23

0

5

10

15

20

25

TYPE I TYPE II TYPE III TOTAL

FEMALE(F)

MALE(M)

F + M



851


2. Oh SJ. Clinical Electromyography Nerve

Conduction Studies. Baltimore: Williams

Wilkins; 1993; Ed. 2; 314-333

3. Gutmann L. AAEM Minimonograph:

Important anamolous innervation of the

extremities J Muscle Nerve. 1993; 16:339-347.

4. Uchida Y, Sugiyoka Y, Electrodiagnosis of

Martin Gruber Connection and its clinical

importance in peripheral nerve surgery, J

hand surg. 1992; 17(1):54-59.

5. Hatice Rana Erdem, Sevin, Ergurk, Cigdem

Erturk and Sumru Ozel.”Electrophysiological

Evaluation of the Incidence of Martin Gruber

Anastomosis in Healthy Subjects.” YonseiMedical Journal.2002; 43: 291-295.

6. De Lisa JA, Lee HJ, Baran EM, Lai KS,

Speilholz N. Manual of Nerve Conduction

Velocity and Clinical Neurophysiology. New

York: Rven Press; 68-92.

7. Mannerfelt. Studies on the hand in ulnar

nerve paralysis. A clinical experimental

investigation in normal and anomalous

innervation. Acta Ortho Scand.1966;87:23-

142.

8. Crutchfeild CA, Gutmann L. Hereditary

aspects of median-ulnar nerve

communications. J Neural Neurosurg

Psychiatry1980; 229-235.

9. Gutmann L, Gutierez A, Riggs JE. The

contribution of median-ulnar nerve

communication in diagnosis of mild carpal

tunnel syndrome. J Muscle Nerve. 1986; 9

(4) :319-321.10. Wilburn AJ, Lambert E. The forearm median

to ulnar nerve communication:

electrodiagnostic aspects (1976); 26: 368.

11. Lambert EH, Diagnostic value of electrical

stimulaton of motor nerves. J.EEG clinical

neurophysiology. 1962;22:9-16.



852

Lilian Ebele Chris-ozoko et al., Int J Med Res Health Sci. 2013;2(4):852-856


&

Health Sciences

www.ijmrhs.com Volume 2 Issue4Oct-Dec Coden: IJMRHS Copyright @2013 ISSN:2319-5886Received: 23

rdAug 2013 Revised: 17


thSep 2013

Research article

PREDICTION OF WEIGHT OF CHILDREN AGED UP TO TWO YEARS BASED ON FOOT

LENGHT IN ETHIOPE EAST LOCAL GOVERNMENT AREA OF DELTA STATE OF SOUTH-

SOUTH NIGERIA

Lilian Ebele Chris-ozoko

Department of Human Anatomy, Faculty of Basic Medical Sciences, College of Health Sciences, Delta

State University Abraka, Nigeria.

Corresponding author email: [email protected]

ABSTRACT

Introduction: When a child is in a critical condition, it may not be hundred percent possible to

determine the body weight using weighing scale. Under such a condition, paediatricians estimate weight

using the age of the child. Material and Method: The weight was measured using a weighing scale. In

cases where the babies were too small and unable to stand on the weighing scale alone, the mother was

weighed alone and while carrying the baby and the weight of the baby was determined by subtractingthe weight of the mother from the weight of the mother and the baby. Results: Mean weight for male

children is 10.98kg, Mean foot length for male children is 5.04 inches, R2

= 0.61, F statistics = 7.57,

Probability = 0.0001531, Standard deviation of weight for males is 5.2, Standard deviation of foot length

is 0.009 Conclusion: Base on Foot length, weight of children below two years can be predicted in

emergency condition.

Keywords: Weight, Foot length, Children

INTRODUCTION

In emergency situations drug dosage is very

difficult to calculate for children who are

incapacitated, because their weight, surface areas

and length which are the present available means

of estimating appropriate drug dosages may not

be readily assessable. Although early researchers

have predicted age-based formulas which were

predominantly used for estimation of children’s

weight under emergency medical treatment.1

This method of drug dosage estimation is even

less specific and hence less accurate than the

preceding ones most especially because of the

variability of weight of children across differenttribe and economic situations.

Haftel et al2

carry out a study on “hanging leg-

weight” method for weight estimation in

children. Though the method was not like other

work proposed and used before, but could not

attract further interest. For obvious reasons

Mathur et al,3

showed that foot length can be

used to predict the gestational age of very

premature aborted foetuses.Bavdekar

4in India conducted a study on a

novel technique using foot-length to predict the

DOI:10.5958/j.2319-5886.2.4.136



853


weight of children under the age of 2 years was

developed in India.

Foot length measurement is a potential tool for

evaluating children with low birth weight.5

Embleton et al6

work on a research study on the

relationship between foot length and nasotracheallength. They came out to show that foot length is

a reliable predictor of nasotracheal length.

Other researchers (Amamturk et al7also

conducted a study on the relationship between

foot length and body weight in adults age

between 17.6 and 82.9 years. And found a

significant relationship between both.

The aim of this study therefore, is to establish a

relationship between foot length and weight of children below two years in Ethiopia East local

Government Area of Delta State; south-south

Nigeria.

MATERIAL AND METHOD

Sample size : Sample size of the research study

is hundred and ten. Sixty four (64) males and

females (46) were included in the present study.

All the children used in the study were under two

years and their ages ranged from three months to

two years. Healthy children without deformity

were used after permission was obtained from

parents and teachers of sure foundation nursery

and primary school, Abraka- Delta State.

Procedure for weight measurement: The

weight was measured using a weighing scale. In

cases where the babies were too small and unable

to stand on the weighing scale alone, the mother

was weighed alone and while carrying the baby

and the weight of the baby was determined bysubtracting the weight of the mother from the

weight of the mother and the baby.

Procedure for measurement of foot length:

Foot length was measured as a direct distance

from the prominent point of the back of the heel

to the tip of the hallux or to the tip of the second

toe, when the second toe is longer using a vernier

calliper.

Statistical analyzing data: The data obtainedwas analyzed using mean, bar chart, frequency

polygon, standard deviation, body mass index,

linear regression and correlation analysis.

Statistical analysis performed using the ordinary

least squares (OLS) technique with its desirable

property of the best linear unbiased estimator

(BLUES) being adopted.

RESULT

Data analysis : Mean weight for male children is

10.98kg, Mean foot length for male children is

5.04 inches, R2

= 0.61, F statistics = 7.57,

Probability = 0.000153, Standard deviation of

weight for males is 5.2, Standard deviation of

foot length is 0.009

Table 1: Showing Weight, foot length and Weight Predicted using regression formula for males

Weight Foot length Weight predicted using regression formula

8kg 2.05 inches 6kg

9kg 3.83 inches 10kg


14kg 5.72 inches 14.7kg


Table 2: Summary of Regression Result for Male

Independent

variable

Dependent variable (Foot length male)

Coefficient Standard Error t-statistics Probabilities

Weight 0.07 0.03 2.88 0.01Constant 77927 6248.207 12.47 0.00



Lilian Ebele Chris-ozoko et al.,

The result in table 4.1 shows tha

weight has a linear relationshi

length. Thus an increase in weig

increase the foot length by 0.07 u

The R2

is the coefficient of dete

explains the fitness of the eqsuggests that 63 percent of the

length have been explained by

means that the equation repres

This is because the unexplained

thirty seven percent (1-063).

adjusted R2

for degrees of f

suggests that sixty one percent o

foot length have explained by wei

Table 3: Showing Weight, Foot le

Weight Foot len

11.5kg 1.09 inc

5kg 2.37 inc

7kg 3.67 inc

12kg 4.21 inc

10kg 5.80 inc

Table 4: Summary of Regression

Independentvariable

Dependent v

Coefficient

Weight 0.81

Constant 2794.7

The results in this table suggest t

positive linear relationship with f

an increase in the weight by a u

the foot length by 0.81 units.

Fig 1: Foot length and weight of M

Int J Med Res Health S

t the increase in

with the foot

t by a unit will

nits.

mination and it

ation. The R2

changes in foot

weight. This

nts a good fit.

variation is just

The R2

is the

reedom and it

f the changes in

ght.

The F test is used to te

of the equations. The

calculated (7.57) > +

(2.01). This is an i

significant in explain

length.R

2= 0.81, R

-2= 0.7

Probability = 0.00019

9.58kg

Female mean foot len

deviation of weight in

deviation of foot length

gth and Weight Predicted using regression fo

gth Weight predicted using r

hes 4kg

hes 5kg

hes 7.8kg

hes 8.6kg

hes 11.2kg

esult for Female

ariable ( Foot length male)

Standard Error t-statistics

0.05 16.25

1183.3 2.36

at weight has a

oot length. Thus

it will increase

The regression

linear equation relating

y = 2.4x + 1 and y = 1

average body mass in

and for females is 17.2

ales Fig 2: Foot length and wei

854

i. 2013;2(4):852-856

st the overall significance

result showed that the F

critical (2.01) + critical

ndication that weight is

ing the changes in foot

9, F statistics = 10.67,

, Female mean weight is

th is 4.04inches, Standard

females is 3.9, Standard

in females is 0.009

mula for Females

egression formula

robabilities

.0000

.0228

foot length to weight was

.6x + 1.9 for females. The

dex for males was 15.70

ht of Females



855


DISCUSSION

The finding in this present study shows that the

mean weight in males is higher than the mean

weight in females, while the mean foot length in

males is higher than the mean foot length infemales.

Sandeep et al,8

working with Indian children

under two (2) years found a coefficient of

determination to be 0.88 while James D.K. et al9

working in Manchester found a correlation

coefficient of 0.95. This work arrived at a

correlation coefficient of 0.62 in males and 0.81

in females. This is quite similar to the above

finding and suggests that all variability in weight

can be explained by a linear regression model.

The average body mass index for females was

17.28 and for males was 15.70, this all falls

within the fifth percentile for children under two

(2) years which is considered as normal (CDC,

2009). This work also gives a regression line

equation for children under two years in Nigeria.

It is our hope that other writers will derive

equations for other parts of Nigeria since this

work x-rays Ethiope East local Government Areaof Delta State in South- South Nigeria.

The importance of this study cannot be

overemphasized, because it provides the

parameters measured for estimation of weight

and thereby estimation of dosage of drugs for

emergency purposes in health cares. The results

have shown some important implications. It

showed that both for females and for males, the

weight plays significant role in influencing thechanges in foot length for both males and

females. The result showed that when the weight

of the females changes by a unit, the foot length

of males increases by 0.86 units. The result also

indicates that when the weight of the females

changes by a unit, the foot length of males will

increase by 0.07 units.

From the equations derived for both males and

females, it shows that if any of the variables are

known, the other can be determined.

Weight was estimated using the regression

equation derived and was compared with the

actual weight and they were all within the same

range.

CONCLUSION

In conclusion, this study is most useful in

emergency cases for determination of weight for

calculation of drugs doses especially in rural

Nigeria where adequate facilities are not

available in our paediatric wards and the age of

the child is in doubt.

REFERENCES

1. Lubitz DS, Seidel JS, Chameides L, Luten

RC, Zaritsky AL, Campbell FW. A rapid

method for estimating weight and

resuscitation drug dosages from length in the

paediatric age group. Ann Emerg Med

1988;17:576-581

2. Haftel AJ, Khan N, Lev R, Schonfeld N.

Hanging leg weight -- a rapid technique for

estimating total body weight in pediatric

resuscitation. Ann Emerg Med1990;19(5):523-526

3. Marthur A, Suresh K. Foot length – a newer

approach on neonatal anthroprometry.

Journal of Tropical pediatrics. 1984; 30(6):

333 – 36.

4. Bavdekar SB, Sathe S, Jani P. Prediction of

weight of Indian children aged up to two

years based on foot-length: implications for

emergency areas. Indian Pediatr

2006;43(2):125-30.

5. Marchant T, Jeanie J, suzzane P, Marcel T,

Joanna A S. Measuring newborn foot lengths

to identify small babies in need of extra care:

A cross – sectional hospital based study with

community follow up in Tanzania. BMC

Public health. 2010;10: 624.

6. Embletonn et al. Foot length an accurate

predictor of nasotracheal tube length in

neonates. Arch des child fetal, neonatal ed

2001: 85: F60 – F64.

7. Atamturk D. And duyar, I. (2008). Age-related factors in the relationship between

foot measurement and living stature and body



856


weight. Journal of forensic sciences, 53:

1296 -1300.

8. Sandeep B, Shefalis Pranar J. Prediction of

weight of India children aged up to two years

based on foot length: implication for

emerging areas. J. Clin. Pediatrics. 2005; 10:100 – 06.

9. James K, Dryburgh F, Chiswick M. Foot

length – a new and potentially useful

measurement in the neonate. Arch dis child.

1979; 54: 226 -30.



857

Rajsri et al., Int J Med Res Health Sci. 2013; 2(4):857-860


&

Health Sciences




thSep 2013

Research article

A STUDY ON PULMONARY FUNCTION TESTS IN WEAVERS

*Rajsri TR1, Gokulram N

1, Gokulakrishnan K

1,Chandrasekar M

2, Nikhil Chandrasekar

3

1II

ndYear M.B.B.S.,

2Dean,

3Department of Anesthesia, Meenakshi Medical College and Research

Institute, Enathur, Kanchipuram, Tamilnadu, India,


ABSTRACT

Occupation is the one in which person not only earn his daily bread but also spend one third of average

adult life. As the number of industries is on the increase, several industries like cement industries,

chemical industries, textile industries etc, serves mainly man for comfortable living. Health hazards

caused due to a particular occupation is yet to gain importance in public health measures. These diseases

are termed occupational hazards. Weavers are constantly exposed to fine cotton dust generated from the

weaving unit. Inhalation of this dust compromises their lung function greatly. Occupational exposure to

cotton dust has been a great threat to the respiratory function. Pulmonary function tests are set of parameters to assess the lung function. It measures the function of lung capacity and chest wall

mechanics to determine a fault in lung function. Materials & Method: Spirometry is used to determine

airway disorders and is capable of predicting early damage in lung function. This paper discusses about

the lung impairment in female weavers of below age groups, corresponding to minimum 5 years of

exposure to cotton dust. 50 non smoking female weavers of age groups 25-40 years are chosen

respectively. Pulmonary function was assessed using computerized spirometry and compared with same

age, healthy non weavers. Conclusion: The pulmonary function parameters such as FVC, FEV1,

FEV1/FVC, and FEF25-75 were significantly reduced in weavers.

Key words: Pulmonary function tests, Spirometry, Occupational hazards, etc

INTRODUCTION

Weavers play an important role in a community.

Weaving either its manual or mechanized has

been important in a society which fulfill the

clothing needs. Several studies have found that,

on average, lung function is lower in cotton

workers than in the general population and in

general in those with a history of byssinosis. A

mortality study reported in 1985 of women agedbetween 15 and 74 years found a marked excess

in the proportional mortality ratio (PMR) from

all causes of respiratory disease, including

byssinosis, in textile workers, particularly in

those employed as labourers and in fibre

preparation, whose PMR was more than 200 (i.e.

more than twice expected; a PMR of 100 is

equivalent to no excess mortality). The

Occupational Health Decennial Supplement

published in 1995 reported a PMR for chronic

bronchitis and emphysema in female textileworkers of 119 and of byssinosis of 1140.

DOI:10.5958/j.2319-5886.2.4.137



858


Prevalence of byssinosis was 10.5%, chronic

cough 7.5%, chronic phlegm 12.9%, wheeze

with shortness of breath 22.3%, shortness of

breath (grade 2) 21%, chest tightness ever

33.3%; whereas, a low prevalence of asthma

(4%) was identified in this population1.

Karjalainen et al studied the impact of

occupational factors in the inception of adult

onset persistent asthma, and consequently the

potential for prevention is much larger and more

widely spread than generally assumed2.DrAsaad

Ahmed Nafees et al3studied the pattern and

predictors for respiratory illnesses and symptoms

and lung function among textile workers in

Karachi, Pakistan. This was a cross-sectional

survey of 372 adult male textile workers from the

spinning and weaving sections of 15 textile millsfrom Karachi. Data were collected from

November to December 2009 through a

structured, pretested questionnaire and

spirometry3.

Christiani et al conducted their research in

People's Republic of China. Pulmonary function

tests were performed pre and post work shift on

887 textile workers with at least two years of

employment in two cotton mills and one silk mill

in Shanghai, the People's Republic of China.

Environmental sampling was performed withvertical elutriators, and pulmonary function was

performed with standardized techniques. Cotton

textile workers were found to have greater

across-shift decrements in forced expiratory

volume in 1 s (FEV1.0) than silk workers.

Increasing duration of exposure resulted in

increasing acute decrements in FEV1.0, although

significant acute decrements were found in

workers with less than five years of exposure.

The acute changes in FEV 1.0 were noted in both

symptomatic and asymptomatic cotton workers,though the difference between the across-shift

change in FEV1.0 (delta FEV1.0%) of the

byssinotics and non byssinotics increased as

work duration increased. There was no differencein pres hift FEV1.0 between the cotton and silk

workers, but several selection factors likely

influenced the observations4.

Boskabady et al evaluated the respiratory and

allergic symptoms in 66 Iranian carpet weavers

and 66 controls with similar age and gender

characteristics using a questionnaire includingquestions on work-related respiratory symptoms

in the past year, allergies, smoking habits, and

work exposure duration. A total of28 carpet

weavers (42%) reported work-related respiratory

symptoms. Incidences of all respiratory

symptoms and most allergic symptoms were

significantly higher in carpet weavers than in

controls (p<0.05 - p<0.001). Moreover, most

respiratory and allergic symptoms in carpet

weavers were significantly more prominent

during working hours (p<0.01 - p<0.001).

Pulmonary function test results ofthe carpet

weavers showed significant impairment

compared with controls (p<0.05 - p<0.001)5.


Cotton weaving has been a major occupation of

people in Thirupparkadal village in Velloredistrict over generations. Almost all the members

of the family are involved in weaving. Cotton

weaving causes excessive development of fine

dust of cotton. Continuous exposure to this fine

dust over years has caused a threat to their lung

function. Reduction in lung function is directly

proportional to years of exposure to cotton dust.

This study mainly focuses on proving that over

the years there is severe impairment in lung

function.

Study population: Present study was conductedin weaving units at Thirupparkadal village in

Vellore district, Tamilnadu in India. .

Institutional Ethical committee of Meenakshi

Medical College and Research Institute

(MMCH&RI), Enathur Kanchipuram has given

approval for the study. Study group consist of

non smoking female weavers

Group I: female weavers aged 25- 40 yrs (n=50)

Group II: female non weavers aged25-40yrs

(n=50). From all weavers informed consent was

obtained and procedure of the research was

properly explained. Subjects with clinical

abnormalities of the neuromuscular diseases,

known cases of gross anemia, diabetes mellitus,

pulmonary tuberculosis, bronchial asthma,

chronic bronchitis, bronchiectasis, emphysema

and malignancy were excluded from the study.

The subjects who had undergone abdominal or

chest surgery were also excluded from the study.

Inclusion criteria: Non smoker, corresponding

to minimum 5 years of exposure to cotton dust.Exclusion criteria: Subjects with clinical

abnormalities of the neuromuscular diseases,



859


known cases of gross anemia, diabetes mellitus,

pulmonary tuberculosis, bronchial asthma,

chronic bronchitis, bronchiectasis, emphysema

and malignancy were excluded from the study.

The subjects who had undergone abdominal or

chest surgery were also excluded from the study.

Pulmonary function test: The pulmonary

function tests was carried out using a

computerized spirometer (Helios 401 RMS)

using the standard laboratory methods. The

spirometer was calibrated regularly and a brief

physical and general examination was carried out

and the anthropometric parameters (name, age,

sex, height, weight, occupation, and smoker /

nonsmoker) were entered in the computer. All

the pulmonary function tests were done on the

subjects comfortably in an upright position.During the test, the subject was adequately

encouraged to perform their optimum level and

also a nose clip was applied during the entire

maneuver. Tests were repeated three times and

the best matching results were considered for

analysis. The parameters measured by the

apparatus were the Forced vital capacity (FVC),

Forced Expiratory Volume in 1st second (FEVI),

FEVI /FVC, Forced Expiratory Flow in 25% -

75% (FEF25 -75%) with graphic curves were

obtained.

Statistical analysis

The data of pulmonary function tests were

presented as the Mean ± Standard Deviation for

each of the parameter. The two groups were

compared by using student t test by SPSS

software. The values obtained are statistically

significant.

RESULT AND DISCUSSION

Parameters Group I Group II(control group) P Value

FVC 66.65 ± 4.793 83.26±2.5 < 0.01*

FEV 1 76.24 ± 5.180 86.25 ± 6.292 < 0.01*

FEV 1 / FVC 115.8 ± 2.600 87.9± 10.17 < 0.01*

FEF 25 - 75 40.88 ± 4.442 70.64 ± 2.019 < 0.01*

*significantThe mean values of pulmonary function

parameters of weavers are given in above table.

The table depicts the comparative decline in lung

parameters of group I compared with group II.

The FVC, FEV, FEF25-75, FEV1/FVC (as a

percentage of predicted) was seen to significantly

decreased in group I than group II. The Present

study demonstrates that there is altered lung

function in weavers due to chronic exposure.

When compared to the predicted values there

was statistically significant decline in the valuesof FVC, FEV, FEF25-75 and FEV1/FVC.

Inhalation of dust is an important cause of

interstitial lung disease in India.6

The present

study demonstrates that there is a significant

decrease in lung function as the years of

exposure to cotton dust increases. The probable

cause for the decrease in pulmonary function test

is the accumulation in peri bronchial lymphoid

and connective tissues along with varying

degrees of wall thickening and remodeling in

terminal and respiratory bronchioles arising from

each pathway. Bronchiolar walls with marked

thickening contained moderate to heavy amounts

of carbon and mineral dust and wall thickening is

associated with increase in collagen and

interstitial inflammatory cells including dust-

laden macrophages.7

The study by Edwards et al

has shown that in larger bronchi of the bysinotics

there was a higher percentage of muscle and

glands with corresponding lower percentage of

connective tissues and cartilage. While in

segmental bronchi no significant changes were

observed.12 Decrese in FVC, FEV1andFEV1/FVC indicates an obstructive pattern of

lung disease. Decrease in FEF indicates a

pathology involving the larger airways due to

cotton dust. Studies have shown that cotton dust

induces histamine release or immunological

reaction antigen-antibody reaction as mechanism

of cotton dust disease. A growing number of

literatures have confirmed that endotoxin is the

main mediator in byssinosis and obstructive lung

diseases.13- 15.



860


CONCLUSION

The data suggests that cotton dust inhalation can

account for substantial decrease in lung function.

In order to prevent these among weavers the

strategies of use of mask, regular health check up

and proper awareness about the symptoms of aparticular lung dysfunction can be done

ACKNOWLEDGEMENT

Rajsri thanks Department of Physiology,

MMCH&RI for their guidance. Also thanks

Mr.M.G.K. Danacheriyan, Panchayat president

and Smt. Baby, VHN of thiruparkadal village for

helping out on the field.

REFERENCES

1. The Occupational Health Decennial

Supplement published in 1995.

2. Karjalainen A, Kurppa K, Martikainen R,

Klaukka T, Karjalainen J. Work is related to

a substantial portion of adult-onset asthma

incidence in the Finnish population. Am

JRespirCrit Care Med. 2001;164(4):565-8.

3. Asaad Ahmed Nafees. Pattern and predictors

for respiratory illnesses and symptoms and

lung function among textile workers in

Karachi, Pakistan. Occup Environ Med:2013; 10.1136/oemed-2011-100561; 99-107.

4. Christiani DC, Eisen EA, Wegman DH, Ye

TT, Gong ZC, Lu PL et al., Respiratory

disease in cotton textile workers in the

People's Republic of China. II. Pulmonary

function results, Scand J Work Environ

Health. 1986;12(1):46-50.

5. Boskabady MH, Karimiani EG, Vostacolaei

HA. Respiratory symptoms and pulmonary

function changes among carpet weavers in

Iran.Int J Occup Environ Health. 2007;

13(4):369-75.

6. Jindal SK, Aggarwal AN, Gupta D. Dut-

induced intertitial lung diease in the tropics.

Curr Opin Pulm Med.2001; 7: 272-77.

7. Pinkerton KE, Green FHY, Saiki C,

Vallyathan V, Plopper CG, Gopal V et al.

Distribution of particulate matter and tissue

remodeling in human lung. Environ Health

Perspect 2000; 108:10639.

8. Kauffmann F, Drouet D, Lellouch J, Brille D.Twelve years spirometric changes among

Paris area workers. Int J Epidemiol 1979;

8:201-12.

9. Mahmoud TM, Hosnia. Abd El – Maged. A

study of occupational health hazards among

assuit spinning factory workers; Ass. Univ.

Bull Enviro. Res.2004;1: 63-75.

10. Paramasvam Parimalam, Narayani

Kamalamma and Anind kumar Ganaguli

knowledge, attitude and practices related to

occupational health problems among

Garment workers in Tamilnadu, India.

Journal of occupational health. 2007: 49 (6):

528-534.

11. Calvin S, Joseph B. Occupational Related

accidents in selected Garment Industries in

Bangalore city: Indian journal of community

medicine.2006;31(3):150.12. Edwards C, Macartney J, Rooke G, Ward F,

The Pathology of lung in byssinotics. Thorax

1975:30: 612-23.

13. Khan AJ, Nanchal R, Cotton Dust Lung

Diseases, Corr Opin Pul Med 2007: 13(2);

137-41.

14. Rylander R, Haglind P, Lundholm M,

Endotoxin in Cotton Dust and Respiratory

function on decrement among cotton workers

in an experimental cardroo Am Rev Respir

Dis 1985; 131; 209-213.15. Niven R McL, Pickering CAC. Occupational

Lung Disease-6; Byssinosis; a reviw: Thorax

1996: 51(6): 632-37.



861

Minhas et al., Int J Med Res Health Sci. 2013; 2(4):861-869


&

Health Sciences




thSep 2013

Research article

A STUDY OF ANTHROPOMETRIC MEASUREMENTS AND PREVALENCE OF

OVERWEIGHT AMONGST GIRLS IN AN URBAN SCHOOL

*Sukhmeet Minhas1, Priyanshi Chaudhary

2, Harinder Sekhon

3, George Koshy

4, Vandana Gangadharan

5

1Reader, Dept of Community Medicine, Armed Forces Medical College, Pune, Maharashtra, India

2Intern, MH Secunderabad,3 Psychiatrist, Composite Hospital, Central Reserve Police Force, Jammu, Jammu & Kashmir

4OIC, Station Health Organisation, INS Rajali, Arakkonam, Tamil Nadu

5Assistant Professor, Department of Pathology, Meenakshi Medical College & Research Institute,

Enathur, Tamil Nadu


ABSTRACT

Background: Individuals whose Body Mass Index exceeds the age-gender-specific 95th

percentile are

overweight; while those with BMI between the 85

th

and 95

th

percentiles are at risk of overweight. Theprevalence of obesity is increasing worldwide. Children are becoming overweight at younger age.

Currently 10% of children worldwide are either overweight or obese. The present study was undertaken

to study the anthropometric measurements and determine the prevalence of overweight amongst school

girls in the age group of 5-8 years in a school of Pune. Methods: Anthropometric measurements of the

study subjects were studied by conducting a cross sectional descriptive study. All the 312 girl students,

aged 5 to 8 years enrolled in the school during the study period were studied. Results: 15.4% of the girls

were found to be overweight while 5.4% are at risk of overweight. Conclusion: With increasing age,

more girls become overweight and at risk of overweight. This increase is steady as the age increases

from 5 to 8 years.

Keywords: Anthropometry, overweight, children, urban, girls

INTRODUCTION

Overweight and obesity are by definition,

abnormal or excessive fat accumulation that may

impair health1,2

or simply as a state of excess

adipose tissue3.Another definition says that

obesity is an excessive accumulation of adipose

tissue containing stored fat in the form of triglycerides

4.Limited research has been carried

out in case of childhood overweight. However,

evidence based on surveys indicates that the

rising incidence of overweight and obesity

among children parallels that among adults5.The

prevalence of obesity is increasing worldwide in

almost every country in all the age groups and

children are becoming overweight at a younger

age6. Blood pressure, blood lipid levels, and

DOI:10.5958/j.2319-5886.2.4.138



862


obesity in childhood “track” into adulthood. The

increase in type 2 diabetes among children and

adolescents is directly related to the obesity

epidemic1,7,8

. There is a secular trend of

childhood obesity to adult life; 41% of obese

adults have been overweight or obese duringtheir childhood also

7,8. The rate of childhood

obesity has increased to a great extent in the last

two decades9. At present, about 10% of children

the world over are either overweight or obese10

.

Among Canadian children, the rate of overweight

has increased from 11% in 1980s to over 30% in

1990s. Amongst Brazilian children it has

increased from 4% (1980s) to 14% (1990s)11

. In

India, available studies from Chennai, Delhi andBhavnagar have shown the prevalence of obesity

as 6.2%, 7.4% and 5.55% respectively. The

prevalence of combined overweight and obesity

is more in girls (16.66%) than in boys

(12.48%)12

. A "double burden" of disease exists

now. This is faced more so by many low- and

middle-income countries. While they continue to

deal with the problems of infectious diseases and

under-nutrition, there is a significant increase in

chronic disease risk factors. An upsurge in

obesity and overweight is particularly found in

urban settings. Very often there is under-nutrition

and obesity existing side-by-side within the same

country, the same community and even within

the same household2. According to one study, the

overall prevalence of overweight in urban

children in New Delhi has shown an increase

from 16% (2002) to about 24% (2006-2007)12

. In

another study, the prevalence of overweight inchildren was 16.75 % in boys and 19.01 % in

girls respectively. Besides, it was observed that

both overweight and obesity started manifesting

as early as 5 years of age13

. At the time of entry

to school at 5 years of age, about 9% of boys and

girls were overweight and about 5% were

obese13

. Another study found the overall

prevalence of obesity and overweight as 11.1%

and 14.2% respectively

14

. Similar study foundthe prevalence of overweight to be 17.8% in boys

and 15.8 % in girls; and the prevalence of obesity

was 3.6% in boys and 2.7% in girls15

. Yet

another study found the prevalence of

overweight among school girls to be significantly

higher compared to the boys of the same age

group16

. The available data therefore suggests

that Indian children today are taller and heavierthan their counter parts were fifteen years ago

13.

The present study was undertaken to study the

anthropometric measurements and determine the

prevalence of overweight amongst school girls in

the age group of 5-8 years in an urban school.

Assessment of overweight: In the case of

children aged 5 to 8 years, emphasis is placed on

the assessment of physical status by the

measurement of height, weight and mid-upper

arm circumference17

.

The anthropometric measurements recommended

for the children aged 5 to 8 years are:

Weight, Height, Body Mass Index, and Mid

Upper Arm Circumference18

.

BMI has been recommended as the preferred

measure by many expert and advisory groups, for

evaluating overweight among children and

adolescents 2 to 19 years of age20

. BMI isrecommended since it can be obtained easily, is

co-related strongly with body fat percentage

(especially at extreme BMI levels), is associated

only weakly with height, and it identifies the

fattest individuals correctly, with acceptable

accuracy at the upper end of the distribution (e.g.

≥85thor ≥95th

percentile for age and

gender)19,20,21

.

The BMI is a derived index and is calculated as

per the guidelines given by the WHO as

follows17

:

BMI = Weight (in Kgs) / Height2

(in meters)

Using the above equation, BMI is calculated

until the second decimal value.

Classification

The most commonly used parameter is BMI

which is calculated as weight in kg divided by

the square of the height in meters. After BMI is

calculated, the number is plotted on the CDC



863


BMI-for-age growth charts to obtain a percentile

ranking. These charts are separate for girls and

boys. Percentiles are the most commonly used

indicator to assess the size and growth patterns of

individual children. Percentile indicates the

relative position of a particular child’s BMInumber in comparison to children of the same

sex and age. The growth charts show the weight

status categories used with children. They depict

underweight, healthy weight, at risk of over

weight, and overweight, as shown in Table 121

.

Table 1: CDC Classification of Weight Status

According to the Percentile Range

Weightstatus

category

Percentile range

Underweight Less than 5th

percentile

Healthy

weight

5th

percentile up to the 85th

percentile

At risk of

overweight

85th

to less than 95th

percentile

Overweight Equal to or greater than the 95th

percentile

Aims and Objectives:

The study was undertaken with the following

aims and objectives:

1. To study the anthropometric measurements of

school girls in the age group of 5-8 years.

2. To determine the prevalence of overweight.


The anthropometric measurements of school girlsin the age group of 5-8 years in an urban school

were studied by conducting a cross sectional

descriptive study. All the 312 girl students, aged

5 to 8 years enrolled in the school during the

study period were studied. Before start of the

study, ethical clearance was obtained from

institutional ethics committee, informed consent

was taken from the parents and the relevant

authorities of the school were briefed about the

scope of the study, with a view to solicit their co-

operation. The age was recorded to the nearest

completed year (6 months and above being

rounded off to the next year and less than six

months to the previous year) as per the official

records of the school. Record of the educational

status of the child was restricted to the class in

which the child was studying at the time of datacollection. Anthropometric Measurements

recorded during the conduct of the study were

weight, height, Body Mass Index (BMI), Mid

Upper Arm Circumference (MUAC) and was

done with the full uniform on, less the belt and

shoes and was conducted on the guidelines

issued by the World Health Organisation13

. Data

was analysed using Epi Info software.

RESULTS

It was observed that out of the total of 312

subjects examined, all the subjects aged 5 years

were studying in class 1, 97% of those aged 6

years were in class 1, while the remaining 3%

aged 6 years were in class 2. 57.1% of those aged

7 years were in class 1, 36.3% in class 2, and the

remaining 6.6% were in class 3, as shown in

Table-2. Out of the 8 year old subjects, 1.6%

were in class 1, 36.3% in class 2 and the

remaining 62.1% were in class 3, respectively.

The distribution of BMI percentiles according to

age of the subjects is as shown in Table – 2. It was

observed that based on BMI criteria as defined,

overall, 16.7%, 42.4%, 33.0% and 16.5%

subjects had BMI <5th

percentile at the age of

5,6,7, and 8 years, respectively. 83.3%, 45.5%,

51.6% and 57.7% subjects had BMI ≥5 th- <85

th

percentile at the age of 5, 6, 7, and 8 years,

respectively. 9.1%, 9.9% and 19.8% subjects had

BMI ≥85th- <95

thpercentile at the age of 6, 7,

and 8 years, respectively. 3.0%, 5.5% and 6.0%

subjects had BMI ≥95thpercentile at the age of 6,

7, and 8 years, respectively. It was found that

BMI percentile categories as shown in the table

were homogenous with respect to age (p<0.05).

The distribution of mean MUAC and standard

deviation of the subjects by age, is as shown inTable – 3. It was observed that the mean MUAC



864


of the subjects decreased till 7 years and

increased thereafter. Similarly, the median

MUAC decreased from 5 to 6 years of age, and

increased thereafter. It was found that mean

MUAC, median MUAC and standard deviation

as shown in the table were homogeneous withrespect to age of the subjects (p<0.05).

The distribution of percentiles of weight of

subjects according to age is as shown in Fig –

1.On plotting the percentile distribution of

weight with respect to age of the subjects; it is

observed that there is an increasing trend in

respective percentile with respect to age. The

weight at 5, 6, 7, and 8 years of age being 17, 14,

14, and 16 kg at the 5

th

percentile; the same being21, 18, 20, and 24 kg at the 50

thpercentile; and

the corresponding weight at the 95th

percentile

being 23, 36, 35 and 40 kg. There is a gradual

decrease till the age of 7 years, after which there

is a rapid increase observed to 8 years of age.

Further, this increase in the weight is more

marked at the higher percentiles.

The distribution of percentiles of height of

subjects according to age is as shown in Fig-2.On

studying the percentile distribution of height with

respect to age of the subjects, it is observed that

there is generally an increasing trend in

respective percentile with respect to age. The

height at 5, 6, 7, and 8 years of age being 115,

101, 104, and 106cms at the 5th percentile; thesame being 118, 113, 117, and 124cms at the 50

th

percentile; and the corresponding height at the

95th

percentile being 121, 129,137, and 140cms.

The distribution of percentiles of BMI of subjects

according to age is as shown in Fig – 3.On

studying the percentile distribution of BMI with

respect to age of the subjects; it is observed that

there is an increasing trend in respective

percentile with respect to age, except for a slightdip around 6 years of age. The BMI at 5, 6, 7,

and 8 years of age being 12, 10, 12, and 10 kg/

m2

at the 5th

percentile; the same being 14, 14,

14, and 15 kg/ m2

at the 50th

percentile; and the

corresponding BMI at the 95th

percentile being

16, 22, 23 and 24 kg/ m2. The fall and rise in the

BMI is more marked at the lower percentiles.

Table 2: Distribution of BMI percentiles according to age

Age BMI Percentiles Total

<5th

≥5th

- <85th

≥85th

- <95th

≥95th

5 1 (16.7) 5 (83.3) 0 0 6 (100)

6 14 (42.4) 15 (45.5) 3 (9.1) 1 (3.0) 33 (100)

7 30 (33.0) 47 (51.6) 9 (9.9) 5 (5.5) 91 (100)

8 30 (16.5) 105 (57.7) 36 (19.8) 11 (6.0) 182 (100)

Total 75 (24.0) 172 (55.1) 48 (15.4) 17 (5.4) 312 (100)X

2= 20.6024, df = 9, p < 0.05

Note: As per CDC 2000 guidelines, percentile of the BMI define Underweight, Healthy weight, At risk

of overweight and Overweight in case of children. The figures in parenthesis refer to the percentages.

Table: 3 Distribution of MUAC Mean ± Standard Deviation according to age of the subject

Age

(completed years)

Observations Mean ± SD

5 6 17.66±1.40

6 33 16.99±2.07

7 91 16.96±2.55

8 142 17.99±2.47



865


X2

= 21.0258, df = 3, p < 0.05

Fig 1: Distribution of percentiles of weight of subjects according to age

Fig 2: Distribution of percentiles of height of subjects according to age

Fig: 3Distribution of percentiles of BMI of subjects according to age

0

5

10

15

20

25

30

35

40

45

P5

P25

P50

P75

P95

W e i g h t ( k g )

5 6 7 8

Age in completed years

80

90

100

110

120

130

140

150

P5

P25

P50

P75

P95

5 6 7 8


H e i g h t

( c m s )

0

5

10

15

20

25

30

P5

P25

P50

P75

P95

B M I

5 6 7 8




866


Table 4: Comparison of median height of subjects

Age Present

Study

Agarwal et

al26

Rath et al29

Marwaha

et al13

Vijaya

Raghavan et al28

CDC23

WHO31

5 117.83±0.0223 104.92±27.38 109.69±4.84 111 112.24±3.91 108 110

6 114.76±0.0639 110.5±44.34 118.78±4.65 117 117.73±5.08 115 115

7 116.70±0.0633 115±42.10 122.99±4.74 122 122.65±5.79 122 121

8 124.40±0.0582 123.8±35.51 127.79±6.83 128 127.22±6.58 128 127

Note: The values in parenthesis correspond to the mean and SD. The values of SD are not available in

respect of the other studies.

Table 5: Comparison of median weight of subjects

Age PresentStudy

Agarwal etal

26Rath et al

29

Marwahaet al

26VijayaRaghavan et al

28CDC

23

WHO31

5 20.33±2.14 15.77±11.14 18.72±2.4 19 18.67±1.89 18 18

6 19.08±4.21 17.89±18.72 21.72±3.85 21 21.56±3.44 20 20

7 20.15±4.09 19.34±23.40 23.03±3.49 24 24.45±4.41 23 22

8 23.82±4.54 22.34±22.56 26.39±6.11 27 25.97±4.87 26 25



Table 6: Comparison of median BMI of subjects

Age Present Study WHO CDC Marwaha et al

5 14.63±1.32 13 13 12

6 14.38±2.05 13 13 12

7 14.72±2.07 13 13 12

8 15.30±2.13 13 13 13



Table 7: Comparison of means of MUAC of subjects

Age Present Study Shrivastava et al32 Rath et al29 Vijaya Raghavan et al28

5 17.66 1.40 15.3 1.1 16.34 1.24 16.3 1.31

6 16.99 2.07 15.9 1.3 17.72 1.71 16.96 1.60

7 16.962.55 16.5 1.2 17.58 1.76 17.70 2.14

8 17.992.47 17.2 1.5 18.57 2.82 18.00 2.16

DISCUSSION

The comparison of median height of subjects is

as shown in Table – 4.On comparing with otherstudies, it was observed that the median height of

the subjects in the present study is higher at all

ages than that observed by KN Agarwal et al26, 27

whereas it is lower at all ages than that observed



867


by Marwaha et al13

, VijayaRaghavan et al28

and

Rath et al23

at all ages except at the age of 5

years. On the whole, it was observed that the

median height of the girls in the present study is

comparable to the other studies.

The comparison of median weight of subjects isas shown in Table – 5.On comparing with other

studies, it was observed that the median weight

of the subjects in the present study is higher at all

ages than that observed by KN Agarwal et al26

whereas it is lower at all ages than the median

weight observed in the other studies, except at

the age of 5 years.

The comparison of median BMI of subjects is as

shown in Table – 6.On comparing the medianBMI with respect to age of the subjects, it was

observed that the median BMI of subjects in the

present study is generally more than that in the

CDC standards23

, the WHO standards31

, and the

BMI observed by Marwaha et al13

at all ages.

The comparison of MUAC of subjects is as

shown in Table – 7.On comparing with other

studies, it was observed that the mean MUAC of

the subjects in the present study is higher at 5

years of age, than the mean MUAC of the

subjects observed in the studies by DK

Shrivastava et al32

, Rath et al29

and

VijayaRaghavan et al28

. However, there is a dip

at 6 and 7 years of age, after which it again rises.

CONCLUSION

In the present study we have observed that at the

age of 6 years, 3.0% of the subjects are

overweight while 9.1% of the subjects in the

study population are at risk of overweight.

Similarly, at the age of 7 years, 5.5% of the

subjects are overweight while 9.9% of the

subjects in the study population are at risk of

overweight. The similar figures at 8 years of age

are 6.0% and 19.8% respectively. Overall, 15.4%

of the girls were found to be overweight while

5.4% are at risk of overweight. From the present

study we can conclude that with increasing ageduring childhood, more girls become overweight

and at risk of overweight. This increase is steady

as the age increases from 5 to 8 years.

ACKNOWLEDGEMENT

This study is part of a research project funded by

grant from the Indian Council of Medical

Research.

REFERENCES

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Richard, Kleigman M Robert and Jenson B

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311/en/

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7. Ramachandra A, Snehalata C, Vinitha R.Prevalence of overweight in urban Indian



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adolescent school children. Diabetes Res

ClinPract 2002; 57: 185- 90.

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39: 449-452.9. Han JC, Lawlor DA, KimmSY. Childhood

obesity. Lancet. 2010;375:1737-48.

10. Bessesen DH. Update on obesity. J Clin Endo

crinol Metab. 2008;93(6):2027-34.

11. Flynn MA, McNeil DA, Maloff B. Reducing

obesity and related chronic disease risk in

children and youth: a synthesis of evidence

with 'best practice' recommendations. Obes

Rev. 2006;7(Suppl 1):1-5.12. Shah C, Diwan J, Bhabhor M, Gokhale P,

Mehta H. Assessment of obesity in school

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13. Bhave S, Bavdekar A, Otiv M. IAP National

Task Force for Childhood Prevention of

Adult Diseases: Childhood Obesity. Indian

Paediatrics.2004; 41: 559-75.

14. World Health Organisation. Obesity:

preventing and managing the global

epidemic, Geneva; June 1997: 3-5.

15. Chhatwal J, Verma M, Riar SK. Obesity

among pre-adolescent and adolescents of a

developing country (India). Asia Pac J

ClinNutr. 2004;13(3):231-35

16. Heird CW and Donohoue AP. Nutrition. In:

Behrman E Richard, Kliegman M Robert and

Jenson B Hal editors. Nelson: Textbook of

Pediatrics. 17th

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17. World Health Organisation. “Physical Status:

The use and interpretation of

Anthropometry”. WHO Tech Report Series,

No. 854. WHO Geneva 1995.

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publications/physical_status/en/index.html

18. Jelliffe BD and Jelliffe EFP editors.

Anthropometry: methods. In: CommunityNutritional Assessment. Oxford Medical

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19. Bhasin SK, Singh S, Kapil U. Height and

Weight of ”Well – to – do Children in

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20. Krebs N, Himes JH, Jacobson D et al.

Assessment of Child and AdolescentOverweight and Obesity. Pediatrics 2007;

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Health Statistics .National Health and

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bmi/

24. Reaven GM. Role of insulin resistance in

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Pediatrics. 1970; 7 (3): 146 – 55.

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R, Grewal K, Mani K. A study of growth

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MC. Heights and Weights of Well- nourishedIndian School Children. Indian Journal of

Medical Research. 1971; 59 (4): 648-654.



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Health Examination of primary School

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Hemalatha et al., Int j Med Res Health Sci. 2013; 2(4): 870-873


&

Health Scienceswww.ijmrhs.com Volume 2 Issue4 Oct - Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886

Received: 24th Aug 2013 Revised: 16th Sep 2013 Accepted: 28th Sep 2013

Research article

EVALUATION OF TRENDS IN THE PROFILE OF GYNAECOLOGIC MALIGNANCIES AT

A TERTIARY CARE HOSPITAL IN KARNATAKA, SOUTH INDIA

Hemalatha AL1, Gayathri MN

2, *Deepthi B Ramesh

3, Neelima P Chamarthy

3,Giripunja M

3, Nayana

NS3



3Post Graduate, Department of Pathology, Mysore Medical

College and Research Institute, Mysore, Karnataka, India


ABSTRACT

Objective: Comprehensive estimates of the incidence of gynecological malignancies reported from

India are very limited due to limitation in record maintenance. Auditing of the results on the incidence

rates provided by the Population Based Cancer Registries has shown variation in the patterns of

gynecologic malignancies. The present study was undertaken to establish the profile of gynecologic

malignancies reported in our centre, with reference to incidence, histological subtypes and frequency of

involvement at various sites. Another objective was also to compare the procured data with those from

other national and international centers. Materials and Methods: In this descriptive study, the records

pertaining to all the pathological specimens categorized as ovarian, uterine corpus and uterine cervical

cancers from January 2003 to December 2012 at our tertiary center were studied and compared with the

available international data. Results: Cervical malignancies were the commonest at our center, as

compared to the uterine malignancies, which were commoner as per the data available from Surveillance

Epidemiology and End Result (SEER) programme of the United States and the European Union.

Keywords: Gynecological malignancy; South India; Cervical Malignancy.

INTRODUCTION

The cancer has already emerged as one of the

most important health problems with an alarming

rate of over 800,000 new cases occurring every

year.1

According to the data collected the Cancer

Registries, it has been noted that >70% of the

cancers in women according occurs in middle

aged women ranging from 35 to 64 years,

thereby suggesting the impact of cancer as a

major public health issue in the most productive

age group of women. Data from the population

bases registries under the National Cancer

Registry Program indicate that the leading sited

of cancer among women are the cervix, uterus,

breast and oral cavity.2

70% of women present at an advanced stage of

the disease, which results in poor survival and

high mortality rates.2

India, being one of the

developing countries, need to take active

measures to decrease the rate of gynecological

malignancies, thereby decreasing the rate of

DOI:10.5958/j.2319-5886.2.4.139



871


morbidity in women. The first step in this

process is to assess the incidence and prevalence

of cancers. It is of utmost importance in our

country to detect the cancers early and take

active treatment measure. But illiteracy, lack of

awareness about the symptoms of the underlyinggrave disease and lack of access to health centers

with treatment and prevention facilities,

prevalence of poverty, results in failure to elicit

the expected response and results in Indian

women.

Regional variability in cancer incidence, the

mean age at which women present with

gynecological symptoms, stage at presentation,

the common sites of occurrence is noted from thedata available from the a good number of centers

worldwide. Studies regarding these issues are

available in registries from developed countries

but reliable data from developing countries, such

as India, is lacking. Keeping this need in view,

the present study was designed to determine the

relative frequency of the malignant tumors of the

female genital tract to study the various

histological types and characteristics of these

tumors among the patients at our center. An

attempt has also been made to compare our data

with those available from cancer registries in

India and across the world.


Detailed relevant information regarding the

clinical history and findings such as patient age,

site of affliction, histopathological diagnosis and

subtypes were collected. The 475 cases includedin the study had a definite histological diagnosis,

made either on biopsy or resection specimens.

Cancer diagnosed by aspiration and cervical

scrape smears but not followed by

histopathological confirmation were excluded

from the study.

The data was analyzed using Microsoft Excel

Software and SSPS 16. For the purpose of

comparison of incidence, our data was curtailedto the corresponding periods, for which the

international data was also available.

RESULTS

A total of 475 cases of gynecologic malignancies

were reported and treated at our centre, in

between January 2003 to December 2012. The

age ranged from 7 to 85 years (Median age = 47).

The sites of involvement in the order of prevalence of occurrence included Cervix (358),

Ovary (73), Corpus Uteri (27), Vagina (9) and

Vulva (8).

Out of the total number of 475 cases, the cervix

was a common site affected (Median age = 48

years). Patients between 25 years and 35 years of

age constituted the commonest age group

affected. 8.4% of the cervical cancers occurred in

women <30 years of age.Ovarian malignancies constituted 14.94% of all

the gynecological malignancies reported, with a

median age of 45 years. The histological

subtypes encountered in the study are as shown

in the table. Uterus was the primary site of

involvement in 5.6% of cases. Nine malignancies

of vaginal origin and 8 malignancies of the

vulval origin were identified. Two cases of

bilateral Krukenberg tumor of the ovary were

encountered.

Table 1: Histologic distribution of gynecologic

malignancies

Histologic types No. of cases %

Uterine cervix 358 75.36

Squamous cell

carcinoma

339 71.36

Adenoma 16 3.36

Others 3 0.36

Ovary 71 14.94

Epithelial 36 11.78

Germ cell 7 1.47

Stromal 8 1.68

Uterus 27 5.68

Epithelial 24 5.05

Mesenchymal 3 0.63

Vagina 9 1.89

Vulva 8 1.68

Secondary tumors 2 0.42



872


DISCUSSION

Gynecological malignancies form a huge burden,

contributing significantly to the morbidity and

mortality around the world. Studies based on

cancer incidence in India revealed that theincidence is >70 per 100,000 population.

1, 3

Nearly 70% of the Indian population lives in

rural areas where the socioeconomic living

standards are low and the quality of health care is

limited. Owing to these factors, women in India

are more vulnerable to most of the risk factors

for cervical cancer such as early marriage, early

childbirth, multiparity and chronic infections

with genital disease, mostly transmitted

sexually.3,4 In the cohort of patients in our study,

cervix was the commonest site of affection

among the gynecologic malignancies. Other

registries in India and South Asia also reported

similar observation.5,6

Cervical cancer remains the commonest

gynecologic cancer and the second most

common cancer among females, first being the

breast cancer as recorded in the consolidated

report from the National Cancer RegistryProgramme.

7,8The small number of cases of

vulval and vaginal cancer in our study is not

suitable for making statistical comparison or

estimated due to their small numbers.

Ovary was the second commonest site amongst

gynecologic malignancies at our center. The age

specific incidence rate of ovarian cancer revealed

that, the disease increases from 35 years of age

and reaches a peak between the ages of 55 to 64

years.9

Western data from the GLOBOCAN

2002 reveals a higher number of cases of ovarian

malignancies recorded as compared to the data

recorded in our study, and also the NRCP and

other cancer registries in India.7,8,10

Uterine malignancies were the commonest ones

reported as per the SEER programme of United

Stated and European Union which was

significantly higher in their population as

compared to those reported at our center.11,12 It

was also noted that all the gynecological

malignancies expect those involving the cervix

affected the younger age group in our study as

compared to the studies done in United States

and other developed countries.

Table 2: Leading sited of cancers in females,pooled aar/100,000 in india

3

SITE AAR

Breast 25.1

Cervix 21.2

Ovary 6.7

Oral cavity 6.4

Esophagus 5.5

Stomach 3.4

Gall bladder 3.2Leukemia 2.9

Lung 2.7

Corpus uteri 2.5

CONCLUSION

The present study includes an extensive data of

gynecologic malignancies. Although the

comparative study with the population basedinternational registries like Seer and Globocan

may not offer a totally accepted comparison,

considering the vast socio-economic and cultural

differences, it nevertheless provides a

comprehensive understanding of the current

scenario of gynecological malignancies in India.

In our country, lack of widespread population

based data has led to a greater reliance on

hospital based registries for the epidemiological

information. The need of the hour is more studies

on gynecologic cancer to help formulate better

cancer detection strategies towards specific age

groups and risk factors.

ACKNOWLEDGEMENTS

We acknowledge the technical help in the

statistical calculations, extended by Dr. Sumanth

MM, Assistant Professor, Department of

Community Medicine, Mysore Medical College

and Research Institute, Mysore.



873


REFERENCES

1. Consolidated report of hospital based cancer

registries 2001-3, national cancer registry

program. New Delhi; Indian Council of

Medical Research; 2007.2. Uma Devi K. Current status of gynecological

cancer care in India. Journal of Gynecologic

Oncology.2009; 20(2), 77-80.

3. Agarwal S, Malhotra KP, Sinha S, Rajaram

S. Profile of gynecologic malignancies

reported at a tertiary care center in India over

the past decade: Comparative evaluation with

international data. Indian journal of cancer.

2012;49(3); 298.

4. Momtahen S, Kadivar M, Kazzazi AS,

Gholipour F. Assessment of gynecologic

malignancies: A multi-center study in

Tehran. Indian journal of cancer.2009; 46(3):

226.

5. Nandakumar A, Ramnath T, Chaturvedi M.

The magnitude of cancer cervix in

India.2009;

6. Moore MA, Ariyaratne Y, Badar F, Bhurgri

Y, Datta K, Mathew A et al. Cancerepidemiology in South Asia-past, present and

future. Asian Pac J Cancer Prev.2010;11(2),

49-66.

7. Indian Council of Medical Research

(homepage on the internet). Bangalore:

National Cancer Registry Programme – 2007.

Consolidated Report of Hospital Based

Cancer Registries 2001-2003. Available

from: www.icmr.nic.in/ncrp/report.

8. Chhabra S, Sonak M, Prem V, Sharma S.

Gynaecological malignancies in a rural

institute in India. Journal of Obstetrics &

Gynaecology. 2002;22(4), 426-29.

9. Murthy NS, Shalini S, Suman G, Pruthvish S,

Mathew A. Changing trends in incidence of

ovarian cancer-the Indian scenario. Asian Pac

J Cancer Prev. 2009;10:1025-30.

10. Ferlay J, Bray F, Pisani P, Parkin DM.

Globocan: Cancer Incidence, Mortality and

Prevalence Worldwide. Lyon, France: IARC

Press; 2004.

11. Seer.cancer.gov (homepage on the internet).

Bethesda, Maryland: North American

Association of Central Cancer Registries;

c2000. SEER Cancer statistics review 1975-2007. Available from: http://www.seer.

cancer.gov/resources

12. Boyle P, Ferlay J. Cancer incidence and

mortality in Europe, 2004.Annals of

oncology.2005;16(3), 481-488.



874

Nazir A khan et al., Int J Med Res Health Sci. 2013; 2(4): 874-882


&

Health Sciences




thSep 2013

Research article

A PROSPECTIVE STUDY OF AN EFFECT OF SEPTORHINOPLASTY /RHINOPLASTY ON

DEVIATED EXTERNAL NASAL PYRAMID IN KASHMIRI POPULATION

Nazir A khan1, AyazRehman

1,MushtaqSangoo

1, Sajad Hamid

2

1Department of Otorhinolaryngology,

2Department of Anatomy, SKIMS Medical College, Bemina


ABSTRACT

Most studies show that objective measures to quantify and determine surgical success in the treatment of

External nasal deformity with /without nasal obstruction do not correlate with subjective improvement

as reported by patients. Aim: To evaluate the subjective& objective improvement in patients undergoing

septorhinoplasty or rhinoplasty Materials and Methods: It is a prospective study in which we evaluate

100 patients who had to undergone septorhinoplasty /rhinoplasty; various angles of nose & face were

evaluated both preoperatively & postoperatively. In cases selected for Septorhinoplasty, the patients

answered a questionnaire preoperatively and 2 months after surgery with questions about the main

symptoms of nasal obstruction (nasal obstruction, coryza, pruritus, sneezing, facial pain, snoring, sleep

disorders, daytime drowsiness), and a score of each. The intensity of symptoms was scored from 1 to 4,

as follows: 1 - absence of symptoms; 2 - mild symptoms; 3 - moderate symptoms; 4 - severe symptoms.

Results: An improvement of all symptoms was observed after surgery, where there was nasal

obstruction associated with external nasal deformity i.e; NOSE (Nasal obstructive symptom evaluation

were 45.0±10.2 (preoperatively) &10. 0±4.23 (post-operatively) with p- value < 0.005 whereas NASE

(Nasal appearance surgical evaluation) were 41.8±11.25 (pre-operatively) &7. 8±5.29 (post-

operatively) with p-value < 0.005 Conclusions: The external nasal appearance as well as symptoms of

nasal obstruction (in c/o =septorhinoplasty) improved.

Keywords: nasal septum, External nasal deformity, NOSE score, NASE

INTRODUCTION

Patients seeking nasal surgery come for a variety

of reasons. Some have trouble breathing through

the nose. Others have suffered injuries of some

sort, and would like to restore better symmetry

and correct the damage. Finally, many are

looking to alter the size or shape of the nose tomake it more harmonious with their features, to

improve their appearance. The goal of

rhinoplasty is to improve the nose aesthetically,

creating harmony with the other facial features.

Before the nose is altered, a young patient must

reach full growth, usually around age fifteen or

sixteen. Exceptions are cases in which breathingis severely impaired.

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875


Before deciding on rhinoplasty, additional

surgery might be recommended to enhance the

appearance of face. Many patients have chin

augmentation in conjunction with rhinoplasty to

create a better balance of features.

In cases of Nasal obstruction associated withexternal nasal deformity, the nasal septum

deviation is one of its most frequent causes.

Other causative conditions are: adenoid

hypertrophy; turbinate hypertrophy; nasal

tumors; and nasal polyps1. Nasal septum

corrective surgery (Septoplasty) was started in

the 19th

century, and has been modified and

improved since. The techniques have attempted

to provide maximum functional and respiratoryimprovement at the same time preserving other

physiologic functions of the nose (filtering,

warming, and moisturizing the air) to improve

nasal flow.2

Submucosal resection (SMR) was first defined

by Freer in 1902, as the resection of

quadrangular cartilage, the perpendicular lamina

of ethmoid bone and total resection of the vomer.

The era of modern septal surgery began in 1940s

with Cottle, Goldman, and Smith who recognised

the disadvantages of submucous resection.3

The

inadequate surgery for nasal obstruction is still a

dilemma. The surgery specified to the obstructive

pathology should be emphasized. The surgical

correction of nasal septum does not always

guarantee a successful outcome. The literature

supports a reevaluation of surgical paradigms in

patients with the physical findings of both a

septal deviation and turbinate hypertrophy.2,4

The corrective nasal valve surgery results in

significant improvement in disease specific

quality of life and the high satisfaction level.5

Some other studies have been performed to

assess the impact of the surgery for nasal

blockage on the quality of life of the patient.6,7

Objective measures to quantify and establish the

success of surgery have been a challenge.

Several methods have been proposed; the twomost common are rhinomanometry and acoustic

rhinometry. Rhinomanometry measures nasal

flow resistance during breathing. Acoustic

rhinometry measures nasal permeability and

quantifies the cross-sectional area of the nostrils

up to the nasopharynx, as well as the nasal cavity

volume between any two chosen cross-sections6.

Most studies have shown that these methods donot correlate with the patient's reported

subjective improvement6,7

. A few studies have

shown, however, that septoplasty is generally

effective for treating nasal obstruction, and that

most patient show improvements in nasal

symptoms3,4,7-11

. The aim of this study is to

evaluate the surgery of External nasal deformity

with/ without nasal obstruction in the patient's

perception, and exhibit our results. We used theNasal Obstructive Symptom Evaluation (NOSE)

score and NASE (Nasal angle Surgical

Evaluation) to indicate the impact of surgery.8-10


After approval by the ethics committee of our

hospital, the study was performed prospectively

between 2012 June – 2013 July in a tertiary

hospital. SKIMS Medical college/hospital all

enrolled patients gave signed informed consent.

This study included 100 patients which met the

inclusion criteria as follows: Indications that are

covered:

1) For cosmetic purposes

2) Medically indicated as in

A) When it is being performed to correct a nasal

deformity secondary to congenital cleft lip

and/or palate for patients 18 years of age andyounger.

B) To correct chronic non-septal nasal airway

obstruction from vestibular stenosis

(collapsed internal valves) due to trauma,

disease, or congenital defect, when all of the

following criteria are met:

1. Prolonged, persistent obstructed nasal

breathing; and

2. Physical examination confirming moderate tosevere vestibular obstruction; and



876


3. Airway obstruction will not respond to

Septoplasty and turbinectomy alone; and

4. Nasal airway obstruction is causing

significant symptoms (e.g., chronic

rhinosinusitis, difficulty breathing); and

5. Obstructive symptoms persist despiteconservative management for 3 months or

greater, which includes, where appropriate,

nasal steroids or immunotherapy; and

6. Photographs demonstrate an external nasal

deformity; and

7. There is an average 50 % or greater

obstruction of nares (e.g., 50 % obstruction

of both nares, or 75 % obstruction of one

nare and 25 % obstruction of other nare, or100 % obstruction of one nare), documented

by nasal endoscopy, computed tomography

(CT) scan or other appropriate imaging

modality.

C) When rhinoplasty for nasal airway

obstruction is performed as an integral part of

a medically necessary septoplasty and there

is documentation of gross nasal obstruction

on the same side as the septal deviation.

Revision cases: Patients who have any of the

following conditions or met any of the

following criteria are excluded from the

study: The history of allergy, Adenoid

hypertrophy, Undergoing concurrent

endoscopic sinus surgery, polypectomy, With

a main preoperative complaint other than

nasal obstruction(e.g. snoring, facial pain,

nasal discharge, postnasal drip syndrome,

sinonasal malignancy etc.), nasosinusaltumors, head and neck radiotherapy, nasal

septum; insufficient nasal valve, nasosinusal

granulomatous disease, hyperplasic

pharyngeal tonsils, snoring surgery,

craniofacial malformation, pregnancy.

After selecting, the patients were assessed

preoperatively and on the 7th

, 14th

, 30th

, and

60th

postoperative day. This evaluation consisted

of an otorhinolaryngologica examination,

measurement of NASE (Nasal appearance

surgical evaluation) & NOSE SCORE (Nasal

obstructive symptom evaluation) in cases of

those who underwent septorhinoplasty whereby,

a questionnaire with questions about the main

symptoms of nasal obstruction (nasal

obstruction, coryza, pruritus, sneezing, facialpain, snoring, sleep disorders, daytime

drowsiness), were asked and a score given for

each answer. The intensity of symptoms was

scored from 1 to 4, as follows: 1 - absence of

symptoms; 2 - mild symptoms; 3 - moderate

symptoms; 4 - severe symptoms. Data were

gathered on sex, age, and the degree of septal

deviation. Also, the patient factors are to be

taken into consideration. During assessing apatient for potentialrhinoplasty, a full

concentration was given on the patient’s

expectations prior to performing the

comprehensive facial analysis. Although there

are different methods for integrating the patient

in the surgical process. The computer imaging of

the face was done as it provides an excellent way

to gain a realistic understanding of the

anticipated outcome these images were combined

with standardized anterior, lateral, oblique, and

basal photographs. Nonsteroidal anti-

inflammatory agents and certain herbal

supplements may increase bleeding

complications after surgery and should be

discontinued at least 7 – 10 days before a

rhinoplasty. Furthermore, patients are instructed

to avoid consumption of salicylic derivatives for

3 weeks prior and 1 week following surgery.

A critical facial analysis was also done in orderto preserve nasofacial harmony & any natural

facial asymmetries was pointed out so that the

patient gains a better understanding of what is

present before any operative intervention.12,13

Prior to surgery we convert our operative plan

into a graphic representation to assist us in the

operating room. Modifications to the plan are

documented intraoperatively, transposed to the

graphic depictions postoperatively, and placed inthe patient's chart for future reference. Cefazolin

1 g was administered intravenously as a



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perioperative antibiotic. We prefer general

anesthesia for our patients, though local

anesthesia with intravenous sedation is a viable

alternative. After the administration of

anesthetic, the nasal vibrissae are clipped and the

nares are prepared with povidone iodine solution.The anticipated incision approach is marked and

injected with approximately 10 ml of 1%

lidocaine with 1: 100 000 epinephrine into the

nasal mucosa, along the septum and the soft

tissue envelope. Next, the mucosa is treated with

cottonoidpledgets soaked in oxymetolazone

Operative approach: We select the two basic

incisional approaches to rhinoplasty: 1. The open

technique 2. The closed (endonasal) technique.Each has its advocates who use them

successfully in the practice of rhinoplasty.

The open approach involves a transcolumellar

incision, which can assume varying geometries,

depending on surgeon choice. Our preference is a

stair step configuration, which facilitates

reapproximation while breaking up the scar and

preventing contracture deformities. The open

approach also involves skeletonizing the

underlying osseocartilaginous framework, which

gains enormous exposure for the manipulation

and correction of deformities. The closed (or

endonasal) technique can be performed using a

cartilage-delivery approach or a nondelivery

approach.

Osteotomy techniques: Osteotomies are a

powerful technique in rhinoplasty.14-16

The

indications to perform osteotomies, regardless of

technique are: 1. To narrow the lateral wall of nose 2. To close an open roof deformity (after

dorsal hump reduction) 3. To create symmetry

by straightening the nasal bony framework

Contraindications: 1. Patients with short nasal

bones 2. Elderly patients with thiin fragile nasal

bones 3. Patients with heavily eye glasses

There are several osteotomy techniques,

including medial, lateral, transverse, or a

combination of these. Furthermore, they can beperformed through either an external or internal

approach17-19

Closure: After hemostasis was achieved and any

excess debris removed, the skin envelope was

redropped. If the patient has thick skin, and

especially if the patient is a woman, we choose to

place a single 5-0 Vicryl suture from the dermis

(underside of the skin envelope) to theunderlying cartilaginous framework in an attempt

to recreate a supratip break.

The transcolumellar incision was closed using 6-

0 nylon suture in simple interrupted fashion,

making sure the coaptation of the incision

margins is precise. The stair stepping of the

original incision helps us close this accurately.

The infracartilaginous incisions were

reapproximated using 5-0 chromic suture insimple interrupted fashion. We take special care

to prevent overbiting with the suture, which can

create contour irregularities and notching,

especially in the soft triangle area. In septal

work, we place intranasal silastic splints coated

with antibiotic ointment.

Alar base surgery: In certain cases Alar base

abnormalities were seen &include wide or

excessive nostril sills, a wide alar base,

asymmetric or malpositioned alar bases, or any

combination of these, so alar base surgery was

necessary, & was performed after closure of the

transcolumellar and infracartilaginous incisions,

but before intranasal and external splints are

placed.

Depressor septi translocation: Some patients

had a tension tip (foreshortened upper lip with

decreased tip projection), a depressor septi

translocation was donePostoperative care: All preoperative and

postoperative instructions were given to the

patients in writing before and on the day of

surgery. Postoperatively, we put them on :

Cephalexin 500mg orally, 8 hourly for 3 days,

Medrol dose pack for 7 days to minimize

postoperative edema, Acetaminophen500mg

every 4-6 hourly for post-operative pain, Normal

nasal saline solution for post-operative nasalcongestion. The patient is instructed to keep the

head of the bed elevated at an angle of 45°



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beginning immediately after surgery to help

minimize postoperative swelling. Cool

compresses are used periorbitally during the day

for the first 48 hours. The patient is instructed to

change the drip pad under the nose as necessary

until the drainage stops, at which time the drippad and tape can be discontinued. Any

manipulation of the nose, including rubbing,

blotting, or blowing, is discouraged for the first 3

weeks postoperatively.

Statistical Analysis

Analyses were conducted in NCSS (Number

Cruncher Statistical System) 2007&PASS 2008

Statistical Software (Utah, USA). The predictors

of improvement for quantitative data, parameters

showing the normal distribution between groups

compared with the One-way Anova test. As wellas descriptive statistical methods (mean, standard

deviation) are used. Parameters which are not

showing the normal distribution between groups,

Mann-Whitney U test is used. To assess the

qualitative data, chi-square test is used. A p<0.05

is considered as statistically significant.

RESULTS

Table 1: Showing information regarding various parameters among selected cases

Parameter No of patients

Sex distribution Male 67

Female 33

Area-wise distribution Rural areas 70

Urban areas 30

Types of cases Primary cases 86

Revision cases 14

Main indications Saddle nose deformity 20

Dorsal hump 55Supratip depression 5

Nasal valve area weakness 20

Type operative procedure Septorhinoplasty 80

Rhinoplasty only 20

Type of operative

approach

Open 55

Close 45

Chief complaints External nasal deformity with nasal obstruction 80

External nasal deformity 20

Aetiological factors Post-traumatic 54

Developmental 40

Post-operative 5

Post-infective 1

Table 2: Shows the type of graft material used

Graft material used ( only in 45 cases)

Autologous septal cartilage 35

Autologous Conchal cartilage 5

Autologous iliac crest 1Autologous septal bone 4



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Table 3: Shows the different techniques used

Various surgical techniques used

Dorsal augmentation Only graft

Supratip augmentation Goldhen’s tip procedure

Spreader graft Intra & Inter dermal suturing

Table 4: Shows evaluation of operation in terms of pre-operative and post-operative nasal angles

Nasal angles Pre-operative Post-operative p-Value

Nasolabial 94.2 ±7.7° 97.1±6.8° 1.042

Nasofrontal 134.5±7.4° 133.1±6.9 1.058

Nasofacial 32.0 ±5.2° 31.2 ±4.9 1.020

Table 5: Shows evaluation of operation success by analysing pre-operative & post-operative NOSE score

and NASE score23,24

Score Pre-operative Post-operative p- Value

NOSE (Nasal obstructive symptom evaluation) 45.0±10.2 10.0±4.23 < 0.005

NASE (Nasal appearance surgical evaluation) 41.8±11.25 7.8±5.29 < 0.005

Fig. 1a: Deviated External nose (pre-op.) 1b: Corrected deformity (Post-op.)

Fig 2a: Deviated External nose (pre-op.) 2b: Corrected deformity (Post op.)



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Fig 3a: Deviated External nose (pre-op.) 3b: Corrected deformity (Post op.)

DISCUSSION

Owing to its central location on the face, the nose

plays an intimate role in all social interactions.Early surgical correction of nasal deformities

improves psychosocial development and

opportunities for normalized social integration

and removes the stigma of an abnormal

appearance. Pre and intraoperative planning are

essential in order to achieve good results; the

surgeon must carefully examine the nose in order

to determine which pathological condition there

is and which surgical procedure is needed

20.

In the present study 67% of patients were male

vs. 33% female. (Table 1) This agrees with the

study for objective evaluation of a deviated

septum, Erdem & Ozturan21

reported that the

number of males was more than females,21

that

may be explained because this study dealt only

with patients seeking functional correction of

deviated septum which is more common in males

due to more exposure to trauma. (Table 4) In

contrast to females, male patients seem to lack a

clear body concept and an in-depth awareness of

their physical appearance. As a result, they often

have difficulty articulating their objectives for

cosmetic surgery.

In the current study there was a statistically

significant difference between pre-operative and

postoperative measurements for nasofacial,

nasolabial & naso frontal angles. (Table 4) This

agrees with Okur, et al.22

who stated that theangle measurement method may be helpful in

evaluating the effectiveness of surgical

techniques and the results for correction22. Inanother study by Ozkul & Ozkul et al.,

23five

parameters (nasofrontal, nasomental, nasolabial,

nasofacial angles and nasal projection ratio) were

used to induce a facial harmony index, which is

to generate a score for the patient before and

after the rhinoplasty operation so that the

improvement due to rhinoplasty operation can be

determined objectively23

.

In the current study, we found that 20% of patients with saddle nose deformity, 55% had

dorsal hump, 5% had supratip depression & 20%

had nasal valve area v weakness. (Table 1) And

excellent results were seen in in post-operative

measurements. This agrees with Okur et al.

(2004) who found that 66.7% of the patients with

crooked noses had good and excellent results

after surgery.

Also, Erdem & Ozturan (2008) found that 27.7%

of his patients had excellent results and 30.5%

had good results after measuring the angle of

septal deviation post-operatively21,22

. The

approach for the management were open (55%)

& close approach in (45%) (Table 1)with the

operative procedure septorhinoplasty done in

(80%) cases & rhinoplasty alone in (20%) cases

(Table 1) & includes wide exposure through

external septorhinoplasty, release of all

deforming forces for the septum, straightening of the septum while maintaining an adequate dorsal



881


and caudal strut, realigning and reinforcing the

nasal structures with sutures or grafts, and

performing adequate osteotomy.

Although not being necessary for indicating

surgery, the classification of patients as being

candidates or not to the procedure, may predictresults which are more or less satisfactory.

Patients with high scores in the pre-op may not

be very pleased after the surgery, and they may

even have a risk of worsening in their initial

situation. This agrees with Izu, et al.24

CONCLUSION

This study along with other studies emphasizes

the importance of using the evaluative tools tosubjectively and objectively assess patients

undergoing septorhinoplasty / rhinoplasty. Both

subjective and objective evaluation tools are

important for identifying the best candidate for

rhinoplasty operation, though most of the

surgeons depend on their aesthetic eye only. It

should be taken into consideration that the

aesthetic eye is a skill that needs a lot of time to

be developed.

REFERENCES

1. Uppal S, Mistry H, Nadig S, Back G,

Coatesworth A. Evaluation of patient benefit

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obstruction. AurisNasus Larynx.

2005;32(2):129-137

2. Dinis PB, Haider H. Septoplasty: Long-term

evaluation of results. Evaluation studies. Am

J Otolaryngol 2002;23:85 – 90.3. Devaiah AK, Keojampa BK. Surgery of the

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4. Harrill WC, Pillsbury HC, McGuirt WF,

Stewart MG. Radiofrequency turbinate

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5. Rhee JS, Poetker DM, Smith TL, Bustillo A,

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measurement of attitudes. Archives of

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11. Constantian MB, Brian CR. The relative

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primary and secondary rhinoplasty. Plast

Reconstr Surg 1996;98(1):38 – 54

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and facial analysis. In: Dallas rhinoplasty:

nasal surgery by the masters, St

Louis: Quality Medical Publishing; 2002:53.

13. Rohrich RJ, Gunter JP, Shemshadi H: Facial

analysis for the rhinoplasty patient. Dallas

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14. Goldfarb M, Gallups JM, Gerwin JM: Perforating osteotomies in rhinoplasty. Arch

Otolaryngol Head Neck Surg 1993; 119:624-

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15. Parkes ML, Kamer F, Morgan WR: Double

lateral osteotomy in rhinoplasty. Arch Oto

laryngol 1977;103:342-48.

16. Sullivan PK, Harshbarger RJ, Oneal RM: Na

salosteotomies. In: Gunter JP, Rohrich RJ, A

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17. Rohrich RJ, Janis JE, Adams WP. An update

on the lateral nasal osteotomy in rhinoplasty:

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external versus the internal approach. PlastReconstr Surg 2003; 111:2461-62

18. Rohrich RJ, Krueger JK, Adams WP. Achiev

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Karagiannidis K, Kontzoglou G. Long term

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21. Tamer Erdem, Orhan Ozturan. Objective

measurement of the deviated nose and a

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Rhinology. 2008; 46; 56-61

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Keerti S et al., Int J Med Res Health Sci. 2013; 2(4): 883-886


&

Health Sciences




thSep 2013

Research article

A STUDY ON MORBIDITY PROFILE OF SCISSOR MANUFACTURING WORKERS

*Keerti S Jogdand1, Pravin N Yerpude

1, Mohini Jogdand

2

1Associate Professor, Dept of Community Medicine, Gujarat Adani Institute of Medical Sciences, Bhuj,

Gujarat, India2Assistant professor, Dept of Community medicine, SRTR Medical College and Hospital, Ambajogai,

Maharashtra, India


ABSTRACT

Introduction: In India, the life of the vulnerable and the marginalized working population is at risk as

there is a lack of awareness about occupational safety and environmental hazards. The scissor

manufacturing workers sector is one of the important but unorganized parts of industry of India and

mainly run by private establishments. The scissors manufacturing workers hardly ever benefit from

occupational health and safety provisions. Materials and methods: The present community based,

cross-sectional study was conducted among 218 scissor manufacturing workers of small scale industry

of urban slum area, Malvani in South Mumbai. The study period was from June 2010 to September

2010. Results: In the present study, 52.75% workers were in the age group of 20-30 yrs followed by in

the age group of 30-40 yrs (32.57%). Majority, 92.66% were males. Regarding the history of addiction,

77.52% workers were using tobacco related products. The commonest health problem present in

workers was acute respiratory infection (ARI) (34.86%) followed by musculoskeletal problems in

25.68% workers. Conclusion: As scissor manufacturing workers suffering from various morbidities, it

is necessary to monitor the occupational environment and health status of the workers periodically. It is

also necessary to create awareness regarding the ill effects of industrial hazards.

Key words: Morbidity profile, scissor manufacturing workers

INTRODUCTION

In the world, one of the leading causes of

morbidity and mortality is occupational health

risks and they are more common in developing

countries1.

In India, the life of the vulnerable and

marginalized working population is at risk as

there is a lack of awareness about occupational

safety and environmental hazards. In small scale

industries worldwide, over 1000 million people

are employed.2

The scissor manufacturing workers sector is one

of the important but unorganized parts of

industry of India and mainly run by private

establishments. The scissors manufacturing

DOI:10.5958/j.2319-5886.2.4.141



884


workers hardly ever benefit from occupational

health and safety provisions. As they work for

long hours, they may suffer from various health

problems. Most of the health problems among

them are due to the dust particles produced

during various processes like heat treatment,processing, grinding, polishing, plating, edging,

packing. Scissor manufacturing workers mostly

suffer from various illnesses such as respiratory

problems, musculoskeletal problems, eye

diseases, skin problems. The various

socioeconomic factors such as poverty, lack of

education, poor diet, addictions, and poor

working conditions also contribute to the ill

health of the workers

3.

The present study wasconducted among scissor manufacturing workers

with the objective of finding common morbid

conditions among them.


The present community based, cross-sectional

study was conducted among scissor

manufacturing workers of small scale industry of

urban slum area, Malvani in South Mumbai. The

study period was from June 2010 to September

2010. Before the start of the study, ethical

clearance was taken from the Institutional Ethics

Committee. The study consists of 218 workers

working in scissor manufacturing units. This

includes all workers involved in all stages of

scissor manufacturing. The workers involved in

other units like cotton were not included in the

study. Out of 218 workers, 202 were males and

16 were females. A pre-designed, pre-tested semi

structured schedule was used during interview of

the workers. Before interview of the workers,

they were explained clearly the purpose of the

study and then verbal consent was obtained fromthem. Health status of the workers was assessed

by asking questions regarding their health

problems in the past 3 month period followed by

clinical examination that included respiratory

examination, eye check up. The data was

analyzed using Microsoft excel and the results

were expressed in percentages.

RESULTS

In the present study, 52.75% workers were in the

age group of 20-30 yrs followed by in the age

group of 30-40 yrs (32.57%). Majority, 92.66%

were males. Religion wise, the majority were

Muslims (90.83%). 12.39% were illiterate,

74.77% were married (Table1).

Regarding history of addiction, 77.52% workers

were using tobacco related products. 17.43%

were alcoholics. The commonest health problem

present in workers was acute respiratory

infection (ARI) (34.86%) followed by

musculoskeletal problems in 25.68% workers.

Asthma was present in 23.39% workers.

Tuberculosis was present in 8.26% workers. Skin

diseases were present in 16.05% workers. Eye

problems were present in 10.55% workers

(Table 2).

Table1: Socio-demographic characteristics of workers

Characteristics No (%)

Age (years) 20-30 115 (52.75%)

30-40 71 (32.57%)

Above 40 yrs 32 (14.68%)

Sex Male 202 (92.66%)

Female 16 (7.34%)

Religion Muslim 198 (90.83%)

Hindu 20 (9.17%)

Education Illiterate 27 (12.39%)

Literate 191 (87.61%)

Marital status Married 163 (74.77%)

Unmarried 55 (25.23%)



885


Table 2: Morbid conditions of workers

Diseases No (%)

Persistent cough 76 (34.86%)

Asthma 51 (23.39%)

Tuberculosis 18 (8.26%)

COPD 6 (2.75%)

Musculoskeletal problems 56 (25.68%)

Skin diseases 35 (16.05%)

Eye problems 23 (10.55%)

DISCUSSION

In the present study, Majority, 92.66% workers

were males. Religion wise, the majority were

Muslims (90.83%). 12.39% were illiterate.

74.77% were married. Similar results were found

in a study done in Meerut on the health status of

scissor workers by Goel K et al4.

The prevalence of tobacco use among workers

was 77.52%. In a study by Goel K et al4in

Meerut , the prevalence of tobacco use was found

to be 85%. According to NFHS III, in India,

55.8% males in the age group of 12-60 years

have been found to be consuming tobacco. The

reasons of tobacco consumption may be loweducational status, occupation involving hard

labour work during night shift work and low

socioeconomic status.

In our study, 34.86% workers were having cough

followed by asthma in 23.39% workers. TB was

present in 8.26% workers. In a study by Goel K

et al4on scissor manufacturing workers in

Meerut,40% worker were suffering from

persistent cough .Asthma was present in 28%

workers. In a study of Qurratul et al5,100 %

workers were suffering from lung diseases. The

reason for such high prevalence may be due to

reason that the workers working in the scissors

industry come in direct contact with the iron

sparkles, suspended particles of metal, iron and

cotton dust and fumes of acids, kerosene oil.

In our study apart from respiratory infections,

other health complications present were

musculoskeletal problems (25.68%), skindiseases (16.05%) and ear problems

(10.55%).Mismatch between man and machine

may be one of the major factor contributing to

musculoskeletal problems.

CONCLUSION

In scissor manufacturing workers, commonest

morbidities detected were respiratory and

musculoskeletal problems. In scissor industry,

several hazardous conditions exist like poor

ventilation, overcrowding and poor illumination

which synergistically affects the health and

comfort of the workers ultimately decreasing the

work efficiency and hence productivity. It is

necessary to monitor the occupationalenvironment and health status of the workers

periodically. It is also necessary to create

awareness regarding the ill effects of industrial

hazards. Use of personal protective equipments

(PPE) like masks or respirators, ear plugs,

earmuffs should be regularly used by workers.

ACKNOWLEDGEMENT

We would like to thank the study participants fortheir co-operation

Conflict of interest: Nil

REFERENCES

1. World health report, 2002.Reducing risks,

promoting healthy life. Geneva WHO; 2002.

Available from http://www.who.int/peh/

occupational health4. htm2. Occupational health: The workplace health

and environment in sustainable



886


development. Geneva WHO; 1997.

Available from http://www.who.int/peh/

occupational health2.htm

3. ILO Encyclopedia. Occupational health and

safety 4th

ed.1998.pg.89-90.

4. Goel K, Ahmad S, Goel P, Parashar P,Maroof KA, Ali AA. Study on social and

health status of scissor manufacturing

workers of Meerut, UP. International J of

Contemporary Medicine 2003;1(1):51-54.

5. Qurratul A, Shama P, Verma RK.

Prevalence of lung disease in the workers of

scissors manufacturing industries in Meerut

city. The Pharma research. 2009;4(3):57-60.



887

Nitesh Mohan et al., Int J Med Res Health Sci. 2013; 2(4):887-892


&

Health Sciences

www.ijmrhs.com Volume 2 Issue4 Oct - Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886Received: 24



thSep 2013

Research article

CLINICO HISTOPATHOLOGICAL CORRELATION WITHIN THE SPECTRUM OF

HANSEN'S DISEASE: A MULTICENTRIC STUDY IN NORTH INDIA

*Nitesh Mohan1, Nitin Mishra

2

1Associate Professor, Department of Pathology, Rohilkhand Medical College & Hospital, Bareilly, U.P.

India2Assistant Professor, Department of Dermatology, SRMS Institute of Medical Sciences, Bareilly, U.P.,


ABSTRACT

Background: Leprosy is one of the oldest and chronic infectious diseases known to human being

caused by Mycobacterium leprae. Leprosy is widely prevalent in all parts of India and it presents with

different clinico-pathological forms. However a great variation is seen in interpretation of clinical and

histopathological examination of these lesions. The present research was taken to study the correlations

between the clinical and histological diagnosis and to evaluate the importance of skin biopsy as animportant diagnostic and spectrum defining tool. Methods: A prospective hospital based study was

conducted among patients attending Dermatology OPD of two tertiary care centres in this region over a

period of two years. All clinically suspected new leprosy patients were included in the study. A detailed

clinical history and examination was carried out and skin biopsies were taken from the most active part

of lesions. Sections were stained with Hematoxylin & Eosin stain and Fite-Feracco stain.

Histopathological findings were compared with clinical diagnoses. Results: A total of 190 cases were

studied, out of which 137(72.10%) were males and 53(27.9%) were females. The histopathological

diagnosis of leprosy was established in 99.47% of clinically diagnosed cases. Clinico-histopathological

concordance was seen maximum in LL (97.22%), followed by BT (79.76%), TT (71.43%), BL(66.67%), BB (66.67%) and least in IL (50.00%). Overall concordance was 56.54% Conclusion:

Clinical diagnoses of Leprosy still pose a significant problem, especially the Intermediate subtypes of

the disease spectrum. Histopathological examination of the active skin lesions should be done in all new

cases to confirm the spectrum of disease and expected duration of therapy.

Keywords: Leprosy, Lepromatous leprosy, Skin biopsy

INTRODUCTION

Leprosy is one of the oldest and chronic

infectious diseases known to human being caused

by Mycobacterium leprae. The disease still

carries a grave social stigma and ostracism which

compels the patients to hide the disease. Leprosy

DOI:10.5958/j.2319-5886.2.4.142



888


continues to be an important public health

problem in most parts of Asia, especially India.1

Leprosy is a progressive, chronic granulomatous

disease of the peripheral nerves and skin and

other tissues such as mucous membranes,

muscles and reticuloendothelial system. Thedisease presents in various clinico-pathological

forms depending on the immune status of the

host. The disease spectrum has been

characterised in a number of classification

systems, most widely being the Ridley-Jopling

classification. In this classification, leprosy has

been divided into five groups as

Tuberculoid(TT), Borderline tuberculoid(BT),

Mid-bordrline (BB), Borderline Lepromatous(BL), and Lepromatous (LL).

2

The Classification has been accepted worldwide

and is highly recommended. Though the clinical

diagnosis is based on characteristic skin lesions

with sensory loss, a great variation is seen in

interpretation of these lesions, both clinically and

histopathologically.3

The present research was taken to study the

correlations between the clinical and histological

diagnosis of the tissue sections from clinically

suspected patients in this region, and to evaluate

to the importance of skin biopsy as an important

tool in diagnosing leprosy in these patients.3


A prospective hospital-based study was

conducted among patients attending

Dermatology OPD of Rohilkhand Medical

College & Hospital, Bareilly and SRMS Institute

of Medical Sciences, Bareilly and few others

private hospitals in this region, between January

2012 to December 2012. The study was approved

by the Institutional Ethics Committee, and is

informed consent from taken from all the

participants

Unit of Study: Both sex patients of all age groups

between 2 to 70 years, having clinically

suspected leprosy were included in the study.

Exclusion criteria: Patients already treated with

anti-leprosy medications at any time earlier were

excluded.

Nature of Study: The study includes all patients

with clinically diagnosed leprosy and was

subjected to history and examination after taking

informed consent and approval from Institutions’Ethical Committee.

Sample Size: Total no. of cases studied was 190.

Study Schedule: A detailed clinical history and

examination was carried out. Clinical

examination included the type, number and site

of lesion, type of disease and neural involvement.

All the patients were subjected to skin biopsies

from the most active part of the lesions. Biopsies

were fixed in 10% formalin & processed. Serial

sections of 5µ thickness were cut and stained

with routine Haematoxylin and Eosin and Fite-

Feracco stains. The Ridley & Jopling

classification was followed in both clinical and

histopathological diagnosis. Histopathological

evaluation included invasion of epidermis,

involvement of sub-epidermal zone, character &

extent of granulomas, density of lymphocytic

infiltrate, epitheloid cells and other cellular

elements, nerve involvement and presence of M.leprae.

RESULTS

Table 1: Clinical presentation in various types of leprosy

Clinical diagnosis Hypopigmented

patch (No. of cases)

Erythematous plaque/

papule/nodule (No. of cases)

No.of

cases

%

Tuberculoid Leprosy (TT) 06 09 15 7.89

Borderline Tuberculoid (BT) 75 11 86 45.26

Mid Borderline (BB) 02 02 04 2.12

Borderline Lepramatous (BL) 10 16 26 13.68

Lepramatous Leprosy (LL) 16 29 45 23.68Intermediate Leprosy (IL) 08 06 14 7.37



889


Table 2: Histopathological distribution of leprosy cases

Table 3: Observation of AFB in different types

Type of Leprosy No. of Positive cases Percentage

Tuberculoid Leprosy (TT) -- --

Borderline Tuberculoid (BT) 08 8.42

Mid Borderline (BB) 11 11.58

Borderline Lepramatous (BL) 28 29.47

Lepramatous Leprosy (LL) 34 35.79

Intermediate Leprosy (IL) 14 14.73

Total 95 100

No acid fast bacillus could be demonstrated in any case of TT

Table 4: Distribution of Site of lesions

Site of Lesion Number of cases Percentage

Head & Neck 40 21.05

Upper limb 65 34.21

Lower limb 30 15.79

Trunk 25 13.16

Multiple sites 30 15.79

Total 190 100

Table 5: Comparison of clinical and histopathological diagnosis

Histological

Types

Clinical Types Percentage

of

concordanceTT BT BB BL LL IL

TT (14) 10 04 71.43

BT (84) 03 67 - 10 04 - 79.76

BB (03) 01 02 66.67

BL (24) 03 01 16 04 66.67

LL (36) 01 35 97.22

IL (28) 02 11 01 14 50.00

Total (189) 15 86 04 26 45 14

Histopathological diagnosis No. of cases %

Tuberculoid Leprosy (TT) 14 7.40

Borderline Tuberculoid (BT) 84 44.44

Mid Borderline (BB) 03 1.6

Borderline Lepramatous (BL) 24 12.70

Lepramatous Leprosy (LL) 36 19.05

Intermediate Leprosy (IL) 28 14.82

Total 189 100



890


Table 6: Comparison of Sex Distribution

Authors Males (%)

Moorthy et al (2001) 65.05

Bhushan et al (2008) 72.34

Mathur MC et al (2011) 53.8

Gridhar M et al (2012) 77.6

Present study (2013) 72.10

Table 7: Comparative Analysis of Overall Concordance with other similar studies

Studies Year Overall Concordance %

Kalla G et al 2000 60.6

Tailor et al 2008 58

M Giridhar et al 2012 60.23

Present Study 2013 56.54

Fig1: Grenz zone and macrophage granuloma in

Borderline tuberculoid leprosy (H&E)

Fig 2: Non caseating granulomas & Langhans

Fig3: A case of BT leprosy with satellite lesion

Fig 4: Case of Mid Borderline Leprosy



891


DISCUSSION

In the present study, a total of 190 clinically

diagnosed leprosy patients were examined and

were subjected to clinical and histopathological

examination, which included various aspects of

the lesions, like number and site of lesions, typeof disease.

The studied showed the most common clinical

presentation to be with hypopigmented patch

(61.58%) followed by erythematous plaque or

nodule (38.42%). This correlated well with study

done by M Gridhar et al.3

and Ocampo and

Francisco.4

The sex ratio was heavily skewed towards males

(72.10%). This is similar to other Indian studiesundertaken by Gridhar M et al (77.6%)

3]&

Bhushan et al (72.34%)5. Mathur MC et al.

2

however observed 53.8% males in their study

while Moorthy et al. observed 65.05% males.6

In the present study concordance between

clinical and histopathological diagnosis for

individual type of leprosy was found to be TT

(71.43%), BT (79.76%), BB (66.67%), BL

(66.67%), LL (97.22%) and IL (50.00%).

Maximum concordance was observed in LL type

of leprosy, which was similar in studies by

Mathur MC et al.2, Gridhar M et al

3and Moorthy

et al.6

However, concordance differed variably

when compared with other types of Leprosy,

which may be due to more precise diagnostic

criteria laid down in histopathology with

emerging microbiological and immunological

techniques. The observations strongly suggest the

importance of histopathological diagnosis inthese cases, as lesions are easy to diagnose

clinically towards Lepromatous pole of the

disease.4

In our study, histological diagnosis of leprosy

was established in 99.47% cases. One case

(0.53%) was diagnosed as Lupus Vulgaris.

Similar observations have been made by different

authors in their studies, however with lesser

specificity. The discrepancy, whenever seen maybe due to clinical overdiagnosis of leprosy and

misinterpretation of many skin lesions presenting

with hypopigmented patches.3,4,6

CONCLUSION

Leprosy is a chronic granulomatous disease

widely prevalent in India and is present in

different clinico-pathological forms. Study of

these lesions has contributed a great deal in

understanding the disease. Many cases can be

diagnosed clinically; especially those towards the

Lepromatous pole of the disease, however, other

types of Leprosy pose a significant problem in

clinical diagnosis. Histopathological examination

of the lesions confirms the exact subtype of the

disease and should be done in all cases so as tofacilitate the institution of accurate mode of

therapy.

REFERENCES

1. Mohite RV, Mohite VR, Durgawale PM.

Differential Trend of Leprosy in Rural and

Urban Area of Western Maharashtra. Indian J

Lepr. 2013;85:11-18.

2. Mathur MC, Ghimire RBK, Shrestha P,Kedia SK. Clinicohistopathological

Correlation in Leprosy. Kathmandu Univ

Med J. 2011;36(4):248-51.

3. Giridhar M, Arora G, Lajpal K, Chahal KS.

Clinicohistopathological concordance in

Leprosy- A Clinical, Histopathological and

Bacteriological study of 100 cases. Indian J

Lepr 2012;84:217-25.

4. Vargas-Ocampo, Fransisco. Analysis of 6000

Skin Biopsies of the National Leprosy

Control Program in Mexico. Int J Lepr Other

Mycobact Dis. 2004;59:28-35.

5. Bhushan P, Sardana K. Diagnosing

multibacillary leprosy: A comparative

evaluation of diagnostic accuracy of slit-skin

smear, bacterial index of granuloma and

WHO operational classification. Indian J

Dermatol Venereol Leprol 2008; 74:322-26.



892


6. Moorthy BN, Kumar P, Chatura KR.

Histopathological correlation of skin biopsies

in leprosy. IJDVL 2001; 67:299-301.

7. Kalla G, Salodkar A, Kachhawa D. Clinical

and histopathological correlation in leprosy.

Int J Lepr 2000; 68:184-85.8. Pandya A, Tailor HJ. Clinico

histopathological correlation of leprosy.

Indian J Dermatol Venereol Leprol 2008;

74:174-76.



893

Jankar DS et al., Int J Med Res Health Sci. 2013; 2(4):893-898


&

Health Sciences




thSep 2013

Research article

A STUDY ON HEARING LOSS IN TYPE II DIABETICS

Jankar DS1*

, Bodhe CD2, Bhutada TB

3

1MD Physiology,

2Asst. Professor,

3Asso. Professor, Dept. of Physiology, Govt. Medical College, Miraj,

Maharashtra, India


ABSTRACT

Diabetes-related sensorineural hearing impairment affects people’s ability to hear and understand

sounds. We carried out this case control study with the purpose of determining the hearing loss in type II

diabetes mellitus in relation to the age and gender of the patients and duration of the illness using tuning

fork tests and pure tone audiometry. Aim: To study the hearing loss in type II diabetics and controls.

Objectives:1. To study the hearing loss in relation to different age groups in diabetics and controls. 2.

To study the hearing loss in relation to gender in diabetics and controls. 3. To study the hearing loss in

relation to duration of diabetes. Material and Methods: 200 diabetic patients and 200 age and sexmatched controls took part in the study. They were evaluated by Tuning fork tests and Pure Tone

Audiometry. Results: The hearing of diabetics was significantly impaired than the non-diabetic control

group. This hearing impairment was noted in all the frequencies tested. The hearing acuity was not

influenced by the duration of diabetes, age or sex of the subjects. Discussion: The possible mechanisms

underlying the hearing loss in diabetic individuals are microangiopathy, demyelination, hyperglycemia,

etc. Conclusion: Type 2 diabetes causes significant hearing loss in the patients, but it is not affected by

the age and sex of the patient or duration of the illness.

Key words: Audiometry, Diabetes, Sensorineural hearing loss

INTRODUCTION

Diabetes mellitus is a heterogeneous group of

metabolic disorders characterized by chronic

hyperglycemia that results from defects in insulin

secretion, insulin action or both. Diabetes

mellitus leads to long term damage, dysfunction

and failure of various organs, especially the eyes,

kidneys, heart and blood vessels.1

Diabetes-related sensorineural hearing

impairment affects people’s ability to hear and

understand sounds. Although evidence from as

early as the mid-19th century linked diabetes

with hearing loss, a degree of controversy has

surrounded this association.2

Various tests are available for the clinical

assessment of hearing loss. Localization and type

DOI:10.5958/j.2319-5886.2.4.143



894


of hearing loss can be known by use of simple

tests like the tuning fork tests, while audiometry

gives the graphic recording of hearing

quantitatively and qualitatively.3-5

We carried out this case control study with the

purpose of determining the hearing loss in type IIdiabetes mellitus in relation to the age and

gender of the patients and duration of the illness

using tuning fork tests and pure tone audiometry.

Aim: To study the hearing loss in type II

diabetics and controls.

Objectives:

1. To study the hearing loss in relation to

different age groups in diabetics and controls.

2. To study the hearing loss in relation togender in diabetics and controls.

3. To study the hearing loss in relation to

duration of diabetes.


The present study was conducted on patients

attending the ENT and Medicine OPD and IPD

of civil hospital, Miraj after proper consent. 200

diagnosed diabetic patients (Fasting plasma

glucose ≥ 126 mg/dl or 2 hour plasma glucose ≥200 mg/dl during an oral glucose tolerance test)

and 200 age and sex matched controls took part

in the study. The Ethical Committee of the Govt.

Medical College and Hospital, Miraj approved

this study.

Inclusion criteria: Case: Diagnosed cases of type

2 diabetes, Age above 40 yrs, both genders.

Control: non-diabetic healthy controls, Age

above 40 yrs, both genders.

Exclusion criteria: Diabetes other than type2,

patients with conductive hearing loss, or hearing

loss associated with other causes.

Interpretation of tuning fork tests3-5 Initialscreening of hearing loss in the study and control

group was done by tuning fork tests.

Then they were subjected to pure tone

audiometry

Pure Tone Audiometry3-5

: Instrument:- Elkon

EDA-3N3 Giga 3 Audiometer5a

was used in the

study.

I. Air conduction tests: The Conventional “5-

up-10-down method” was followed. In thisprocedure the tones are lowered in 10 dB

steps and increased in 5 dB steps for each

frequency. The exact hearing threshold is

obtained when one gets at least 3 out of 5

responses correct.

II. Bone conduction tests: Technique:- the “5-

up-10-down method” is followed for bone

conduction study.

Participants were labeled as having sensory-

neural hearing impairment if the average of the

pure-tone thresholds in either ear exceeded 25 dB

HL and the air – bone gap less than 15 dB.5

Statistical Analysis: Analysis was done by ‘chi

– square’ test using Microsoft Office Excel 2010.

A ‘p’ value of < 0.05 was considered statistically

significant.

Table1: Interpretation of tuning fork tests

Test Normal Conductive deafness Sensori-neural deafness

Rinne AC > BC BC > AC AC > BC

Weber Not lateralized Lateralized to poorer ear Lateralized to better ear

ABC Same as examiner’s Same as examiner’s Reduced

RESULTS

Table 2: mean age of Diabetic and non-diabetic (controls)

Diabetics Non-diabetics

Total no. 200 200

Mean age (years) 50.30 ± 5.78 50.25 ± 5.69



895


Table 3: Age and sex wise distribution of Diabetics and Non-diabetics

Diabetics Non-diabetics

Males Females Males Females

Age 41-50 yrs 60 40 60 40

Age 51-60 yrs 60 40 60 40

Table 4: Duration wise distribution of Diabetics

Duration < 5 years 79

Duration > 5 years 121

Total 200

Table 5: Comparison of hearing loss in diabetics and non-diabetic controls (chi square test) (Odd’s

ratio: 2.398)

Hearing Loss Diabetics Non-diabetics P value

Present 72 38 0.0001*absent 128 162

Total 200 200 -

p value: 0.0001 (highly significant)

Table 6: Comparison of hearing loss in relation to different age groups in diabetics and non-diabetic

controls (chi square test)

Age Diabetics Non-diabetics P value

41-50 years 29 160.852

51-60years 43 22

Total 72 38 -

Table 7: Comparison of hearing loss in relation to sex in diabetics and controls. (chi square test).

Sex Diabetics Non-diabetics P value

Male 42 24 0.6233*

Female 30 14

Total 72 38 -

Table 8: Comparison of hearing loss in relation to duration of diabetes in diabetics. (chi square test).

Duration Hearing loss No Hearing loss P value

< 5 yrs 25 54 0.2999

> 5 yrs 47 74

Total 72 128 -

DISCUSSION

The results of the present study showed that the

hearing of diabetics was significantly impaired

than the non-diabetic control group. All the

frequencies tested demonstrated this hearing

impairment. The hearing acuity was not

influenced by the duration of diabetes, age or sex

of the subjects.



896


Thus, statistically highly significant hearing loss

has been observed in the diabetic group than in

the non-diabetic control group and Odd’s ratio of

2.398. This finding coincides with the findings of

other workers – Taylor I and Irwin J6, Wackym

PA7, Kurien M etal 8, Dalton DS etal 9,Rózańska-Kudelska

10, Kakarlapudi V etal

11,

Panchu P12

, Bainbridge KE et al13

.

Diabetes-related hearing loss is a progressive,

sensorineural impairment typically affecting

audiometric thresholds between 500 and 8,000

Hz.7,13

The pathophysiology underlying diabetes-

associated hearing loss may involve the effect of

diabetes-related microvascular disease on thecochlea.

14Few microscopic studies (obtained

post-mortem) show sclerosis of the internal

auditory artery, thicker vessel walls of the stria

vascularis and of the basilar membrane, damage

to the outer sheath (demyelination) of the

cochlear nerve, and atrophy of the spiral

ganglion (linking the cochlear nerve and the

brain).7,15

One study among autopsied diabetic patients

shows atrophy of the spiral ganglion and

demyelination of the eighth cranial nerve

indicating a neurological etiology to diabetes-

related hearing impairment.15

Hyperglycemia itself via elevated glucose levels

in the cerebrospinal fluid or in the perilymph can

lead to cochlear dysfunction in diabetic patients.

This is independent of angiopathic or

neuropathiclesion.8

Study on severe diabetic neuropathy has reporteda reduction of Nerve Growth Factor (NGF) in

neuropathic diabetics causing limitation of

axonal retrograde transport and nervous fibres

demyelinization.16,17

Thus, the possible mechanisms underlying the

hearing loss in diabetic individuals from the

above discussion are as follows:

1. Microvascular disease affecting the stria

vascularis,2. Thickening of the basilar membrane,

3. Damage to the outer sheath (demyelination)

of the cochlear nerve,

4. Atrophy of the spiral ganglion,

5. The loss of outer hair cells,

6. Neuronal degeneration or diabetic

encephalopathy,7. Hyperglycemia,

8. Hyperactivity of oxygen free-radicals,

9. Reduction of Nerve Growth Factor (NGF),

10. Atherosclerotic narrowing of the internal

auditory artery.

The effect of age on auditory thresholds in

diabetic subjects was statistically not significant.

Kakarlapudi11

Dalton9

Rózańska-Kudelska10

, and

P. Panchu

12

showed similar findings in theirstudy. Thus, age of the patient is not related to

hearing loss in diabetics.

The effect of sex on auditory thresholds in

diabetic subjects was statistically not significant.

Similar findings were reported by Kathleen E.

Bainbridge et al.13

Thus, there is no sex

difference as far as occurrence of hearing loss in

diabetics is concerned.

When hearing loss in diabetics is compared with

relation to duration of diabetes, the difference in

the two groups was statistically not significant.

Thus the duration of diabetes does not alter

hearing thresholds. Similar findings were noted

by Pallavi Panchu12

, Kurien M et al8, Dalton S et

al9, Taylor IG and Irwin J.

6

The degree of hypergylcemia and the duration of

uncontrolled hyperglycemia are gaining more

importance as causative factors than the duration

of the disease itself as indicated by the studies of Kakarlapudi

11Frisina et al

18, Hsueh

19, Panchu

P12

, Bainbridge et al.13

Thus, the age or sex of the

subject or the duration of diabetes are not related

to hearing loss in diabetics but the duration and

degree of uncontrolled hyperglycemia may be

related to hearing loss in diabetic patients and it

needs further study.



897


CONCLUSION

The present study shows that type II diabetes

causes significant hearing loss in the patients, but

it is not affected by the age and sex of the patient

or duration of the illness.

ACKNOWLEDGEMENT

Authors thankful to Dr. Aundhkar VG, Professor

and Head, Dept. of Physiology for his constant

support and valuable guidance; Dr. Bhagwat,

Professor and Head, Dept. of Medicine, Dr.

Mahure, Professor and Head, Dept. of ENT for

allowing me perform this study and their timely

guidance. I am very much thankful to thetechnical staff of Audiometry and ENT. I am

thankful to the participants without whom this

study would not have been possible.

REFERENCES

1. Wild S, Roglic G, Green. Global percentage

of diabetes: estimates for the year 2000 and

projections for 2030, Diabetes care 2004; 27:

1047-1053

2. Kathleen Bainbridge. Hearing impairment –

an under-recognized complication of

diabetes? Diabetes Voice.2009;54(1): 13-16

3. Dhingra PL. Diseases of ear, nose and throat,

assessment of hearing. 2004, 3rd

Ed:Chapter

5: 23-32

4. Bhargava KB, Bhargava Sk, Shah TM. A

short textbook of ENT diseases. Examination

of the ear; 2003; 6th

Ed; Chapter 4: pg 23-32

5. Anirban Biswas, clinical audio-

vestibulometry 2nd Ed for Otologists and

Neurologists: Pure Tone Audiometry: 1996,

pg 1-17

6. Taylor IG, Irwin J. Some audiological

aspects of Diabetes mellitus, Journal of

Laryngology and Otology.1978; 92;99-113

7. Wackym PA, Linthicum FH. Diabetes

mellitus and hearing loss: clinical and

histopathologic relationships. Am J Otol.1986;7(3):176-82.

8. Kurien M, Thomas K, Bhanu TS. Hearing

threshold in patients with diabetes mellitus. J

Laryngol Otol. 1989;103(2):164-8

9. Dalton DS, Cruickshanks KJ, Klein R, Klein

BE, Wiley TL. Association of NIDDM and

hearing loss. Diabetes Care. 1998;21(9):154010. Rózańska Kudelska M, Chodynicki S,

Kinalska I, Kowalska I. Hearing loss in

patients with diabetes mellitus type II.

Otolaryngol Pol. 2002;56(5):607-10.

11. Kakarlapudi V, Sawyer R, Staecker H., The

effect of diabetes on sensorineural hearing

loss., Otol Neurotol. 2003;24(3):382-86

12. Panchu P. Auditory acuity in type 2 diabetes

mellitus. Int J Diabetes Dev Ctries.2008;28(4):114-20.

13. Bainbridge KE, Hoffman HJ, Cowie CC.

Diabetes and hearing impairment in the

United States: audiometric evidence from the

National Health and Nutrition Examination

Survey, 1999 to 2004. Ann Intern Med.

2008;149(1):1-10

14. Lisowska G, Namysłowski G, Morawski K,

Strojek K. Cochlear dysfunction and diabetic

microangiopathy. Scand Audiol Suppl.

2001:52:199-203

15. Makishima, Tanaka. Pathological changes of

the inner ear and central auditory pathways in

diabetes. Annals of Otology, Rhinology and

Laryngology1971; 80, 218-28.

16. Tomlinson DR, Femyhough P, Diemel LT,

Maeda K. Deficient neurotrophic support in

aetiology of diabetic neuropathy. Diabet

Med.1996;13S:679-8117. Salvinelli F, Casale M, Greco F, Trivelli M,

Di Peco V, Amendola Tetal., Nerve growth

factor serum level is reduced in patients with

sensorineural hearing impairment: possible

clinical implications. J Biol Regul Homeost

Agents.2002; 16(3):S176-80

18. Frisina ST, Mapes F, Kim S, Frisina DR,

Frisina RD. Characterization of hearing loss

in aged type II diabetics. Hear Res.2006;211(1-2):103-13



898


19. Hsueh W, Abel ED, Breslow JL, Maeda N,

Davis RC, Fisher EAet al. Recipes for

creating animal models of diabetic

cardiovascular disease. Circ. Res.

2007;100:1415-2



899Vedavathi et al., Int J Med Res Health Sci. 2013; 2(4):899-904


&

Health Scienceswww.ijmrhs.com Volume 2 Issue 4 Oct-Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886Received: 25th Aug 2013 Revised: 17th Sep 2013 Accepted: 29th Sep 2013

Research article

COMPARATIVE STUDY ON TEACHING OF BIOETHICS TO HEALTH CARE PERSONS

USING DIFFERENT METHODOLOGIES

Vedavathi H 1, Tejasvi TS2, * Shreenivas P Revankar3

1Associate Professor, 3Assistant Professor, Department of Pharmacology, Shimoga Institute of MedicalSciences, Shimoga, Karnataka, India2Assistant Professor, Department of General Medicine, Shimoga Institute of Medical Sciences,Shimoga, Karnataka, India

* Corresponding author email:[email protected]

ABSTRACT

Introduction: Bioethics has gained lots of importance in the present days and especially very important in thefield of medical research. Doctors, medical students, nursing staff and other paramedical staff are directly orindirectly involved in the clinical and research activities. A proper training in bioethics is very essential especiallyfor medical students nursing and other paramedical staff. There are various teaching methodologies like a blackboard (lecturing), power point presentations, case discussions, group discussions and film/movie clipping related

to bioethics .Each of the teaching methodology is effective in a particular group. Materials and methods: Fourdifferent teaching methodologies were used to teach bioethics in four different categories namely MBBS students,doctors/interns, nurses and lab technicians. All were exposed to all types of teaching methodology. An evaluationwas done by performance based and choice based evaluation system. Results: Case discussion was most popularchoice of MBBS students and Doctors/Interns. Among nurses and lab technician’s film discussion was best in

terms of performance and choice. Conclusion: Bioethics covers more about abstract issues related to the healthdiscussion on this topic help in better understanding and clarification.

Keywords: Bioethics, Teaching Methods, Evaluation

INTRODUCTION

Bioethics is a study of typical controversialissues brought about by advances in biology andmedicine, it relates to medical policy, practiceand research. In general context ethics is aboutgiving priority to individual needs and moralvalues in an attempt to curb and control potentialsocietal abuses. 1 The term bioethics was coinedin 1927 by Fritz Jahr.2 Van Ransseller Pottergave it a broader meaning and coined the wordglobal ethics. It is a link between biology,ecology medicine and human values in order to

attain the survival of human beings and otheranimal species.2,3 The scope of bioethics canexpand with biotechnology including cloning,gene therapy, life extension, human geneticengineering and manipulation of basic biologythrough altered DNA, RNA and proteins.4

The fundamental principles of bioethics includedin Belmont report are autonomy, beneficence and

justice the others which were added later on arenon malfeasance and sanction of life.5 Medicalethics is study of moral values and judgements. It

DOI:10.5958/j.2319-5886.2.4.144




encompasses its practical applications in clinicalsettings as well as work on its history,philosophy, theology and sociology.6 Bioethicshas addressed a broad swath of human enquiryranging from debates over the boundaries of life

care (eg.abortion, euthanasia, surrogacy,allocation of scare health care resources) to theright to refuse medical care.7

Teaching and learning are the two sides of thesame coin. There are various teaching methodslike lectures, power-point presentations, groupdiscussion, seminars, role play, film ordocumentary presentations, case discussions etc.8

Each of them has their own advantages and

disadvantages.

9

The teaching methodology to beused also depends on the topic to be covered; i.e.for a particular topic a particular methodologymay be effective. The effectiveness of teaching isdependent on individual interest, but more overthe methodology used is also important. 10

The most accepted criterion for measuring goodteaching is the amount of student learning thatoccurs. Teaching in the absence of learning istalking; effective teaching is that which produces

beneficial and purposeful student learningthrough the use of appropriate procedures.11

Students are most qualified sources to report onthe extent to which the learning experience wasproductive, informative, satisfying andworthwhile. A meta-analysis of 41 researchesprovides validity that, student ratings tend to bereliable, valid, unbiased and useful.12 Health careprofessionals are the ones who are constantly

exposed to various issues related with bioethics.This group includes the doctors, nurses, andlaboratory technicians, medical and nursingstudents. The ability to understand the conceptsof bioethics varies in each of these health carepersonals. There is a need for identifying theproper teaching methodology for each of thisgroup; hence the present study was undertaken.


The study population was divided into fourgroups which included participants fromdifferent categories like medical students,

intern/junior doctors, nursing staff and labtechnicians from the medical college andhospital. A group consisted of ten candidateseach from each category, It included ten MBBSstudents, ten interns/junior doctors, ten nurses

and ten lab technicians (N=40). Boys and girlswere equally distributed in each group. A totalof 160 participants were included in the study.Inclusion criteria: Students from second yearMBBS were chosen, taking into considerationthat they sufficient knowledge of basic medicalscience. Random selection of fourty students wasdone; majority of the students had secured firstclass in first year examinations. Hence the bias in

selection of the participants was ruled out. Juniorresidents/internees, forty in number wererandomly distributed in four groups with tenmembers in each group. They had betterknowledge on ethical issues.The nurses included in the study were fromdiploma (General nursing and midwifery)background, had fair knowledge and goodcommunication skills in English.Laboratory technicians, who had completed

DMLTC (diploma in lab techniques course) wereincluded in the in the study. They had sufficientknowledge of understanding and communicatingin English but knew very little about ethics. Atotal of forty members working in the variousdepts. were included in the study.Exclusion criteria: Those who lacked the abovecriteria’s were excluded from the study. Nursing

staff had no theoretical knowledge of bioethics.

Topics chosen were easy to understand andformed the core of bioethics. The four topicschosen were Informed consent, Medicalnegligence, and ethical issues of HIV/AIDS andClinical trials.13 Four different teachingmethodologies used in the study were Blackboard /lecturing, Power-Point presentations, Casediscussions and film clippings followed bydiscussions. Lecture is a talk or a verbal

presentation given by a lecturer, trainer or aspeaker to an audience. This method iseconomical, can be used for a large number of




students, material can be covered in a structuredmanner and the teacher has a great control of time and material. Power-point presentationsmake use of computer and LCD-projector,material to be covered is restricted. Discussion is

a free verbal exchange of ideas between groupmembers or teacher and students. In case-discussion a case related to the topic is explainedfollowed by discussion. In film discussion a filmor documentary related to the topic is screenedfor 25 minutes, followed by discussion on theethical issues relatedAn evaluation was done by two types of analysesi.e. performance based and choice based.

Performance based evaluation, scores of pre andpost evaluation test were taken into considerationto access the performance.14,15 Pre and postevaluation tests were done with the help of questionnaires designed in each of the topics.The topic to be taught was not informed to theparticipants. Pre-evaluation test was givensimultaneously to all the groups i.e. all the 160

members had to take the pre-evaluation test atthe beginning of the day. Post evaluation wasdone immediately at the end of their respectiveclasses. The type and number of questions askedin the pre and post evaluation test were same, the

time duration of the class was restricted to fortyfive minutes only which was followed by postevaluation test for fifteen minutes. The questionsasked were of multiple choice and of yes/no type.The questions were displayed on the screenusing LCD projector. Improvement wascalculated based on difference in pre and postevaluation scores.15

A choice based evaluation was done on the last

day, after exposing all the candidates to differentteaching methodologies. In this system thecandidates were asked to rate different methodsof teaching used by their teachers on a scale of 1-4, one being the least important and 4 being themost important teaching method. The results of the study were compiled and analyzed bypercentage method.16, 17

Table 1: Schedule of the study

Teaching methodologyTopic Lecture

classPower pointpresentation

Casediscussion

Film clip followedby discussion

Day1 Informed consent Group 1 Group2 Group 3 Group 4Day2 Medical negligence Group 2 Group 3 Group 4 Group 1Day3 Ethical issues of HIV/ AIDS Group 3 Group 4 Group 1 Group 2Day4 Clinical trials Group 4 Group 1 Group 2 Group 3

RESULTS

Table 2: Results of performance based evaluation

TeachingMethod

MBBS students Junior residents/internsPost# Pre* Diff* % imp Post* Pre* Diff * % imp*

Lecture 14.025 9.65 4.375 21.87 15.7 12.45 3.25 16.25Power point 14.050 9.55 4.5 22.50 15.85 12.40 3.45 17.25

Case disc# 14.55 10.10 4.45 22.25 15.55 12.55 3.00 15.00Film/disc# 14.15 9.20 4.95 24.75 14.85 11.85 3.00 15.00

Nurses Lab technicians

Lecture 9.00 6.00 3.00 15.00 5.62 3.37 2.25 11.25Power point 8.75 5.50 3.25 16.25 6.00 3.25 2.75 13.75Case disc# 9.75 6.00 3.75 18.75 4.87 3.12 1.75 8.75

Film/disc# 10.25 6.25 4.00 20.00 7.75 3.25 4.50 22.50Pre*-average pre evaluation score; Post*-average post evaluation score, Diff*-difference between averagepre and post evaluation scores, %imp$-percentage of improvement ; disc#-discussion




Results of the performance based evaluation:The major improvement in performance wasseen by medical students. It was above 20% withall teaching methodology used, Maximum withfilm discussion (24.75) and minimum with

lecture class (21.87). The other two teachingmethods showed almost same improvement(22.5). The improvement percentage in juniordoctors/interns was less but almost in the samerange with different methods. It was highest withpower-point (17.25), followed by a lecture(16.25), while it was 15% with case discussionand film-discussion. In this category it was notedthat the pre-evaluation scores were in higher

range compared to other categories. So therelative improvement was less.Among the nurses highest improvement (20%)was seen with film-discussion followed with case

discussion (18.75) and power-point (16.25).They showed less improvement with lectureclasses (15%). As nurses had limited knowledgeon bioethics their pre-evaluation scores were lesscompared to doctors and medical students. Lab

technicians had very low improvement comparedto other categories. The pre-evaluation scoreswere least as they had no knowledge aboutbioethics. The improvement percentage were8.75 with case discussion,11.25 with lectures and13.75 with power-point presentations but film-discussion brought about marginal improvementof 22.5%Results of choice based evaluation: Table

showing the preferences given by differentcategories (MBBS, junior doctors/interns, nursesand lab technicians) for different teachingmethods.

Table 3: Results of choice based evaluation

Teachingmethod

Lecture Power point Case discussion Film-discussion

Preferences 1 2 3 4 1 2 3 4 1 2 3 4 1 2 3 4MBBS 13 12 8 7 8 11 16 5 16 15 5 4 3 2 11 24Junior dr

/internees8 8 13 11 8 14 15 3 18 09 7 6 6 9 5 20

Nurses 9 13 8 10 9 8 14 8 8 5 13 14 14 13 5 8Labtechnicians

4 8 8 20 6 8 16 10 12 14 10 4 18 10 6 6

Table 4: Scores and percentage share of different teaching methods

Lecture Power point Casediscussion

Film/discussion

Score %share

Score %share

Score %share

Score %share

MBBS 111 27.75 102 25.5 123 30.75 64 16.00Junior.doctors/interns 93 23.25 107 26.75 119 29.75 81 20.25Nurses 101 25.25 99 24.75 87 21.75 113 28.25

Lab technicians 76 19.00 90 22.50 114 28.50 120 30.00

All candidates 381 23.81 398 24.87 443 27.69 378 23.63Table 5: Concluding results of the study

Slno

Category Best teaching methodology based on

Performance -evaluation Choice-evaluation

1 MBBS Film followed by discussion Case discussion

2 Junior.doctors/internees Power point Case discussion3 Nurses Film followed by discussion Film followed by discussion4 Lab technicians Film followed by discussion Film followed by discussion




Scoring was calculated based on the preferencesgiven by the candidates. It was calculated onallocation of points i.e. the 1st preference wasallotted four points, three points for 2nd

preference, two points for 3rd preference and one

point for 4th preference. The sum obtained wasthe overall score for each methodology undereach categoryThe majority of the medical student’s preferredcase discussions which accounted for highestscore of 123, lectures were their second choice toscore 111 followed by PowerPoint in 102. Filmdiscussion was their last choice. Doctors/internsalso liked case discussions very much, power-

point and lectures were subsequent choice andfilm-discussion was the last choice. Filmdiscussion was a popular choice among thenurses and lab technicians. Nurses hated the casediscussions while lab technicians did not likelectures the most.

DISCUSSION

In our study the participants were exposed to allthe four different types of teaching methodology.

The topics chosen were also of similar categorythere is every possibility of bias as a particulartopic is taught effectively by a particular method.To overcome this we had opted for a two wayevaluation system i.e. performance based andchoice based evaluation system as compared tosome of the studies. The performance basedevaluation took into consideration theperformance of candidate in pre and post

evaluation. In choice based evaluation system wegave freedom to the candidates to grade theteaching methodology.When overall results were taken intoconsideration it was found that film discussionand case discussion as teaching methodology is amost effective means of learning compared to thelectures and power point presentations.Discussion involves more participation; learningis more effective and develops creativity amongparticipants. This may be contradictory to someof the studies conducted on teaching

methodologies. 9 Lecture as a teaching methodcreates new ideas, are good for large class butuseful only when the concept and views of thetopic are clear. Bioethics has more of abstractconcepts.1, 3 In this study, case discussions and

film presentations followed by discussion faredwell mainly because they provide a platform forbetter understanding of abstract concepts in asimplified way.8 Bioethics as such need not berestricted to health care; it involves various fieldsso there is need to evaluate similar studies inother areas. In our study only four teachingmethods were tried, this study can be improvedupon by experimenting with other methods of

teaching.CONCLUSION

In our study we found that lectures and powerpoint presentations are not much importance inimparting the knowledge of bioethics. Theconcepts involved in bioethics are abstract and itrequires more of discussion for betterunderstanding and clarifications. The topics of bioethics must be reserved for panel discussionsin the CME and workshops, so as to improve theknowledge of bioethics among medical andparamedical personnel.

ACKNOWLEDGEMENTS

We thank ICMR (Indian council of medicalresearch) for giving me an opportunity toparticipate in a one month long trainingprogramme and taking up the above study as a

part of project. My special thanks to Dr Nandinikumar and Dr Vasanta Muthuswamy of ICMR.

REFERENCES

1. Andre, Judith Bioethics as Practice, ChapelHill and London: University of NorthCarolina Press. 2002; Pg no35-37

2. Appel, Jacob, A Supreme Cou-forrt forBioethics. Huffington Post. August 9, 2009;

http://huffingtonpost.com/jacob-m-appeal/a-supreme-court-for-bioet_b_228967.html




3. Aulisio, Mark; Arnold, Robert; Younger,Stuart. Ethics Consultation; from theory topractice, Baltimore, London: Johns HopkinsUniversity Press, 2003: pg 54

4. Glad Joh. Future Human Evolution: Eugenics

in the Twenty-First Century, HermitagePress, 2008; pg 41-44.

5. Crowley, Mary. From Birth to Death andBench to Clinic: The Hastings CenterBioethics Briefing Book, Garrison, NewYork: The Hastings Center. 2008 Ed; 71-75.

6. Beauchamp Tom, Childress James. Principlesof Biomedical Ethics, Oxford, New York:Oxford University Press, 2001; pg 152-54.

7. Häyry Matti, Tuija Takala, Peter Herissone-Kelly, Gardar Árnason. Arguments andAnalysis in Bioethics. Amsterdam/NewYork: Rodopi; 2010

8. Kochkar, S.K. Methods and Techniques of Teaching. Sterling press New Delhi:2000; 13.

9. McCarthy P. Common Teaching Methods.1992; Retrieved July 24, 2008, from.http://honolulu.hawaii.edu/intranet/committees/FacDevCom/guidebk/teachtip/comteach.ht

m10. Hoyt MP, Pallett WH. Appraising teaching

effectiveness: Beyond student ratings;Kansas State University, Center for FacultyEvaluation and Development; 1999 Pg No.36.. Retrieved June 1, 2002, fromhttp://www.idea.ksu.edu/products/Papers.html.

11. Centra JA. Reflective faculty evaluation. San

Francisco, CA: Jossey-Bas; 199312. Cohen PA. Student Ratings of Instruction and

Student Achievement: A Meta-Analysis of Multisection Validity Studies. Review of Educational Research. yr 1981; 51, 281-309.

13. Singer PA, Viens AM. Cambridge Textbookof Bioethics, Cambridge: CambridgeUniversity Press, 2008; pg 276-78

14. Arreola RA. Developing a comprehensive

faculty evaluation system. Bolton, MA:Anker Publishing;1995; 37-40.

15. Ory JC. Faculty thoughts and concerns aboutstudent ratings; Techniques and strategies forinterpreting student evaluations. NewDirections for Teaching and Learning, 2001;no. 87. Pg 3-15.

16. Doyle T. Evaluating Teachers Effectiveness.Retrieved July 24, 2008, fromferris.edu/fctl/Teaching_and_Learning_Tips/ EvalTeachEffec.htm.

17. Theall M, Franklin J. Student Ratings of Instruction: Issues for Improving Practice.New Directions for Teaching and Learning,1990; 43.

18. Hamm PH. Teaching and Persuasive

Communication: Class Presentation Skills.The Harriet W. Sheridan Center for Teachingand Learning: Retrieved July 24, 2009, fromhttp://www.brown.edu /Administration

/Sheridan_Center /publications /preskils.



905

Rahul et al., Int J Med Res Health Sci. 2013; 2(4):905-910


&

Health Sciences




thSep 2013

Research article

LEVELS OF STRESS AMONGST THE SCHOOL TEACHERS IN A PUBLIC SCHOOL OF

RURAL WESTERN MAHARASHTRA

* Kunkulol Rahul R1, Rusina Karia

2, Prashant Patel

3,Abhinav David

3

1Associate Professor, Department of Pharmacology, Secretary, Research Cell, PIMS-DU, Loni

2MBBS Student, Rural Medical College, PIMS-DU, Loni, Maharashtra

3Resident, Department of Pharmacology, Rural Medical College, Loni, Maharashtra


ABSTRACT

Objectives: Teachers are among the professions reporting highest level of work-related stress, the study

was undertaken to evaluate the levels of stress amongst school teachers in a public school of rural

western Maharashtra Methods: Prospective survey based study was carried out amongst school teachers

of rural western Maharashtra using Copenhagen Psychosocial Questionnaire (COPSOQ).The survey was

carried out on 3 scheduled visits over a period of 2 months after the Institutional Ethical committeeapproval. Total 110 Primary and secondary school teachers, satisfying inclusion and exclusion criteria

were randomly selected for the study. All the questions in the Copenhagen Psychosocial Questionnaire

(COPSOQ) were graded according to 1 (Always-0), 2 (Sometimes-25), 3 (Often-50), 4 (Seldom-75) and

5 (Never-100). The scale value was calculated as the simple average. More the average score less the

stress and vice versa Results & Conclusion: Inability to understand the meaning and importance of

work, improper clarity about the job, inability to cope with the problems were found to be the factors

always contributing to stress of teachers.

Keywords: School teacher, Job related stress, COPSOQ, Personal Stressors

INTRODUCTION

“

Work-related stress has been identified at

international and national levels as a concern for

both employers and workers”. Occupational

stress is known as stress at work. It occurs when

there is a discrepancy between the demands of

the workplace and that of an individual. Such

individuals under occupational stress, experienceof negative emotional states such as frustration,

worry, anxiety and depression attributed to work

related factors.1

Occupational stress in the human

service professions, particularly teachers, has

been a focus of study in the last decades. Most

surprisingly, school teachers have been

considered to be under stress and undergoing the

process of burnout.2

Teaching is a physically andmentally challenging job. The daily chores in the

DOI:10.5958/j.2319-5886.2.4.145



906


classroom coupled with personal and family

commitments require a lot of energy and

forwards a lot of stress to the teacher.3

Undoubtedly, teachers are among the professions

reporting the highest level of work-related stress.

The increasing workload on teachers, the roleoverload, the increased class size per teacher and

an increasing number of pupils behaving in an

unacceptable way are some of the trends

identified in several countries as leading to a rise

in stress-related illnesses.4

Teachers are exposed to a wide variety of multi-

dimensional predisposing factors leading to

stress which can be classified as job related and

related to the personal events.

5

Job relatedcontributory factors can be like inadequate

working conditions , role conflict and ambiguity,

pupil (student related) problems, time pressures ,

threat of redundancy, work pressure, little

participation in decision-making and distribution

of tasks , stereotypes and discrimination against

minority groups, inadequate salaries.5

Those related to the personal events are

Marriage, Divorce, Pregnancy, Death of a loved

one, change of residence and others if any. In

addition, it has been found that job satisfaction

and teacher stress are strongly correlated.6

The

amount of stress and degree of satisfaction

experienced by teachers influences the quality of

life and may create various stress related health

problems like Hypertension, cardiac disorders,

Acid peptic diseases, psychological disorders.7,8

Work involving responsibility for other people

creates potential stress as it may heightenexpectations for job performance and emotional

availability. The complexity and diversity of

teachers’ work, clearly links workload and stress

not only to the quantity of hours worked, but also

to the diverse nature and demands placed on

teachers.5-8

In view of above mentioned etiological factors

and detrimental adverse effects of stress among

school teachers, it was thought prudent toevaluate levels of stress amongst them by using

Psychosocial Questionnaire (COPSOQ) a well-

structured questionnaire developed by the

Psychosocial Department, National Institute of

Occupational Health, Copenhagen, Denmark.9

Hence a study was planned with the following

aims and objectives

Aims and objectives1. Evaluate levels of stress amongst school

teachers in a public school of rural

western Maharashtra

2. Find out various stressors or

predisposing factors responsible for stress

among them.

3. To find out the most common stressor or

stress indicator if any amongst primary

and secondary school teachers in a publicschool of rural western Maharashtra


This was a prospective survey based study. This

survey was carried out school amongst the

teachers in a public school of rural western

Maharashtra. The School was selected on the

basis of ease and access. Consent from the school

authorities and Institutional ethical committee

approval were obtained before the

commencement of the study. The primary and

secondary school teachers were selected on the

basis of following inclusion and exclusion

criteria.

Inclusion criteria:

1. Primary and secondary school teachers of

Public School (Standard L.K.G to X)

2. Teachers willing to participate in the study

3. Ready to give written informed consent

4. Teachers completing the survey, i.e present on

the days of data collection

Exclusion criteria:

1. The teachers of XI Std. onwards.

2. The teachers who were absent on either day

during data collection.

3. The teachers suffering from debilitating

physical or psychiatric illness

4. Teachers with history of addiction, drughistory or any chronic illness



Rahul et al.,

Study tool:

Psychosocial Questionnaire (C

scales of the COPSOQ were fo

the points of the individual q

scales by giving equal weights t

In most cases the questions haoptions.

The Questionnaire was divided

Job related Questionnaire

stressor Questionnaire. The s

calculated as the simple average

Respondent absent for any

considered as a drop out

Study conduct: Data was

scheduled visits approximatelyTable 1: Psychological Questio

RESULTS

Fig 1: Mean scores of job related s

0

Meaning of Work

Possibilities for Development

Cognitive Demands

Commitment to workplace

Predictability

Influence at Work

Emotional Demands

Demands for Responsibility

Degree of Freedom of Work

M

P

G

1

2

3

4

5


OPSOQ): The

med by adding

uestions of the

each question.

five response

into two types:

and Personal

cale value was

from 0 to 100.

ne visit were

ollected in 3

7 days apart

according to the conve

by the school authoritie

Visit-1: 1. Introduc

Explanation of the

consent

Visit-2: Job related queVisit-3: Personal stress

Study period: 2 m

approval of the study

Committee


pooled, subjected t

analysis and conclusio

Sample size: Out of t

for the study effectivenaire

tressors

20 40 60

11.76

23.40

26.81

27.35

32.94

34.44

37.50

52.98

an Scores of Job related stressors (%

ychosocial Questionnaire (COPSOQ):9

rade Score Interpretation

0 ALWAYS

25 SOMETIMES

50 OFTEN

75 SELDOM

100 NEVER

907

ci. 2013; 2(4):905-910

nient date and time given

s.

ion of the project 2.

tudy Tool 3. Obtaining

stionnaire or questionnaire

nths from the date of

y the Institutional Ethical

The data was collected,

appropriate statistical

s were drawn

otal 110 teachers enrolled

ample was 78

80 100

74.49

)



Rahul et al.,

Fig 2: Mean score of personal stre

DISCUSSION

Among all the Job related stress

for meaning of work (11.76),

development (23.70) were Gr

always causing stress.(Fig I)

Teachers were of the opinion that

development were very less an

them the most. The school au

give emphasis on understanding

meaning and clarity about the j

that the teachers can give the

school.

The personal stressors with mea

between (0-24) were Role C

focused coping and social supGrade I stressors always causing

Many of the teachers were not c

own role and revealed an inabilit

to day problems resulting in s

consistent evidence that teach

support from others experience l

burnout10

and teachers facing pot

demands, conflicts and pro

workplace, having support froreduce the impact of the pr

individuals well-being.11,12

0

ROLE CLARITY

PROBLEM FOCUSED COPING

SOCIAL SUPPORT

JOB SATISFACTION

SELECTIVE COPING

GENERAL HEALTH

ROLE CONFLICTS

SENSE OF COHERENCE

MENTAL HEALTH

BEHAVIOURAL STRESS

COGNITIVE STRESS

SOMATIC STRESS

M


sors

ors mean score

possibilities of

de I stressors

possibilities for

was worrying

thorities should

the importance,

b and work so

ir best for the

n score ranging

larity, Problem

port thus were tress.(Fig II)

lear about their

y in coping day

tress. There is

ers with more

ower strain and

ntially stressful

lems in the

m others may ssures on the

This study reveals inc

coping with day to

should incorporate ha

balance between th

professional life The

neccesity of analysin

training. Workshops

positive attitude s

periodically. It is ne

support for the teac

through social gatherin

A lack of appropri

specifically where t

implement new praongoing training in ord

increasingly diverse

source of stress.

The factors that influe

health status were w

modern societies, high

community that are

becoming unrealistic

given to teachers

13

.sources of burnout a

environment are rel

20 40 60

16.57

22.68

23.07

25.99

37.02

40.03

46.50

47.65

52.18

54.67

61.62

an scores of Personal stressors (%)

908

ci. 2013; 2(4):905-910

rporation of measures for

day problems.Teachers

bbit of keeping Proper

personal, family and

e is a requirement and

the system of teacher

on stress management,

ould be incorporated

essary to provide social

ers for their betterment

gs.

te professional training

achers are required to

ctices with inadequate er to meet the needs of an

opulation is a particular

nced the teachers’ mental

rkload. In urbanised and

demands by parents and

constantly increasing is

ith the resources that are

An study indicated that d stress in the working

ated to role conflicts,

80 100

2.38



909


professional isolation, lack of support, ineffective

teaching aids, student disciplinary and

behavioural problems, inadequate working

conditions and general lack of respect for the

teacher’s role. Our results were consistent with

with Shankar and Famuyiwa (1991)14

Stress affects the efficiency of the individual. So,

there is a need to provide a proper conducive

environment and support for teachers to maintain

individual stress at their workplace. Positive

attitude of teachers in facing their challenges will

help them in improving their functional skills and

reduce stress. Regular assessment of stress level,

direct physiological measures of stress like

diagnostic tests and consultation with medicalprofessionals and preventive measures should be

taken accordingly. Besides that, the institution or

management should check that, supervision,

support and relationship with the teachers is

properly taken care of and enhanced most

strongly. Most importantly, it is recommended

that principals and supervisors should investigate

the causes of stress and evaluate the

organizational climate of the school. They should

also suggest ways, like workshops and seminars

to alleviate and cope with stress.1

Limitations:

• Similar studies should be done using larger

samples in different region including both

private and public schools

• The accuracy of the research results should

be checked by other methods (interviews,

observations, etc.)

CONCLUSION

The factors always causing stress like job related

clarity, ability to cope with problems, inadequate

social support should be tackled by various

measures at the individual and institute level.

ACKNOWLEDGEMENT

Authors dually acknowledge the teachers,

Principal and the Director of a Public school inrural western Maharashtra for their support and

participation in the study for the betterment of

teachers

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1. Mariya Aftab, Tahira Khatoon. Demographic

differences and occupational stress of secondary school teachers. European

Scientific Journal.2012: 8(5):159-75

2. Olivier MAJ, Venter DJL. The extent and

causes of stress in Teachers in the George

region. South African Journal of Education.

2003;23(3) 186-92.

3. Surinder Kaur. Comparative Study of

Occupational Stress among Teachers of

Private and Government Schools in Relation

to their Age, Gender and Teaching

Experience. International Journal of

Educational Planning & Administration.

2011;1(2):151-160

4. ETUC, UNICE/UEAPME and CEEP - the

Framework Agreementon work-related

stress. 8 October 2004.

www.etuc.org/IMG/pdf/Brochure_stress_EN

-3.

5. Marais JL. Faktore wat stress veroorsaak byonderwysers in die Oranje-Vrystaat en

Kaapprovinsie. Suid Afrikaanse Tydskrif vir

Opvoedkunde. 1992:12: 305-09.

6. Hittner A. Teachers in distress: Perceptions

of stress and life satisfaction. Maryland:

Associated Press. 1981Incomplete reference

7. Liina Osila, Kirsti Nurmela. EWCO

comparative analytical report on Work-

related Stress. European Working ConditionsSurvey, European Foundation for the

Improvement of Living and Working

Conditions, on-line database,

http://www.eurofound.europa.eu/ewco/surve

ys/index.htm

8. Constantinos M Kokkinos. Job stressors,

personality and burnout in primary school

teachers. British Journal of Educational

Psychology. 2007:77, 229 – 243

9. Nübling M, Vomstein M, Haug A, Nübling

T, Adiwidjaja A. European-Wide Survey on

Teachers Work Related Stress – Assessment,



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Comparison and Evaluation of the Impact of

Psychosocial Hazards on Teachers at their

Workplace. FFAS:ETUCE Teacher pilot

study 2011,1-63

10. Lee R, Ashforth B. A meta-analytic

examination of the correlates of the threedimensions of job burnout. Journal of

Applied Psychology .1996: 81,123-33.

11. Jarvis M. Teacher stress: a critical review of

recent findings and suggestionsfor future

research directions (2002). Teacher Support

Network, 14(1). Retrieved Nov.13, 2003

from http //www.google.com/ searc

:www.teachersupport.org.uk/index.

12. Olivier MAJ, Venter DJL. The extent andcauses of stress in Teachers in the George

region. South African Journal of Education.

2003;23(3) 186-192

13. Sveinsdottir H, Gunarsdottir H, Fridriksdottir

H. Self-Assessed Occupational Health and

Working Environmental of Female Nurses,

Cabin Crew and Teachers. Scandivian

Journal of Caring Science, 2007; 27:262-73.

14. Shankar J, Famuyiwa OO. Stress among

Factory Workers in a Developing Country.

Journal of Psychomotor Research.

1991;35(2/3): 163-71.



911

Pradeep et al., Int J Med Res Health Sci. 2013; 2(4):911-916


&

Health Sciences




thSep 2013

Research article

A STUDY ON PREVALENCE OF GROUP B STREPTOCOCCI AS A COLONISER IN

WOMEN OF REPRODUCTIVE AGE GROUP

*Sobhana Surya Pradeep M1, Vishnuvardhana Rao K

2


2Associate Professor, Department of Microbiology, Dr.Pinnamaneni Siddhartha

Institute of Medical Sciences & Research Foundation Chinnaoutapalli, Gannavaram Mandal, Krishna

District, Andhra Pradesh, India


ABSTRACT

The present study was undertaken to detect the presence of Group B streptococci (GBS) as a coloniser

among women of reproductive age group attending to outpatient clinic in Obstetrics and Gynaecology at

Dr.PSIMS &RF general hospital, Chinnaoutapalli. Methods: Two low vaginal swabs were collected

from 200 women in the age group of 15-45 years and the swabs were subjected to microscopy, culture,

Christie, Atkins and Munch-Peterson test (CAMP) and antibiotic susceptibility testing by Kirby-Bauerdisc diffusion method. Results: Of the total 400 vaginal swabs collected from 200 women 7 were found

to be colonized with Group B streptococci which were mostly susceptible to ceftriaxone and

erythromycin and all were resistant to penicillin except strain 1.Conclusion: Detection of colonization

with GBS and treatment helps in reducing the incidence of neonate acquiring GBS infection.

Keywords: Streptococci, colonization, CAMP test, neonatal meningitis, antibiotic sensitivity

INTRODUCTION

Women of reproductive age group are at risk of

acquiring urogenital infections. The microbes

present in the normal gastrointestinal flora are

the most common etiological agents. The

proximity between the anus and vagina facilitates

entry these microbes into urogenital tract.

Several bacteria are implicated as the common

agents causing urogenital infections among

women of reproductive age group especially

pregnant women.1

These organisms produce

urinary tract infections, bacteraemia and

endometritis and related complications such as

pre maturity and pre-term labour and even to

meningitis and pneumonia in the newborn with

high rate of mortality.1

Group B streptococcus (GBS) is a facultative

gram positive coccus known to be responsible for

bovine mastitis (1930’s). It is non-pathogenic

commensal of human flora of female genital

tract. By 1970’s group B streptococcus was

recognized as one of the leading causes of

neonatal mortality and morbidity.2

It is estimated

to be responsible for neonatal infections with

case fatality ratio of 50% and at a frequency of 2-

DOI:10.5958/j.2319-5886.2.4.146



912


3 per 1000 live births.2

It is said to be the leading

cause of neonatal sepsis, meningitis and

pneumonia. Streptococcal colonization as a risk

factor for pre-term delivery is a subject of

conflicting opinions.1

This bacterium is normally

found in vagina and rectum of 15% - 40% of allhealthy women of reproductive age group. Those

women who test positive for group B

streptococcus are said to be colonized. The vast

majority of group B streptococcal infections are

acquired during childbirth when a baby comes

into direct contact with bacteria which are carried

by mother as normal vaginal flora.2As estimated

12000 infants in US will become infected with

group B streptococcus each year and will resultin deaths of an estimated 2000 infants yearly,

while leaving others with physical or mental

disabilities. Group B streptococcus usually

causes infant illness within first 7 days of life,

but late onset infections may occur up to 3

months of age. Performance of a caesarean

section will not eliminate the risk of infection.3

That is why many western countries like USA,

Canada have made a national policy to screen

women of reproductive age group especially

pregnant women to detect group B streptococcus

vaginal colonization which was backed by CDC.

Few countries have also formed a national

protocol for prophylactic antibiotic treatment for

such women. Such national policies have brought

down rates of group B streptococcal infections in

reproductive age group women, pregnant women

and neonatal sepsis markedly.4

Group B

streptococcal infections are more common thanother illnesses for which pregnant women are

screened such as Rubella, Down’s syndrome,

Spina bifida etc. Yet, group B streptococcus

remains generally unknown to public.

Geographical, ethnical, social, economic

conditions and rate of group B streptococcal

colonization has also been studied and also the

rate of acquisition of group B streptococci by

infants was related to the heaviness of vaginalcarriage in the mother during labour and total

acquisition rate was found to be ranging from 4%

to 48%.5

Further detailed research in this

direction would help in understanding

epidemiology of group B streptococcal

colonization.

Group B streptococcal vaginal colonization is

detected in the majority of post pubertal women.Group B streptococcus has also been detected on

the external genitalia of men. With a degree of

colonization increasing among women of

reproductive age group there is increased

frequency of urinary tract infections. The degree

of colonization in pregnant women and rates of

neonatal sepsis are directly proportional.6

In

women of reproductive age group it may cause

symptoms irrespective of the time of acquisition(colonization). In pregnant women neonatal

transmission rate is less in early colonization.

But acquisition after 24 weeks of gestation, the

chances of neonatal transmission is more.6,7

Though many western researchers have been

working on group B streptococcal colonization,

only few Indian studies are available on this

problem.

This attempt is made at DR.PSIMS & RF to find

out the incidence of group B streptococcus as a

colonizer among women of reproductive age

group.

MATERIALS & METHODS

Subjects: 200 women of reproductive age

attending to obstetrics and gynaecology OPD at

Dr. PSIMS and RF during the period of May

2009 to February 2011 were included in this

study.15-45 yrs of age (post-pubertal or

reproductive) group was taken as inclusion

criteria. 83 pregnant women and 117 in non-

pregnant women were included in the present

study. Out of 83 pregnant women, 41 were third

trimester, 29 were in second trimester and

thirteen were in first trimester. Women having

any type of bleeding disorders like Dysfunctional

uterine bleeding (DUB) etc. were excluded.



Pradeep et al.,

METHODS

After taking informed consent

participants; two vaginal swabs

subjects and the swabs wer

transported to the microbiology l

Direct Microscopy: One swabinoculate 5% sheep blood agar a

wet mount and gram stainin

preliminary microscopic exa

recorded. The other swab

enrichment culture with Brain

(BHI) broth with antibiotics

mcg/ml and Nalidixic acid-8

after 24hrs incubation was inoc

sheep blood agar.

8

After overnight incubation the g

were read and suspected colonie

were subjected to catalase t

staining. Gram positive and c

colonies were subjected to C

confirmation was done by Late

using latex suspension coated

(Bio-merieux).9

Plates which

growth of streptococci were furth

24 hours, read and processe

suspected colonies. The enrich

subcultured and read and proc

Specimens yielding group B stre

on direct inoculation or on

enrichment medium were recorde

Antibiotic susceptibility of the i

streptococci was done by emp

Bauer disc diffusion method.8

Fig 1: Christie, Atkins and Mun

(CAMP test)


from all the

taken from all

e immediately

boratory.

was used to d then used for

. Findings of

ination were

was used for

Heart Infusion

(gentamicin-15

mcg/ml) which

lated on to 5%

rowth on plates

s on blood agar

st and Gram

talase negative

AMP test and

x agglutination

ith anti-serum

did not yield

er incubated for

similarly for

ent broth was

ssed similarly.

tococcus either

subculture of

d as positive.

olated group B

loying Kirby –

ch-Peterson test

Fig 2: Antibiotic SenBauer Disc diffusion t

RESULTS

200 women in the rep

included in the study.

(41.5%) women were

were nonpregnant wo

GBS was isolated fro

an incidence of 3.5%.

were positive for GB

age group of 23-24

between 20-37 weeks.

pregnant and belonged

yrs.

Antibiotic sensitivity t

isolated group B stre

disc diffusion method

SD013, C-SD010) onand the diameter of t

disc was measured un

measuring scale and

susceptible(S), interm

per the CLSI criteria.8

913

ci. 2013; 2(4):911-916

itivity testing by Kirby- echnique

roductive age group were

Out of the 200 women 83

pregnant and 117 (48.5%)

en.

7 women which indicate

Out of the 7 women who

, 3 were pregnant in the

yrs and gestational age

The other four were non

to the age group of 30-35

sting was done for all the

ptococci by Kirby Bauer

(Himedia, P-SD028, E-

% sheep blood agar plates he clear zone around the

der transmitted light with

results interpreted as

diate (I), resistant(R) as



914


Table 1: Standard zone size interpretation chart for the antibiotics tested against GBS8, 10

Drug PotencyZone of inhibition (in mm)

Sensitive Intermediate Resistant

Penicillin 10U 28 20-27 (≤ )19

Erythromycin 15mcg 21 16-20 (≤ )15

Ceftriaxone 30mcg 27 25-26 (≤ )24

Table 2: Antibiotic sensitivity patterns of group B streptococcal isolates (total no.7)

Strain No. Penicillin Erythromycin Ceftriaxone

002 I(24) R(14) S(28)

003 I(25) S(25) S(28)

050 I(25) S(25) S(27)

055 I(25) R(14) R(24)

117 S(29) S(22) S(29)

131 I(27) S(21) S(28)

180 I(23) S(22) S(28)

*Figures in brackets indicate the zone of inhibition (in mm)

DISCUSSION

GBS is one of the common agents causing

urogenital infections among women of

reproductive age group especially pregnant

women and also is the leading cause of neonatal

infections in the western hemisphere. These

infections in turn lead to UTI, bacteremia,

endometritis in women of reproductive age group

and in pregnant women UTI, endometritis,

amnionitis, post-partum wound infections and

neonatal complications such as prematurity,

preterm labor GBS pneumonia and meningitis1.

The recognition that maternal colonization with

this organism is a key factor in the occurrence of GBS infections associated with neonatal

mortality and morbidity was a milestone in the

history of perinatal health. In fact this awareness

has created a radical change in antenatal health

practice, but the spectrum of GBS disease

remains largely an under recognized problem.

The CDC advocated the prevention of GBS

infection in reproductive age group women,

especially in pregnancy by chemoprophylaxis inwomen with culture evidence of recent rectal or

vaginal colonization. According to them even

women without a known GBS status but

delivering before 37 weeks of gestation with

PROM or intrapartum fever are also advised to

be given antimicrobial prophylaxis presumably

to prevent GBS infection. Even women who are

not pregnant and present with UTI, endometritis

should be screened for GBS colonization through

culture for evidence of rectal/vaginal swabs3.

Very few Indian studies are available where an

attempt for detecting GBS colonization has been

done in women of reproductive age group. Even

the studies on pregnant women do not throw

light on the time of colonization, efficiency of transmission and the incidence of neonatal

disease. The Indian studies available for review

have reported lower colonization and infection

rates in general. However on closer analysis

taking into consideration use of adequate culture

techniques and microbiological media some of

the GBS colonization rates reported from India

and other developing countries are similar to

those reported in the United States. In our studyout of 200 samples, 7 samples yielded the growth

of GBS which accounts for 3.5%.In the present



915


study, utmost care was taken for processing the

samples and standard guidelines were followed.

A further prospective study in this direction and

screening of newborn babies for GBS

colonization would help in knowing the

magnitude of GBS related problems. Ourstatistics correlate with results of R Mhasker Rita

et al who have reported an incidence of 1.65%

vaginal colonization.10

Kulkarni et al has

observed a low rate of GBS colonization

(2.52%).11

El Kersh et al observed a rate of 2.6% GBS

vaginal colonization among 151 cases who were

negative for GBS colonization in earlier visits.

Findings of authors are correlating with that of Mhaskar Rita et al

10Kulkarni et al

11and with

findings of El Kersh et al. 12

High rates of GBS colonization were detected

among Saudi women (25.7%). Similarly a very

high GBS colonization rate was identified by J

Motlova et al (29.3%)13

, Orett FA (32.9%)14

in

their respective studies. Most of the studies

detected that GBS colonization occurred in

pregnant women more frequently during late

stages of pregnancy. These workers also opined

that early colonization of GBS has no

significance in prematurity or abortion.13, 14

Orett FA14

has observed a higher rate of

colonization among women of East Indian origin.

Most studies in India detected only 1.5%-2.5% of

GBS colonization among Indian women which

was correlated with the present study. But other

international studies revealed vaginal

colonization rate as 21.7% and anorectal carriageas 24.4 %

13.

In the present study author could not follow up

the positive cases, especially pregnant women to

detect whether neonatal transmission has

occurred or not. Based on the findings of the

present study and the findings of other Indian

reports it can be presumed that GBS related

problems in women of reproductive age group is

at a low rate in our country. However anationwide multicenter study is needed to

substantiate this finding. A nationwide screening

for GBS colonization in women of reproductive

age group, especially in pregnant women may

not be cost-effective and may not be necessary

keeping the low rates of reported colonization

rates which are confirmed.

However it is difficult to arrive at such aconclusion based on very few studies available.

There is a need for government/non-government

organization funded projects to the screen,

especially all antenatal women for urogenital

pathogens, like Chlamydia, Mycoplasma, Urea

plasma etc. along with GBS. Screening of GBS

in 3rd

trimester in pregnancy helps in detection of

colonization and also in preventing neonatal

diseases. Performance of Caesarian section willnot eliminate the risk of infection. So a national

policy to screen women of reproductive age

group especially pregnant women to detect for

GBS vaginal colonization and a protocol for

prophylactic antibiotic treatment should be

designed which would help to bring the rate of

GBS colonization and neonatal sepsis markedly.

Prophylactic immunization with Group B

streptococcal vaccines in prevention of

colonization in women of reproductive age group

and neonatal disease should be evaluated.

CONCLUSION

To conclude, there are very few studies in

literature which throw light on detecting GBS

colonization in women of reproductive age

group. In the present study, an attempt was made

to provide knowledge regarding prevalence of

GBS colonization in women of reproductive agegroup which also included pregnant women.

Although this study was not interventional and

the positive cases were not followed, a further

study for screening of GBS colonization will be

helpful in preventing intra-partum, post- partum

and neonatal complications. Present study also

provides implications for giving prophylactic

antibiotics before caesarian sections which would

have a paramount contribution in preventingneonatal meningitis.



916


REFERENCES

1. Maniatis AN, Palermos J, Kantzanou Ml.

Streptococcus agalactiae: A vaginal

pathogen? J Med Microbial 1996; 44: 199-

202.2. Gregary J locksmith, Penny Clark, Patrick

Duff. Maternal and neonatal infection rates

with three different protocols for prevention

of group B Streptococcal disease. Am J

Obstetrics Gynecology 1999; 180(2): 416-

422.

3. Anne Schuchat. Group B streptococcus.

Lancet 1999; 353: 51-55.

4. Sara Kenyon, Brocklehurst P, Blackburn A,

Taylor DJ. Antenatal screening and

intrapartum management of Group B

Streptococcus in the UK. BJOG 2004; 111:

226-230.

5. Ancona RJ, Ferrieri P, Williams PP. Maternal

factors that enhance the acquisition of Group

B Streptococci by newborn infants. Journal

of Medical Microbiology 1980; 13: 273-280.

6. Anitha Shet and Patricia Ferrieri. Neonatal

and maternal group B Streptococcalinfection: A comprehensive review. Indian J

Med Res 2004; 120: 141-150.

7. Regan JA, Klebanoff MA, Nugent RP,

Eschenbach DA, Blackwelder WC et al.

Colonization with Group B Streptococci in

pregnancy and adverse outcome. American

Journal of Obstetrics Gynecology 1996; 174:

1354-60.

8. Bailey and Scotts. Diagnostic microbiology,

11th ed. Andrew Allen, Mosby, Inc.2002;

167.

9. Anthony BF, Okada DM, Hobel CJ.

Epidemiology of group B Streptococcus:

Longitudinal observation during pregnancy.

Journal of infectious diseases 1978; 137:

524-530.

10. Mhaskar Rita, Sharad S, SriKanth N,

Swarnarekha B, Ranjani S. Selective risk

factor based screening of pregnant women

for group B Streptococcal colonization in a

teaching hospital in south India. Indian J

Obstetrics Gynecology 2005; 55(4): 336-38.11. Kulkarni AA, Pawar SG, Dharmadhikari CA,

Kulkarini RD. Colonization of pregnant

women and their new born infants with group

B Streptococci. Indian Journal of Medical

Microbiology, 2001; 19(2): 1-4.

12. El-Kersh TA, Nuaim LA, Kharfy TA,

Shammary FJ, Saleh SS, Zamel FA et al.

Detection of genital colonization of group B

Streptococci during late pregnancy. SaudiMed J 2002; 23(1): 56-61.

13. Motlova J, Strakova L, Urbaskova P,Sak P,

Server T. Vaginal and rectal carriage of

Streptococcus agalactiae in the Czech

Republic: Incidence, serotypes distribution

and susceptibility to antibiotics. Indian J Med

Res, 2004; 119: 84-87.

14. Orrett FA. Colonization with group B

Streptococci in pregnancy and outcome of

infected neonates in Trinidad. Pediatr Inf

2003; 45(3): 319-23.



917

Prashant V et al., Int J Med Res Health Sci. 2013; 2(4):917-922


&

Health Sciences




thSep 2013

Research article

PREVENTIVE MEASURES NEEDED FOR LONG TERM USE OF CARBAMAZEPINE TO

LOWER THE RISK FOR CORONARY HEART DISEASE

*Paunipagar Prashant V1, Babu Ramesh B

2, Sharma Rahul P

3

1Professor and HOD, Department of Biochemistry, ESIC Medical College, Gulbarga, Karnataka, India

2Associate Professor, Department of Psychiatry, Raichur Institute of Medical Sciences, Raichur

3MBBS Student, Raichur Institute of Medical Sciences, Raichur, Karnataka, India


ABSTRACT

Present cross sectional study was carried out with a view to evaluate the Carbamazepine risk for

coronary heart disease. Lipid profile and Framingham point scores were studied in 60 Epilepsy patients

on Carbamazepine. The epileptic patients were compared with age and sex matched 60 healthy controls.

Framingham Point Scores were estimated by taking into consideration several parameters i.e. Age, Sex,

Systolic blood pressure, HDL levels, Total cholesterol, and smoking history, as per guidelines of theFramingham Heart Study group We conclude that this drug significantly increases the risk for coronary

heart disease in patients with respect to lipid profile and other parameters as described by the

Framingham study group. Altogether, this drug may be one of the reasons for the high prevalence of

CHD, which is increasing day-by-day due to the globalization.

Keywords: Carbamazepine, Epilepsy, Lipid Profile, Coronary heart disease

INTRODUCTION

In Latin seizure means "to take possession of".Seizure by definition is a paroxysmal event due

to abnormal, excessive, hyper synchronous

discharges from an aggregate of central nervous

system (CNS) neurons1. Epilepsy describes a

condition in which a person has recurrent

seizures due to a chronic, underlying process.

About 50 million people worldwide have

epilepsy, with almost 90% of these people being

in developing countries2. In India itself,

approximately 6 million people suffer from

Epilepsy. Anticonvulsant drugs like

Carbamazepine are in use since 1962

3

for longterm antiepileptic therapy. This long term

treatment may be associated with various

metabolic abnormalities involving connective

tissues, endocrine system and liver.

Coronary Heart Disease is defined as

“impairment of heart function due to inadequate

blood flow to the heart compared to its needs,

caused by obstructive changes in the coronary

circulation to the heart. Framingham heart study4

started during the 1950s has played a major role

in establishing the nature of CHD risk factors

DOI:10.5958/j.2319-5886.2.4.147



918


and their relative importance. The major risk

factors of CHD are elevated serum cholesterol,

smoking, hypertension, and sedentary habits.

Previous studies by Framingham Heart Study

group have shown that alterations in serum lipids

predisposes to coronary heart disease4. Thus,Influence of Carbamazepine on serum lipids has

been investigated many times leading to

contradictory reports5-9

. Moreover, alterations in

lipid profile may vary in different populations

and not many studies have been done in Indian

scenario. Hence present study was carried out

with a view to determine the association between

long term use of Carbamazepine & changes in

Lipid/Cholesterol metabolism and also to findthe magnitude of risk for coronary heart disease

as an effect of alterations in Lipid/Cholesterol

metabolism by this drug, if any.


Study Design: Cross-sectional study.

Setting: Psychiatry OPD and Department of

Biochemistry of Raichur Institute of Medical

Sciences, Raichur (Karnataka)

Study Subjects: A total of 120 subjects aged

between 20 - 40 years were taken into study. 60

Epileptic patients who are exclusively on

Carbamazepine (in a dosage of 200 mg BD) were

compared with age and sex matched similar

number of Healthy Controls.

Only subjects classified as Epileptic as per ILAE

classification11

and those exclusively taking

Carbamazepine for epilepsy for a period of 6-12

months were included in the study. Whereassubjects having co-morbid conditions like

hypertension, Diabetes, Tuberculosis, Obesity,

etc. were excluded from the study.

Before carrying forward the subject selection,

Institutional Ethics committee approval was

taken.

Diagnostic Criteria: Epilepsy: The subjects areclassified as per ILAE classification

11,

Diagnosed by Psychiatry Department of Raichur

Institute of Medical Sciences, Raichur.

Estimation of Lipid Profile: Total cholesterol,

HDL-c and Triglycerides levels estimation done

using Randox kits by Daytona Randox fully

automated analyzer. LDL-c levels calculated as

per formula by Friedewald et al.10

Collection of Blood sample: 12 hour overnightfasting blood sample in plain bulb is collected in

the morning from anticubital vein using 21 gauze

5ml disposable syringe using a tourniquet and

with all aseptic precaution.

Estimating the risk for coronary heart

disease: Framingham Point Scores were

estimated by taking into consideration several

parameters i.e. Age, Sex, Systolic blood pressure,

HDL levels, Total cholesterol, and smoking

history, as per guidelines from Framingham

Heart Study group4

Statistical Analysis: Data collected was

analyzed using student t-test and chi square test.

Values <0.05 were considered statistically

significant.

RESULTS

Estimation of Lipid profile in Epilepsy patients

on Carbamazepine and their Framingham score

and related risks are tabulated in following tables

Table 1: Lipid Profile in Epilepsy patients on Carbamazepine, compared with Controls

Parameter Cases (n=60) Controls (n=60) P Value

Total Cholesterol (mg/dl) 174.15 ± 14.43 164.27 ± 13.19 <0.001

HDL(mg/dl) 43.36 ± 5.26 45.65 ± 6.03 0.03

LDL(mg/dl) 104.74 ± 13.08 94.52 ± 15.09 <0.001

Triglycerides (mg/dl) 130.18 ± 15.13 120.45 ± 10.76 <0.001

TC/HDL 4.06 ± 0.51 3.67 ± 0.57 <0.001

LDL/HDL 2.45 ± 0.44 2.12 ± 0.51 <0.001

Framingham Risk % 0.45 ± 0.96 0.27 ± 0.76 0.17



919


Table 2: Age & Sex wise Distribution of Epilepsy patients on Carbamazepine

Age (yr) Parameter Male (n=15) Female (n=24) P – Value

20-30 Total Cholesterol (mg/dl) 161.93 ± 16.49 178.29 ± 11.52 0.003

HDL (mg/dl) 43.33 ± 4.87 42.83 ± 4.94 0.759

LDL (mg/dl) 94.76 ± 15.01 108.5 ± 10.60 0.005

Triglycerides (mg/dl) 119.2 ± 13.54 134.79 ± 12.52 0.001

TC/HDL 3.76 ± 0.44 4.20 ± 0.45 0.005

LDL/HDL 2.21 ± 0.41 2.56 ± 0.40 0.013

30-40 Male (n=9) Female (n=12)

Total Cholesterol (mg/dl) 182.22±11.78 175.08±9.83 0.199

HDL (mg/dl) 45.89 ± 5.08 42.58 ± 6.45 0.205

LDL (mg/dl) 109.27 ± 13.35 106.33 ± 8.99 0.579

Triglycerides (mg/dl) 135.33 ± 23.50 130.83 ± 5.63 0.588

TC/HDL (%) 4.02 ± 0.58 4.18 ± 0.55 0.535

LDL/HDL (%) 2.41 ± 0.47 2.55 ± 0.46 0.524

Table 3: Framingham point scores depict the estimated 10-year % risk(4)

for development of Coronary

heart disease in Epilepsy patients on Carbamazepine

10 year

% Risk

Males Females

Total point

scores

Cases Controls Total point

scores

Cases Controls

<1 <0 8 19 <9 36 30

1 0-4 10 9 9-12 - -2 5-6 4 1 13-14 - -

3 7 - - 15 - -

4 8 1 - 16 - -

5 9 1 1 17 - -

>6 >10 - - >18 - -

Total 24 30 36 30

Table 4: Age and Sex wise distribution of Framingham score in cases

Male Female p-Value

Overall 1.125 ± 1.26 0 0.000225

20-30 0.73 ± 0.79 0 0.003

30-40 1.77 ± 1.64 0 0.011

Total cholesterol (TC), LDL and Triglycerides

level were elevated very significantly (p < 0.01)

in the cases, whereas significant (p < 0.05)

reduction in protective HDL levels were noted.

Further leading to significant elevation in TC:

HDL and LDL: HDL ratios. Overall increase in

framingham risk % is noted in the cases as

compared to controls.

In age group of 20-30 years, very significant (p <

0.01) elevation is noted in TC, LDL and

Triglycerides in Females when compared to

males of the same age group. However, changes

in levels of HDL are not in statistically



920


significant range. Overall, it leads to very

significant change in TC: HDL (p < 0.01), and

significant change in LDL: HDL ratios (p <

0.05).

However, in age group of 30-40 years, sex-wise

no significant changes noted in lipid profileparameters. Very significant (p < 0.01) rise in 10

year % risk is noted in male cases. However,

when divided into subgroups of age 20-30 and

30-40 years, significant ( p < 0.05 ) elevation in

risk is observed in 30-40 years group with very

significant( p < 0.01) rise in the young age group

of 20-30 years is observed. Inspite of this

difference in significance values, the mean

increase in risk % is more in higher age group of 30-40 years.

In case of female study group, no significant

difference noted in two groups of cases and

controls,with all the females having < 1 % risk of

developing CHD in 10 year period.

Fig 1: 10 year Framingham % risk comparison in

Males

Fig 2: 10 year Framingham % risk comparison in

Females

DISCUSSION

The action of Carbamazepine and its metabolites

is now well understood with the advancement in

pharmacological field. Neurons are allowed to

communicate for long distance by the voltage –

gated sodium channels which generate an action

potential. The sodium channels which opens with

generation of action potential are inactivated

essentially by closing the channels.

Carbamazepine acts by stabilizing the inactivated

state of sodium channels. Thus the neurons are

less excitable because very few channels are

available to open subsequently. GABA receptor

alpha 1, beta 2 and gamma 2 subunits are

potentiated with carbamazepine.12 The intake of

carbamazepine not only affects the neurons but

also other systems by inducing liver microsomal

enzymes leading to alteration in metabolism of

lipids, bile acids and bilirubin13

If Carbamazepine increases the risk of Coronary

Heart Disease, it might lead to increase in

patients’ burden which they are already having.

Hence, present study was carried out to evaluate

the safety or risk of these drugs. For this purpose,we evaluated lipid profile in patients between age

group of 20-40 years, receiving Carbamazepine

for more than 6 months. From the study we

found, statistically highly significant increase in

Total Cholesterol (TC), LDL-c, and

Triglycerides (Tg) level. However, there was

also statistically significant fall in HDL-c levels,

leading to increase in atherogenic ratio (TC/HDL

and LDL/HDL ratio) in the study group. This can

attribute to increase in Total cholesterol to

increased levels of LDL and not because of the

HDL levels, as reported previously in many

reports5-8

. This is consistent with the reports by

Zeilthoper S et al.(9)

who also attributed

increased Total Cholesterol to increased LDL-c

levels.

10 year % risk for development of Coronary

heart disease by Framingham Point score reveals

a score in Epilepsy patients on Carbamazepine tobe less than 2% in the majority of the patients



921


(58 of 60), which reveals the safety of this drug;

if other modifiable factors are in control like

smoking habits, blood pressure.

CONCLUSION

Assessing and stratifying the risk for CHD, entire

constellation of factors needs to be considered,

not only just lipid profile. As Carbamazepine

used in the treatment of Epilepsy is significantly

raising Total cholesterol, LDL and Triglycerides

level, routine lipid profile estimation is required

in these patients. Moreover, due to various other

predisposing factors for the risk of CHD and a

significant increase in atherogenic ratios,

periodic Lipid Profile estimation should bemandatory in the cases with presence of other

risk factors like hypertension and smoking

history, particularly in males. Other measures

like the addition of Lithium Carbonate and

Vitamin E14

can be suggested in the treatment

regimens to decrease the Carbamazepine dosage

and hence its atherogenic effects and better

outcome for the patient, as the prevalence of

CHD is increasing day-by-day due to increased

Globalization.

REFERENCES

1. Lowenstein DH. Seizures and epilepsy. In:

Kasper DL, Fansi AS, Lango DL, Jameson

LJ, Braunwald E, Hauser SL, editors.

Harrison’s Principles of Internal Medicine.

16th

edn. (Vol II). United States of America:

McGraw Hill Companies; 2005.p.2357.2. WHO Factsheets – Epilepsy-1

stSept, 2010

http://www.who.int/mediacentre/factsheets/fs

999/en/

3. Murali MS. Epidemiological Study of

Prevalence of Mental Disorders in India.

Indian Journal of Community Medicine

2001; 26 (4): 10-12

4. Framingham Heart Study; a project of

National Heart, Lung and Blood Institute and

Boston University. Last updated: June

29,2010

http://www.framinghamheartstudy.org/

5. Nakken KO, Kornstad S. Do Males 30-50

Years of Age with Chronic Epilepsy and on

Long-Term Anticonvulsant Medication Have

Lower-Than-Expected Risk of DevelopingCoronary Heart Disease?, Epilepsia. 1998;

39(3):326-330,

6. Aggarwal A, Kumar M, Faridi MMA. Effect

of Carbamazepine on Serum Lipids and Liver

Function Tests; Indian Pediatrics, 2005;

42:913-918.

7. Nikolaos T, Stylianos G, Chryssoula N, Irini

P,Christos M, Dimitrios T, et al. The effect of

long-term antiepileptic treatment on serumcholesterol (TC, HDL, LDL) and triglyceride

levels in adult epileptic patients on

monotherepy. Med Sci Monit 2004; 10: 50-

52.

8. Mintzer S, Skidmore CT, Abidin CJ, Morales

MC, Chervoneva I, Capuzzi DM, Sperling

MR. Effects of antiepileptic drugs on lipids,

homocysteine, and C-reactive protein. Annals

of Neurology. 2009;65: 448 – 56.

9. Zeilthoper S, Doppelbauer A, Tribl G, Leitha

T, Deecke L. Changes in serum lipid pattern

during long term anticonvulsant treatment.

Clin Invest 1993; 71: 574-78.

10. Friedwald WT, Levy RI, Frederickson DS.

Estimation of the concentration of LDL-c in

plasma without use of the preparative

ultracentrifuge. Clin Chem, 1972; 18: 499-

02.

11. ILAE’s 1989 International Classification of Epilepsies and Epileptic Syndromes,f rom

(1989). Proposal for revised classification of

epilepsies and epileptic syndromes.

Commission on Classification and

Terminology of the International League

Against Epilepsy. Epilepsia.1989;30(4); 389-

99

12. Granger P, Bilton B, Faure C, Vige X,

Depoortere H, Graham D. et al. Modulationof the gamma-aminobutyric acid type A



922


receptor by the antiepileptic drugs

carbamazepine and phenytoin. Mol.

Pharmacol. 1995; 47(6): 1189 – 96.

13. Havel RJ, Kane JP. Structure and metabolism

of plasma lipoproteins. In: Secriver CR,

Beaudet AL, Sly WS, Valle D (eds). TheMetabolic and Molecular Basis of Inherited

Disease, 7th edn, vol II. New York, McGraw-

Hill, 1995; pp 1841-51.

14. Megrabian AA, Mkhitarian VG, Amadian

MG, Badalian GE, Avakian SL. Use of

lithium carbonate and vitamin E in the

complex treatment of epileptics. Zh

Nevropatol Psikhiatr Im S S

Korsakova. 1986; 86(9):1407-10.



923

Khan et al., Int J Med Res Health Sci. 2013; 2(4):923-930


&

Health Sciences




thSep 2013

Research article

SCREENING OF ANTIBIOTIC RESISTANT GRAM NEGATIVE BACTERIA AND PLASMID

PROFILING OF MULTI-DRUG RESISTANT ISOLATES PRESENT IN SEWAGE

ASSOCIATED WITH HEALTH CARE CENTERS

Khan Md. Anik Ashfaq, Sutradhar Pijush, Islam Mohammad Majharul, Ojha Ravi Kant, Biswas Gokul

Chandra*

Department of Genetic Engineering and Biotechnology, Shahjalal University of Science andTechnology, Sylhet-3114, Bangladesh


ABSTRACT

Background: Healthcare effluent acts as the store house of harmful infectious agents such as the

pathogens and microorganisms possessing multiple drug resistant genes. Potential health risk includes

spreading of diseases by these pathogens and wide dissemination of antimicrobial resistance genes.

Gram-negative bacteria are particularly important for causing most of the hospital and community

acquired infections. Aim: This study was carried out to highlight the incidence of antibiotic resistantbacteria in hospital generated effluent discharged into municipal sewage system of Sylhet city,

Bangladesh. Methodology: Standard biochemical tests were used to isolate and identify 29 gram

negative bacteria from 6 effluent samples. Antibiotic susceptibility test was assessed by Kirby-Bauer

disc diffusion method. Plasmid isolation and gel electrophoresis were performed using standard

protocols. Results: Antibiogram study showed that the percentage of isolates resistant to amoxicillin,

ceftriaxone, ciprofloxacin, gentamicin, imipenem, azithromycin, andsulphamethoxazole-trimethoprim

were 93.10%, 55.17%, 27.6%, 24.14%, 20.7%, 13.8% and 10.34% respectively. Ten of the isolates

showed resistance to three or more commonly used antibiotics. Plasmid profiles of the multi-drug

resistant isolates showed to harbor two or more plasmids and almost all of them showed a common band

for plasmid DNA size of 24.5kb. Conclusion: Resistance to the bacterial pathogens causing community

acquired infections may, thus, exert a serious public health threat through confining the antibiotic pool.

Hospitals should follow, monitor and regulate proper sanitary measures of hospital generated effluents

to forestall the dissemination of multi drug resistant bacteria transfer from hospital waste to the

environment.

Keywords: multi-drug resistance, hospital effluents, antibiogram, plasmid profiling.

INTRODUCTION

Waste effluent from hospitals and clinics contain

high numbers of resistant bacterial strains and

residual antibiotics at a concentration to which

susceptible bacterial growth is inhibited.1

One

study by Schwartz et. al.,2 has evaluated the

microbiological content of hospital and

DOI:10.5958/j.2319-5886.2.4.148



924


household waste quantitatively and qualitatively

and found that general hospital waste contains

bacteria with pathogenic potentials for humans

compared to household waste.2

Grabow and

Prozesky3

showed that two mechanisms,

introduction and selection for resistant bacteriaresults in increased number of resistant bacteria

in the sewers where hospital effluents are

immediately discharged3. Excretion mechanism

is responsible for the addition of a significant

amount of un-metabolized antibiotics.4

Long-

term exposure of microorganisms to low

concentrations of antibiotics in wastewater and

surface water has the potential for the

development of antibiotic resistance, which wasreported by Smith et. al.,

5If the hospital effluents

are not treated, concentrated forms of infectious

agents and antibiotic resistant microbes are shed

into communities resulting in water borne

diseases such as cholera, typhoid fever,

dysentery and gastroenteritis.6

Grabow and

Prozesky stated that, although, sewage treatment

reduces the number of bacteria in wastewater but

the effluent generally contains a large number of

both resistant and susceptible bacteria3.

The basic principle of underlying wastewater

management is the strict limit on the discharge of

hazardous liquids into sewers without prior

treatment so that living pathogenic organisms are

not introduced into the environment.7

In

Bangladesh, at present no government rule is

prevailing for regulating the hospital waste

management. No institutional mechanism is

working on the government side specially forhandling this kind of waste, which was reported

by ‘Prism Bangladesh.8

Also, unfortunately,

there is no structured form of medical waste

treatment in Bangladesh, and most wastes are

dumped in open areas for natural degradation or

re-sold by scavengers9, although, hospitals

usually maintain local measures (e.g.,

incineration, chemical sterilization etc.) of waste

treatment before disposal. The sewerage network of Sylhet city consists of many small drains

connected with some natural hilly channels,

which fall into the Surma River.10

Therefore,

even if the hospitals are discharging their health

care liquid waste into the sewerage system, it

mixes with the sewage and gets in surface water

without proper treatment.Haque (1994) reported that some 5.2 million

people (including 4 million children) die each

year from waste-related diseases in

Bangladesh.11

Therefore, untreated hospital

liquid waste discharges into surface water

directly or indirectly have been causing

additional problems. Gram-negative bacteria are

crucial in this aspect because they are the most

common causes of hospital and communityacquired infections and they are inherently

resistant to many hydrophobic antibiotics.12-15

In

such scenario, this study was carried out to

screen the antibiotic susceptibility pattern of

gram-negative bacterial isolates from healthcare

liquid waste generated in Sylhet metropolitan

area of Bangladesh and investigate on their role

in developing antibiotic resistance.


Sample collection, isolation and identification

of bacteria: A total of six sewage samples

associated with hospital and clinical effluents

were collected from six different spots in the

Sylhet Metropolitan area, where hospitals

effluents are immediately discharged. Sample

from each site was collected in 150 ml sterile

containers and transported to the laboratory

within an hour of collection in cold conditions.

100 ml diluted samples were spread over

MacConkey agar media that inhibits the growth

of gram positive bacteria and incubated for 24

hours at 37ºC. Differentiation as lactose

fermenter and non-lactose fermenter could be

made on Mackonkey agar for the isolates based

on pigmentation.16

Five colonies from each plate

were selected with different colony morphologies

by using five-colony method and further purifiedtwice.

17A total of twenty nine isolates thus



925


obtained were identified on the basis of

morphological characteristics, gram staining and

biochemical tests according to Bergey´s Manual

of Determinative Bacteriology.18

Other media

used in this study include Eosine Methylene Blue

Agar (EMB), Salmonella Shigella (SS) Agar andThiosulfate Citrate Bile Salts (TCBS) agar.

Antibiotic sensitivity test: Antimicrobial

susceptibility testing of all 29 bacterial isolates

was performed following the modified Kirby-

Bauer disk diffusion method on Muller-Hinton

against selected antibiotics namely Amoxicillin

(AMX) 10µg, Ceftriaxone (CTR) 30µg,

Azithromycin (AZM) 15µg, Gentamycin (CN)

10µg, Imipenem (IPM) 10µg, Ciprofloxacin(CIP) 5µg and Sulphamethoxazole-Trimethoprim

(SXT) 10 µg. Klebsiella ATCC and

Pseudomonas ATCC were the only standard

controls used to screen antibiotic resistance of

Klebsiella sp. and Pseudomonas sp. isolates

respectively. Inhibition zone size was interpreted

using standard recommendation of the National

Committee for Clinical Laboratory Standards19

now known as the Clinical Laboratory Standard

Institute (supplementary data: Table 1).

Plasmid analysis: The present study emphasized

on investigation on the correspondence between

antibiogram and plasmid profile of the multiple

drug resistant (MDR) isolates. Therefore,

plasmid DNA of MDR isolates was extracted

from cultured cells following alkaline lysis

method of plasmid preparation.20

The samples

were processed using gel electrophoresis to

identify the number of plasmid copies present indifferent isolates. Agarose gel electrophoresis

was carried out in a horizontal gel apparatus (My

Run Cosmo bio co. ltd, IMR-201). After

electrophoresing of all the plasmids in 0.7%

agarose (Merck, Mumbai), the gel stained with

ethidium bromide were visualized by Ultraviolet

Transilluminator (UVP, High Performance

transilluminater; USA)and photographed by

Samsung camera. The number and molecular

sizes of the plasmid DNA were determined on

the basis of mobility through agarose gel and was

compared with the mobility of Supermix DNA

Ladder, (Genei Pvt. Ltd., Bangalore, India)

which was used to estimate the plasmid size.

RESULTS

In the present study, we collected effluent

samples from hospitals and clinics which were

immediately released into the corresponding

municipal sewerage. As gram negative bacteria

are the most common causes of hospital and

community acquired infections15

, an effort was

given to isolate and identify gram negative

probable pathogens. Of the 29 isolates, eight(27.58%) were found to be of Pseudomonassp.,

followed by seven (24.14%) of Escherichia coli,

six (20.69%) of Klebsiella sp., three (10.74%) of

Shigella sp., two (6.90%) each of Yersinia sp.

and Vibrio sp., and one (3.49%) of Serratia sp.

respectively.

Antibiogram study of the 29 isolates

(supplementary data: Table 2, 3, 4) showed that

the percentage of isolates resistant to amoxicillin,

ceftriaxone, ciprofloxacin, gentamicin,

imipenem, azithromycin and sulphamethoxazole-

trimethoprim were 93.10%, 55.17%, 27.6%,

24.14%, 20.7%, 13.8% and 10.34% respectively.

Highest rates of sensitivity pattern were found to

imipenem (68.96%), followed by SXT (65.52%),

ciprofloxacin (62.06%) and azithromycin

(62.06%) (Fig. 2). Among the predominant

isolates (Pseudomonas sp., E. coli, and

Klebsiella sp.), The highest percentage of

resistance to ciprofloxacin and azithromycin was

shown by E. coli isolates (42.86%) whereas

66.66% of Klebsiella sp. showed resistance to

ceftriaxone and gentamycin which was highest

(supplementary data: Table 2). All of the isolates

of Pseudomonas and Klebsiella sp. expressed

resistance pattern to amoxicillin whereas in case

of E. coli it was 85.71%.



Khan et al.,

(A)

Fig. 1: Antibiogram of two of th

Although, imipenem showed hi

pattern to the isolates, both of tsp. expressed resistance to

Bacterial isolates resistant to thre

Fig. 2: Comparati

Plasmid profiling of ten isolat

eight of the isolates show pl

varying sizes (1.5 kb to 24.5

Table 1). One of the isolates

band of plasmid while others ha

with different sizes as shown in t

other hand, only two isolates h

even though they were resistan

0

10

20

30

40

50

60

70

80

90

100

CTR AZM

% o

f S u s c e p

t i b i l i t y


e isolates- (A) Klebsiella sp. and (B) Pseud

hest sensitivity

e two Yersinia this antibiotic.

e or more of the

antimicrobial agents

resistant (MDR) were(34.48%) out of 29.

ve antibiogram study of twenty nine isolat

s showed that

smid DNA of

kb) (Fig. 3and

ossessed single

more than one

he table. On the

ave no plasmid

t to antibiotics.

Almost all of the isol

of plasmid contained c

of 24.5kb. Earlier, anti

isolates showed that al

amoxicillin. Four of th

ciprofloxacin and thre

and K-6-4) harbored

around 2kb.

GEN IPM CIP SXT AM

Antibiotics

926

ci. 2013; 2(4):923-930

(B)

monas sp.

tested, hence multi-drug

found to be 10 in number

d bacteria.

tes that showed presence

ommon plasmid DNA size

biogram of MDR bacterial

l isolates were resistant to

e isolates were resistant to

e of them (P-1-3, K-1-2

a plasmid each of size

Resistant

Moderately

sensitive

Sensitive



927


Fig. 3: Agarose gel eletrophoresis of plasmid DNA from ten MDR isolates.

*L= Ladder DNA, † P-A=Pseudomonas ATCC, ‡K-A= Klebsiella ATCC

Table: 1. Plasmid profiling and correlation with antibiogram.

*P=Pseudomonas sp., † E= E. coli,

‡S=Shigella sp.,

§Y=Yersinia sp.,

||K=Klebsiella sp.

DISCUSSION

Both lactose fermenting and non-lactose

fermenting bacteria were isolated and identified

in which most predominant was Pseudomonas

sp. with 27.58%, followed by Escherichia coli-

24.14%, and Klebsiella sp.- 20.69%. One of the

hospital effluent studies carried out in India

involved isolation of gram negative bacilli, in

which E. coli (37.19%) was predominant

organisms, which is contrasted to this study

whereas percentages of Pseudomonas Sp.

(22.31%) and Klebsiella sp. (19.83%) were fairly

consistent. The study carried out in India showed

higher percentage of resistant isolates from

hospitals to ciprofloxacin (42.97%) and

gentamicin (27.27%) whereas the less percentage

of isolates was found to show resistance to

imipenem (16.66%).21 In contrast to this, less

percentage of isolates showed resistance to

Isolates Antibiotics resistance

pattern

No. of

bands

Band size (kilo base pair)

*P-4-5 AMX, CTR, SXT 0 -

P-1-3 AMX, CTR, CIP,

SXT

4 7kb, 4.2kb, 2.4kb, 1.7kb

† E-1-4 AMX, CTR, AZM 0 -

E-3-1 AMX, CTR, CIP 2 24.5kb,7kb‡S-6-2 AMX, CTR, IPM 1 24.5kb§Y-4-4 AMX, CTR, IPM, CN 2 24.5kb, 14.5kb||K-1-2 AMX, CTR, CIP, CN 2 24.5kb, 2kb

K-3-2 AMX, SXT, CN 2 24.5kb, 2.8kb

K-2-2 AMX, CTR, CN 2 24.5kb, 9kb

K-6-4 AMX, CTR, CIP 2 24.5kb, 2kb

ATCC-Pseudomonas AMX 0 -

ATCC- Klebsiella AMX 0 -



928


ciprofloxacin (27.6%) whereas almost same

pattern of resistance was found in the present

study in case of gentamycin (24.14%).

Amoxicillin was the antibiotic to which highest

number of resistant bacteria (93.1%) was found,

followed by ceftriaxone (55.17%). Discharge of antibiotic residues from hospitals and households

usage into effluent and municipal sewage

provides an indication of a selection pressure on

bacteria.22

Islam et al (2008) carried out a similar

type of study in Bangladesh and found that the

resistance development was directly related to

the use of antibiotics.23

It can be assumed that

isolated organisms in this study have been

persistently exposed to the antibiotic residuesand as a result, they might have developed

resistance mechanisms to them. Walton (1988)

pointed out that hospital environment appears to

be the origin of MDR bacterial strains and the

selective pressure responsible for expanding such

bacterial populations in hospitals must have been

through the use of drugs in humans and

veterinary and agricultural uses are not

responsible.24

Therefore, the results suggest that

the MDR bacteria containing multi drug resistant

genes present in the hospital effluent of this

particular locality may act as a possible source of

transfer of these resistant genes to the bacterial

population.

Plasmid profiling of two of the MDR isolates did

not show up any visible band. Possibly, some

resistant genes were not located on plasmid and

perhaps exist on the bacterial chromosome as it

is known that genetic origin of drug resistancemay be plasmid or chromosomal.

25Beta-lactams

are particularly important because they are the

most prevalently used antibiotics all over the

world, and because clinical crisis resulted due to

resistance to this antibiotic.26 β-lactamases,

including extended-spectrum β-lactamases

(ESBLs), AmpC β-lactamases (AmpC) and

metallo-β-lactamases (MBLs) genes that are

responsible for prevalent emergence of antibioticresistance in gram-negative bacteria are most

often carried on plasmid, thus, facilitate rapid

spread between microorganisms.27

Being the

types of beta-lactam, this may be attributed to the

widely dissemination of amoxicillin, ceftriaxone

and imipenem resistant genes, because a

significant percentage of bacterial isolates tend toshow resistance to antibiotics in the present

study. It is suggested to carry out further research

including plasmid curing and transformation in

order to examine plasmid-mediated mode of

resistance to the antibiotics used in this study.

As this study was performed over limited number

of samples and isolates, studies in broad manner

are needed to fully understand the extent to

which hospitals and clinics in big cities of Bangladesh contribute to resistance properties of

bacterial strains. In addition, the samples were

collected from the spots where the effluents

immediately discharged into municipal sewage,

with a view to isolating those bacteria which

have a better chance to come from effluents or

persist to effluent materials i.e., antibiotic

residues. In this circumstance, some other

bacterial strains that have attained resistant

properties from other sources other than hospital

effluents may be mixed. Despite the possibility

of this rare pitfall, the present observations

suggest that hospital effluents may contribute to

health hazard by adding MDR bacteria to city

sewage of this particular locality, which

ultimately falls into river.

CONCLUSION

The present study was carried out on a

preliminary basis, in order to investigate on the

development of antibiotic resistance and their

possible mode of dissemination. Finally, it can be

concluded that the isolated strains were showing

resistance mechanisms against various antibiotics

especially to beta lactams and these drug

resistant strains may cause to induce health

hazard. Hence, solution to the problem of MDR

bacteria in healthcare liquid waste is crucial.Good safety sterilization methods should be



929


implemented before releasing of waste materials

to the environment or sewage. Proper regulation

and monitoring of an integrated health care liquid

waste management practice is essential in order

to diminish the risk of disseminating multiple

drug resistant microorganisms for the safeguardof public health.

ACKNOWLEDGEMENTS

This research work was carried out both in the

former ‘USDA laboratory’ and in the

‘Microbiology, Fermentation and Environmental

Biotechnology laboratory’ of the Department of

Genetic Engineering and Biotechnology,

Shahjalal University of Science and Technology,Sylhet. We want to thank the personnel of both

laboratories for their support and technical help.

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J Pharm Clin Res. 2013; 6(3):42-46.

22. Kummerer K, Henninger A. Promoting

resistance by the emission of antibiotics from

hospitals and households into effluent.

ClinMicrobiol Infect. 2003; 9(12):1203-14.

23. Islam MJ, Uddin MS, Hakim MA, Das KK

and Hasan MN. Role of Untreated Liquid

Hospital Waste to the Development of Antibiotic Resistant Bacteria. Journal of

Innovation and Development Strategy. 2008;

2(2):17-21.

24. Walton JR. The Veterinary Record.1988;

122:249-51.

25. Oktem IM, Gulay Z, Bicmen M and Gur D.

HITIT project study group qnrA prevalence

in extended spectrum beta-lactamase-positive

enterobacteriaceae isolates from Turkey. JapJ Infect Dis.2008; 61:13-17.

26. Jean SS, Teng LJ, Hsueh PR, Ho SW, Luh

KT. Antimicrobial susceptibilities among

clinical isolates of extended-spectrum

cephalosporin-resistant Gram-negative

bacteria in a Taiwanese University Hospital.

J AntimicrobChemother.2002; 49:69-76.27. Gupta, V. An update on newer beta-

lactamases. Indian J Med Res. 2007;

126(5):417-27.



931

Ankita etal., Int J Med Res Health Sci. 2013;2(4):931-934


&

Health Scienceswww.ijmrhs.com Volume 2 Issue 4 Oct-Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886

Received: 27thAug 2013 Revised: 16th Sep 2013 Accepted: 28th Sep 2013Research article

AN EVALUATION OF ORAL HEALTH IN ADOLESCENTS OF AHMEDABAD CITY

Parekh Paras A1,

*Shah Ankita P2

1Post Graduate student, Department of Physiology, B.J.Medical College, Ahmedabad, Gujarat, India.

2Former Graduate student, Govt. Dental College & Hospital, Ahmedabad, Gujarat, India

*Corresponding Author email: [email protected]

ABSTRACT

Context: The present study evaluated oral hygiene & anomalies of tooth formation and eruption in

adolescents. This was a cross-sectional study, with the primary data was collected from two different

schools in Ahmedabad, Gujarat, India. Aims: Aim of the study was to evaluate oral health that includes

maintenance of oral hygiene and dental anomalies in adolescents of Ahmedabad city. Methods and

Material: In this study, total 500 healthy male and female subjects between 14-16 years of age were

selected for the study and examined for the oral hygiene in the form of cleaning of teeth after all meal,

flossing and regular visit to dentist for check-up. Also they were observed for dental anomalies which

were divided into three types viz. dentitional, occlusal and space anomalies. Comparison of outcomeparameters was calculated with significance test. Results: Awareness of oral hygiene was found

improper in more than half of all adolescents. Occlusal anomalies were found in 48.8% of males &

50.8% of females which were most common among all anomalies. Though all anomalies were more

prevalent in female than male subjects, dentitional anomalies were significantly more in female subject.

Conclusions: Awareness for oral hygiene in adolescent of Ahmedabad city is found to be less. Females

are even less aware than male. Malocclusion is the most common anomaly. All anomalies are more

common in females.

Keywords: Oral hygiene, Anomaly, Mal-occlusion

INTRODUCTION

Oral hygiene is the practice of keeping the mouth

clean and healthy by brushing and flossing to

prevent the build-up of plaque, the sticky film of

bacteria and food that forms on the teeth. Plaque

adheres to the crevices and fissures of the teeth

and generates acids that, when not removed on a

regular basis, slowly eat away, or decay, the

protective enamel surface of the teeth, causing

holes (cavities) to form.1,2 The primary and

permanent dentitions are subject to considerable

variations in the number, size and form of teeth

and the structure of the dental tissue. These

developmental anomalies may be genetically

determined or brought about by environmentally

induced systemic or local changes or possibly by

combination of these factors. One of the

etiological factor of malocclusion is the dental

anomalies.3,4

Malocclusion is classified into three

main groups (1) Dentitional anomalies -

anomalies restricted to individual teeth

DOI:10.5958/j.2319-5886.2.4.149



932


(2) Occlusion anomalies - anomalies in the

positional relationship between the dental arches,

and (3) Space anomalies.5,6

The present study

was planned out to assess oral hygiene and the

anomalies of tooth formation and eruption in

males and female of age group of 14-16 years

and to compare these anomalies in both sexes.

SUBJECTS AND METHODS

This study was carried out in two different

schools in Ahmedabad City in India.

All procedures followed were in accordance with

the ethical standards of experimentation and with

the Helsinki Declaration of 1975, as revised in

2000.7

Selection of study participant was done

randomly. Prior permission from the authority of

each school was obtained. Total number of 250

boys and 250 girls between 14 to 16 years of age.

Inclusion criteria: In whom permanent teeth

except third molar tooth be fully erupted and are

not undergone orthodontic appliance therapy,

irrespective of simultaneous extractions were

selected for dental examination. Written consent

was obtained and data collection forms were

distributed.Then personal and family history that includes

frequency of brush and floss in a day, frequency

of visit to dentist for regular dental check-up etc.

was recorded. The boys and girls were examined

in the premises of the school during health camp.

Intra-Oral Examination:

Soft tissue: The condition of oral mucosa is

good indicator of general health. Examination of

mucosa of palate, tongue and cheeks for

inflammation, any swelling, white or red patches,

ulcers etc was done.

Periodontal tissue: Examination of periodontal

pocketing, oral hygiene, tooth mobility was done.

Teeth: The teeth present were counted and

recorded in full dental charting. The

supernumerary or missing teeth were looked for.

If any missing or supernumerary tooth was found

its location was noted. After counting teeth, oral

cavity was observed crowded teeth and their

location was noted. Oral cavity was searched for

the spacing of teeth, and if present, it was noted

whether they were in upper or lower arch. The

size and shape of the crown of teeth were

inspected. Tooth size was diagnosed as

anomalous when the norms for the sex and racial

group concerned were exceeded. The teeth were

inspected for discoloration, after taking the

history and grouped under intrinsic/extrinsic

discoloration.

Occlusion8: Inspecting the distance between the

upper and Lower incisors in the horizontal plane

identified the over jet. The Maxillary or

mandible over jet and distal medial molar

occlusions were looked for. The overbite was

identified inspecting vertical overlap of the upper

and lower incisors when viewed interiorly, The

overbite which was greater than one half was

described as being increased, and was noted asoverbite, The over bite which was less than one

third, was described as being reduced. Open bite

was identified by space vertically between the

incisors when the buckle segment teeth were in

occlusion. Cross bite was identified by buccal

cusps of the lower premolars and/or molars

occluded buccal cusp of the upper premolars

and/or molars. Scissor bite were identified by

buccal cusps of the lower Premolars and/or

molars occluded lingual to the lingual cusps of

the upper premolars or molars.5

Data was

analyzed using Graphpad prism (6.0.3) software.

RESULTS

Table 1: Number of visits to dentist for regular dental check-up

Male subject Female subject

Number Percentage % Number Percentage %

No any visit in a year 169 67.6 195 78

<3 visits in a year 55 22 46 18.43 or more visits in a year 26 10.4 9 3.6

Total 250 250



933


Table 2 : Different anomalies found in Male and Female subjects.

Anomalies Male Female P value

Number % Number %

Dentitional anomalies 83 33.2 103 41.2 < 0.05*

Occlusal anomalies 122 48.8 128 50.8 > 0.05

Space anomalies 108 43.2 112 44.8 > 0.05*Significant

Awareness of oral hygiene is less in females.

Occlusal anomalies are more predominant among

all anomalies. All anomalies are more prevalent

in females. Dentitional anomalies are

significantly more in females

DISCUSSION

Maintaining oral hygiene should be a lifelonghabit. With proper brushing and flossing, oral

hygiene may be maintained and oral health

problems may be avoided. Regular oral care

preserves speech and eating functions, thus

prolonging the quality of life. Variations of teeth

have been an enduring interest to a clinical

practitioner. No two teeth are alike. It is the odd,

peculiar, and stranger arrangement of teeth on

which we focus our attention here. They are

called anomalies. The primary and permanent

dentitions are subjected to considerable

variations in the number, size, and form of teeth

and the structure of dental tissue. These

developmental anomalies may be genetically

determined or systematic, prenatal, postnatal

environmental and may be due to local causes.3

The anomalies may be symmetrical or

asymmetrical and indifferent degrees of severity.

Variation in the morphology, number, time andorder of eruption of the teeth are important

etiologic factors in the establishment of

malocclusion.9

The prevalence of dental

anomalies observed in deciduous dentition is

lower than in the mixed and permanent

dentitions. Probably in part due to the fact that

many conditions do not develop or become

clearly apparent before the age of 7 to 8 years or

even later.3,9

This study suggested a fact that

recognition of dental anomalies is essential in

determining appropriate treatment for each

patient. Early diagnosis and timely intervention

could reduce or eliminate the need for

orthodontic treatment and prevent serious

complications. It also determines the type,

prevalence and relative severity of the condition

in the population. This study gives the health

authorities positive information concerning the

need for and the progress of dental health

programs. Malocclusion is variation from ideal

occlusion, which has a dental health and / or

psychosocial implications for an individual.9,10

It

is a condition where teeth do not erupt in normal

position causing unsightly appearance.11,12

An

epidemiological study done by Sven Helm

(1968)5

in Danish children showed that the

frequency of dentitional anomalies in males was

33.5% and 42.2% females. In the present study

the figure for males was 33.2% and for females41.2%.The results are almost matching. The

occlusion anomalies that recorded by Sven Helm

were present in 50.1% males and 50.4% in

females. In the present study it was present in

48.8% of males and 50.8% females. According

to Helm the space anomalies were present in

47.1% males and 47.4% in females.

CONCLUSION

From present study it may be concluded that

awareness of oral hygiene in adolescents needs to

be increased through health check up camps and

electronic media to decrease overall burden on

their pockets in future. Occlusal anomaly is the

most common anomaly in both sex while

dentitional anomalies are signifcantly more

common in females. Though this is pilot study,

there is requiring more detail research in

response to larger sample size and statistical

analysis in India.



934


ACKNOWLEDGEMENT

We would like to thank Principals of both

schools who have given permission to arrange

health check-up camp in their schools, and also

to all students who have actively participated in

our study.

REFERENCES

1. American Dental Association. 211 E.

Chicago Ave., Chicago, IL 60611. (312) 440-

2500. http://www.ada.org

2. American Dental Hygienists' Association.

444 North Michigan Ave., Chicago, IL

60611. (800) 847-6718.

3. Winter GB. Anomalies of tooth formation

and eruption, Paediatric denstistry. Oxford

University Press 1997:1st

ed,;251-270.

4. Buschang PH, Thrackmork GS. Does

malocclusion affect masticatory performance.

Angle orthod. 2002:72(1): 21 – 27.

5. Sven H. Malocclusion in Danish children

with adolescent dentition. An epidemiologic

study. Am. J. Orthodontics 1968 , volume 54

Number 5, 40-476. Seipal CM. Variation of tooth position,

Svensktabdl-hdskr, 1946;39.:50-57.

7. Declaration of Helsinki. http://www.who.int

/bulletin/archives/79(4)373.pdf

8. Riolo and Avery. Essentials for Orthodontic

practice. First edition: Chapter 6: 163-178

9. Laury M. Cross bite, An introduction to

orthodontics, Oxford University Press Inc.

New York: 1996: First Edition 130-137.10. Mills LF. 1455 School children in dental

arech. Dimensions Expressed on the basis of

tooth eruption as a measure of biologic age.

J. D. Res. 1965;44 : 120-141,

11. Munblatt MA. A statistical study of dental

occlusion in children. Dental Items of

Interest. 1943:65 : 43-63.

12. Miyosh S, Tanaka S, Kunimatsu H.: An

epidemiological study of supernumerary

primary teeth in Japanese children. A review

of racial differences in the prevalence. Oral

Dis 2000: 6 (2): 92-102.



935

Manikanta Reddy. V et al., Int J Med Res Health Sci. 2013; 2(4):935-940


&

Health Sciences

www.ijmrhs.comVolume 2 Issue 4 Oct-Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886Received: 27



thSep 2013

Research article

PREVALENCE AND PATTERN OF ABNORMALITIES OCCURRING IN PLACENTA AND

UMBILICAL CORD

*Manikanta Reddy. V1, Senthil Kumar. S

1, Sanjeeva Reddy. N

2

1Department of Anatomy,

2Department of Reproductive Medicine, Sri Ramachandra Medical College

and Research Institute, Chennai, Tamilnadu, India


ABSTRACT

A hospital based cross sectional study has been conducted in 975 cases to evaluate the prevalence and

pattern of Placental and Umbilical cord abnormalities. All the Placentas with Umbilical cords were

examined for different abnormalities immediately after delivery. Out of 975 specimens, a total of 262

(26.87%) were identified to have various types of abnormalities. Of which, 232 (23.79%) specimens

showed single abnormalities and the remaining 30 (3.07%) specimens were with multiple abnormalities

(more than one abnormalities in each specimen). Prevalence of most of the abnormalities in the presentstudy is in co ordinance with previous studies and all the abnormalities are distributed among the

specimens in two different forms i.e. specimens with any single abnormally and specimens with multiple

abnormalities.

Keywords: Placental abnormalities, Umbilical Cord abnormalities, IUGR, Circumvallate, Velamentous,

Battledore Placenta

INTRODUCTION

The Placenta and Umbilical cord plays an

efficient role alongside maternal health condition

and genetics of the parents in controlling the

growth and health of the developing fetus by

holding nutritive, respiratory, endocrine,

immunological and excretory functions. Any

abnormality in the Placenta and Umbilical cord

may lead to the impairment of the fetal growth

and health by disturbing the fore said functions.

The literature review of Placenta and Umbilical

cord abnormalities suggests its strong associationwith different conditions of the fetus like IUGR,

Pre Term delivery, IUD, Fetal Anomalies and so

on1.

In such condition, we felt the necessity of

knowledge on the prevalence and pattern of

abnormalities among Placenta and Umbilical

cord, which will reinforce the prenatal care by

health providers in addressing the adverse

outcome caused by these abnormalities.

The current study has been designed to estimate

the prevalence and pattern of different

abnormalities occurring in Placenta andUmbilical cord, to address the wide variations

regarding, in the existing literature.

DOI:10.5958/j.2319-5886.2.4.150



936



A hospital based cross sectional study was

conducted in the Department of Obstetrics and

Gynaecology, Sri Ramachandra Medical College

and Research Institute, Chennai, over a period of

15 months (April 2012 – June 2013).

Institutional Ethical Committee (IEC) approval

has been acquired for the study. A total of 975

patients, who met with selection criteria were

enrolled in the study after their written Informed

Consent.

Selection Criteria: All the pregnancies of > 32

weeks of Gestational Age onwards. Specimens

(Placenta with Umbilical Cord) were collected

immediately after the delivery. Chorioamniotic

Membranes were examined for the Blood

Vessels or any Placental masses. Then, all the

Placental discs were examined for the insertion

of Chorioamniotic Membranes, Umbilical Cord

Insertion and extra lobes. Then the Umbilical

Cord length (i.e. length of the Cord with Placentaand Baby) has been measured with an Inch Tape.

All the Umbilical Cords were checked for the

presence of Knots and Coiling. Finally Umbilical

Cords were severed transversely at its Placental

end and examined for the presence of Wharton’s

Jelly and number of Umbilical Vessels.

DATA were recorded and analyzed. Specimens

with abnormalities were photographed.

RESULTS

Table 1: Placental and Umbilical cord abnormalities

Type of abnormality

Number of

abnormalities

(292)

Percentage (%)

in 975 cases

(29.74%)

Percentage (%) of each

abnormality among total

abnormalities (In 292

Abnormalities)

PLACENTAL [82 (8.41%)]

Bilobed 11 1.12 3.76

Accessory lobe 19 1.96 6.5

Placenta extrachorialisCircumvallate

Circumvallate Complete 12 1.23 4.1

Circumvallate Partial 13 1.33 4.45

Circummarginate

Circummarginate

Complete

13 1.33 4.45

Circummarginate Partial 14 1.43 4.79

UMBILICAL CORD [210 (21.53%)

Marginal 72 7.4 24.65

Velamentous 9 0.9 3.08

Furcate 7 0.7 2.39

Single Umbilical Artery 7 0.7 2.39

False Knots 42 4.3 14.38

True Knots 2 0.2 0.68

Uncoiled Cords 18 1.84 6.16

Absent Jelly 7 0.7 2.39

Short Cords (≤ 35cm) 24 2.46 8.21

Long Cords (≥75cm) 22 2.25 7.53





938


Fig 5a: True Knot

Fig 5b: False Knot

Fig 6: Circumvallate Placenta Arrows showing the

circumvallation

Fig 7: Circumvallate with Marginal Insertion Upper

and Lower

(Arrows showing the Circumvallation middle arrowshowing the Marginal Insertion of Umbilical Cord)

Out of 975 specimens, a total of 262 (26.87%)

were with different abnormalities, among 262

specimens with abnormalities, 232 (23.79%)

showed single abnormalities and 30 (3.07%)

specimen [Table 2] were with multiple

abnormalities (two abnormalities in each

specimen).

In the total 292 abnormalities 82 (8.41%) werePlacental and 210 (21.53%) were Umbilical Cord

abnormalities.

DISCUSSION

Most of the Placental and Umbilical cord

abnormalities are quoted to have an association

with IUGR, IUD, Low Birth Weight, Small for

Gestational Age, Pre Term delivery, Congenital

anomalies and so on1

.In the review of literature, Placenta Previa,

Abruptio placentae, Cord prolapse,

Malignancies, Tumors and pathology of Placenta

and Umbilical cord also included under the

heading of abnormalities2. We have omitted the

above conditions in the current study by adding

only developmentally malformed conditions

under the heading – Abnormalities.

In our study all the abnormalities (29.7%) are

classified into two categories:

1. By affected organ wise:

a. Placental abnormalities

b. Umbilical cord abnormalities

2. Considering the number of abnormalities

in each specimen:

a. Specimens with any single

abnormality

b. Specimens with multiple

abnormalities

We have not compared Placental and Umbilical

cord abnormalities as a whole with existing

literature as the reason mentioned earlier that

Placental and Cord pathology also included

under the heading - abnormalities. Instead, we

compared the individual abnormalities of

Placenta and Umbilical cord in the subsequent

text.

Different types1

of Umbilical cord abnormalitiesare as follows, Short cords (<35 cm), Long Cords



939


(>75 cm), 2 Vessels cords, Multi Vessels cords,

Straight cords (Uncoiled cords), Hypo & Hyper

coiled cords, Cords without Wharton’s Jelly,

Velamentous, Marginal/Battledore Placenta and

Furcate cords. Among these, we have excluded

Hypo and Hyper coiled cords as there was much

fluctuation in the number of coils with time,

postnatally.Different types of Umbilical cord abnormalities

observed in our study are Marginal (Fig. 1),

Velamentous (Fig. 2), Furcate cords (Fig. 3),

Single Umbilical Artery (Fig. 4), True Knots

(Fig. 5a) and False Knots (5b) occurred in

7.38%, 0.92%, 0.71%, 0.71%, 0.20% and 4.3%

rates respectively.

Michale K Fritsch3

and Cunningham et al4

mentioned the prevalence of Marginal cord as7%, which is coinciding with our study.

Jason H Collins et al5

quoted the prevalence of

Velamentous as 0.5 – 2.7%, Furcate as 0.5 – 1%.

Jason H Collins et al5, Michale K Fritsch

3and

Fernando Heredia et al6

stated the prevalence of

Umbilical cords with Single Umbilical Artery as

0.2 – 2%. Whereas True Knots occurs in the rate

of 0.3 – 2.1%1,7, 8

The present study showed Uncoiled, Long and

Short cords in 1.84%, 2.25% and 2.46%. But

Jason H Collins et al3

placed the occurrence of

Uncoiled cords at 4.3% and 5%, Michale K

Fritsch5, BalkawadaNileshUnmesh et al

9found

the prevalence of Long and Short cords in 5 -

5.3% and 5.9% respectively. Jason H Collins, et

al1

mentioned the prevalence of Short cords at

3%.

Among the 8.41% of Placental abnormalities in

our study, Bilobed (Placenta Bilobata) were1.28%, Accessory lobes (Placenta Succenturiata)

were 1.96% and Placenta Extrachorialis with

5.33% of prevalence. Placenta Succenturiara

have been classified into Complete and Partial

Circumvallate (Fig. 6) (occurred in 1.22% and

1.33%) and Complete & Partial

Circummarginate (occurred in 1.33% and 1.43%)

placenta. Michale K Fritsch3

quoted the

occurrence of Bilobed Placenta at 2 - 8%.

Whereas Michale K Fritsch3

and Joan M.

Mastrobattista et al10

stated the prevalence of

Accessory lobe as 5 - 6%, which are not in

correlation with the present study.

Michale K Fritsch3

mentioned the prevalence of

Complete and Partial Circumvallate Placenta in

co -ordinance with our study as 1 - 5% but his

finding of Circummarginate Placenta as 25% are

not in correlation with the present study. Robert

D. Harris et al11 found the rate of occurrence of Complete Circumvallate Placenta at 2% and

Partial Circumvallate at 19%, in line with present

study findings.

Prevelance of Circummarginate is poorly quoted

in the literature. In the available literature it has

been coined as 25% [Michale K Fritsch3] which

is far high from the present finding.

Nevertheless in the literature, we encountered

specimens with multiple abnormalities in 3.07%of cases. All these specimens (Table. 2) showed

the combination of two different abnormalities in

each. According to the author’s opinion, the

degree of impairment of blood supply to the

developing fetus or impairment of the fetal heath

will be higher in this kind of cases.

Among all the abnormalities Umbilical cord

abnormalities occurred in higher rate (71.9%), in

which Marginal Insertion/Battledore cords were

predominant (24.65%). In Placental

abnormalities, Partial Circummarginate Placentas

(4.79%) occurred in higher rate. Amides

specimens with multiple abnormalities

combination of Marginal with Short cords

(23.33%) were predominant.

The limitation of this study is that it is a hospital

based study and further research on evaluating

the outcome in above abnormalities, with high

sample is recommended.

CONCLUSION

The prevalence of Placental and Umbilical cord

abnormalities in the present study is in line with

earlier studies.

Umbilical cord abnormalities are more

predominant (71.9%) among the Placental and

Cord abnormalities. Occurrence of Marginal

cords/Battledore cords (24.65%) is more among

Umbilical cord abnormalities. Similarly

prevalence of Partial Circummarginate placentas



940


(4.79%) is higher among Placental abnormalities

(28.1%).

Specimens with multiple abnormalities were

found in 3.07%, which has not been reported in

the literature to the best of our knowledge.

The frequency of occurring Marginal with Short

cords (23.33%) is high among the specimens

with multiple abnormalities.

ACKNOWLEDGEMENT

I wish to thank INSPIRE division, Department of

Science and Technology for funding, All the

subjects of our study, Dr. S. MelaniRajendran

(Professor of Anatomy, Madha Dental College),

Dr. V. Sankar (Head, Department of Anatomy,

PGIBMS), Dr. Rameshkumar Subramanian

(Head, Department of Anatomy), Dr. PushpaLatha Barua (Professor of Obstetrics and

Gynaecology, Sri Ramachandra University) for

their support.

Conflict of interest: None declared

REFERENCES

1. Jason H Collins, Charles L. Collins, Candace

C. Collins. (2010). Umbilical cord Accidents.

Available From: http://www.preginst.com/ UmbilicalCordAccidents2.pdf .

2. Bettye Wilson. Sonography of the Placenta

and Umbilical cord. Radiologic Technology.

2008; 79(4): 333 – 45.

3. Michale K Fritsch. Placental Pathology.

Available From: http://pathology.bsd.

uchicago.edu/PedsPath/2012/Files/handouts/

Placental%20Pathology-Fritsch%202012.pdf.

4. Cunningham, Levono, Bloom, Rouse,

Sponge. Abnormalities of Placenta,

Umbilical cord, Membranes. In:

Cunningham, Leveno, Bloom, Hauth, Rouse,

Spomg. (23ed). Williams Obstetrics.

McGraw Hill, New Delhi. 2010: P 577 – 587.

5. Jason HC, Charles LC, Candace CC. Silent

Risk. Issues about Human Umbilical cord.

Available From: http://www.preginst.com/

silentrisk.pdf

6. Fernando Heredia, Philippee Jeanty.

Umbilical cord Anomalies (2002). Available

From: http://sonoworld.com/fetus/page.aspx

?id=1149

7. Alain Goriely. Knotted Umbilical cords.

Available From: http://math.arizona.

edu/~goriely/Papers/2005-knotbook

(umbilical).pdf 8. Spellacy WN, Graven H, Fish RO. The

Umbilical cord Complications of True Knots,

Nucal coils, Cords around the Boby, Am J

Obstet Gynaecol.1966; 94(8): 1136 – 42.

9. Balkawade NU, Shinde MA. Study of Length

of Umbilical cord and Fetal outcome: A

Study of 1,000 of 1000 Deliveries. The

Journal of Obstetrics and Gynaecology of

India.2012; 62(5): 520 – 25.10. Joan M. Mastrobattista, Eugene CT.

Placenta, Cord and membranes. In: Arthor C.

Fleischer, Eugene C. Toy, Wesley Lee. (7ed).

Sonography in Obstetrics and Gynaecology.

McGraw Hill, New Delhi. 2011:155 – 84.

11. Rodert D. Harris, Wendy A. Wells, William

C. Black, Jocelyn D. Chertoff, Steven C.

Poplack, Steven K. Sargent, Harte C. Crow.

Accuracy of Prenatal Sonography for

Detecting Circumvallate Placenta. American

Journal of Radiology.1997: 168: 1603-08.



941

Baradol etal., Int J Med Res Health Sci. 2013;2(4):941-948


&

Health Sciences




thSep 2013

Research article

HYPERTENSION AS AN EMERGING HEALTH PROBLEM AMONGST SCHOOL

CHILDREN AND ADOLESCENTS

*Ravikumar V Baradol1, Anand Ranagol

2, Patil SV

3

1Asst Professor,

2Asst Professor,

3Professor & Head, Dept. of Pediatrics, BLDEU’S S. B. M. Patil

Medical College, Bijapur, Karnataka, India


ABSTRACT

Introduction: Hypertension is a common non communicable disease in developed countries. But

nowadays even in developing countries like India its prevalence is increasing in adults as well as in

childhood population. Objective: To find out the prevalence of Pre hypertension and Hypertension

amongst school children and adolescents. Study Design: Randomised, Cross-sectional, observational

multicentric School based study. Methodology: In this study 3 schools were selected by simple random

sampling method from Urban and rural region of Bijapur district which is a part of North Karnataka.Total 2800 children were screened in the age group from 10-16 years. General data and Blood pressure

were recorded for each child. Blood pressure values are compared with reference charts given by

National High Blood Pressure Education Programme working group of American heart association 2004

and grouped as prehypertensive (PHTN) and Hypertension (HTN). Results: In Rural school children,

Prevalence of systolic PHTN was 2.2% and prevalence of systolic HTN was 1.8%. Among urban school

children prevalence of systolic PHTN was 3.92% and prevalence of systolic HTN was 3.79%.

Prevalence Diastolic PHTN in rural school children was 2% and that of Diastolic HTN was 1.5%. In

case of urban school children, the prevalence of Diastolic PHTN was 4.28% and that of Diastolic HTN

was 3.86%. In our study the prevalence of hypertension in males was more than female in both rural &urban school children. Also the prevalence of HT was more in urban than in rural population.

Conclusions: Prevalence of hypertension in school children is increasing even in developing countries.

In feature to prevent morbidities, early intervention strategies for promoting healthy eating, physical

activities and health education should be undertaken from school age group. This primordial prevention

should be considered as an important public health issue in our developing country.

Keywords: Prehypertension, Hypertension, North Karnataka, Primordial prevention.

INTRODUCTION

Hypertension is of importance mainly as a risk

factor for cardiovascular and cerebrovascular

disease. High blood pressure in the adult

population has been shown to relate to the risk of

stroke, renal disease and occlusive

atherosclerotic vascular disease.1

Efforts have

DOI:10.5958/j.2319-5886.2.4.151



942


been made to reduce the blood pressure level

than to prevent their development.

Although it is obviously better to prevent than to

cure a disease, it is only recent years that interest

has been focused on primary prevention of high

blood pressure. Efforts should be made toprevent the development of hypertension during

childhood only. This primordial prevention is of

utmost important thing that should be considered

in developed as well as in developing countries.

Systemic hypertension is an important condition

in childhood, with estimated population

prevalence of 1-2% in the developed countries.2

Data is lacking from India; small surveys in

school children suggest a prevalence rangingfrom 5-10 %.

3, 4

In the recent years numbers of studies of blood

pressure have appeared for the most part these

studies have attempted to establish value of

blood pressure measurement for the purpose

clinical diagnosis. Comparatively few studies

have considered blood pressure and its relation to

the increasing age or adolescent period and

etiology and incidence of hypertension in this

age group.5-7

So we carried out the study to find out the

prevalence of hypertension amongst school

children and adolescents in north Karnataka. The

findings of this study will be useful for initiation

of primordial prevention in this developing part

of India.

MATERIALS & METHODOLOGY

It was a Randomised, Cross-sectional,multicentric study done in school children of the

age group of 10 to 16 years during 9 months of

study duration. 1400 Children were selected from

rural areas and 1400 children of same age groups

from the urban areas in and around Bijapur City

which is part of North Karnataka. Out of 10

affluent schools in Bijapur City and rural areas, 3

schools were selected based on simple random

sampling method. The total sample size was2800. Exclusion criteria: Children with Renal

diseases, acute illness, systemic diseases,

students who are unwilling, children who are

known hypertensives and who are on

antihypertensive medication and children taking

medications which can modify blood pressure

measurement were excluded from the study.

Before initiation of the study, the study protocolcontaining proforma was approved by

Institutional Ethics Committee. Data was

collected in a pretested proforma meeting the

objective of the study. Informed consent was

taken from the parents of all children, Head of

the Institution before examining school children.

The importance of the study was explained to the

school management, staff and teachers. The age

of the school children was obtained from theschool records. The name and other particulars

were entered in a pretested proforma.

Blood pressure was measured in all 10 to 16

years school children between 8AM to 11AM in

sitting position after 10 minutes of rest as per

American Heart Association Guidelines.8

Systolic blood pressure was determined as

appearance of 1st

Korotkoff sounds and diastolic

blood pressure was taken at the point of muffling

of heart sounds (4th Korotkoff sounds). Three

measurements were taken at an interval of five

minutes each and mean of these readings were

taken as average systolic blood pressure and

average diastolic blood pressure. Blood pressure

values were compared to the values given by the

update of 1987 task force report of the National

high blood pressure Education Programme Co-

ordinating Committee9. Children were classified

into three groups as follows:9

• BP < 90th

percentile - Normal (N) Blood

pressure (compared to age, sex and height

percentile in each age group)

• BP = 90 - 95th

percentile - Prehypertension

(PHTN)

• BP > 95th

percentile - Hypertension (HTN)

In those children whose systolic and or diastolic

BP value was found to be more than 95th

percentile for age, sex and height, two sets of BPreading were taken at an interval of 4 weeks. If

systolic and or diastolic BP was found to be



943


persistently more than 95th

percentile for age,

sex, and height then child was classified as

having sustained hypertension. Those children

who had sustained hypertension were subjected

to further investigations with informed parental

consent. Investigations were done after takingconsent from the parents in a format, after

explaining the parents about the need for

investigations and treatment aspects. Following

investigations were done: Lipid profile, Blood

Urea/serum creatinine, Urine albumin, urine

sugar, urine microscopy, USG of abdomen.

Statistical analysis: Data were analyzed for

prevalence rate & Frequency distribution. All the

statistical operations were done through SPSS

(Statistical Presentation System Software) for

Windows, version 10.0 (SPSS, 1999. SPSS Inc:

New York). A value of P < 0.05 was considered

as statistically significant.

RESULTS

In the present study total 2800 students were

screened. Out of these 1400 were Rural & 1400

were urban school children. Out of 2800, 1514

were male children and 1286 were female

children. In male children, 731 students were

from rural school and 783 students were from

urban school. Also, in case of female students

669 students were from rural school, while 617

students were from urban school.

Table 1: Prevalence of Systolic Hypertension in Rural & Urban Children according to age*.

Age

(years)

Rural school children Urban school children

Normal PHTN HTN Total Normal PHT HT Total

10 407 2 1 410 338 2 2 342

11 219 1 1 221 292 4 4 300

12 128 4 2 134 222 4 7 233

13 124 6 5 135 111 9 13 133

14 198 8 8 214 89 11 9 109

15 182 4 4 190 156 9 7 17216 85 6 5 96 84 16 11 111

Total 1343 31 26 1400 1292 55 53 1400

(*All values are in absolute numbers) PTHN: Prehypertension, HTN: Hypertension

Table 2: Prevalence of Systolic Hypertension in Rural & Urban Children according to sex (*)

SexRural school children Urban school children

Normal PHTN HTN Total Normal PHTN HTN Total

Male 697 19 15 731 717 33 33 783

Female 646 12 11 669 575 22 20 617

Total 1343 31 26 1400 1292 55 53 1400


Table 3: Prevalence of diastolic hypertension in Rural & Urban Children according to age (*)

Age

(years)

Rural school children Urban school children

Normal PHTN HTN Total Normal PHT HT Total

10 408 1 1 410 335 4 3 342

11 215 4 2 221 295 3 2 300

12 131 2 1 134 222 5 6 233

13 126 4 5 135 103 8 12 133

14 208 5 3 214 87 12 10 109

15 178 6 6 190 154 10 8 172

16 88 5 3 96 80 18 13 111

Total 1353 27 20 1400 1286 60 54 1400




Baradol etal.,

Table 4: Prevalence of diastolic hy

Sex Ru

Normal

Male 703

Female 650

Total 1353

(*All values are in absol

Fig1: Prevalence of Systolic Hyper

Fig 2: Prevalence of systolic hyper

As shown in Table no. 1, Preval

prehypertension (PHTN) wa

prevalence of systolic hypertens

1.8% in rural school childrenobserved that, systolic BP incre

99.28 99.1

0.48 0.40.24

0

10

20

30

40

50

60

70

80

90

100

10 11

p r e v a

l e n c e ( i n % )

98.83 97.33

0.58 1.34

0.58 1.

0

10

20

30

40

50

60

70

80

90

100

10 11

p r e v a l e n c e ( i n % )

Int J Med Res Heal

pertension in Rural & Urban Children accord

ral school children Urban schoo

PHTN HTN Total Normal PHTN

17 11 731 716 36 3

10 9 669 570 24 2

27 20 1400 1286 60 5

ute numbers)

tension in Rural School Children according to

tension in urban school children according to

ence of systolic

s 2.2% and

ion (HTN) was

. It was also ses with age in

both male & female.

hypertensive and preh

above 13 years of age.

% prevalence of systgroup.

95.5291.12 92.42 95.8

2.98 4.44 3.74

2.10.45 1.5

4.44 3.74 2.1

12 13 14 15

Age groups (in yrs)

95.28

83.46 81.65

90.7

1.72

6.76 10.195.23

.33 3

9.78 8.26

4.0

12 13 14 15Age Groups (in yrs)

944

th Sci. 2013;2(4):941-948

ing to sex (*)

l children

TN Total

1 783

3 617

4 1400

age.

ge.

lso, maximum number of

ypertensive were seen in

Figure no.1 describes the

lic hypertension in each

87.5

6.256.2

16

Normal

PHTN

HTN

75.68

14.419.91

16

Normal

PHTN

HTN



945


Among rural school children, it was found that

Prevalence of systolic prehypertension in males

was 2.6% compared to 1.79% in females. The

prevalence of hypertension in males was 2.05%,

while in females it was 1.64%.

Among urban school children, prevalence of systolic PHTN was 3.92% and prevalence of

systolic HTN was 3.79%. As compared to rural,

the prevalence of prehypertension and

hypertension was more in urban population in all

age groups. The maximum numbers of

hypertensive were found in 16 years of age

group. (As shown in table no. 1 & figure no.2)

It was observed in our study that, the prevalence

of Systolic hypertension was predominantly seenin males (4.21%) compared to females (3.24%)

in Urban school children. Also, the prevalence of

systolic prehypertension was more in males

(4.21%) as compared to females (3.56%).

In case of diastolic BP measurement, Prevalence

of Diastolic PHTN in rural school children was 2

% and that of Diastolic HTN was 1.5%. It was

also observed that, diastolic BP increases with

age in both male & female. Also, maximum

number of diastolic hypertensive and

prehypertensive were seen in above 13 years of

age.

When the difference between the prevalence

rates of different sex was examined, it was found

that the male prevalence of diastolic

hypertension was 1.5% as compared to 1.34% in

female.

In case of urban school children, the prevalence

of Diastolic PHTN was 4.28 % and that of Diastolic HTN was 3.86 %. The maximum

numbers of prehypertensive and hypertensive

were found in 16 years of age group.

In the urban school children, the prevalence of

diastolic PHTN in male was 4.6% while the

prevalence of HTN was 3.96%. In female, the

prevalence of PHTN was 3.89% and the

prevalence of HTN was 3.72%.

DISCUSSION

Hypertension is a common non communicable

disease. It is also risk factor for various disorders

including cardiovascular disorders like

myocardial infarction, angina and

cerebrovascular disorders like stroke,haemorrhage etc. It is very important to diagnose

and to treat the hypertension at early stage only,

so as to decrease the morbidity and mortality

following these disorders. Therefore detection of

childhood hypertension carries utmost

importance. Population changes in health-related

behaviours, including the childhood obesity

epidemic, indicate that the rates of hypertension

in the young are increasing.

1

Although theprevalence of HT is less common in children

than in adults,10, 11

there are studies which had

proven that the origin of essential HT start

childhood.11-15

But studies indicative of current

status of hypertension in north Karnataka are not

available in literature. Therefore, we decided to

undertake the present study to highlight the rising

problem, hypertension in both rural and urban

area of north Karnataka.

Considerable advances have been made in

detection, evaluation, and management of high

blood pressure (BP), or hypertension, in children

and adolescents.8

The level of ‘normal’ BP varies

in different studies due to number of variables

such as the size of the rubber bladder within the

cotton cuff, type of sphygmomanometer, arm

position, whether the fourth or the fifth phase of

Korotkoff's sound is used to obtain the DBP, and

place and time of BP measurement.12-13

In thepresent study, BP was recorded by mercury

sphygmomanometer using standardized method.8, 9

In the present study, both SBP & DBP showed

increase in the value as with increase in age.

Similar findings were reported by Sharma et al15

The age-related increase in BP may be

attributable in part to increase in body mass.16

A

trend of increase in SBP and DBP with age in the

present study was observed in both sexes. An

increase in SBP and DBP with age has also been



946


reported in Indian children by other authors.17-

20Gupta et al

21, observed a spurt in SBP between

13 – 15 years in both sexes. The spurt in SBP

between 13 – 15 years is mainly related to certain

biological and psychosocial factors, and puberty

timing.22-23 In our study, we observed that therewas increase in both SBP & DBP value above 13

years of age with maximum BP at the age of 16

years. Also, there was no significant difference in

BP measurement between male & female of

same age group. The differences in BP between

males and females of same age groups are

probably related to certain biological and

psychosocial factors.16

The appearance of

secondary sex characters together with themenarche is associated with a high level of

anxiety resulting in higher SBP values in girls.

However, there are no appreciable differences in

the level of the BP of children, aged 5 – 14 years,

between the two sexes.24-27

We found that, the prevalence of systolic

prehypertension (PHTN) & hypertension (HTN)

in rural school children were 2.2% and 1.8%,

respectively, while in urban area, they were

3.92% & 3.79%, respectively. The prevalence of

HT in children has been reported to vary between

0.41% to 11.7%.17, 21

The prevalence of HT in

urban population was found to be more than rural

population. The contributing factors could be

dietary habits like junk foods, lack of physical

activity, and peer pressures16

. Similar findings

were noted about diastolic HT.

But in our study has some limitations. All BP

measurements were taken by single observer.This can be a bias source. Also we did not

include factors such as physical activity, diets

and salt intake. These factors significantly affect

the BP readings. In our study, we did not studied

that among the hypertensive children, how many

of children require antihypertensive medications,

do they develop any cardiovascular disease or

other morbidity. We referred these children to

hospital with all their recorded data. Furtherresearch can be done in this aspect.

The study of childhood HT is important for

several reasons: i) sequelae of long-term HT are

irreversible and associated with significant

morbidity and mortality, ii) childhood BP is the

best predictor of adult BP. iii) helps in planning

primordial preventive strategies.16, 28-31

Therefore, this study can help to plan various

health care strategies to prevent hypertension

related comorbidities in developing countries like

India.

CONCLUSION

The findings of this study suggest that there is

increasing prevalence of hypertension both in

rural as well as in urban part. The prevalence of HT in urban children is more than rural children.

Maximum number of hypertensive and

prehypertensives are present in more than 13

years of age. So there is need of further research

in large scale to raise the issue of early childhood

hypertension to start the primordial prevention as

early as possible.

REFERENCES

1. Munter P, He J, Cutler JA, Wildman RP,

Whelton BK. Trends in blood pressure

among children and

adolescents. JAMA. 2004; 291:2107 – 13.

2. Mohan B, Kumar N, Aslam N, Rangbulla A,

Kumbkarni S, Sood NK, et al. Prevalence of

sustained hypertension and obesity in urban

and rural school going children in

Ludhiana. Indian Heart J.2004; 56:310 – 4.3. Arvind Bagga. Evaluation and management

of hypertension. Indian paediatrics.

2007;17:111-12.

4. Hari P, Bagga A, Srivatsava RN.

Hypertension in children. Indian pediatrics

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5. Sidhu S, Kaur N, Kaur R. Overweight and

obesity in affluent school children. Ann Hum

Biol 2006;33: 255-259.

6. Chhatwal J, Verma M, Rair SK. Obesity

among pre-adolescent and adolescents of a



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developing country (India). Asia Pac J Clin

Nutr 2004; 13: 231-33

7. Ross JG, Pate RR, Lohman TG, Christenson

G M. Changes in the body composition of

children.J Phys Educ Rec Dance 1987;58:74-

778. National High Blood Pressure Education

Program Working Group on High Blood

Pressure in Children and Adolescents. The

Fourth Report on the diagnosis, evaluation

and treatment of high blood pressure in

children and adolescents. Pediatrics. 2004;

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9. Update on the 1987 Task Force Report on

High Blood Pressure in Children andAdolescents: A working group report from

the National High Blood Pressure Education

Program. National High Blood Pressure

Education Program Working Group on

Hypertension Control in Children and

Adolescents. Pediatrics.1996; 98:649 – 58.

10. Bernstein D. Systemic hypertension. In:

Kliegman RM, Behrman RE, Jenson HB,

Stanton BF, editors. Nelson text book of

pediatric. 18th ed. Philadelphia: W.B.

Saunders Co. 2007;1988 – 96.

11. Rocchini AP. Childhood hypertension,

etiology, diagnosis and treatment. Pediatr

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12. Canner PL, Borhani NO, Oberman A, Cutler

J, Prineas RJ, Langford H. The hypertension

prevention trial assessment of the quality of

blood pressure measurements. Am J

Epidemiol.1991; 134:379 – 92.13. Sinaiko AR, Gomez Marin O, Prineas RJ.

Diastolic fourth and fifth phase blood

pressure in 10-15-year-old children: The

children and adolescents blood pressure

program. Am J Epidemiol.1990;132:647 – 55

14. Sarin D, Chaturvedi P. Normal blood

pressure and prevalence of hypertension in

school going children. J MGIMS. 1997;

1:32 – 5.

15. Sharma BK, Sagar S, Wahi PL, Talwar KK,

Singh S, Kumar L. Blood pressure in school

children in North-West India. Am J

Epidemiol. 1991; 134:1417 – 26.

16. Amar Taksande, Pushpa Chaturvedi, Krishna

Vilhekar, and Manish Jain; Distribution of blood pressure in school going children in

rural area of Wardha district, Maharashatra,

India; Ann Pediatr Cardiol. 2008; 1(2): 101 –

106.

17. Anand NK, Tandon, L Prevalence of

hypertension in school going children. Indian

Pediatr.1996; 33:337 – 81.

18. Badaruddoza, Afzal M. Age-specific

differences in blood pressure among inbredand non-inbred north Indian children. J

Bioscience. 1999;2:177 – 84.

19. Verma M, Chatawal J, George SM.

Biophysical profile of blood pressure in

school children. Indian Pediatr. 1995;32:749 –

54.

20. Chahar CK, Shekhawat V, Miglani N, Gupta

BD. A study of blood pressure in school

children at Bikaner. Indian J

Pediatr. 1982;49:791 – 4.

21. Gupta AK, Ahmad AJ. Normal blood

pressures and the evaluation of sustained

blood pressure elevation in childhood. Indian

Pediatr. 1990;27:33 – 42

22. Shubi MD. Blood pressure profile and

hypertension in Iraqi primary school

children. Saudi Med J.2006;27:482 – 6.

23. Nichols S, Cadogan F. Blood pressure and it's

correlates in Tobagonian Adolescents. WestIndian Med J. 2006;55:2 – 8

24. Bernstein D. Systemic hypertension. In:

Kliegman RM, Behrman RE, Jenson HB,

Stanton BF, editors. Nelson text book of

pediatric. 18th ed. Philadelphia: W.B.

Saunders Co. 2007;1988 – 96.

25. Rocchini AP. Childhood hypertension,

etiology, diagnosis and treatment. Pediatr

Clin North Am.1984;31:1259 – 73.



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26. Canner PL, Borhani NO, Oberman A, Cutler

J, Prineas RJ, Langford H., et al. The

hypertension prevention trial assessment of

the quality of blood pressure

measurements. Am J Epidemiol. 1991;134:

379 – 92.27. Sinaiko AR, Gomez Marin O, Prineas RJ.

Diastolic fourth and fifth phase blood

pressure in 10-15-year-old children: The

children and adolescents blood pressure

program. Am J Epidemiol.1990;132:647 – 55

28. Task Force 1987 on Blood Pressure control

in children: Report of the Second Task Force

on Blood Pressure Control in

Children. Pediatrics. 1987;79:1 – 25.29. Kochanek KD, Smith BL. Deaths:

Preliminary data for 2002. Natl Vital Stat

Rep. 2004; 52:1 – 47.

30. Inglfinger JR. Pediatric antecedents of adult

cardiovascular disease: Awareness and

interaction. N Engl J Med. 2004; 350:2123 –

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31. Atwood K, Colditz GA, Kawachi I. From

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Placing science in its social and political

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949

Kavitha etal., Int J Med Res Health Sci. 2013;2(4):949-954


&

Health Sciences




thSep 2013

Research article

THE EFFECT OF DIFFERENT BOUTS OF EXERCISE ON WEIGHT LOSS IN

OVERWEIGHT INDIAN FEMALE UNDERGRADUATES

*Kavitha U1, Navin Rajaratnam

2, Suzanne Maria D’cruz

3, Chandrasekhar M

2

1Department of Physiology, Sri Venkateswaraa Medical College Hospital and Research Centre, Pondicherry,

India2Department of Physiology, Meenakshi Medical College Hospital and Research Institute, Kanchipuram,

Tamilnadu, India3Department of Physiology, Sri Muthukumaran Medical College Hospital and Research Institute, Chennai,

Tamilnadu, India


ABSTRACT

Background: The prevalence of obesity is increasing globally and in India with lack of sufficient time

for continuous exercise being one of the causes. Performing multiple short bouts of exercise has been

introduced as an alternative method to reduce weight gain. Aim: To determine the effects of different

bouts of supervised exercise accumulated in 30 minutes on weight loss, in overweight Indian female

undergraduate students, without dietary restriction. Methods and Material: Sixty otherwise healthy

overweight female undergraduate medical students aged 18 to 25 years, with a body mass index (BMI)

of 25 to 29.9 kg/m2

were randomly selected and divided into four groups of 15 students each as follows:

Group I: Non-exercising group (controls); Group II: Participants performed one 30 minute bout of

exercise (1×30 =30min/day); Group III: Participants performed two 15 minute bouts of exercise (2×15

=30min/day); Group IV: Participants performed three 10 minute bouts of exercise (3×10=30min/day).

Participants performed moderate intensity exercise using a bicycle ergometer for 16 weeks and their

weight and Body Mass Index were measured before and after the exercise programs and statisticallyanalyzed. Results: There was a significant weight reduction (p<0.05) in Group II, Group III and Group

IV. Conclusion: Our study revealed that there was significant weight reduction in participants who

performed single or multiple bouts of exercise. The use of accumulated short-bouts of moderate

intensity exercise can therefore be recommended to young overweight females who have difficulty

doing a single long-bout of exercise.

Key words: Exercise; overweight; short-bouts; weight loss.

INTRODUCTION

The prevalence of obesity is increasing globally.

In their review highlighting the Asian Indian

body composition with regards to obesity,

Chopra et al concluded from different studies

DOI:10.5958/j.2319-5886.2.4.152



950


that women have higher prevalence of

overweight and obesity (15-61%) when

compared to men (12-54%) in India.1

They also

found that obesity was increasing in the youth.1

The Centers for Disease Control and Prevention

(CDC) and the American College of SportsMedicine (ACSM) has provided new physical

activity recommendations for the public, that

adults should accumulate 30 minutes of

moderate-intensity physical activity with at least

four hours interval between the bouts for 5 days

in a week.2, 3

Jakicic et al showed that short-bouts of exercise

enhance exercise adherence and may be

preferred when prescribing exercise to obeseadults.

4Schmidt et al proved that that exercise

accumulated in several short-bouts had similar

effects as one continuous bout with regard to

aerobic fitness and weight loss during caloric

restriction in overweight, young women.5

Woolf-

May K et al6

found like Ebisu7

that there was

little difference in the effect of continuous and

accumulated exercise, although their findings on

the effect on lipid profile varied. Woolf-May K

et al 8 further investigated the effects of single

and accumulated short-bouts of walking on

aerobic fitness and lipid profile. They found that

there were similar changes in aerobic fitness

among long, intermediate and short walkers and

recommended the incorporation of accumulated

bouts of moderate intensity exercise for health

promotion since it might be easier for the

individuals than single prolonged bouts.8

Murphy

et al compared the effects of short and long-boutsof brisk walking in sedentary females and found

that changes in anthropometric parameters did

not differ between short- and long-bout walkers.9

De Busk compared the effect of 30 minutes of

moderate exercise per day in 18 men with the

effect of three 10 minute bouts of exercise per

day and found that multiple short bouts of

exercise significantly increased peak oxygen

uptake.

10

Quinn et al found that an intermittent exercise

program, which is incremental in nature,

provided comparable, and in some cases greater,

health and fitness benefits than those expected

following traditional continuous exercise

training.11

Jakicic et al, in addition, investigated

the effect of combining intermittent exercise with

the use of home exercise equipment.12 Theyfound that access to home exercise equipment

facilitated the maintenance of multiple short-bout

exercise, although subjects in the short-bout

group did not experience improved long-term

weight loss when compared with the long-bout

group.12

In a randomized controlled trial

involving 21 sedentary male and 19 female

subjects, Osei-Tutu proved that while both long

bout walking and short bout walking producedsimilar and significant improvements in VO2

max, long bout walking was more effective at

reducing percent body fat.13

Darling et al proved

that intermittent bouts of moderate exercise in

young, healthy college-aged males result in the

same energy expenditure as continuous exercise

of the same intensity.14

Schmidt et al concluded

that current data appear to generally agree that

though the magnitude of benefit is unclear,

multiple short bouts of exercise per day appeared

to increase aerobic capacity and were effective in

decreasing weight.5

In view of the higher prevalence of obesity and

overweight in Indian women and the increased

prevalence among the youth; and in view of the

above studies, we decided to study the effect of

different bouts of exercise on weight loss in

overweight Indian female undergraduate

students. However, as Schmidt et al5

advised, wedecided to verify both the actual time spent and

the intensity of exercise done (as it was felt that

this would be more informative than relying on

unsupervised or self monitored exercise by the

participants), and to include a non-exercising

group also. The aim of the present study was

therefore to determine the effect of different

bouts of supervised exercise accumulated in 30

minutes on weight loss, in overweight Indianfemale undergraduate students, without dietary

restriction.



951


METHODS

This study was conducted in the Department of

Physiology of Meenakshi Medical College

Hospital and Research Institute in Kanchipuram

in South India, with the approval of theInstitutional Ethics Committee. Informed consent

was obtained from the all participants.

Sample Size: Sixty otherwise healthy overweight

female undergraduate medical students aged 18

to 25 years, with a body mass index (BMI) of 25

to 29.9 kg/m2

who satisfied the following

inclusion and exclusion criteria were selected

and divided into four groups of 15 students each

by using random sampling method.

Inclusion criteria: Female under graduate

medical students in the age group 18 to 25 years

who were overweight with a BMI of 25 to 29.9

kg/m2

who were staying in the hostel and eating

food provided from the same hostel mess.

Exclusion criteria: Students suffering from

diseases like diabetes mellitus, systemic

hypertension, heart disease, bronchial asthma or

medical problems that could influence heart rate

and/or exercise capacity were excluded from the

study. Students with history of smoking or

alcohol or nicotine intake; or current intake of

any medication; and students following regular

physical exercise or weight reduction programs

were also excluded from the study.

Screening of the participants (consisting of

detailed history including dietary history and

clinical examination) was done. The participants’

height was measured by using a calibrated, wall-mounted stadiometer while standing straight and

looking forward; weight was measured using a

weighing scale and body mass index was

calculated. Participants were randomly assigned

to the following four groups:

Group I: Non-exercising group (controls)

Group II: Participants performed one 30 minute

bout of exercise per day (1×30=30 min/day).

Group III: Participants performed two 15 minute

bouts of exercise per day (2×15 =30 min/day).

Group IV: Participants performed three 10

minute bouts of exercise per day (3×10=30

min/day).

All participants were advised to eat food

provided from the same hostel mess and not to

eat food from elsewhere. The participants’weight and body mass index were measured

before and after the 16 week period of exercise

(Group II, III and IV) and after 16 weeks in the

non-exercising group (Group I) also. Subjects

who belonged to Group II, III and IV were asked

to do moderate intensity of exercise on a bicycle

ergometer for 5 days a week for 16 weeks. The

intensity of the exercise was monitored by taking

the participant’s heart rate 10 seconds post-exercise, at the halfway point, and at the end of

each session and comparing with the resting

heart rate. The exercise was considered as

moderate exercise if the participant’s heart rate at

the end of the session increased to 50-75% of

the resting heart rate. Means and standard

deviations of age, height, weight and BMI were

calculated.

Statistical analysis: Data was analyzed by using

SPSS 17. ANOVA was used to examine

differences between the four groups and the

paired Student’s t test was used to compare the

participants’ weight and BMI before (pre-

training) and after the 16 week period (post-

training). Statistical significance was accepted at

the 5% level.

RESULTS

There was no significant difference (p>0.05) in

age, height , weight and Body Mass Index (BMI)

of participants measured at the start of the study,

in all four groups, which indicated homogeneity

between the groups in all parameters (Table 1).

Significant differences (p<0.05) were found on

comparison of the pre-training and post training

body weight and BMI (Table 2) of participants in

Group II, III and IV.



952


Table 1 - Baseline characteristics of participants in all four groups of the study

Parameter Group I Group II Group III Group IV

Age (years) 18 ± 0.98 18 ± 0.75 18 ± 0.12 18 ± 1.22

Height (cm) 158.93±3.45 158.92±2.62 158.42±5.24 157.68±5.22Weight(kg) 71.46±3.09 70.36±4.6 70.36±4.6 71.32±5.00

BMI(kg/m ) 28.40±1.08 27.34±1.22 28.76±1.02 28.91±1.03

Data presented as mean ± standard deviation

Table 2 - Comparison of the pre-training and post-training body weight of participants

Data presented as mean ± standard deviation. *Significant ( p < 0.05 ).

DISCUSSION

Our study done to determine the effects of

different bouts of supervised exercise

accumulated in 30 minutes on weight loss, in


students, without dietary restriction, revealed that

significant weight reduction occurred in

participants in Group II (who performed one 30

minute bout of exercise per day), Group III (who

performed two 15 minute bouts of exercise per

day ie. 2 × 15 = 30 min/day) and Group IV (who

performed three 10 minute bouts of exercise per

day ie. 3 × 10 = 30 min/day) over a period of 16

weeks.

Schmidt et al also found that that exercise

accumulated in several short bouts in overweight,

young women had similar effects on weight loss

as one continuous bout.5

However, their study

differed from ours in that they subjected their

participants to caloric restriction, while our

participants did not have any dietary restriction,

although uniformity in diet was maintained.Woolf-May K et al

6and Ebisu

7also found that

there was little difference in the effect of

continuous and accumulated exercise. Murphy et

al compared the effects of short- and long-bouts

of brisk walking in sedentary females and found

that changes in anthropometric parameters did

not differ between short- and long-bout walkers.9

The findings of our study differ however from

those of Osei-Tutu who found that long bout

walking was more effective at reducing percent

body fat13

and Jakicic et al who found that

subjects in the short-bout exercise group did not

experience improved long-term weight loss when

compared with the long-bout group.12

Excess post-exercise oxygen consumption

(EPOC) and exercise induced anorexia could be

the reasons for the weight reduction in Group II,

III and IV of our study. There is a possibility of

equal energy expenditure in both single and

multiple bouts of exercise. Following each bout

of exercise, the slight elevation in body

temperature directly stimulates metabolism to

increase recovery oxygen consumption.Moreover, restoration of pulmonary ventilation

and circulation and redistribution of calcium,

Groups Weight (kg) BMI (kg/m )

Pre-training Post-training Pre-training Post-training

Group I 71.46±3.09 73.63±4.82 28.4±1.68 29.02±2.33Group II 70.36±4.60 66.42±3.4* 27.34±1.22 25.95±1.00*

Group III 70.36±4.60 67.42±4.54* 28.76±1.02 27.05±1.26*

Group IV 71.32±5.00 67.69±4.6* 28.91±1.09 27.75±0.98*



953


potassium and sodium ions within muscle and

other compartments also require additional

energy.

The main effect of exercise is negative energy

balance due to both increased energy expenditure

and also decreased energy intake.14, 15, 16 Acutemoderate intensity exercise has been known to

increase the secretion of polypeptide YY (PYY),

glucagon-like peptide (GLP-1), and pancreatic

polypeptide (PP) and suppresses the hunger score

in the post exercise period.14, 18

Although it is

generally accepted that the role of exercise is

mainly to prevent weight gain,19

exercise also

causes moderate weight reduction even without

dietary restriction due to exercise inducedanorexia.

18In our study also, the weight

reduction that was achieved in the groups

performing different bouts of exercise, without

dietary restriction could be due to the exercise

induced anorexia.

In our study, as Schmidt et al5

advised, we had

verified both the actual time spent in exercising

and the intensity of exercise done by the

participants. We had included a non-exercising

group also in whom it was found that there was

an increase in weight, which however was not

statistically significant. The results of our study

therefore assume more significance. In view of

the increased prevalence of obesity in females

and the youth in India,1

it is recommended that

short-bouts of exercise accumulated in 30

minutes can be adopted by young overweight

Indian females in order to reduce their weight.

Using accumulated bouts of moderate intensityexercise has been recommended by others too,

since it is easier (than single prolonged bouts)

and since similar changes in aerobic fitness have

been found among long, intermediate and short

walkers,8

and since short-bouts of exercise also

increase the adherence to the exercise

programme.4

Limitations of this study include the

small sample size and duration of exercise;

failure to measure exact calorie intake, VO2 maxand lipid profile; and the fact that the results of

this study may not necessarily be applicable to

other age groups or even to males in the same

age group.

CONCLUSION

Our study done to determine the effects of

different bouts of supervised exercise

accumulated in 30 minutes on weight loss, in


students, without dietary restriction, revealed that

significant weight reduction occurred in

participants who performed a single bout of 30

minutes of exercise and those who performed

two 15 minute bouts of exercise or three 10

minute bouts of exercise per day over a period of

16 weeks. The use of accumulated bouts of

moderate intensity exercise can therefore be

recommended to young overweight females who

have difficulty doing a single long bout of

exercise.

REFERENCES

1. Chopra SM, Misra A, Gulati S, Gupta R.

Overweight, obesity and related non-

communicable diseases in Asian Indian girlsand women. Eur J Clin Nutr. 2013:67(7):688-

696

2. American College of Sports Medicine

Exercise prescription In ACSM’s Guidelines

for Exercise Testing and Prescription 7th Ed,

2006.

3. Report of the Surgeon General. Atlanta GA.

Centers for Disease Control and Prevention

Physical Activity and Health US Department

of Health and Human Services 1996 (S/N

017-023-00196-5)

4. Jakicic JM, Wing RR, Butler BA, Robertson

RJ. Prescribing exercise in multiple short

bouts versus one continuous bout: effects on

adherence, cardiorespiratory fitness, and

weight loss in overweight women. Int J Obes

Relat Metab Disord.1995;19(12):893-901.

5. Schmidt WD, Biwer CJ, Kalscheuer K.

Effects of long versus short bout exercise onfitness and weight loss in overweight

females. J Am Coll Nutr 2001;20:494 – 501



954


6. Woolf-May K, Kearney EM, Jones DW,

Davidson RCR, Coleman D, Bird SR. The

effect of two different 18-week walking

programmes on aerobic fitness, selected

blood lipids and factor XIIa.Journal of Sports

Sciences 1998;16(8):701-107. Ebisu T. Splitting the distance of endurance

running:on cardiovascular endurance and

blood lipids. Japanese Journal of Physical

Exercise 1985;37.

8. Woolf-May K, Kearney EM, Owen A, Jones

DW, Davison RC, Bird SR. The efficacy of

accumulated short bouts versus single daily

bouts of brisk walking in improving aerobic

fitness and blood lipid profiles. HealthEduc.Res. 1999 Dec;14(6):803-15.

9. Murphy MH, Hardman AE. Training effects

of short and long bouts of brisk walking in

sedentary women. Med.Sci.Sports Exerc.

1998;30(1):152-7.

10. DeBusk RF, Stenestrand U, Sheehan M,

Haskell WL.Training effects of long versus

short bouts of exercise in healthy subjects.

Am.J.Cardiol. 1990;65(15):1010-13.

11. Quinn TJ, Klooster JR, Kenefick RW. Two

short, daily activity bouts vs. one long bout:

are health and fitness improvements similar

over twelve and twenty-four weeks?

J.Strength Cond Res. 2006;20(1):130-35.

12. Jakicic JM, Winters C, Lang W, Wing RR.

Effects of intermittent exercise and use of

home exercise equipment on adherence,

weight loss, and fitness in overweight

women: a randomized trial. JAMA 1999;282(16):1554-60

13. Osei-Tutu KB, Campagna PD. The effects of

short- vs. long-bout exercise on mood,

VO2max, and percent body fat. Prev.Med.

2005;40(1):92-8.

14. Darling JL, Linderman JK, Laubach LL.

Energy expenditure of continuous and

intermittent exercise in college-aged males. J

Exer Physiol online 2005;8(4):1-8.15. Quinn TJ, Vroman NB, Kertzer R. Post-

exercise oxygen consumption in trained

females: effect of exercise duration. Med Sci

Sports Exerc. 1994;26(7):908-13

16. King NA, Tremblay A, Blundell JE. Effects

of exercise on appetite control: implications

for energy balance. Med Sci Sports Exerc.

1997;29(8):1076-89.17. King NA, Lluch A, Stubbs RJ, Blundell JE.

High dose exercise does not increase hunger

or energy intake in free living males.

European Journal of Clinical Nutrition

1997;51(7):478-83.

18. Martins C, Morgan LM, Bloom SR,

Robertson MD. Effects of exercise on gut

peptides, energy intake and appetite. Journal

of Endocrinology 2007;193(2):251-58.19. Katsuura G, Asakawa A, Inui A. Roles of

pancreatic polypeptide in regulation of food

intake. Peptides 2002;23:323-29.

20. Miller WC, Koceja DM, Hamilton EJ. A

meta-analysis of the past 25 years of weight

loss research using diet, exercise or diet plus

exercise intervention. International Journal of

Obesity1997; 21(10):941-47

21. Haapanen N, Miilunpalo S, Pasanen M, Oja

P, Vuori I. Association between leisure time

physical activity and 10-year body mass

change among working-aged men and

women.International Journal of Obesity1997;

21(4): 288-96.



955

Rakate etal., Int J Med Res Health Sci. 2013;2(4):955-959


&

Health Sciences




thSep 2013

Research article

COMPARATIVE STUDY OF THE DERMATOGLYPHIC PATTERNS IN TYPE II DIABETES

MELLITUS PATIENTS WITH NON DIABETICS

*Rakate NS

1, Zambare BR

2

1Tutor,

2Professor & Head, Department of Anatomy, Padmashri Dr Vitthalrao Vikhe Patil Medical

College, Ahmednagar, Maharashtra, India


ABSTRACT

Aim: To compare the differences in the finger print patterns viz., total finger ridge count (TFRC), a-b

ridge count and atd angle in patients with type II diabetes mellitus with non-diabetic as control group

Materials and methods: The study is conducted in 75 type II diabetic patients and 75 non-diabetic

persons as a control group. A sample of 51 male and 24 female patients suffering from type II diabetes

mellitus in the age group of 30 to 60 years has been examined and compared with 75 normal persons (47

males and 28 females) in the same age group to know the difference in fingerprint patterns. We havealso compared total finger ridge count, a-b ridge count and atd angle. For collection of palmar prints

‘Purvis Smith’ method has been used. Results: Increase in number of whorls, total finger ridge count, a-

b ridge count along with wider atd angle in type II diabetes mellitus patients. The result of the present

study is more or less coincides with the observations of the earlier researchers. Conclusion: This

inference may be widely applied clinically for the early diagnosis of type II diabetes mellitus mainly in a

mass screening of a population as an additional diagnostic tool.

Keywords: Type II Diabetes mellitus, Dermatoglyphic patterns, Total finger ridge count, a-b ridge

count, atd angle.

INTRODUCTION

Diabetes mellitus, or simply diabetes, is a

metabolic disorder in which a person has high

blood glucose level, either because the pancreas

does not produce enough insulin, or because cells

do not respond to the insulin that is produced.1

Type 2 Diabetes mellitus results from insulin

resistance, it is a condition in which cells fail to

utilise insulin properly, sometimes combined

with an absolute insulin deficiency.2

This form of

diabetes was previously referred to as non

insulin-dependent diabetes mellitus (NIDDM) or

"adult-onset diabetes".

Dermatoglyphics is the study of skin markings

produced by the ridges on hands and feet.

Dermatoglyphics is used as a way of measuring

gene expression determined by the early pre-

natal environment.3On each fingertip, the number

of dermal ridges (the ridge count) provides a

DOI:10.5958/j.2319-5886.2.4.153



956


measure of fingertip growth activity during the

early foetal period. These dermal ridges are

formed during gestational weeks 12 – 19, and the

resulting fingertip ridge appearance (i.e.,

Fingerprint) is fixed permanently and because of

these reasons dermatoglyphics becomes an

identification marker for Diabetes.4

According to

Henry’s6classification the dermatoglyphic

patterns can be mainly recognised in to 3 forms,

those are named as arch, whorl and loop. Arch is

the pattern in which ridges are arranged in such a

way that the delta is absent. Whorl is the pattern

in which two deltas are present and ridges are

arranged circularly from the core. The loop is

formed when the ridges pass on the same side

from where it originate, in this pattern one delta

is present along with core. The arch is again

divided in to plain arch and tented arch. The

whorl is subdivided into five types, these are

plain whorl, meet whorl, double loop whorl,

central pocket loop whorl and accidental whorl,

likewise, the loop is having two types these are

radial loop and ulnar loop.

The present study is aimed to analyse the

dermatoglyphic patterns of the patients sufferingfrom type II diabetes mellitus and compare with

a random non diabetic population. The

observations of the present study may apply

clinically in the mass screening of diabetic

mellitus patients in a random population in

addition blood glucose level.

Fig1: Dermatoglyphic patterns of finger


Sample for the present study comprises palmar

prints of 75 clinically diagnosed Type II Diabetic

patients of age group between 30-60years out of

them 51 were males and 24 were female

compared with same age group of 75 non-

diabetic persons as control the group, Out of

them 47 males and 28 females. The study was

carried out in Vikhe Patil Hospital, Ahmednagar,

Maharashtra, during the period of June 2012 to

December 2012. Informed consent was obtained

from the participants and ethical clearance was

obtained from the institutional ethics committee

prior to this study.

Exclusion criteria: Eliminated co-morbid

patients with associated cardiac, renal and other

life threatening diseases.

To collect the palmar prints black coloured

duplicating ink, rubber roller, glass, bond paper

were used. Patients were asked to wash their both

hands with soap water. Then ink was spread on

the glass with the help of roller and applied on

their hands carefully. Afterwards palmar prints

were taken on the bond paper by using ‘Purvis-

Smith method’.7

The ridges present on fingertip are counted from

core to delta for each finger. The Triradius

present below medial four fingers are nameda,b,c and d starts from index finger to little

finger, the Triradius present between thenar and

hypothenar eminence were named as t. From the

finger prints, the type of the pattern of the print,

TFRC, a-b ridge count along with atd angle were

find out, the results were recorded and

photographed.7

Fig 2: atd angle measurement.



957


RESULT

In the sample of 75 type II Diabetes Mellitus

patients, we observed an increase in the number

of whorls of both hands in males and females of

compared with control group, while the

frequency of ulnar loop was more in controlgroup than diabetic patients. It has been found

that total finger ridge count increased in diabetic

patients along with a-b ridge count and atd angle

when compared with normal population.

Average of total finger ridge count measured in

males is 74.62 in Rt hand, 73.60 in Lt hand and

in females is 72.70 in Rt hand, 74.54 in Lt hand

which is more as compared to 75 non-diabetic

population, which shows average total finger

ridge count of 67.02 on Rt hand and 69.17 on Lt

hand in males while in females Rt hand 65.71

and Lt hand 61.89. The average a-b ridge count

of diabetic patients is 36.00 on Rt hand, 37.00 on

Lt hand in males and in females it is 34.66 on Rt

hand, 35.33 on Lt hand which is more as

compare to non-diabetic males counted 34.42 on

Rt hand and 35.44 on Lt hand, in females 35.85

on Rt hand, 36.78 on Lt hand. The atd angle is

wider in diabetic patients found in males 37.98°

on Rt hand, 38.34° on Lt hand and in females

36.41° on Rt hand, 36.95° on Lt hand compared

with non-diabetic males 37.98° on Rt hand, 39°

on Lt hand and in females 36.41° on Rt hand,

36.95° on left hand.

Table 1: Fingerprint patterns in Diabetic population, Non Diabetic population (N=75)

Table 2: Ridge count and atd angle in Diabetic population, Non Diabetic population

Diabetic population Non Diabetic population

Male Female Male Female

Right

hand

Left

hand

Right

hand

Left

hand

Right

hand

Left

hand

Right

hand

Left

hand

Total finger ridge count 74.62 73.60 72.70 74.54 67.02 69.17 65.71 61.89

a-b ridge count 36 37 34.66 35.33 34.42 35.44 35.85 36.78

atd angle 37.98 39 36.41 36.95 36.19 36.40 37.14 37.75

Pattern Diabetic population Non Diabetic population

Male Female Male Female

Right

hand

Left

hand

Right

hand

Left

hand

Right

hand

Left

hand

Right

hand

Left

hand

Arch Plain 05 10 00 00 03 02 05 02

Tented arch 05 06 00 00 09 05 00 04

Total 26 00 19 11

Loop Ulnar 121 117 69 56 164 172 89 88

Radial 03 06 01 04 03 04 02 06

Total 247 130 343 185

Whorls

Plain Whorl 79 78 34 43 40 12 22 16

Meet whorl 07 02 02 00 03 03 01 00

Central pocket loop 22 24 12 14 16 10 13 12

Double loop 12 12 02 03 10 13 08 11

Accidental 01 00 00 00 00 01 00 01

Total 347 110 108 84



958


DISCUSSION

Several authors have studied the Dermatoglyphic

patterns in type II Diabetes Mellitus patients and

their findings were matching with the

observations of the present study. Sant et al8

reported an increased number of Whorls and

decreased number of ulnar loops in type II

Diabetic mellitus patients. The findings are

similar with Knussmann et al9

and Hirsch5. Barta

et al10

found higher TFRC in type II Diabetic

patients. Vadgaonkar Rajinigandha et al11

found

increase TFRC in type II Diabetic patients. Rt

hand 53.85, Lt hand 54.73 compared with control

group Rt hand 44.73, Lt hand 44.70. She also

observed wider atd angles in diabetes 52.13 in Rt

hand and 52.51 in Lt hand which was compared

with control group 43.60 in Rt hand and 44.26 in

Lt hand. Iqbal et al12

reported increased TFRC in

non-insulin dependent diabetes mellitus patients.

Sarthak Sengupta et al13

reported increased

frequency of whorls in male type II diabetic

patients. However, Banarjee et al14

Chakravartti15

found a higher frequency of loops.

CONCLUSION

The current work emphasises increased number

of whorl, decreased number of loops and arch in

type II diabetes mellitus patients along with

increased TFRC, a-b ridge count and wider atd

angle in male while in females decreased tfrc, a-b

ridge count and narrower atd angle as compared

with non-diabetic population.

AKNOWLEDGEMENT

With a deep sense of gratitude I hereby

acknowledge the support render by Principal and

Management of Dr. Vikhe Patil Medical College.

REFERENCES

1. Gardner DG, Dolores. Greenspan's basic &

clinical endocrinology. New York. McGraw-

Hill Medical. pp. 2011;9:17.

2. Diabetes mellitus type 2

http://en.wikipedia.org/wiki/Diabetes_mellitu

s_type_2

3. Ravindranath R, Joseph AM, Fluctuating

asymmetry in dermatoglyphics of non-insulin-dependent diabetes mellitus in

Bangalore-based population. Ind J Human

Genetics.2005;11:3: 149-153.

4. Kahn HS, Graff M, Stein AD and Lumey LH.

A fingerprint marker from early gestation

associated with diabetes in middle age. The

Dutch Hunger Winter Families Study.

International Journal of Epidemiology.2009;

38(1):101 – 09.5. Hirsch W. Dermatoglyphics and creases and

their relationship to clinical syndromes, A

diagnostic criteria in dermatoglyphics an

international perspective. J. Mavalwala

Jamshed.1978; 263 – 282

6. Henry ER. Classification and uses of

fingerprints. London http://www.clpex.com/

Information/ Pioneers/henry-classification.

pdf. 1900.

7. Purvis-Smith SG. Finger and Palm printing

techniques for the clinician. Med J Aust

1969;2:189.

8. Sant SM, Vare AM, Fakruddin S,

Dermatoglyphics in Diabetes Mellitus. J

Anatomical society India. 1983;35(1): 29-32.

9. Knussmann R, Nach ZF, Zwisehen B.

Diabetes Mellitus and Hautleisten system In

Hautleisten and Krankheiten 1971.

10. Barta L, Vari A, Susa E, Dermatoglyphicpatterns of Diabetic children. Acta Paediatric

Acad Sci Hung 1970;11:71-74.

11. Vadgaonkar R, Pai M, Saralaya PL, Vasudha.

Digito-palmar complex in Non-insulin

dependent Diabetes mellitus. Turk J Med Sci

2006;36(6):353-55.

12. Iqbal MA, Sahay BK, Ahuja YR. Finger and

palmar ridge counts in Diabetes mellitus.

Acta Antropogenetica. 1978;2:35-38.



959


13. Sengupta S, Boruah J. Finger dermatoglyphic

patterns in Diabetes mellitus J.Hum.Ecol.

1996;7(3):203-06.

14. Banerjee AR, Banarjee N, Sarkar NC, Pal,

Gupta M. Dermatoglyphics in disease

diabetes mellitus. Ind J Phys, Antrop HumGen. 1985;11:165-70.

15. Chakravartti MR. Association between

Diabetes mellitus and dermatoglyphics.

1967;157-60.



960

Puja Bansal etal., Int J Med Res Health Sci. 2013;2(4):960-966


&

Health Sciences

www.ijmrhs.com Volume 2 Issue4Oct- Dec Coden:IJMRHS Copyright @2013 ISSN: 2319-5886Received: 10



thAug 2013

Review article

HERPES – ZOSTER: AN UPDATE

*Bansal Puja1, Bhargava Deepak

2, Ali Sheeba

3

1Reader,

2Professor & Head,

3Postgraduate student, Department of Oral Pathology & Microbiology,

School of Dental Sciences, Greater Noida, India


ABSTRACT

Herpes zoster (HZ) is the reactivated form of the Varicella zoster virus (VZV), the same virus

responsible for chickenpox. The condition produces a striking picture, with a blistering, crusting rash

confined to well demarcated areas of the body. Latency is typically life long, and Herpes Zoster is

caused by viral reactivation from the latent state. The survival of Varicella Zoster Virus in human for

several million years attests to its success. Present review provides an overview of the natural history,

epidemiology and possible complications of varicella zoster virus along with diagnosis, prophylaxis and

different treatment modalities.

Keywords: Varicella, Herpes, Shingles

INTRODUCTION

The term herpes comes from the ancient Greek

word meaning to “creep or crawl”. The human

herpes family is officially known as

Herpetoviridae .1

Eight different types of herpes

viruses are known whose primary hosts are

humans. They have been officially designated

‘Human herpes types 1-8.2

Human herpes

simplex viruses type 1 and type 2, both, are

cytolytic in nature and have neurons as the site of

latent infection, whereas human herpes viruses

type 4 (Epstein barr virus), type 6 and type 7

have lymphoproliferative effect. The only known

human herpes virus which is cytomegalic is type

5, commonly known as a Cytomegalo virus

(Table 1). 2,3 In 1889, Von Bokay suggested that

varicella (chickenpox) and herpes zoster (HZ)

are different manifestations of same virus

infection.2

Varicella Zoster Virus, a neurotropic

human herpes virus causes chicken pox and then

remains latent for decades in cranial nerve,

dorsal root and autonomic nervous system

ganglia. The virus gets reactivated after a

variable period of time usually ranging from 5-40

years in 15% patients and causes herpes zoster.4

Herpes Zoster is more commonly known as

shingles, from the Latin cingulum, for “girdle”.

This is because a common presentation of HZ

involves a unilateral rash that can wrap around

the waist or torso like a girdle. Similarly, the

name zoster is derived from classical Greek,

referring to a belt-like binding (known as a

zoster) used by warriors to secure armor.3

DOI:10.5958/j.2319-5886.2.4.154



961


Table.1: Classification, cytopathology, site of latent infection and common associated diseases of human

herpes virus.2,3

Species Cytopathology Site of latent

infection

Common associated diseases

Herpes simplex virus-

Type I

Cytolytic Neurons Oral herpes lesions


Type 2

Cytolytic Neurons Genital herpes lesions

Herpes virus- Type 3

Varicella zoster virus

Cytolytic Neurons Chickenpox, shingles

Herpes virus- Type 4

Epstein- barr virus

Lymphoproliferative Lymphoid tissues Infectious mononucleosis


Type 5

Cytomegalo virus

Cytomegalic Secretory glands,

kidneys etc

CMV mononucleosis


Type 6

Lymphoproliferative Lymphoid tissues Roseola, mononucleosis

syndromes


Type 7

Lymphoproliferative Lymphoid tissues Currently, no human disease

definitely linked


Type 8

- - Suspected association with

Kaposis sarcoma

STRUCTURE

Varicella zoster virus belongs taxonomically to

the group of alpha herpes viruses. It has double-

stranded, linear DNA, consisting of about 125-

kilobase pairs, encased within an icosahedral

protein capsid, composed of 162 capsomers. The

nucleocapsid is surrounded by a pleomorphous

outer shell (tegument with envelope membrane),

which is rich in phosphoprotein. Diameters vary

between 150 and 180 nm due to the variability of

the outer shell.5

EPIDEMIOLOGY

A systemic review published in 2004 found the

overall incidence of zoster among

immunocompetent subjects ranged from 1.2-4.8

per 1000 people; recent studies from United

Studies and France have also reported disease

incidences within this range.6

The estimated

annual incidence of HZ in Cebrián-Cuenca et al.

(2010) study was 4.1 per 1,000 persons >14 years

of age.7 The increased risk of zoster among older

individuals may be due to waning of specific

immunity with increasing time since primary

infection (varicella), or may occur as part of the

generalized decay in cell-mediated immunity that

occurs with age (immunosenescence), an

important factor in the increased susceptibility to

infections, malignancies, and autoimmune

disorders in the elderly. Little is known about the

determinants of either generalised or VZV-

specific immune decay.8

CLINICAL MANIFESTATIONS

The prodromal syndrome stage presents assensations described as burning, tingling, itching,

boring, prickly or knife-like occurring in the skin

over the affected nerve distribution.9

Pain is the

most annoying symptom of herpes zoster. It

often precedes and generally accompanies the

rash.10

Zoster rash is a vesicular eruption on an

erythematous base in one to three dermatomes,

usually accompanied by severe, sharp,

lancinating, radicular pain, itching, and

unpleasant, abnormal sensations (dysesthesias).

Patients may also have decreased sensation in the



962


affected area, while the skin is exquisitely

sensitive to touch (allodynia).11

Within 3 to 5 days of the initial symptoms, an

erythematous maculopapular rash erupts

unilaterally in the nerves of sensory dermatomes

adjacent to the involved ganglia. Over the next 7to 10 days, the rash progresses to pustules and

ulceration, with crusts, scabbing, or both, this can

persist for up to 30 days in the acute phase. At

the end of the healing process, altered (post

inflammatory) pigmentation may develop along

the affected dermatome.12

Complete healing may

take more than 4 weeks.13

The cutaneous

eruption is unilateral and does not cross the

midline. Simultaneous involvement of multiplenoncontiguous dermatomes virtually never

occurs in immunocompetent patients, although

lesions overlap adjacent dermatomes in 20

percent of cases.14

DIAGNOSIS

Differential diagnosis: Definitive diagnosis

involves a process of elimination, with several

likely aetiologies in the differential diagnosis. A

differential diagnosis should include trigeminal

neuralgia, maxillary sinusitis, periodic migraines

neuralgia, myocardial pain, atypical facial pain

and Munchausens syndrome.9

Laboratory diagnosis: Histopathologicalfeatures; cytologic alterations are virtually

identical to those of human herpes simplex virus.

Intranuclear inclusions- lipschutz bodies may be

seen in smears prepared by scraping of the base

of the early vesicles (Tzanck smears) and stained

with toulidiene blue, Giemsa or PAP. Infected

cells exhibit acantholysis, nuclear clearing and

nuclear enlargement that is ballooning

degeneration. Connective tissue showsinflammatory cells infiltate.

1,2

On the basis of histological features one cant

rule out the definite diagnosis of herpes zoster

infection form herpes simplex. Co-relation with

clinical features is required. Table 2 enumerates

some differences between herpes zoster and

recurrent herpes simplex infection.

Table 2: Difference between herpes zoster and recurrent herpes simplex15

Characteristic Herpes Zoster Recurrent Herpes Simplex

Sites of latent infections Sensory neurons in all sensory

ganglia

Sensory neurons in trigeminal and

sacral sensory ganglia

Viral gene expression

during latency

Several “immediate early”

and “early” VZV proteins are

synthesized

No HSV proteins are synthesized; only

“latency-associated transcripts”

Symptomatic reactivation of

latent virus

Infrequent (rarely involves the

same dermatome)

Frequent (usually involves the same

dermatome)

Asymptomatic reactivation

with asymptomatic virus

shedding

None Frequent

Proportion of the affected

dermatome involved by rash

Large (sensory fields of many

neurons)

Small (often the sensory field of a

single neuron)

Consequences of

reactivation of latent virus

Extensive ganglionic

pathology and neuronal death

No obvious ganglionic pathology or

neuronal death

Postherpetic neuralgia Common Extremely rare

Frequency of symptomatic

reactivation

Increases with increasing age

(and time after primary

infection)

Decreases over time after primary

infection



963


In most cases, a diagnosis of VZV infection is

based on the characteristic prodrome of

symptoms and the pattern of skin eruptions.

Virus isolation can be attempted from the buccal

or cutaneous lesion in the early stages by

inoculating human amnion, human fibroblasts,HeLa or Vero cells but typically viral culture

test.2

Viral culture, antigen detection test by

using modified Tzank technique. Serological test

via ELISA or latex agglutination, polymerase

chain reaction (PCR) is useful to detect VZV

DNA.16

COMPLICATIONS

Postherpetic Neuralgia (PHN): Postherpetic

neuralgia (defined as pain that persists more than

30 days after the onset of rash or after cutaneous

healing) is the most feared complication in

immunocompetent patients.14

Clinically

significant PHN was described by R. Edgar

Hope-Simpson in 1975 as a chronic neuropathic

pain syndrome that may contribute recovery

from an acute attack of herpes zoster.17

Although

it has a high morbidity, the mechanism causing

PHN remains unknown, its occurrence cannot bepredicted at the time of zoster and its treatment is

still highly unsatisfactory and generally

ineffective.18

Cutaneous complications: Cutaneous dissemina-

tion of herpes zoster defined as more than 20

vesicles outside the area of primary or adjacent

dermatomes and occurs in approximately 10% of

immunocompromised persons.10

Acute and

chronic complications involving the skin are

frequent. The skin is predominantly affected by

bacterial secondary infections in the acute stage.

Ecthymiform ulcerations may develop. Other

cutaneous complications include: hemorrhages

(zoster hemorrhagicus), purulent gangrene

(zoster gangrenosus), and persistence of lesions

and dissemination (zoster disseminatus) in

immunocompromised patients. A manifestation

of psoriasis vulgaris (Kobners phenomenon)

may occur with chronic hypo-pigmented and

depigmented scar formation.19

Herpes zoster ophthalmicus (HZO): Herpes

zoster ophthalmicus occurs when reactivation of

the latent virus in the trigeminal ganglia involves

the ophthalmic division of the nerve.20

While

HZO does not necessarily affect the structures of

the eye, many of the acute and long-termcomplications associated with the disease are the

result of direct viral toxicity to the eye or the

ensuing inflammatory response within the eye.21

Hutchinsons sign is defined as skin lesions at the

tip, side, or root of the nose and is a strong

predictor of ocular inflammation and corneal

denervation in HZO, especially if both branches

of the nasociliary nerve are involved.22

Ramsay Hunt syndrome and other neurological syndromes: Less common manifestations of

zoster include the Ramsay Hunt syndrome

(involvement of the geniculate ganglion of the

facial nerve) which manifests as vesicles in the

external auditory canal and palate associated

with loss of taste to the anterior two-thirds of the

tongue and facial weakness.23

Neurologic symptoms (headache, fever,

vomiting, and altered sensorium) most often

occur about 1 week after the onset of the

varicella rash. The onset of symptoms may be

abrupt or gradual and is accompanied by seizures

in 29% – 52% of cases.24

Prophylaxis

The live attenuated Oka vaccine was developed

in 1974 by Takahashi in Japan. Virus from a

child with varicella was serially passaged at low

temperature (34°C) in human fibroblasts,

followed by a passage in guinea pig embryo

fibroblasts and the production of a standardized

seed lot in human diploid cells. Production of the

vaccine is now standardized according to the

World Health Organizations’ “good

manufacturing process”.25

Recommended dose for children 1-12 yrs is a

single subcutaneous dose, while in case of adults

and adolescents 2 doses (6-10weeks apart)

should be given.2



964


TREATMENT

The objectives of treating HZ are to control acute

pain, accelerate rash healing, minimize systemic

complications and reduce the risk of PHN and

other complications.26

In most cases, HZ is self-

limiting and treatment with analgesics suffices.

Based on level I evidence, antiviral medication

might have some effect on the severity of acute

pain and the duration of skin lesions.27

Most

commonly used drugs used in treatment of

herpes infections are given in Table 3.

Table 3: Treatment of Acute Herpes Zoster.13

Class of agent and usual

dose

Patients in whom treatment is indicated Comments

Antivirals

*Famciclovir: 250 mg orally

3 times daily for 7 days.

*Valacyclovir: 1 g orally 3

times daily for 7 days.

*Acyclovir: 800 mg orally 5

times daily for 7 days.

*In immunocompromized

patients/disseminated

disease: acyclovir, 10 mg/kg

intravenously every 8 h

until resolution of cutaneous

/ visceral disease

*All who present within 72 h of rash onset.

*Consider antivirals in those who present

>72 hrs after rash onset if they have the

following characteristics:

- Age >50 y

- Immunocompromised status

- Severe pain at presentation

-High-risk lesions (involving tip of

nose/eye)

Antivirals reduce both

acute symptoms and

subsequent risk of PHN.

Glucocorticoids

Prednisone: 60 mg orally

for 7 d, then taper for next 2

weeks.

Those who are older and/or those with

severe pain as long as no contraindications

exist.

Corticosteroids have no

effect on the subsequent

development of PHN and

should be used with

antivirals, never alone;

significant adverse effects

are possible.

*Pain medications

*Tramadol

*Oxycodone/acetaminophen

Most will require some type of pain

medication.

Opioids should be used

with caution in elderly

patients.

Prophylactic laxatives andstool softeners should be

considered when

prescribing opioids.

CONCLUSION

Herpes zoster represents a mode of evolutionary

adaptation by the VZV which is an obligate

human parasite. Normal aging, poor nutrition,

and immunocompromised status correlate with

outbreaks of herpes zoster, and certain factors

such as physical or emotional stress and fatigue

may precipitate an episode. In small countries,

the susceptibilities are completely eliminated by

varicella infection in childhood. Therefore, the

ability of the virus to remain latent and reappear

as zoster years later confers on it a great survival

advantage.



965


REFERENCES

1. Neville BW, Damm DD, Allen CM, Bouquot.

Viral infections. Oral and Maxillofacial

Pathology. 3rd

ed. Reed Elsevier India Private

Limited. Noida. 2009. p.2402. Ananthanaryan R, Paniker CKJ. Virus-Host

interactions: Viral infections. Textbook of

Microbiology. 7th

ed. Orient Longman Private

Ltd. Chennai. 2006.p.474

3. Roxas M. Herpes Zoster and Postherpetic

Neuralgia: Diagnosis and Therapeutic

Considerations. Altern Med Rev.

2006;11(2):102-13.

4. Raza N, Iqbal P, Anwer J. Recurrence of

Herpes Zoster In An Immunocompetent

Adult Male. J Ayub Med Coll Abbottabad.

2005;17(3):80-81.

5. Wittek M. Advances in the diagnostics of

Varizella Zoster Virus and Importance of

Vaccination. J Lab Med. 2008;32(4). doi

10.1515/JLM.2008.041et

6. Forbes HJ, Thomas SL, Langan SM. The

Epidemiology and Prevention of Herpes

Zoster. Curr Derm Rep. 2012;1:39 – 477. Cebrián-Cuenca AM, Díez-Domingo J,

Rodríguez MSM, Puig-Barberá J, Navarro-

Pérez J. Epidemiology of Herpes Zoster

Infection among Patients Treated in Primary

Care Centres in the Valencian Community

(Spain). BMC Family Practice. 2010;11:33.

8. Thomas SL, Hall AJ. What does

epidemiology tell us about risk factors for

herpes zoster? Lancet Infect Dis. 2004;4:26 –

33

9. Tidwell E, Hutson B, Burkhart N, Gutman

JL, Ellis CD. Herpes zoster of trigeminal

nerve third branch: a case report and review

of literature. International endodontic journal.

1999;32:61-66.

10. Kutlubay Z, Göksügür N, Engin B, Tüzün Y.

Complications of Herpes Zoster. J Turk Acad

Dermatol. 2011;5(2):115-21

11. Nagel MA, Gilden DH. The protean

neurologic manifestations of varicella-zoster

virus infection. Cleveland Clinic Journal of

Medicine. 2007;74(7):489-500

12. Kenneth R. Cohen KR, Salbu RL, Frank J,

Israel I. Presentation and Management of

Herpes Zoster (Shingles) in the Geriatric

Population. P T. 2013;38(4):217-2413. Sampathkumar P, Drage LA, Martin DP.

Herpes Zoster (Shingles) and Postherpetic

Neuralgia. Mayo Clin Proc. 2009;84(3):274 –

80

14. Gnann JW Jr, Whitley RJ. Herpes Zoster. N

Engl J Med. 2002;347(5):340-46.

15. Oxman MN. Herpes Zoster Pathogenesis and

Cell-Mediated Immunity and

Immunosenescence. J Am Osteopath Assoc.2009;109(6):(Suppl 2):13-17

16. Srikrishna K, Prabhat MPV, Balmini PR,

Sudhar S, Ramarjun D. Herpes Zoster:

Report of a treated case with review of

literature. J Indian Aca Oral Med Radiol.

2012;24(1):51-55

17. Hempenstall K, Nurmikko TJ, Johnson RW,

A'Hern RP, Rice ASC. Analgesic Therapy in

Postherpetic Neuralgia: A Quantitative

Systematic Review. PLoS Med. 2005; 2(7)

:e164.

18. Kennedy PGE, Montague P, Scott F, Grinfeld

E, Ashrafi GH. Varicella-Zoster Viruses

Associated with Post-Herpetic Neuralgia

Induce Sodium Current Density Increases in

the ND7-23 Nav-1.8 Neuroblastoma Cell

Line. PLoS ONE. 2013;8(1):e51570.

19. Singh BS, Scholand SJ. Herpes Zoster: A

Clinical Review. J Infect Dis AntimicrobAgents. 2011;28(3):211-21

20. Shaikh S, Christopher N, Evaluation and

Management of Herpes Zoster Ophthalmicus.

Am Fam Physician. 2002;66(9):1723-30

21. Catron T, Hern HG. Herpes Zoster

Ophthalmicus. WestJEM. 2008;9:174-176.

22. Liesegang TJ. Herpes Zoster Ophthalmicus

Natural History, Risk Factors, Clinical

Presentation, and Morbidity. Ophthalmology.2008;115:S3 – S12



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23. Wehrhahn MC, Dwyer DE, Herpes Zoster:

epidemiology, clinical features, treatment and

prevention. Aust Prescr. 2012;35:143-7.

24. John W, Gann Jr. Varicella-Zoster Virus:

Atypical Presentations and Unusual

Complications. J InfectDis. 2002;186(1):S91-8.

25. Breuer J. Vaccination to prevent varicella and

shingles. J Clin Pathol. 2001;54:743-747.

26. Whitleya RJ, Volpib A, McKendrickc M,

Wijckd AV, Oaklander AL. Management of

Herpes Zoster and Post-Herpetic Neuralgia

now and in the future. Journal of Clinical

Virology. 2010;48(S1):S20 – S28

27. Opstelten W, Eekhof J, Neven AK, VerheijT. Treatment of Herpes Zoster. Can Fam

Physician 2008;54:373-7.



967

Dhananjay et al., Int J Med Res Health Sci. 2013;2(4):967-969


&

Health Sciences

www.ijmrhs.com Volume 2 Issue 4 Oct - Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886Received: 24



ndAug 2013

Case report

SEVERE PETER PLUS SYNDROME: A RARE CASE REPORT

Dhananjay Y Shrikhande1, *Amol Pokharkar

2, Jayshree Jadhav

3, Divyank Pathak

2, Vivek Dholakiya

2,

Amit Narkhede2


2Post graduate student,

3Associate Professor, Department of Pediatrics, Pravara

Institute of Medical Sciences, Loni, Maharashtra, India


ABSTRACT

Severe Peter plus Syndrome is a rare autosomal recessive condition that is characterized by ocular

anomaly and associated with other systemic major or minor anomalies. Mutations of B3GALTL gene

encoding beta 1,3 glucosyltransferase have been seen in patients with Peter Plus Syndrome.1

We report

a male patient with unusually severe manifestations of Peter Plus Syndrome including prominent

forehead, long area between nose and mouth (philtrum), pronounced double curve of the upper lip,

Anterior Eye Staphyloma (Bilateral), retrognathia, widely spaced nipples and Fallot’s tetralogy. To our

knowledge Fallot has not been reported previously in Peter plus Syndrome and bilateral anterior

staphyloma, a most severe anterior chamber eye defect i s also apparently rare in this syndrome. Our

patient might represent a new variant of severe Peter plus syndrome wi t h anterior eye Staphyloma and

Fallot’s tetralogy.

Key words Severe Peter Plus syndrome, Fallot’s tetralogy, Anterior eye staphyloma, Retrognathia

INTRODUCTION

Severe Peter Plus syndrome is a very rareautosomal recessive condition characterized by

ocular anolamly, disproportionate short stature,

developmental delay, cleft lip/palate and other

systemic major or minor anomalies. “Peter plus

syndrome” is also known as Krause-van

Schooneveld – Kivlin syndrome. 1-3

We report a male patient with unusually severe

manifestations of Peter Plus Syndrome including

prominent forehead, long area between nose and

mouth (philtrum), pronounced double curve of

the upper lip, Anterior eye staphyloma(Bilateral), retrognathia, widely spaced nipples

and Fallot’s tetralogy.

CASE

A term male neonate (birth weight: 2.9Kg),

normal delivery, born to non consanguineous

parents at 7th

week of gestational age was

brought to our hospital on 1st

day of life with

complaints of protrusion of right eyeball.

Examination revealed prominent forehead, long

DOI:10.5958/j.2319-5886.2.4.155



968


area between nose and mouth (philtrum),

pronounced double curve of upper lip (Cupid’s

bow), bilateral anterior eye Staphyloma, webbed

neck, retrognathia & micrognathia, short stature.

Systemic examination revealed a single second

sound in pulmonary area, systolic murmur, nocyanosis. 2D- ECHO findings revealed

Tetralogy of Fallot.

Fig.1: Widely spaced nipples, depressed nasal

bridge, cupid’s bow

Fig.2: Large forehead, long philtrum, right eyestaphyloma

DISCUSSION

Mutations of B3GALTL gene encoding

beta 1,3glucosyltransferase have been seen in

patients with Peter Plus Syndrome4. Less than 70

people with this condition have been reported

worldwide. Patients with this syndrome may also

have shortened upper limbs i.e. rhizomelia and

shortened fingers and toes (brachydactyly)5. It is

also noticed that intellectual disability may be

present which may be mild to severe, although

some individuals may have normal

intelligence6. We report a male patient

(neonate) with unusually severe manifestations

of Peter plus Syndrome.7

Fallot’s Tetralogy hasnot been reported previously in Peter Plus

Syndrome. Bilateral Anterior Staphyloma, a most

severe anterior chamber eye defect is also

relatively rare in this syndrome.8

Our patient

might represent a new variant of Severe Peter

plus Syndrome with anterior eye Staphyloma and

Fallot’s tetralogy.9,10

REFERENCES

1. Aliferis K, Marsal C, Pelletier V, Doray B,

Weiss MM, Tops CMJ. A novel nonsense

B3GALTL mutation confirms Peters plus

syndrome in a patient with multiple

malformations and Peters anomaly.

Ophthalmic Genetics. 2010;31(4):205 – 08.

2. Boog G, Le Vaillant C, Joubert M. Prenatal

sonographic findings in Peters-plus

syndrome. Ultrasound Obstet Gynecol.

2005;25:602 – 06.

3. Frydman M, Weinstock AL, Cohen HA,

Savir H, Varsano I. Autosomal recessive

Peters anomaly, typical facial appearance,

failure to thrive, hydrocephalus, and other

anomalies: further delineation of the Krause-

Kivlin syndrome. Am J Med Genet.

1991;40:34 – 40.

4. Kosaki R, Kamiishi A, Sugiyama R, Kawai

M, Hasegawa T, Kosaki K. Congenitalhypothyroidismin peters plus syndrome.

Ophthalmic Genet. 2006;27:67 – 5.

5. Kozma K, Keusch JJ, Hegemann B,

Luther KB, Klein D, Hess D, Haltiwanger

RS, Hofsteenge J. Identification and

characterization of abeta1,3-

glucosyltransferase that synthesizes the Glc-

beta1,3-Fuc disaccharide on thrombospondi

type 1 repeats. J Biol Chem.2006;281:36742 – 51.



969


6. Krause U, Kovisto M, Rantakillio P. A case

of Peters' syndrome with spontaneous corneal

perforation. J PediatrOphthalmol. 1969;

6:145 – 9.

7. Maclean K, Smith J, St Heaps L, Chia N,

Williams R, Peters GB, Onikul E, McCrossinT, Lehmann OJ, Adès LC. Axenfeld-Rieger

malformation and distinctive facial features:

Clues to a recognizable 6p25 microdeletion

syndrome. Am J Med Genet A. 2005;132:381

8. Maillette de Buy Wenniger, Prick LJ,

Hennekam RC. The Peters' plus syndrome: a

review. Ann Genet. 2002;45:97 – 103

9. Traboulsi E. Peters anomaly. In: Stevenson

RE, Hall JG, eds. Human Malformations

and Related Anomalies. 2nd ed. New

York, NY: Oxford University Press;

2006:313-14.

10. Yang LL, Lambert SR, Lynn MJ,

Stulting RD. Surgical management of

glaucoma in infants and children with Peters'

anomaly: long-term structural. J AAPOS.

2000;4(4):205-10.



970

Babu et al., Int J Med Res Health Sci. 2013;2(4):970-972


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Health Sciences




thAug 2013

Case report

IDIOPATHIC NEONATAL RECTAL PERFORATION: A CASE REPORT

*Nyamannawar Babu1, Nagathan Vikram

2, Vallabha Tejaswini

3

1Associate Professor of Surgery,

2Resident in Surgery,

3Professor & Head, Department of Surgery,

Shri B.M.Patil Medical College, Bijapur, Karnataka, India


ABSTRACT

Idiopathic perforation of rectum in newborns is extremely rare. Etiology of spontaneous neonatal rectal

perforation is unknown. We report a case of idiopathic rectal perforation in a neonate who presented

with signs of perforative peritonitis. This case is reported because of its rarity.

Keywords: Rectal perforation, Spontaneous gastrointestinal perforation.

INTRODUCTION

Perforative peritonitis is one of the common

neonatal emergencies encountered. It is life

threatening condition. Such perforations are

explained by mechanical distal obstruction like

anorectal anomalies1, Hirschsprung’s disease

2,

mechanical injury like rectal thermometer usage,

and administration of contrast enema3.

Perforations are commonly observed in small

intestine, followed by large intestine, andstomach

4. Perforation of the rectum without a

known etiological factor such as injury,

iatrogenic cause, inflammatory disease, and

distal obstruction is defined as the idiopathic

perforation of the rectum4. We report a case of

idiopathic neonatal rectal perforation for its

rarity.

CASE REPORT

A day one, term, home delivered male babypresented to hospital with complaints of

distension of abdomen noticed at 6 hours after

Shri B M Patil Medical College Bijapur. There

was no history of resuscitation, or rectal

instrumentation. Child had normal antenatal

history and care. It weighted 2.5 Kg. Child was

acutely ill, lethargic with cold peripheries,

hypothermia, tachycardia, tachypnea with feeble

peripheral pulses. The abdomen was distended

with signs of peritonitis. Anus was normallysited. Hematological investigations were normal

& radiography revealed massive

pneumoperitoneum (Fig.1). Baby was

resuscitated with correction of fluid deficit,

inotrope support, and broad spectrum antibiotics.

Explorative laparotomy showed.

Pneumoperitoneum, fecal peritonitis with 0.5 cm

wide perforation on the rectum. Closure of rectal

perforation with loop sigmoid colostomy was

done. Postoperative recovery was uneventful.

Histopathology suggested benign nonspecific

DOI:10.5958/j.2319-5886.2.4.156



971


inflammatory pathology. Colostomy closure was

done after 6 months. At follow up the baby has

normal growth development.

Fig.1: Erect x ray abdomen showing gross

pneumoperitoneum (saddle sign)

DISCUSSION

The etiology of spontaneous intestinal

perforation is still being debated. The common

identifiable etiologic factors are mechanical

distal obstruction like anorectal malformations1,

Hirschsprung’s disease2, mechanical injury by

thermometer usage, and contrast enemas2.

However these factors were absent. Ischemicnecrosis, secondary to a localized vascular

accident in the wall of the affected viscus could

explain such spontaneous intestinal bowel

perforations5. They noticed six out of seven

babies had intestinal perforations on the anti-

mesenteric aspect of the bowel, indicating

localized vascular accident as possible etiology.

Congenital segmental absence of intestinal wall

musculature is another proposed etiologic factor

to explain idiopathic neonatal intestinal

perforations6.

Idiopathic intra-peritoneal perforation of rectum

in newborn is extremely rare. There is only one

case reported in literature4. However there are

many reports, describing extra-peritoneal

perforation of rectum which classically presents

as spreading cellulites in perianal and buttock

regions with or without leakage of feces7. In such

a scenario diverting proximal sigmoid stomawith drainage of perianal region is advised.

Defects in pelvic floor are noticed in such babies.

In intra-peritoneal perforation of rectum, early

diagnosis and prompt resuscitation can’t be

overemphasized. Radiography allows earlier

diagnosis and prompt surgical treatment. The

abdominal upright film will show “saddle” or “football” sign due to the massive pneumo -

peritoneum. Isolated rectal perforation can be

managed by closure of perforation, if general

condition is stable. In case of severe sepsis,

proximal diverting sigmoid stoma with closure of

perforation is a safer alternative.

In conclusion there are many factors associated

with Idiopathic neonatal rectal perforation, such

as localized ischemia, and defect in the muscularwall of the bowel. In a given case their relative

significance is difficult to assess. Early

recognition of the perforation is of paramount

importance for a successful outcome. This case is

being reported for its rarity and to inform that

though rare, it can occur.

Conflict Of Interest: Authors do not have

conflicts of interest.

Funding Source: Nil

REFERENCES

1. Sharma SB, Gupta V, Sharma V.

Gastrointestinal perforations in neonate with

anorecctal malformations. Indian J

Gastroenterol. 2004;23:107-08.

2. Khan TR et al. Neonatal pnemopertoneum: a

critical appraisal of its causes and subsequent

management from a developing country.Pediatr Surg Int. 2009;25:1093-97.

3. De Feiter PW, Soeters PB, Dejong CH.

Rectal perforations after barium enema: a

review. Dis Colon Rectum. 2006;49:261-71.

4. Prabhakar G. Spontaneous gastrointestinal

perforation in the neonate. Indian Pediatr.

1991;28:1277-80.

5. Weinberg G, Kleinhaus S, Boley SJ.

Ideopathic intestinal perforations in the

newborn: An increasingly common entity. J

Pediatr Surg. 1989;24:1007-08.



972


6. Husain AN, Hong HY, Gooneratne

S, Muraskas J, Black PR. Segmental absence

of small intestinal musculature. Pediatr

Pathol. 1992;12:407-15.

7. Davies MR, Cywes S, Rode H. Prenatal

perfotion of the extraperitoneal part of therectum associated with a developmental

defect of the pelvic floor. Z

Kinderchir. 1984;39:271-3.



973

Samuel Ponraj et al., Int J Med Res Health Sci. 2013;2(4):973-975


&

Health Sciences




thAug 2013

Case report

CASE REPORT OF A RARE FUNGAL CORNEAL ULCER

Rajvin Samuel Ponraj1, Srinivasan M

2, Sundararajan D

3, Senthamarai S

4, Sivasankari S

5, Anitha C

6,

Amshavathani SK7

1Post graduate student,

2Professor & Head,

3Associate Professor, Dept of Ophthalmology, Meenakshi

Medical College, Kanchipuram, Tamilnadu, India4Associate professor,

5Asst. professor,

6Tutor,

7Professor & HOD, Department of Microbiology,

Meenakshi Medical College, Kanchipuram, Tamilnadu, India


ABSTRACT

The dematiaceous fungi appear to be an increasing cause of human disease. This was a case of a patient

coming with complaints of watering and irritation of right eye following injury to her eye by a stick.

Scrappings from corneal ulcer were sent for gram stain, bacterial and fungal culture. Cladosporium

species of fungus was isolated from a patient who presented with a corneal ulcer not responding tonatamycin drops. Ointment fluconazole was prescribed along with natamycin , moxifloxacin and

atropine drops. The corneal ulcer began to respond and healed completely.

Keywords: Cladosporium, Dematiaceous, Keratomycosis, Conidiophores

INTRODUCTION

Many fungal species can invade the cornea and

result in Keratomycosis which is an infective

condition of the cornea. It is typically a slow

progressive disease. It is mandatory that this be

distinguished from its counterpart namely

bacterial keratitis. Ocular surfaces which have

been compromised or suffered trauma are likely

to be caused by fungus. The type of fungi varies

with the geographic location and the climate.

Due to the profound use of steroids and

antibiotic, its incidence has increased over the

years. Diagnosis and treatment of keratomycosis

has become a challenge to ophthalmologists

because of its resistance to treatment and

difficulty in obtaining drug sensitivity.1,2

CASE REPORT

A 50-year old female patient presented with a

history of a stick injury to her right eye. Her

main complaint was irritation and watering of her

right eye. On examination the affected eye had

oedema of the eye lid, injected conjunctiva, ulcer

on the cornea covered with slough and a sluggish

reaction of pupil to light. Scrapings from corneal

lesion were taken and sent for bacterial and

fungal culture. Gram stain showed few pus cellsand no bacteria was seen. Bacterial culture

showed no growth. Potassium hydroxide mount

DOI:10.5958/j.2319-5886.2.4.157



974


showed actively branching septae and thin

hyphae.

Fungal culture on Sabourand Dextrose Agar

plate showed dark green to black coloured

flattened colonies and rapidly spreading black

coloured colonies on the reverse side.Microscopic findings showed blastoconidia in

branching chains. The patient was on the

following medications during attending the

outpatient clinic. Moxifloxacin eye drops-1 drop

(8 times per day), Natamycin eye drops-1 drop (8

times per day), Atropine (1 drop twice a day).

The lesion did not respond to the above

mentioned treatment. She was prescribed

ointment fluconazole to be applied twice a dayalong with the above mentioned medications.

The ulcer responded to treatment and healed

completely.

Fig 1: Culture growth of Cladosporium colonies

Fig 2: Microscopic appearance of Conidiophores,

Condidia

DISCUSSION

Keratomycosis is most commonly caused by

filamentous fungi which can be further classified

into two types: pigmented (dematiaceous) fungi

which produce characteristic black/brownpigment appreciable clinically and/or on culture

media and nonpigmented (moniliaceous) fungi

which do not produce such pigments3

Cladosporium is a dematiaceous (pigmented)

mould widely distributed in air and rotten

organic material and frequently isolated as a

contaminant on foods. Some species are

predominant in tropical and subtropical regions.

The growth rate of Cladosporium colonies is

moderate on potato dextrose agar at 25°C and the

texture is velvety to powdery. Similar to the

other dematiaceous fungi, the color is olivaceous

green to black from the front and black from the

reverse.4,5

Most of the Cladosporium spp. does

not grow at temperatures above 35°C.

Cladosporium spp. produce septate brown

hyphae, erect and pigmented conidiophores, and

conidia. Cladosporium spp. produce septate

brown hyphae, erect and pigmentedconidiophores, and conidia.

They have a geniculate appearance. In addition,

conidiophores of Cladosporium herbarum bear

terminal and intercalary swellings. Conidia

of Cladosporium spp. in general are elliptical to

cylindrical in shape, pale to dark brown in color

and have dark hila.6

REFERENCES

1. Ibrahim MM, Vanini R, Ibrahim FM, Fioriti

LS, Furlan EM, Provinzano LM, etal.,

Epidemiologic aspects and clinical outcome

of fungal keratitis in southeastern Brazil. Eur

J Ophthalmol. 2009; 19(3):355-61

2. Foster CS. Fungal keratitis. Massachusetts

Eye and Ear Infirmary, Harvard Medical

School, Boston. Infect Dis Clin North

Am. 1992;6(4):851-57

3. Comparative study on the incidence and

outcomes of pigmented versus non



975


pigmented keratomycosis. Ind J Opthalmol

2011 ;59:291-6

4. Dixon DM, Polak-Wyss A. The medically

important dematiaceous fungi and their

identification. Mycoses. 1991;34:1-18.

5. Collier L, Balows A, Sussman M. Topley &wilson’s Microbiology and Microbial

Infections, 1998;9th

ed, vol .4. Arnold,

London ,Sydney , Auckland , New York.

6. Sutton DA, Fothergill AW, Rinaldi MG.

Guide to Clinically Significant Fungi,.1998;

1st

ed. Williams & Wilkins, Baltimore



976

Shilpa et al., Int J Med Res Health Sci. 2013;2(4):976-980


&

Health Scienceswww.ijmrhs.com Volume 2 Issue 4 Oct-Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886

Received: 3rd Aug 2013 Revised: 22nd Aug 2013 Accepted: 3rd Sep 2013

Case report

CASE REPORT OF GIANT CONGENITAL MELANOCYTIC NAEVUS

*Shilpa Reddy, Archana S, Shefali Singhal, Muruganandam TV, Hamedullah A.

Department of Dermatology, Meenakshi Medical College Hospital and Research Institute, Enathur,

Kanchipuram, Tamilnadu, India


ABSTRACT

This is a case of giant congenital melanocytic nevus, associated with a single lipoma & multiple satellite

lesions. Biopsy report showed skin with groups of nevoid cells extending into underlying fat, intimately

associated with the lobules & surrounding many blood vessels. The systemic examination was normal.

This is a typical case of a giant congenital melanocytic nevus with satellite lesions and a lipoma

association. As the surface area is greater than 40cm in diameter; the risk of developing melanoma is

higher.

Keywords: Bathing trunk nevus, Satellite lesions, Lipoma

INTRODUCTION

Congenital melanocytic nevi are benign

proliferation of melanocytes located in different

skin levels that have existed since one's birth.

However, the same lesion can also appear within

the first 2 years of life, in this case it’s called

“nevus tardive”1Congenital melanocytic nevi are

more common in Asian and Black children.2

Theincidence is between 1-2% of newborns

3. A giant

congenital melanocytic nevus has a diameter of

20cm or more & is very rare. One study

including over 5000,000 newborns has shown

that only one baby in 20,000 has a nevus with a

diameter larger than 10cm.4

It is reported to be

associated with leptomeningeal melanocytosis,

meningomyelocoele and spina bifida, ocular

malformations and glaucoma, auricular

malformation,angiomatous lesions,bone atrophy,

musculoskeletal deformities, neurofibromatosis,

diffuse lipomatosis, vitiligo etc5

there are other

case reports of association of garment nevus with

lipoma, neurofibroma & spina bifida occulta.6,7,8

A case of giant naevi with hydrocephalus was

reported in mexico.9

It is said to occur in the

epidermal naevus syndrome.10

A well

substantiated association with neurofibromatosisis documented.

1

CASE REPORT

A 5-year-old girl second born by normal vaginal

delivery (birth weight was 2.8kgs & cried

immediately after birth) to non consanguineous

parents hailing from Papum Pare in Arunachal

Pradesh, India, presented with a large

asymptomatic hyper pigmented lesionencompassing the entire trunk involving the

chest, abdomen, back, buttocks and genitalia

DOI:10.5958/j.2319-5886.2.4.158


http://slidepdf.com/reader/full/ijmrhs-vol-2-issue-4 259/321Shilpa et al.,

covering more than 40% of th

area, present since birth [figure

growing in size with age. The

initially and gradually started be

Distant to the giant nevus, multi

[figure 2] started developing gupper and lower limbs, that wa

the time of birth. Hypertrichosi

over the large pigmented les

toward the midline [figure 3].

palms, soles and nails were nor

no significant family history. Th

of worry was the cosmetic disfig

by the large hyper pigmented

swelling in the left loin which haincreasing in size. [Figure 1] T

first noted by the patient’s mothe

4 years ago, on examination it

size, soft in consistency, non t

skin pinches able over the

diagnosis was made clinic

systemic, ophthalmologic &

examinations were normal. The

MRI Brain were both normal. B

& urine routine were normal .T

swelling in the posterior left f

using a linear transducer & show

defined thickening of the skin a

plane at the site of swellin

vascularity was noted within,

muscular plane appears normal.

swelling in the left loin was sen

biopsy.

Histopathology of the swelling shunderlying groups of cells wit

[figure 4], which extends into th

[figure 5]. The nevoid cells are s

blood vessels in the subcutaneo

extend into the fat intimately as

the lobules & surround many bl

patient was advised to report

changes in symmetry, color, bor

the lesion or any symptoms of itswellings from the lesion w

recorded all the pigmented mol

and are following them up


e body surface

1]. It has been

lesion was flat

coming thicker.

le satellite nevi

adually on the not present at

s was seen all

ion converging

Scalp, mucosa,

mal. There was

patient’s cause

urement caused

lesion & the

been gradually e swelling was

r approximately

was 8×6 cm in

nder, mobile&

swelling. The

ally. General,

usculoskeletal

X-Ray spine &

sic blood work

he USG of the

lank was done

d a diffuse well

d subcutaneous

, no obvious

the underlying

Under GA, the

t for excisional

owed, skin with h pigmentation

underlying fat

en surrounding

s fat. The cells

sociated within

od vessels. The

immediately if

er, diameter of

hing, oozing or re noted. We

s on her body

periodically to

identify malignant cha

technique”11,12. She w

series of diode laser

hypertrichosis. Patien

counseling to deal

disfiguring disease.

Fig 1:Giant congen

involvement) Associate

Fig 2:Satellite lesions

Fig 3:Hypertrichosis sh

convergence.

977

i. 2013;2(4):976-980

ge by the “mole-mapping

as advised to undergo a

treatments to treat the

t is under Psychiatric

with the cons of this

ital naevus(>40% BSA

lipoma.

distant to giant naevus.

wing midline


http://slidepdf.com/reader/full/ijmrhs-vol-2-issue-4 260/321Shilpa et al.,

Fig 4: Histopathology skin with u

of pigmented cells extending

subcutaneous fat. (10x)

Fig 5: The nevoid cells are seen su

vessels in the subcutaneous tissu

the fat intimately associated with

surround many blood vessels. (40x

DISCUSSION

Synonyms: Giant garment nevi

nevi, Giant hairy nevus

Incidence/prevalence: Giant co

very rare. One study including

newborns has shown that onl20,000 has a nevus with a diam

10cm.4

Classification: The American n

of health (NIH) are used to c

according to size – small are

diameter, large between 1.5 and

naevi having a diameter of 20cm

Association with lipoma: The

melanocortin system regulates

metabolism via the beta adrener

the sympathetic nervous system.

outflow shifts substrate metaboli


derlying groups

nto underlying

rrounding blood

, extending into

n the lobules &

)

, bathing trunk

genital nevi are

over 5000,000

one baby in eter larger than

tional institutes

ategorize naevi

nder 1.5cm in

0 cm and giant

or more.13

central nervous

peripheral lipid

gic receptors of

This autonomic

sm to modulate

energy storage and a

explains the occurre

congenital melanocytic

Clinical features: Co

intensely pigmented m

(terminal hair which ithan normal hair

concentrated in the ce

the child grows the n

and the surface may be

into folds & nodules c

nevus.

The bathing trunk nev

definite cosmetic pr

Commonest site is the& a surface area of a d

is involved. This may

numbers of smaller c

areas distant to the gi

number may develop

satellite nevi.

The hairy component,

the lesions, tends to b

late childhood & seem

dense toward the mid

nevus ceases to thicke

The hair growth patt

distribution, often cent

giant nevus in the bac

CNS, ocular and musc

Histopathology: In co

are typically located o

the dermis. Occasio

subcutaneous tissue, wof cells within the

fibres, with a tenden

cutaneous appendages.

Prognosis & complic

spontaneous regressi

adolescence. This

commonly due to im

.Rarely, it may resu

Superficial spreadingmelanosis , raised

hydrocephalus, or s

rapidly growing ulcera

978

i. 2013;2(4):976-980

iposity. This mechanism

ce of lipoma in giant

nevus14

.

ngenital nevi are usually

acules with hypertrichosis

s darker and more coarse ith a tendency to be

tral midline) at birth .As

evus grows in proportion

come warty or get thrown

an develop within a large

s is very rare but poses a

oblem for the patient.

lower back and thigh area iameter greater than 20cm

be accompanied by large

ongenital nevi present in

nt nevus. An increase in

ver time. They are called

which occurs in 95% of

come more prominent in

s to be more centered and

line, but at this stage the

n and may become paler.

rn usually has a vortex

ered on the midline in the

k. It is crucial to rule out

loskeletal deformities.

genital nevi, melanocytes

n the lower two-thirds of

nally they extend into

ith isolated cells or groups eticular dermis collagen

y to be located around

5

tions: Sometimes there is

n during childhood or

remature regression is

munological mechanisms

lt in complications like

elanoma, neurocutaneous intracranial pressure,

ace occupying lesions,

tive tumor called nodular



979


proliferative neurocristic hamartoma

(neuroectodermal & ectomesenchymal origin15

.

Genetic counseling: It is very important to

reassure the parents of a child with a giant

melanocytic naevus that, the risk of recurrence is

very low in subsequent pregnancies but a fewrare cases have occurred which suggest an

inherited tendency.

Diagnosis &Treatment: MRI scans should be

done in babies with nevi over the cranium or

spine to exclude significant leptomeningeal

melanocytosis.16

Regular neurological

examination is crucial. The treatment aims at

improving the cosmetic aspect and balancing the

risk of melanoma by excision which may not bepossible in giant melanocytic nevi & periodic

check up to keep an eye out for changes of

malignant transformation. Dermabrasion may

help with a mild reduction in pigmentation.

REFERENCES

1. Marghoob AA, kopf AW, Rigel DS. Risk of

cutaneous malignant melanoma in patients

with “classic” atypical-mole syndrome:a

case-control study . Arch Dermatol 1994;

130:993-8.

2. Castilla E, Da Graca Dutra M, Orioli-

Parreiras I. Epidemiology of congenital

pigmented naevi: risk factors. Br J Dermatol

1981;104:421-7.

3. Osburn K, Schosser RH, Everett MA.

Congenital pigmented & vascular lesions in

newborn infants. J Am Acad Dermatol

1987;16:788-92.

4. Castilla EE, Da Graca DM, Orioli-Parreiras

IM.Epidemiology of congenital pigmented

naevi, 1: incidence rates and relative

frequencies. Br J Dermatol 1981; 104:307-

15.

5. Zaal LH, Mooi WJ, Sillevis Smitt JH, Van

der Horst CMAM. Classification of

congenital melanocytic naevi and malignant

melanoma transformation:a review of theliterature. Br J Plast Surg 2004;57:707-19.

6. Mc Kie RM. Disorders of the cutaneous

melanocyte . In:Burns T, Breatnach S,Cox N,

Griffiths C,editors.Rook’s Textbook of

Dermatology.7 th ed.London:Blackwell

Science 2004; 18-38.20.

7. Habib A,Razieh SA,Darius M,NasrinS,Payam S.Giant congenital melanocytic

nevus with neurofibroma-like changes and

spina bifida occulta. Int J Dermatol 2006

;45:1347-50.

8. Bhagwat PV, Tophakhane RS, Shashikumar

BM, Noronha TM, Naidu V. Giant congenital

melanocytic nevus (bathing trunk nevus)

associated with lipoma and neurofibroma:

Report of two cases. Indian J DermatolVenereol Leprol 2009;75:495-8

9. Ruiz-Maldonado R, Tamayo L, Laerza AM,

Duran C. Giant pigmented nevi: clinical,

histopathologic, & therapeutic

considerations. J Pediatr 1992; 120:906-11.

10. Carney J, Gordon H, Carpenter P. The

complex of myxomas, spotty pigmentation

and endocrine overactivity. Medicine

1985;64:270-83.

11. Carli P, De Giorgi V,Chiarugi A,et

al.Addition of dermoscopy to conventional

naked eye examination in melanoma

screening : A randomized study .Jam Acad

Dermatol 2004;50:683-9.

12. Kittler H, Binder M. Risks and benefits of

sequential imaging of melanocytic skin

lesions in patients with multiple atypical

nevi. Arch Dermatol 2001;137:1590-5.

13. Anon. Consensus conference: Precursors tomalignant melanoma. JAMA 1984; 251:

1864-6.

14. Nogueiras R, Wiedmer P, Perez-Tilve D,

Veyrat-Durebex C, Keogh JM, Sutton GM, et

al. The central melanocortin system directly

controls peripheral lipid metabolism. J Clin

Invest 2007; 117:3475-8.

15. Mancianti M-L, Clark WH, Hayes FA,

Herlyn M. Malignant melanoma simulantsarising in congenital melanocytic nevi do not

show experimental evidence for a malignant

phenotype. Am J Pathol 1990;136:817-29.



980


16. Foster RD, Williams ML, Barkovich AJ.

Giant congenital melanocytic nevi: The

significance of neurocutaneous melanosis in

neurologically asymptomatic children. Plast

Reconstr Surg 2001:107:933-41



981

Laul et al., Int J Med Res Health Sci. 2013;2(4):981-984


&

Health Scienceswww.ijmrhs.com Volume 2 Issue4 Oct-Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886

Received: 6th Aug 2013 Revised: 25th Aug 2013 Accepted: 5th Sep 2013Case report

TUBERCULOUS MENINGITIS: PRESENTING AS ISOLATED COMPLETE III NERVE

PALSY

* Laul Rohit S1, Avhad Vinod

2,Laul Abhishek S

3, Laul Subodh S

4

1Chief resident, Department of Ophthalmology,

2Chief resident Department of Medicine, Annasaheb

Chudaman Patil Memorial Medical College and Hospital, Dhule, Maharashtra, India.

3 Chief Resident, Pad.Dr Vithalrao Vikhe Patil Medical College, Ahmednagar, Maharshtra, India4 Chief Resident, Dhoot Hosptial, Aurnagabad, Maharasthra, India.


ABSTRACT

Tuberculous meningitis (TBM) is the most common form of central nervous system tuberculosis (TB)

and has very high morbidity and mortality. TBM is a subacute disease with symptoms that may persist

for weeks before diagnosis. Based on the clinical features alone, the diagnosis of TBM can neither be

made nor excluded with certainty. A high clinical suspicion and vigilance is required for early diagnosis

of TBM. The present case report demonstrates a patient with TB meningitis, who presented with clinicalmanifestation of isolated left III nerve palsy. Case: A 32 years female was hospitalized with acute onset

of left sided ptosis, diplopia and mild generalized headache. Neurological examination at admission

revealed isolated left III nerve palsy. CT scan and MRI of Brain showed no specific finding. Lumbar

puncture was performed four days later due severe headache, low grade fever and neck rigidity.

Cerebrospinal fluid (CSF) study, raised ESR and positive Montoux Test confirmed the diagnosis of TB

meningitis. Since TB meningitis is a chronic disease, cranial nerve palsies are common manifestations.

This case report suggests that TB meningitis should be considered as a disease of differential diagnosis

for isolated III nerve palsy.

Keywords : III nerve palsy, Tuberculous meningitis, Oculomotor nerve palsy

INTRODUCTION

India has approximately one fifth of the global

incidence of tuberculosis with an estimated

prevalence of 3million cases annually as per

WHO1. 9.1% of extra pulmonary TB cases in the

adult population are of Tubercular Meningitis

(TBM). The diagnosis of TBM can be difficult

early in its course, often be a diagnosticchallenge. Because of unusual presentation and

delay in diagnosis and seeking care, TBM causes

an increase in morbidity of the treatable

condition. Early diagnosis and prompt treatment

of TB is important to minimize complications

and reduce morbidity and mortality.

The outcome of TBM depends on the degree of

neurological deterioration that has occurred bythe time antitubercular therapy (AKT) is started.

DOI: 10.5958/j.2319-5886.2.4.159



982


Age is an important determinant of the risk of

disease after infection. So in this typical case

report the woman patient adds the landmark to

the rare event in a rural health care sector of

Maharashtra.

CASE REPORT

We report this case of Tuberculous meningitis:

Presenting as isolated complete III nerve palsy

after taking a written valid informed consent

from the patient.

A 32 years female was hospitalized with a

history of acute onset of left sided ptosis,

diplopia and mild headache. No other CNS

symptoms were present. She had a past history of

being operated for swelling in the upper quadrantof the right sided neck region a year before. She

had no history of any other significant medical

illness in the past. On the 4th day of admission

she developed low grade fever, severe headache

and neck rigidity following which L.P. was

performed. Cerebro-spinal fluid examination

confirmed the diagnosis of tuberculous

meningitis. On examination she was found to be

conscious, cooperative and well oriented to time,place and person. Initial observations recorded a

temperature of 98.20

F, a regular pulse of 76

beats/min, Blood Pressure of 104/72 mm of Hg

and Respiratory rate of 18 breaths/min with no

lymphadenopathy. Cardiorespiratory

examination was normal. Abdominal

examination was also within normal limits. CNS

examination revealed signs of complete left sided

third nerve palsy (head deviated to right side,

reduced interpalpebral fissure, drooping of upper

eyelid covering upper half of the cornea,

ipsilateral pupil dilatation of 7mm, loss light

reflex. In primary position, left eyeball appeared

to be in an outward & downward gaze with

normal abduction but restricted adduction,

supraduction, and infraduction) with intact

higher, sensory & motor functions. There was no

neck stiffness or no involvement of any other

cranial nerve.

Laboratory Investigations: Blood tests reported

Hb of 9.6g%, 4200/cu.mm Leucocytes,

180000/cu.mm platelets, ESR of 80mm at the

end of the first hour, urea 16.0mg/dl, Serum

creatine 1.2 mg/dl, Serum sodium 135.2 mEq/L

and Serum potassium 3.6 mEq/L. All other blood

tests including liver function tests were normal.Urine analysis was negative. Montoux test was

positive. CT brain and MRI performed on day 1

showed no any significant abnormal finding.

Repeat CT brain was performed on day 4, this

time with contrast & revealed no abnormality.

CSF examination on day 5 showed cloudy

appearance, elevated opening pressure, high

protein levels (264mg/dl), low sugar levels

(37mg/dl). Cytological examination of CSF

revealed lymphocyte predominance, total cell

count 424cells/micro.litre, (polymorphs 20%,

lymphocytes 20% & RBC’s few). Gram stain &

Ziehl Neelsen stain revealed no any organism.

This confirmed the diagnosis of TBM in addition

CSF culture yielded growth of TB bacilli at 7th

week.

Diagnosis: The initial impression was Isolated

III Nerve palsy under evaluation.

Table.1: Cerebro- spinal fluid analysis

CSF study Appearance

Cell

countProtein Sugar Blood

Sugar

mg/dl

Initial Pressure

P/M % mg/dl mg/dl mm of H2O

5th

Day Cloudy 424 264 16 84 280

14th

Day Clear 168 112 40 105 146

21st

Day Clear 46 58 46 108 68

CSF: cerebro-spinal fluid; P: polymorphonuclear leukocytes; M: mononuclear leukocytes.


http://slidepdf.com/reader/full/ijmrhs-vol-2-issue-4 265/321Laul et al.,

Fig.1:Showing isolated IIIrd nerve

Final diagnosis: TB Meningiti

isolated III Nerve palsy.

Management: The patient was

with i.v. antibiotics & conservwith a lack of response. After the

diagnosis on 4th

day, she was s

drug AKT and i.v. dexamethas

doses. The patient was dischar

with improvement in her clinical

examination at the time of disch

normal limits On discharge pati

to continue AKT4 and was s

Prednisolone 40 mg in tapering d

DISCUSSION

According to an earlier studies,

and colleagues found that

presentations of TBM include he

fever (91.1%), stiff-neck (7

impairment (40.0%), motor we

and cranial nerve palsies (11.

oculomotor nerve palsy has be

quite uncommon (2.2%). Other at

Manifestations include

ophthalmoplegia, psychosis and

presence of focal neuro-logical

indicates that the neurological

persist in the survivors2-6

. Anoth

that cranial nerve palsies occur

patients and may be the presenti

of TBM. The sixth cranial

commonly affected7.

In the present case, acute droo

with dilated pupil suggests the ini


involvement in a case of tuberculous meningi

presenting as

initially treated

ative treatment confirmation of

arted with four

one in tapering

ed on 21st

day

symptoms. CSF

arge was within

nt was advised

hifted on Tab.

ses.

Chotmongkol

initial clinical

dache (95.6%),

7.8%), mental

akness (11.1%)

1%). Unilateral

n found to be

ypical

inter-nuclear

emianopia. The

deficits often

sequale may

r study showed

in 20 – 30% of

g manifestation

nerve is most

ping left eyelid

tial diagnosis of

isolated III nerve pals

scan and MRI along

fever, headache an

developed after admnecessary. The prese

example of the diversi

manifestations in TB

always necessary to ta

whenever there is an a

nerve8-10

.

Many diseases can pre

unilateral III nerve pals

lobe herniation, inf

thrombosis, diabetes, b

multiple sclerosis, tum

malformations, T

migraine, myastheni

cavernous fistula11

a

obtaining detailed hist

examination, brain i

cerebral arteriography.

The prognosis of TB

early initiation of tr

results in poor pro

sequelae. However, e

often difficult and th

from those of bacte

meningo-encephalitis

not impossible, by cli

empiric anti-tubercul

necessary when TBM

If unrecognized TBMcase report shows tha

should be considered

983

ci. 2013;2(4):981-984

tis.

. No abnormalities in CT

with persistent low grade

neck rigidity which

ission made CSF study nt case serves a good

ty and rarity of the initial

eningitis. Therefore, it is

e TBM into consideration

rupt deficit of 3rd cranial

ent with acute or subacute

y like aneurysm, temporal

ction, cavernous sinus

rainstem vascular disease,

or, mellitus, arteriovenous

losa-Hunt syndrome,

gravis and carotid-

d can be excluded by

ory and thorough clinical

aging studies, including

meningitis is related to

eatment any delay may

nosis with neurological

rly diagnosis of TBM is

discrimination of cases

rial meningitis or other

re sometimes difficult, if

ical features alone. Thus,

osis therapy may be

as suspected8-10,12

is uniformly fatal. This t Tuberculous Meningitis

as a differential diagnosis



984


in a case of Isolated III Nerve palsy. The

diagnosis was made on the basis of positive CSF

findings in favour of TBM with supportive

evidence of raised ESR, positive Montoux test

and response to Anti-tubercular Therapy.

The patient recovered rapidly with a resolution of

palsy at the time of discharge. No any

neurological deficit was found after 2 weeks at

the time of follow up.

To summarize for every patient presenting with

sudden onset of unilateral III nerve palsy, TB

meningitis should be in the list of differential

diagnosis since the timing of initiation of

treatment is an important factor in the prognosis.

REFERENCES

1. TB INDIA 2011. Revised National TB

Control Programme. Annual Status Report.

Government of India. Central TB Division.

http://planningcommission.nic.in/reports/genr

ep/health/RNTCP_2011.pdf

2. Chotmongkol V, Panthavasit J, Tiamkao S.

Tuberculous meningitis in adults: a four-year

review during 1997-2000. Southeast Asian J

Trop Med Public Health 2003;34:869-71.

3. Mak W, Cheung RT, Ho SL. Tuberculosis

meningitis in Hong Kong: experience in a

regional hospital. Int J Tuberc Lung Dis

1998;2:1040-3.

4. Souza RD. Franklin D, Simpson J. Atypical

presentation of tuberculosis meningitis: a

case report. Scott Med J 2002;47:14-5.

5. Thwaites GE, Simmons CP, Than Ha Quyen

N. Pathophysiology and prognosis invietnamese adults with tuberculous

meningitis. J Infect Dis 2003;188:1105-15.

6. Daif A, Obeid T, Yaqub B, et al. Unusual

presentation of tuberculous meningitis. Clin

Neurol Neurosurg 1992;94:1-5.

7. Berger JR. Tuberculous meningitis. Curr

Opin Neurol. 1994;7:191 – 200.

8. Clark WC, Metcalf JC Jr, Muhlbauer MS.

Mycobacterium tuberculosis meningitis: a

report of twelve cases and a literature review.

Neurosurgery 1986;18:604-10.

9. Thwaites GE, Chau TT, Stepniewska K. .

Diagnosis of adult tuberculous meningitis by

use of clinical and laboratory features. Lancet

2002;360:1287-92.

10. Holdiness MR. Management of tuberculosis

meningitis Drugs 1990;39:224-33.

11. Brown RB, Lau SK. A 59-year-old diabetic

man with unilateral visual loss and

oculomotor-nerve palsy. N Engl Med

2001;344:286-93.

12. Harris PJ, Saper CB, Anderson C, et al.

Clinical problem solving: diagnosis of

tuberculous meningitis. N Engl J Med

1999;340:1047-9.



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&

Health Sciences




thSep 2013

Case report

SURGICAL RECONSTRUCTION OF CLOACAL MALFORMATION: A CASE REPORT

*Mehul Vikani1, Dattatray Bhusare

2, Aniruddha Bhagwat

3, Sagar Shetty

4, Renu Bakshi

4, Sheetal

Aggarwal6.

1Resident, Department of General Surgery, MGM Hospital, Navi Mumbai

2Professor and Head of Department,

3Assistant Professor, Department of Pediatric Surgery, MGM

Hospital, Navi Mumbai4Resident, Department of Radiodiagnosis, MGM Hospital, Navi Mumbai

5Resident, Department of Pediatrics, MGM Hospital, Navi Mumbai


ABSTRACT

It is a surgical challenge to repair a cloacal malformation. We are reporting a case of cloacal

malformation in which we performed a reconstructive surgery. We performed a reconstructive surgery

in a 5 yr old patient who had got a colostomy done in the neonatal period. The surgical managementincluded purely a posterior sagittal anorectovaginourethroplasty without an abdominal approach.

Keywords: Cloaca, Anorectal malformations, Posterior sagittal anorectovaginourethroplasty.

INTRODUCTION

Persistent cloaca has a wide spectrum of

anomalies including those of urogenital and hind

gut. It is comes under rare malformations in the

Krickenbeck’s classification of anorectalmalformations

1. Clinical presentation consists of

imperforate anus with a single perineal opening

through which urine and meconium are passed.

The surgical correction is very tough and

challenging and urinary and fecal incontinence

are frequent complications following operation.

The ultimate goal of treatment includes

achieving satisfactory bowel and urinary control

as well as normal sexual functions at

maturity1,2,3.

CASE REPORT

A five year old female child, with a full term

normal hospital delivery, colostomised on 2nd

day of life for imperforate anus with single

perineal opening was referred to us for definitive

treatment. Past history and family history was

not relevant.

On local examination – A single opening in the

perineum was present. The labial folds were

fused and the clitoris was well developed. Anal

pigmentation was present. Gluteal cleft was not

well developed. All sacral pieces could be felt.

Per abdomen, a healthy right transversecolostomy was present.

DOI:10.5958/j.2319-5886.2.4.160



986


Fig. 1: Pre-operative picture showing single

perineal opening.

Investigations – CBC, Coagulation profile, Renal

function tests, Liver function tests were normal

with normal routine urine analysis. Ultrasoundof abdomen was normal except for small sized

left kidney. Intravenous Urogram was also

normal except for small sized left kidney. CT

scan and MRI scan pelvis showed atretic

vagina. Uterus was normal for age. Both ovaries

were normal. Genitogram showed that bladder

was filled with contrast and was normal. Contrast

entered the rectum and entire distal colon was

opacified. Internal genitalia could not be

visualized. Recto-urinary fistula with common

channel opening in the perineum was seen.

Distal cologram did not reveal a recto-urinary

fistula. Rectal ectasia was present.

Fig. 2: Genitogram

A diagnostic pan endoscopy was performed

which showed a short channel cloaca with

common channel of about 2.5 cms. Posteriorurethra, bladder neck and urinary bladder were

normal. A short channel communicating with

cloaca and ending with two visible openings

separated by a septum was visualized. Another

third tiny opening was also visualized however

the scope could not be negotiated into this

opening.Operative findings: The patient was in

jackknife position. A posterior sagittal approach

was used. The incision was taken from

midsacrum upto the single perineal opening. All

the structures were divided in midline. The

coccyx was split. The endopelvic fascia was

incised. The rectal pouch was visualized and the

rectum was opened posteriorly; however no

fistulous communication could be seen. Rectumwas separated off vagina so that it could reach

the perineal skin. The common channel was

incised. Per-urethral catheter had entered into the

vagina. The urethra was visualized and bladder

was catheterized. Entire anomaly was laid open

and all openings into the common channel were

seen. Vagina was septate. The vaginal septum

was excised and the septate vagina was

disconnected from the common channel.

Common channel was repaired over a 10F

Foley’s catheter to create a new urethra. Vagina

was quite high and was sharing a paper thin wall

with the urethra. Hence decision was made to

create a vaginal substitute. Various options were

available like using bowel segments, pedicle

graft, split thickness skin graft etc. But the

surgery was performed by perineal route alone

and abdomen was not opened. Surgery was

completed by doing an ano-rectoplasty whichcould accommodate a 12 no Hegar’s dilator.

Rectum was placed in the middle of the sphincter

muscle complex which was identified by muscle

stimulator. The perineal body was reconstructed

anteriorly. The child was turned supine and a Y-

V plasty was performed using labial skin flaps

which were sutured to the native vagina to create

a new vagina over a 10F red rubber catheter. Post

operatively, feeds were started after 6 hours. Postoperative period was uneventful.

Single perineal opening



987


Fig. 3: Intra-operative findings

Fig. 4: Post-operative reconstruction

DISCUSSION

A persistent cloaca is a complex anorectal

and genitourinary malformation, in which

the rectum, vagina, and urinary tract meet and

fuse, creating a cloaca, a single common

channel4. Cloaca’s probably occur in 1 in 20,000

live births5,6

. This defect has been considered one

of the most formidable challenges in pediatric

surgery. The goals of treatment include achieving

bowel and urinary control, as well as normal

sexual function, intercourse, menstruation andobstetric issues. The repair of persistent cloaca

represents a serious technical challenge and

should be performed in specialized centers.

History of the procedure. Hendren has published

the most comprehensive and authoritative reports

on the subject of cloacal malformation repair.

Hendren has described the posterior sagittal

anorectovaginourethroplasty (PSARVUP). For

more complex anomalies, an abdominal

approach is added to mobilize a very high vagina

or rectum.

The etiology of persistent cloaca is unknown.

More than 80% of all patients with a cloaca

experience an associated urogenital anomaly.

Rich et al report the following associatedurogenital anomalies

9- Cloaca, Rectovesical

fistula, Rectoprostatic fistula, Rectovestibular

fistula, Rectobulbar fistula, Rectoperineal fistula

and all malformations.

In most centers, a single stage reconstruction is

the definitive treatment though some surgeons

prefer a two staged approach where they opt for

repairing the anorectal anomaly initially and

perform urogenital sinus repair at a later date.The planning of surgical management includes

carefully identifying the anatomy specially

measuring length of common channel, level of

insertions of urinary channel, vagina and rectum,

and associated urogenital anomalies. Depending

upon the length of the common channel, cloacal

malformations are categorized into two groups.

Patients having common channel lesser than 3

cm (more than 60% of entire group) can be

repaired by posterior sagittal approach. In

patients having a length of the common channel

more than 3 cm, it would be difficult to perform

total urogenital mobilization from perineum to

repair the malformation, so the common channel

is left intact to be used as urethra, and

colovaginoplasty along with anorectoplasty is

performed. The major complication is fecal and

urinary incontinence. The incidence is usually

higher in cases of higher confluence where anabdomino-perineal approach is used

1,2,3,7,8.

Prognostic factors include quality of the sacrum,

quality of the muscles, and length of the common

channel. Total urogenital mobilization is a

technique devised by Alberto Pena; it allows

mobilization of the urethra and vagina as one

structure. This is possible in patients with the

more benign types of cloacae. If total urogenital

mobilization does adequately lengthen thevagina, the vagina and urethra must be separated,

Rectum

Septate Vagina

Urethra



988


which is a technically challenging maneuver.

Vaginourethral fistulae are more likely after this

plane is dissected. Approximately 50% of

patients have various degrees of vaginal or

uterine septation. These can be totally or partially

repaired during the main operation or deferredfor definitive repair until puberty. Approximately

one third of the patients have obstructed

Müllerian structures, which can lead to severe

problems due to retrograde menstruation,

amenorrhea in patients with atretic uteri or

hydrometrocolpos.

ACKNOWLEDGEMENT

We would like to extend our heartfelt gratitude tothe Dept of Pediatric Surgery, Dept of General

Surgery, Dept of Pediatrics and Dept of

Radiology.

REFERRENCES

1. Buhilla P, Torres PC, Bruned BJ, Emparan

G, DeSalazar C, Castro LC. Total

mobilization of the urogenital sinus in the

treatment of cloaca. An Esp Pediatr 2001;55:573-5.

2. Kay R, Tank ES. Principles of management

of persistent cloaca in the female newborn. J

Urol 1977;117:102-4.

3. Masuko T, Higashimoto Y, Iwai J. Single-

stage operation without temporary colostomy

for persistent cloaca with short common

channel. Pediatr Surg Int 2005;21:922-4.

4. Jenkins D, Bitner-Glindzicz M, Thomasson

L. Mutational analyses of UPIIIA, SHH,

EFNB2 and HNF1β in persistent cloaca and

associated kidney malformations. J Pediatr

Urol. 2007;3 (1): 2 – 9,

5. Spitz Lewis, Coran, Arnold G. Operative

Pediatric Surgery (6th ed.), London: Hodder

Arnold, pp. 2006;503 – 519.

6. Ashcroft, Keith; Holcomb, George; Murphy,

J Patrick, Pediatric Surgery. 2005; 4th

ed.

Philadelphia: Elsevier Saunders, pp. 496 –

517.

7. Malik A, Iqbal Z, Hameed S, Khalid C,

Iftikhar A, Hussain M. Persistent cloaca with

complete duplex ectopic ureters: A rare

presentation. J Med Rehabilit 2007;1:7-9.8. Levitt MA, Pena A. Pitfalls in the

management of newborn cloacas. Pediatr

Surg Int 2005;21:264-9.

9. Rich MA, Brock WA, Pena A. Spectrum of

genitourinary malformations in patients with

imperforate anus. Pediatric Surg Intl.

1988;(3):110-113.



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Hemalatha et al., Int J Med Res Health Sci. 2013;2(4):989-992


&

Health Sciences




thSep 2013

Case report

PRIMARY MALIGNANT MELANOMA OF UTERINE CERVIX: A RARE OCCURRENCE

*Hemalatha AL1, Umarani MK

2, Shashikumar SD

3

1Professor & Head,

2Associate Professor,

3Post-graduate student, Department of Pathology, Mysore

Medical College and Research Institute, Irwin Road, Mysore, Karnataka, India


ABSTRACT

Primary malignant melanoma of uterine cervix is a rare and aggressive neoplasm. In women, genital

tract is the site of approximately 3%-7%of malignant melanomas. Majority of these occur in vulva or

vagina, but cervix is a rare site. Cervical melanoma is reported in the age range of 19 to 83 years with

peak incidence between 60 to 70years. Malignant melanoma presents with vaginal bleeding or discharge

and appears as exophytic, polypoid, pigmented or colorless cervical mass. Diagnosis is by histopatholo-

gy which should be confirmed by immunohistochemical staining with S100 protein and HMB45.

Primary cervical melanoma must be differentiated from secondary metastasis of melanoma to the cervixfrom other sites in the body. In general, prognosis of primary cervical melanoma is poor, because it is

diagnosed at an advanced stage. No consensus has been established regarding treatment of primary

malignant melanoma of cervix, because of its rarity. Cervical melanoma is incurable in totality with the

currently available therapies and hence it has to be diagnosed early.

A 60 year old woman presented with white discharge per vagina. On examination, there was a bluish

black colored mass arising from the anterior lip of cervix. Following histopathology and other investiga-

tions, a diagnosis of primary malignant melanoma of uterine cervix was made. The case is reported for

its rarity.

Keywords: Malignant melanoma, primary, uterine cervix

INTRODUCTION

In 1959, Cid reported the presence of melano-

cytes in the cervical epithelium of 3.5% of wom-

en1

.Since then, in the literature, about 78 cases

of primary malignant melanoma of the uterine

cervix have been reported2. Primary malignant

melanoma of the cervix is a rare neoplasm. It

constitutes less than 2% of cases of malignant

melanoma of the genital tract3. The diagnosis

may be missed or delayed as it often presents in

an amelanotic form4. Majority of the patients are

in advanced stage of the disease on presentation

and respond poorly to therapy4. Diagnosis is by

histopathology and immunohistochemistry and

by exclusion of primary melanoma at other sites.

We report for its rarity, a case of a 60 year old

female with primary malignant melanoma of theuterine cervix and describe its clinical and histo-

logical features.

DOI:10.5958/j.2319-5886.2.4.161



990


CASE REPORT

A 60 year old post menopausal woman presented

to the gynaecology department with a history of

white discharge per vagina since 2 months.

On per speculum examination a 4*5centimeter

bluish black colored mass was seen arising from

the anterior lip of the cervix. The clinical diagno-

sis was endometriosis or endometrial polyp.

A punch biopsy of the cervix was done and the

specimen was submitted for histopathological

examination which revealed a diffusely infiltra-

tive malignant neoplasm composed of highly

pleomorphic, round, polygonal to spindle shaped

cells with atypical large irregular nuclei and

prominent nucleoli. Intra and extra cellular finebrown granules of pigment which were Masson

Fontana positive was present. Junctional activity

was seen in the epithelium.

Immunohistochemical staining for HMB 45 was

positive. The histopathological diagnosis was

pigmented malignant melanoma of the cervix.

No melanotic lesions were found in the skin, eye

and other mucosal sites. Abdominal ultra

sonography and chest radiograph were normal.Considering the absence of malignant melanoma

at any other site and presence of Junctional activ-

ity, the diagnosis was given as primary malignant

melanoma of uterine cervix. The patient was re-

ferred to the regional cancer institute for further

management.

Fig.1: Stratified squamous epithelium of cervix

with pigmented cells beneath the epithelium (10X)

Fig.2: Intracellular fine granules of brown pig-

ment (40X).

Fig.3: Pleomorphic cells with prominent

eosinophilic nucleolus (100X).

DISCUSSION

Malignant melanomas are generally found in ar-

eas of skin exposed to the sun but may also pre-

sent in nonexposed sites, such as genital tract and

esophagus, among other sites’3. Approximately,

3-7% of malignant melanomas in women devel-

op within genital tract.6

Majority of them occurin vulva and vagina. Primary cervical melanoma

is a rare entity.

Cervical melanoma arises from melanocytes in

the cervix. The complete spectrum of melano-

cytic lesions, from benign lentigenes to blue nevi

to melanoma can be seen in the cervical epitheli-

um3, 4

.

Primary malignant melanoma of cervix is very

rare4. A cervical melanoma may be either

melanotic or amelanotic .Diagnosis of

amelanotic melanoma may be missed due to the



991


absence of pigment and thereby needs caution.

The present case exhibited classic features of

melanotic melanoma and hence posed no diag-

nostic dilemma.

Patients with malignant melanoma of the cervix

may range between 19 to 83 years, although themajority of them occur between 60 to 70 years.

5,

6In most cases, vaginal bleeding or discharge is

the usual presenting complaint.4

Some patients

may remain asymptomatic. Physical examination

usually reveals a polypoidal exophytic mass

which may be grey, brown, black, blue or red in

color or it may be colorless in amelanotic mela-

noma ,which constitute up to 55% of cases in the

cervix.

7

Recently the morphological features of primary cervical malignant melanoma in pap

smear have been reported as, bizarre and abnor-

mal cells containing pigment, raising the hope

for an early diagnosis.4

Histologically, malignant melanoma in the uter-

ine cervix is similar to malignant melanoma at

other sites and is composed of cells with vary-

ing degree of pleomorphism and prominent

eosinophilic nucleoli. In the melanocytic type,

dark brown intracellular pigments which stain

positive with Masson’s Fontana stain are seen.

In the absence of pigment, the differential diag-

nosis includes anaplastic carcinoma, poorly dif-

ferentiated squamous cell carcinoma, adenocar-

cinoma, rhabdomyosarcoma, leiomyosarcoma,

stromal sarcoma and high grade lymphoma. Mel-

anoma cells are positive for S100 protein (more

sensitive) and HMB45 (more specific).8

They

also stain positively with Melan A, Vimentin,Tyrosinase and MITF (Microphthalmic Tran-

scription Factor). They are usually negative for

epithelial markers Cytokeratin and EMA and

also Desmin. Primary melanoma of cervix must

be differentiated from metastatic melanoma from

other sites of the body including skin and eye6.

Norris and Taylor have suggested the following

criteria to diagnose primary malignant melanoma

of the cervix’ (a) presence of melanin in thenormal cervical epithelium (b) absence of mela-

noma in another site of the body (c) presence of

junctional activity in the cervical epithelium near

the lesion (d) if metastasis is found, it should be

according to the cervical carcinoma patern3, 6

.

Instead of Clark and Breslow scales, the Interna-

tional Federation of Gynecology and Obstetrics

(FIGO) staging system for cervical cancer is usedfor staging of cervical malignant melanoma as

cervix is an unusual site for malignant melanoma

and, the FIGO staging system has better correla-

tion with prognosis.3

There is no consensus on optimal management of

primary malignant melanoma of cervix, because

of its rarity6. Radical hysterectomy with pelvic

and paraarotic lymphadenectomy is the most

common procedure which may be followed byradiotherapy or chemotherapy.

Malignant melanoma of the cervix is a rare and

aggressive neoplasm9.

The prognosis of primary

malignant melanoma is generally poor because

diagnosis is usually made at an advanced stage

and the tumor is highly aggressive in both local

recurrence and wide spread metastases6, 10.

These

patients have an average survival ranging from

6 months to 14years according to world litera-

ture 7.

CONCLUSION

Primary malignant melanoma of the cervix is a

rare neoplasm. However, it should be included in

the differential diagnosis of cervical malignan-

cies. Special staining and immunohistochemistry

should be used to confirm the diagnosis. Treat-

ment of primary malignant melanoma of cervix

is not yet standardized because of its rarity .In

general, prognosis of primary cervical melanoma

is poor, because it is diagnosed at an advanced

stage. Hence early diagnosis of cervical melano-

ma is essential.

REFERENCES

1. Cid JM. Melanoid pigmentation of the

endocervix: a neurogenic visceral argument.

Ann Anat Pathol (Paris) 1959;4:617-28.2. Pusceddu S, Bajetta E, Carcangiu ML,

Formisano B, Ducceschi. A literature review



992


of primary cervical malignant melanoma: an

exceedingly rare cancer. Crit Rev Onccol

Hematol. 2012:81(2) 185-95.

3. Calderon Salazar L, de Leon DC , Montiel

DP, Almogabar-Villagran E, Villavicencio V.

Primary malignant melanoma of the uerinecervix treated with ultraradical surgery : A

case report. ISRN Obstetrics and gynecology

2011 Article ID68 3020

4. Gupta R, Singh S, Mandal AK. Primary ma-

lignant melanoma of cervix - a case report.

Indian J Cancer 2005;42:201-04

5. Clark KC, Butz WR, Hapke MR. Primary

malignant melanoma of the uterine cervix:

case report with world literature review. In-ternational Journal of Gynecological Pathol-

ogy1999; 18(3): 265-73.

6. Yun NR, Park JW, Park JH, Choi SJ, Hwang

SO. Primary malignant melanoma of the uter-

ine cervix: A case report. Korean J Obstet

Gynecol 2012;55(5):343-47.

7. Hinde E F, Amal B, Hannane S, Cherhazade

B, Abdelaziz B. Unusual primary location of

the malignant melanoma, the cervico-vaginal

region: 3 cases and literature review. Open

Journal of Obstetrics & Gynecology 2012(2)

279-282

8. Santoso JT, Kkucera PR and Ray J. Primary

malignant melanoma of the uterine cervix:

Two case reports and a century’s review

.Obstetrical and Gyecolological Survey

1990:45(11)733-39.

9. Teixeira JC, Salina JR, Teixeira LC, Andrade

LA. Primary melanoma of the uterine cervixfigo stage III B. Sao Paulo Med J

1998;116:1778-80.

10. Khurana A, Jalpota Y. Primary malignant

melanoma of the uterine cervix. Indian J

Pathol Microbiol 2009;52:575-6



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Azonobi et al., Int J Med Res Health Sci. 2013;2(4):993-996


&

Health Sciences




stSep 2013

Case report

CORTICAL BLINDNESS FOLLOWING TWO STAB WOUNDS TO THE SCALP IN AN

ADULT: A CASE REPORT

*Azonobi IR1, Odogu V

2

1Niger Delta University Teaching Hospital, Okolobiri, Bayelsa State, Nigeria

2Diete Koki Memorial Hospital, Opolo-Yenagoa, Bayelsa State, Nigeria


ABSTRACT

Visual disturbances have been reported as a consequence of acute severe blood loss. They are related to

hypoperfusion related watershed infarcts in the posterior visual pathway apparatus.

In this case report, we report the clinical course of a young male adult who suffered transient blindness

following an assault in which he sustained deep cuts to the temporal and parietal regions of the scalp. He

was managed in our hospital with copious infusion of intravenous fluid (normal saline) and subsequent

transfusion of 2 pints of whole blood. Blindness persisted from less than one hour following assaut to 96hours post admission. Blindness resolved completely by the 9

thday of admission but was associated

with a homonymous visual field defect.

Keywords: Blindness, cortical, stab wound, blood loss

INTRODUCTION

Sudden onset of bilateral visual loss

characterized by normal pupillary responses and

normal appearances of the ocular fundus isconsidered as blindness of cortical origin until

proven otherwise.

Cortical blindness has been found to be

associated with a host of clinical states and

procedures (Table 1).

They are due to lesions of the geniculocalcrine

visual pathway in the posterior hemisphere1. The

geniculocalcrine visual pathway is known to

occupy a delicately supplied ‘vascular border zone’. Thus, most cases of cortical blindness is

associated with hypo-perfusion related watershed

infarcts2-4

.

We report the case of a young man who suffered

severe blood loss following an assault and

subsequently developed a reversible visual loss.

DOI:10.5958/j.2319-5886.2.4.162



994


Table 1: Causes of Cortical Blindness

Vascular Trauma

Preeclampsia/ecclampsia

Stroke

Hypertensive encephalopathy

Cerebral venous thrombosisSevere hypotensive states

Head trauma

Cervical trauma

Iatrogenic

Post cardiac catheterization

Cardiac surgery

Infections Metabolic

Hypoglycemia

Uraemia / Haemodialysis

Acute intermittent porphyria

Bacteria meningitis

Mumps encephalitis

Cerebral malaria

Toxic Miscellaneous

Iodinated contrast agents

Metrizamide

AmphetamineChemotherapy

Heroin

FK 506

Status epilepticus

Status asthmaticus

Intracranial haemorrhageBrain tumour

Liver cirrhosis and encephalopathy

CASE REPORT

A 25 year old undergraduate of a Nigerian

university had previously enjoyed good vision in

both eyes until that fateful day when he wasassaulted by a known assailant. He sustained

matchet cuts on both sides of his scalp. He was

said to have bled profusely with an estimated

blood loss of about 1.5 liters. He became

disoriented shortly after the assault as he lost

orientation in space. There was no associated

blunt trauma to the head and no bleeding from

any of the craniofacial orifices.

He was rushed to the Niger Delta University

Teaching Hospital (NDUTH) where he was

attended to and admitted. On examination, he

was noticed to be drowsy but rousable,

disoriented and mentally confused. He was very

pale, anicteric and not dehydrated. His cranial

nerves were grossly intact.

He had deep lacerations at the left temporal

region (6cm long) and at the right parietal region

(10cm long). His pulse rate was 140/min,

regular, poor volume. Blood pressure was

90/46mmHg (supine) and Heart sounds were

normal.

Chest and Abdominal examination was normal.

Ocular examination revealed a visual acuity of

no light perception (NPL) in both eyes andexternal eye and anterior segment examination

were normal. Both pupils were round and

reactive. Fundoscopy revealed a pink disc (C/D

ratio of 0.3), round with well defined edges in

both eyes. Both retinea were flat and normal. A

provisional diagnosis of cortical blindness

secondary to severe hypovolaemia was made. He

was resuscitated with I.V Normal Saline and

thereafter transfused with 2 pints of whole blood.

The two stab wounds were repaired with

appropriate sutures.

Investigation ordered included urgent PCV

(23%), Electrolyte and urea (normal), random

blood sugar (normal) and cranial CT Scan (not

done as a result of absence of equipment in our

centre).By the fourth day on admission following

normalization of his cardiovascular status (PR

70bpm, BP 128/80mmHg), visual recovery was

noticed with a visual acuity of hand motion(H.M) in both eyes. Visual recovery became full



995


on the 9th

day of hospital admission (6/6{OD},

6/6+ 4 {OS}). He was then discharged for follow

up at the ophthalmic outpatient.

A visual field analysis requested at this stage

confirmed a homonymous hemianopia first

detected clinically on the 9th day of admission.

DISCUSSION

Cortical blindness is a hallmark of posterior

cerebral arterial border zone infarcts1. It is

caused by hypoxia of the visual pathways at the

territories supplied by the distal posterior

cerebral arteries. The possibility that vascular

factors (a limited capability of the posterior

vascular system to autoregulate blood flow) andcortical tissue vulnerability to hypoxia as being

responsible for the hypoxic damage has been

suggested5.

The dog electromagnetic flow metre study during

hypoxia and hypercapnia has demonstrated a

decrease in the compensatory dilatation response

of the basilar arterial system to occlusion of the

carotid system5. Loss of the normal protective

autoregulation of blood flow was suggested as

one of the pathomechanism of pre-ecclampsia /

ecclampsia induced cortical blindness6. A

sparing effect of chronic hypoxia on the anterior

cerebral artery has been suggested by an

ultrasonic study on fetal brain circulation7.Thus

under chronic hypoxia the frontal lobes are

spared longer than the lateral and occipital lobes.

It has also been shown that the parieto occipital

border zone is most susceptible to

haemodynamic ischaemic damage as it is the

most peripheral region of the distribution of the

anterior, middle and posterior cerebral

circulation8. Posterior cerebral arterial border

zone infarction has been shown to be a

consequence of profound systemic hypotension

and has been found to be associated with cortical

blindness9-12

.

The patient in our case report developed cortical

blindness following an episode of severe bloodloss. Ischaemia and infarction secondary to

hypoperfusion in severe systemic hypotension is

known to lead to cytotoxic oedema in border

zone infarcts. Radiological evidence of neuronal

oedema in hypotension related watershed infarcts

manifests as hypodense lesion on CT images

and hyperintense lesions on T2 weighted MRIimages in very specific “distal field” territories of

the middle and posterior cerebral arteries13

.

Although, it was not possible to obtain a CT or

MRI images in our patient, clinical evidence

suggests that the above radiologic changes are

not unlikely. The clinical and radiologic changes

in posterior border zone infarcts may be

reversible. Clinical recovery is known to precede

normalization of radiologic abnormalities

14,15

. Inour patient visual recovery was noticed on the

fourth day post admission earlier than what was

reported in most studies. This may be due to

aggressive effort in normalization and sustenance

of the patient’s cardiovascular status.

In hypoperfusion related posterior border zone

infarcts, prompt re-establishment of normal

perfusion pressure may be associated with

resolution of the cytotoxic oedema and visual

recovery. In such cases prompt arrest of blood

loss and restoration of normal cardiovascular

functions may improve the prognosis of visual

recovery.

CONCLUSION

Acute severe blood loss could result in cortical

blindness. Prompt restoration of normal

cardiovascular status is a key step that must be

undertaken in such cases in order to ensure or

optimize visual recovery.

REFERENCES

1. Aldrich MS, Alessi AG, Beck RW, Gilman

S. Cortical Blindness: Aetiology, Diagnosis

and Prognosis. Ann Neurol 1987; 21: 149 –

58.

2. Argenta PA, Morgan MA. Cortical blindness

and Anton Syndrome in a Patient with



996


Obstetric Haemorrhage. Obstet Gynaecol

1998; 91: 810 – 12.

3. Belden JR, Caplan LR, Pessin MS, Kwan E.

Mechanisms and clinical features of posterior

border zone infarcts. Neurology 1999; 53:

1312 – 18.4. Boromeo CJ, Blike GT, Wiley CW, Hirsch

JA. Cortical blindness in a Pre-ecclamptic

patient after a caesarean section delivery

complicated by hypotension. Anaesth

Analog 2006; 9: 609 – 11.

5. Shima T, Ishikawa S, Sasaki U, Miyazaki M,

Hibino H. Quantitative measurement of the

basilar arterial flow in the dog

electromagnetic flow metre study of the extraand intracranial arterial occlusion. No

Shinkei Geka 1976; 4: 451 – 57.

6. Schwartz RB, Jones KM, Kalina P et al.

Hypertensive encephalopathy: findings on

CT, MR Imaging and SPECT Imaging in 14

Cases. Am J R Roeentgenol 1992; 159: 379 –

83.

7. Dubiel M, Gunnarsson GO, Gudmundsson S.

Blood redistribution in the fetal brain during

chronic hypoxia. Ultrasound Obstet Gynaecol

2002; 20: 117 – 21.

8. Torrik A. Pathogenesis of watershed

infarction in the brain. Stroke 1984; 15(2) :

221 – 23.

9. Adams JH, Brierley JB, Connor RCR, Treip

CS. The Effect of systemic hypotension upon

the human brain: Clinical and

neuropathologic observations in 11 cases.

Brain 1966 ; 89(2) : 235 – 68.10. Brierley JB, Excel BJ. The effects of

prolonged systemic hypotension upon the

Brain of M Rhesus: Physiologic and

pathologic observations. Brain 1966: 89(2) :

269 – 298.

11. Mofred A, Curan D, dArondel C, Larib K,

Courtarel P, Cassaz C et al. Blindness

following gastrointestinal haemorrhage. Eur J

Gastrointestinal Hepatol 2000; 12(12): 1339 – 41.

12. Argenta PA, Morgan MA, Cortical blindness

and Anton Syndrome in a Patient with

Obstetric Haemorrhage. Obstet Gynaecol

1998; 91: 810 – 2.

13. Golberg HI, Lee SH, Stroke IN, Rao KC,

Zimmerman RA, eds. Cranial MRI and CT.New York: MC Graw-Hill, 1992: 623 – 99.

14. Sharma JA, Bhatt S. Reversible blindness in

severe Pre-ecclampsia and Ecclampsia. JK

Science 2004; 6(1): 43 – 45.

15.Gaurav S, Bhatia R, Sanjiv B, Ajay KW. MR

Findings of Cortical Blindness Following

Cerebral Angiography:Is This Entity Related

to Posterior Reversible Leucoencephalo

pathy? Am J.Neuroradiol.2005;26:193-94.



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Muthubabu K et al., Int J Med Res Health Sci. 2013;2(4):997-999


&

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ndSep 2013

Case report

REGAUDS TUMOUR INVOLVING THE TONSILS: A CASE REPORT

*Muthubabu K, Srinivasan MK, Sakthivel

Department of ENT, Meenakshi Medical College and Research Institute, Kanchipuram, Tamilnadu,

India

*Corresponding author: [email protected]

ABSTRACT

Regauds tumour is a lymphoepithelioma which usually arises in the nasopharynx. Outside the

nasopharynx such lymphoepithelioma like carcinomas are exceedingly rare. Such tumours in the tonsil

are rare. Here we report a 35 year old lady, a case of Regauds tumour involving the Rt. Tonsil.

Tonsillectomy was performed and the patient was subjected to radiotherapy. 2 years follow up showed

no recurrence of tumour.

Keywords: Regauds tumour, Schminkes tumour, Lymphoepithelioma

INTRODUCTION

Non nasopharyngeal Lymphoepithelioma is rare

and when it occurs in the tonsil it is typically

unilateral. Three fourths of the patients have

nodal involvement. Non nasopharyngeal

Lymphoepithelioma affects the younger

population. Histopathology and

Immunohistochemistry is valuable in thediagnosis. These tumours are highly

radiosensitive. This characteristic along with the

classical histological structure and clinical

typicality made it justifiable for a separate group

and name for the neoplasm.1

CASE REPORT

A 35 year old lady presented with complains of

swelling in the right tonsillar region of 4 months

duration, swelling on the right side of the neck

20 days duration. She had uneasiness in the

throat and difficulty in swallowing. There was no

difficulty in breathing. No pain and no change in

voice.

On Examination there was a unilateral

enlargement of the right tonsil. Surface of the

tonsil was smooth and not ulcerated

macroscopically. Left tonsil was absolutelynormal. On palpation the mass was firm in

consistency. Induration was felt. Ear and Nose

were clinically normal. Indirect laryngoscopy

showed normal posterior third of tongue,

vallecula, epiglottis, arytenoids, aryepiglottic

folds, ventricular bands, vocal folds and piriform

fossa. Examination of the neck revealed Right

sided Jugulodigastric node enlargement, Non

tender, mobile and firm in consistency.

Routine blood investigations were normal. CT

scan showed enlargement of the Right side

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998


tonsil. Under General anaesthesia, Tonsillectomy

was performed. Whole tonsil was removed in

toto and the specimen was sent for

histopathology and immunohistochemistry. Post

operative period was uneventful.

Histopathology confirmed the diagnosis thephotomicrograph showing epithelial islands

surrounded by lymphocytes. Immunohisto

chemistry showed cytokeratin showing positivity

for the epithelial cell nests. After confirmation

patient was referred for radiotherapy and

followed up every 6 months for the past 2 years.

2 years follow up showed no evidence of

recurrence or residual tumour.

Fig.1: Epithelial islands surrounded by

lymphocytes.

Fig.2: Immunohistochemistry shows cytokeratin

showing positivity for the epithelial cell nests

Fig.3: Macroscopic appearance of dissected Tonsil

DISCUSSION

Non nasopharyngeal lymphoepitheliomas are

rare. Such lesions have been reported in the base

of tongue2

In 1921 Reverchan and coutard

reported from Regauds clinic tumours of

hypopharynx to which Regaud had given the

name lymphoepithelioma. In the Same year

Schminke also reported a series with the same

name. The name was applied by Regaud and

Schminke apparently independently in view of

the probable origin from the structure described

as lymphoepithelial organs3

. Tracheallymphoepithelioma like carcinoma has also been

reported.4

Relationship with Ebstein Bar virus is

less in Non nasopharyngeal Lymphoepithelioma.

Even if it is related it does not affect the mode of

treatment.

CONCLUSION

Regauds tumour involving the Tonsil is rare. It

affects the younger age group. Lymphnodeinvolvement is common. Diagnosis is made by

CT scan and clinical examination. Confirmed by

Histopathology and Immunohistochemistry.

Tumour is radiosensitive. Removal of the tonsil

and subjecting the patient to radiotherapy is

helpful.

REFERENCES

1. Munro Black JL. The lymphoepitheliomata.

The journal of laryngology And Otology.1938;53 (4) 225 -245.



999


2. Merz H, Marnitz S, Erbersdobler A, Goektas

O. Schminckes tumour, Carcinoma of the

base of the tongue, a case report. Case rep

oncol. 2010;3(1):77 – 82

3. Cappel DF. On lymphoepithelioma of

nasopharynx and tonsils. The journal of pathology and Bacteriology. 1934;39(1):49 –

64

4. Sathyanarayana Pathak. Tracheal

lymphoepithelioma like carcinoma – A case

report. Indian journal of cancer. 2002; 39 (3)

112 -1



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Rajeshwari et al., Int J Med Res Health Sci. 2013;2(4):1000-1002


&

Health Scienceswww.ijmrhs.com Volume 2 Issue 4 Oct-Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886Received: 23rd Aug 2013 Revised: 17th Sep 2013 Accepted: 29th Sep 2013

Case report

INCOMPLETE FORMATION OF POSTERIOR CORD OF BRACHIAL PLEXUS: A CASE

REPORT

*Rajeshwari MS1,Vijay Kumar S

2

1Associate Professor,

2Post Graduate, Department of Anatomy, Bangalore Medical College and

Research Institute, Bangalore, Karnataka, India.


ABSTRACT

Brachial plexus is a network of nerves formed at the root of the neck to provide motor and sensory

branches to the upper limb. The major contribution for this plexus is by the anterior primary rami of

C5,6,7,8 and T1. The roots join to form the trunks which in turn divide into anterior and posterior

divisions to form the cords. The knowledge of brachial plexus is important for the anaesthetists while

administering brachial blocks. During routine dissection in a female cadaver aged 65years, the posterior

division of upper trunk fails to fuse with the posterior divisions of the middle and lower trunk and gives

out four branches independently.

Keywords: Brachial plexus, Posterior cord, Radial nerve, Axillary artery.

INTRODUCTION

Brachial Plexus is a complicated network of

nerves where the ventral primary rami of

C5,6,7,8,T1 confluence at the root of the neck and

then ramify to provide sensory and motor

branches to the upper limb. The roots join toform the trunks, namely the upper trunk formed

by the union of C5 &C6, the middle trunk

formed by the continuation of C7 root and lower

trunk formed by the union of C8 &T1. This

formation takes place in the interscalene space

in the posterior triangle.1

Each trunk gives off

anterior and posterior divisions behind the

clavicle to form three cords viz.., the lateral,

medial and posterior cords. The three cords

enter the axilla and are named according to their

relation with second part of axillary artery. The

lateral cord is formed by the union of anterior

division of upper and middle trunk, the medial

cord is formed by the anterior division of lower

trunk and the posterior cord is formed by the

union of posterior divisions of all the threetrunks.

2The cords branch out to supply the

flexor and the extensor compartments of upper

limb. The branches which arise from the roots

and the trunks are seen above the clavicle and

these are called as supraclavicular and the

branches which arise mainly from the cords are

seen below the clavicle hence these are infra-

clavicular branches. The posterior cord provides

the upper subscapular nerve, thoraco-dorsal

nerve, lower subscapular nerve, axillary nerve

and the continuation of the cord is the Radial

DOI:10.5958/j.2319-5886.2.4.164



1001


nerve. The upper subscapular, lower

subscapular and axillary nerves convey fibers

from C5,6 the thoraco-dorsal nerve conveys

fibers from C6,7,8 and radial nerve conveys fibers

from C5,6,7,8

,&T11

CASE REPORT

During routine dissection for I year MBBS in

the department of Anatomy at Bangalore

Medical College and Research Institute,

Bangalore, during the exposure of axilla in a

female cadaver aged 65years, it was noted on

the left side that the posterior cord of brachial

plexus was not formed completely and the

branches originated independently from theposterior division of the upper trunk, the

branches were traced and photographed.

The Posterior division of upper trunk conveying

fibers from C5 &C6, failed to unite with the

posterior division of middle and lower trunk.

The posterior division of upper trunk provided

four branches directly -upper subscapular, lower

subscapular and axillary nerve, thus carrying

fibers from C5 & C6, it also provided an

additional branch which lies lateral to axillary

nerve course downwards behind the subscapular

artery which is called here, as the inferior

division of radial nerve (fig1).The posterior

divisions of middle trunk and lower trunk unite

and immediately gives out the thoraco-dorsal

nerve. Close to its origin it receives a

communicating branch from the posterior

division of upper trunk (fig2), the rest of the

nerve then courses downwards in front of the

subscapular artery to form the superior division

of radial nerve. At the lower border of

subscapularis muscle the two divisions of radial

nerve unite to continue as the radial nerve thus

comprising of fibers from C5, 6,7,8, &T1. The

two divisions of radial nerve form a loop around

the subscapular artery which is branch of third

part of axillary artery. (fig2)

Fig 1: Four branches from the posterior division

of upper trunk

Fig2: Showing thoraco-dorsal nerve (TDN) and

superior division of radial nerve derived from the

union of posterior divisions of middle and lower

trunk.

Also seen is the thoraco-dorsal nerve receiving

communicating branch (COM.Br) from the posterior

division of upper trunk. (coloured yellow are the

two divisions of radial nerve, pierced by the

subscapular artery)

Abbreviations: Upper subscapular nerve

(USN), Lower subscapular nerve (LSN),

Axillary nerve (AN), and inferior division of

radial nerve (RN) deep to subscapualar artery

DISCUSSION

Posterior cord is formed by the union of the

posterior divisions of upper, middle and lower

trunks. The variations in the formation and

branching patterns of brachial plexus are quite

common and have been reported time and again

by several authors. The variations can occur in

the formation of trunks, divisions, cords, at the



1002


level of branching or its relationship with the

axillary artery; however the make-up of terminal

branches remains unchanged.2

The unusual

formation may be attributed embryologically

where the axons of the spinal nerve grow

distally in different directions to reach the limbbud mesenchyme. Once these developmental

variations are formed they persist post-natally

and appear as variations in adulthood.2

The

radial nerve was formed by the posterior

divisions of middle and lower trunk without any

contribution from the upper trunk 3.

The

posterior cord divided into two roots enclosing

the subscapular artery and the roots fused to

continue as radial nerve

4.

The radial nerve hastwo roots arising from the posterior cord the two

roots unite to continue as radial nerve after

clasping the subscapular artery5. Posterior cord

is formed by the union of posterior division of

upper and middle trunk without any

contribution from lower trunk 6.

CONCLUSION

The variations usually occur at the junction or

separation of individual parts. Variations in

nerves in their course or branching are prone for

entrapment neuropathies. The close relationship

of the variant nerves with the axillary artery

may result in arterial compression leading to

ischemic pain. The knowledge of these

variations is useful for the neurosurgeons while

managing axillary tumors, for orthopedic

surgeons in treating upper limb fractures or for

anesthetists in proper planning of brachialplexus blocks.

REFERENCES

1. Dutta AK. Essentials of human

Anatomy,superior and inferior

Extremities,2nd

edition;1995;51-52.

2. Moore KL, Dally AF. Upper limb in

clinically Oriented Anatomy, 5th

edition,

Lippincott, Williams and Wilkins :2006,

pg774-75.

3. Aktan. A cadaveric study of the anatomic

variations of the brachial plexus nerves in

the axillary region and arm, Turkish Journal

of Medical sciences. 2001;31(2);147-50.4. Bhat KMR. Variation in the branching

pattern of posterior cord of brachial plexus;

Neuroanatomy. 2003;7:10-11.

5. Jamuna M. A rare variation of the branching

pattern of radial nerve; International Journal

of Anatomic Variation 2011;4:22-24.

6. Fazan. Brachial plexus variations in its

formation and main branches; Acta

Cirurgica Brasiliera; 2003;18(5):14-18.



1003

Rupankar et al., Int J Med Res Health Sci. 2013;2(4):1003-1005


&

Health Sciences




thSep 2013

Case report

HYPERSENSITIVITY TO LIGNOCAINE: A CASE REPORT

*Rupankar Nath

1, Sanju Sharma

1, Anshuman Dutta

2, Joydeep Roy

3, Tulika Singh

4

1Department of Anaesthesiology,

2Department of Orthopaedics,

3Department of Dermatology, Silchar

Medical College, Assam, India4Department of Community Medicine, Lady Hardinge Medical College, New Delhi, India


ABSTRACT

Local anaesthetics are a very important group of drugs in the anaesthetists’ armamentarium. They have

very widespread use in many branches like surgery, Orthopaedics, ENT, Obstetrics & Gynaecology.

Most popular amide group representative – lignocaine – is used as its hydrochloride salt at a

concentration of 1 or 2% with or without epinephrine. Though hypersensitivity reactions are rare, they

may occur and varies from life threatening anaphylaxis to less severe delayed type reactions. Here we

are reporting a case of delayed type 4 reaction to lignocaine after supraclavicular brachial plexus block

which was managed conservatively.

Keywords: Lignocaine, Local anaesthetics, Type 4 hypersensitivity, Supraclavicular brachial plexus

block

INTRODUCTION

Local anaesthetics have been very widely used

since the discovery of the anaesthetic effect of

cocaine in 1884. In spite of their widespread use,true hypersensitivity appears to be infrequent.

Most of the adverse reactions are due to

pharmacologic or toxic effects of local

anaesthetics. While type 1 hypersensitivity

reactions to lignocaine are uncommon, type 4

hypersensitivity is reported even less frequently1.

Here we report a case of a patient with no history

of allergy to local anaesthetics, which developed

an allergic reaction after exposure to preservative

free lignocaine.

CASE REPORT

A 45 – year-old male presented for implant

removal from lower third of humerus. He

underwent surgery for fracture lower third of

humerus about a year back under GA which was

uneventful. This time as it was decided for a day

care surgery anaesthetic plan was supraclavicular

brachial plexus block. He had no previous

history of allergic reactions to food or drugs and

was not on any medications. After obtaining

informed written consent supraclavicular

brachial plexus block was administered with 1%30 ml lignocaine with 1:2,00,000 adrenaline.

DOI:10.5958/j.2319-5886.2.4.165



1004


That formulation was preservative free. After the

block was established surgery was allowed to

proceed. Intra operatively he did not receive any

other medication and the surgery was uneventful.

Though the procedure was planned as day -care

but he was not discharged on-request andadmitted. Next day he complained of itching and

rashes in the neck. On examination we found

severe urticarial rashes in the neck and chest

extending to sternum on the side where block

was administered (Fig 1). He was treated

conservatively with anti histaminics and was

discharged on symptomatic relief.

Fig 1: Urticarial rashes on the neck and chest

after supraclavicular brachial plexus block with

lignocaine

DISCUSSION

Local anaesthetics have traditionally been

divided into 2 groups according to their chemical

structure: esters and amides2. Allergic reactions

of local anaesthetics are extremely rare (less than

1%) 3. Aminoesters such as procaine may

produce allergic-type reactions more commonly

than aminoamides. Even with aminoesters, the

vast majority of reactions are not allergic.

Aminoesters, unlike aminoamides, are

derivatives of p-aminobenzoic acid (PABA),

which is known to be allergenic. Allergy to local

anaesthetics may be type 1 immediate

hypersensitivity reaction mediated by IgE

antibodies or type 4 delayed hypersensitivitymediated by lymphocytes.

Lignocaine (Lidocaine, Xylocaine) is an

aminoamide type of local anaesthetic agent. It is

probably the most widely used local anaesthetic

agent not only as a topical and injectable

anaesthetic, but also intravenously in the

treatment of cardiac arrhythmias. Despite itswidespread use adverse reactions to lignocaine

are uncommon. Most reactions are type 1

immediate hypersensitivity1. There are few

published cases of type 4 delayed

hypersensitivity. It is likely that many cases are

not recognized. On January 1, 2001, the North

American Contact Dermatitis Group (NACDG)

added this antigen to their standard tray to assess

the frequency of sensitivity to lignocaine

1

.Adverse reactions to lidocaine and others LAs

are extremely rare and less than 1% of adverse

reactions caused by local anaesthetic drugs are

due to be true allergy. There are a few cases

reported in literature in which the patient had

developed a type 4 hypersensitivity reaction to

injection of lignocaine.

Bircher et al4reported a patient with localized

swelling 24 hours after dental surgery with patch

test showing lignocaine sensitivity.

Whalen5

reported a patient with localized,

pruritic, vesiculobullous delayed type

hypersensitivity reaction on the dorsum of the

hand 12 hrs after lignocaine injection. Patch test

confirmed it.

Briet et al6

described a man who developed

pruritus, swelling erythema at lignocaine

injection sites. Results from prick and

intradermal tests were negative at 20 minutes,but intradermal test results were positive at 48

hours; thus indicating type 4 hypersensitivity.

Downs AMR et al7

described one patient having

immediate hypersensitivity to lignocaine during

an injection for a dental procedure, but patch test

revealed delayed type of hypersensitivity.

Christine L. Mackley et al1

patch tested 183

patients and all those who were positive to

lignocaine were challenged with 0.1 mlpreservative free 1% lignocaine intradermally.

Four cases had positive reaction to lignocaine.



1005


They concluded that delayed type

hypersensitivity to lignocaine may occur more

frequently than previously thought and given its

frequent use, may become widespread.

Duque et al8

described a woman who suffered

eczematous eruption on her face after theadministration of lignocaine and mepivacaine for

dental surgery. Patch test showed delayed type

hypersensitivity to amide local anaesthetics

lignocaine and mepivacaine.

In our case the patient received preservative free

1% lignocaine with adrenaline (1:2, 00,000) for

supraclavicular brachial plexus block. The

intraoperative and immediate postoperative

period was uneventful. The patient developeditching and subsequently skin rashes about 16 to

20 hours after administration of Local

anaesthetic. It was diagnosed as urticarial rashes

and the patient was treated conservatively with

anti allergic medications as soon as the rashes

were reported. Patient was advised patch test for

lignocaine for further evaluation; which he

refused. So we could not proceed for further

testing. On clinical grounds it is assumed to be

because of hypersensitivity to lignocaine. We

suspected lignocaine to be the cause because the

preparation was preservative free and no other

drug or sedative were used to supplement the

block. Adrenaline as causative agent was ruled

out because the reaction was localized and also

delayed. On further enquiring it was found that

the patient had no history of exposure to Local

anaesthetics or allergy to any drug or substance.

Moreover he underwent surgery for once onlybefore this, for putting the implant which he

underwent under general anaesthesia without the

use of local anaesthetic.

After ruling out other probable causes of allergy

we came to conclusion that the reaction was a

true hypersensitivity to lignocaine as the

formulation we used was preservative free. We

finally conclude with a note that allergic

reactions to local anaesthetics though rare can

occur in clinical situations in our day to day

practice to anyone of us and given its widespread

use the incidence is likely to increase. So it is

better to be aware of these adverse reactions and

be prepared for any untoward incident that may

occur during simplest of procedures.

REFRENCES

1. Mackley CL, Marks JG, Jr, Anderson BE.

Delayed-Type Hypersensitivity to Lidocaine.

Arch Dermatol. 2003;139(3):343-346.

2. Miller RD, Ed. 7th

edn, Anesthesia, Churchill

Livingstone Publisher: 2009; 913-15

3. Giovannitti J, Bennett CR. Assessment of

allergy to local anaesthetics. Journal of

American Dental Association.

1979;98:701-76.

4. Bircher AJ, Messmer SL, Surber C, Rufli T.

Delayed-type hypersensitivity to

subcutaneous lidocaine with tolerance to

articaine: confirmation by in vivo and in vitro

tests. Contact Dermatitis.1996;34:387-89.

5. Whalen JD. Delayed-type hypersensitivity

after subcutaneous administration of amideanesthetic. Arch Dermatol. 1996;132:1256-

57.

6. Breit S, Rueff F, Przybilla B. Deep impact

contact allergy after subcutaneous injection

of local anesthetics. Contact Dermatitis.

2001;45:296-97.

7. Downs AMR, Lear JT, Wallington TB,

Sansom JE. Contact sensitivity and systemic

reaction to pseudoephedrine and lignocaine.Contact Dermatitis. 1998;39:33.

8. Duque S, Fernández L. Delayed-type

hypersensitivity to amide local anesthetics.

Allergol et Immunopathol 2004;32(4):233-

34.



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Saxena D et al., Int J Med Res Health Sci. 2013;2(4):1006-1008


&

Health Sciences




thSep 2013

Case report

A RARE CASE OF FAMILIAL ADENOMATOUS POLYPOSIS

Saxena D, Akhtar M, *Kundra DN, Zaki M, Rangwala M

Department of Surgery, NKPSIMS & LMH, Nagpur, Maharashtra, India

* Corresponding author email - [email protected]

ABSTRACT

FAP is an autosomal dominant disease characterized by numerous polyps, numbering from hundreds to

thousands, in intestine. It is a very rare condition with incidence ranging from 1 in 6000 to 1 in 12000

births. In absence of surgical intervention, their malignant transformation is inevitable. We report this

case because of its rarity.

Keywords: Familial adenomatous polyposis, Colonoscopy, Adenomatous polyposis coli gene, Ileal

pouch-anal anastomosis

INTRODUCTION

Colorectal carcinoma is one of the leading cause

of deaths due to malignancy globally. FAP is a

type of inherited colorectal carcinoma which is

autosomal dominant and characteried by

numerous polyps in the epithelium of intestine.

These polyps are benign in beginning and their

malignant transformation is inevitable around the

age of 34-43 years, if no surgical intervention isdone.

1,2

CASE REPORT

A 24 years old male presented with complaints

of tenesmus and passing watery stools since 2 yrs

and passing blood with stools since 4 months.

There was no significant family history .His

vitals were normal and on per-rectal

examination, multiple polyps were palpablearound 2cms from anal verge. On proctoscopy

there was mucoid discharge with multiple polyps

all around. His routine blood investigations were

normal and USG abdomen also did not reveal

any abnormality. On Colonoscopy there were

multiple polyps in rectum, 1-4cms in size, which

were both pedunculated and sessile. There were

more than 100 polyps throughout the colon till

caecum (Fig.1). Their density decreased

proximally. The biopsy report was suggestive of adenomatous polyps. A diagnosis of FAP was

kept and decision to perform exploratory

laparotomy with total proctocolectomy with ileal

pouch – anal anastmosis was planned . Surgery

was performed by midline incision, specimen

was dissected from terminal ileum up to anal

canal, around 2cms from anal verge .Colon was

studded with polyps throughout its length (figure

2,3). Ileal “J pouch” was created (figure 3) andanastmosed with anal canal using circular

staplers. A diverting loop ileostomy was done

DOI:10.5958/j.2319-5886.2.4.166



1007


before closure. The histopathologic findings

were consistent with multiple adenomatous

polyps with mild to moderate dysplasia (figure4).

Patient was regularly followed up and 6 months

later ileostomy closure was planned. A distal

loopogram was done which was within normallimits. Anal continence was checked and

ileostomy closure was done. The immediate

family members of patient could not be screened

as they lived in a different city. Patient has been

followed up to date and no complications have

been detected so far.

Fig 1: Colonoscopic image showing numerous polyps

throughout colon

Fig 2: Photograph of colon after resection

Fig 3: The opened section of specimen showing

numerous sessile and pedunculated polyps

Fig 4: Creating ileal “j-pouch”

Fig 5: Histological appearance of specimen

(magnification x200)

DISCUSSION

FAP is one of the familial causes for colorectal

carcinoma. Sklifasowski published the first

verified case of FAP in 1881 in Russia. Over the

years, with discovery of APC gene FAP has

become a separate entity.3

FAP results from

mutation in the APC (adenomatous polyposis

gene) gene. APC is a tumor suppressor gene

located on the long arm of chromosome 5 inband q21.

4

Symptoms may not present until the adenomas

are large and numerous so as to cause intestinal

bleeding. Patient may complain of change in

bowel habits, constipation/diarrhea, abdominal

pain or weight loss.5

Extraintestinal manifestations may include

Osteomas, which can be identified as occult

radio-opaque jaw lesions, Congenital

hypertrophy of the retinal pigment epithelium

and cutaneous lesions such as fibromas, lipomas,



1008


sebaceous cysts , epidermoid cysts and

nasopharyngeal angiofibromas.3

Association of

gastro-intestinal polyps with other extra intestinal

manifestations is known as “Gardner’s

syndrome”.6

Surveillance examination in patients with familyhistory or suspected cases, is recommended

beginning at age 10-12 years .Sigmoidoscopy is

recommended every year. Once colon polyps are

found, or by age 20-25 years, colonoscopy

should be done. Multiple colonic polyps, usually

more than 100 are diagnostic for FAP. Genetic

testing is useful in confirming a diagnosis of

FAP in those cases where there is some doubt

about the diagnosis.

7

The aim of the surgical treatment of FAP is to

remove the polyps before the transformation to

malignancy occurs. The surgical options are –

1. Colectomy and ileo-rectal

anastomosis(IRA)

2. Proctocolectomy with ileal pouch-anal

anastomosis (IPAA)

3. Proctocolectomy and ileostomy

Choice of surgery depends upon extent of rectal

involvement. IRA is a simple operation with

quick recovery, low complication rates and

minimal lifestyle interference; however the risk

of cancer in rectum mandates yearly surveillance.

IPAA minimizes this risk but adenomas develop

in the ileal pouch so surveillance is still

necessary. A hand sewn IPAA has more

complications and poorer function than a stapled

IPAA. Laparoscopic surgery can be attempted in

cases which are detected early and with lessextensive intestinal involvement.

8

Medical management of FAP is also under

research. Sulindac, a non-steroidal anti-

inflammatory drug, has been shown in studies to

achieve prolonged remission of polyps. However

it is still under investigation and not a routine

treatment replacing surgery. Aptosyn, a

derivative of sulindac and Celecoxib, a COX-2

specific antagonist have also been tried but arenot as effective as Sulindac.9

Genetic counseling should be offered to family

members of a diagnosed patient.

REFERENCES

1. Boia ES, Mejdi R. Familial adenomatous

polyposis (FAP); What must be known and

what should be done-case report. Pediatr J

2008;11:46-9.

2. Srinivasamurthy M, Geethamala K, Kumar

BD, Sudhrao M . Familial adenomatous

polyposis coli and adenocarcinoma of the

colon: A silent synchronous presentation.

Arch Int Surg 2012;2:101-4.

3. Steffen Bulow, Terri Berk, Kay Neale. The

history of Familial Adenomatous Polyposis.Familial Cancer 2006;5:213-220.

4. Groden J, Thliveris A, Samowitz W, Carlson

M, Gelbert L, Albertsen H, Joslyn G, Stevens

J, Spirio L, Robertson M: Identification and

characterization of the familial adenomatous

polyposis coli gene. Cell 1991, 66:589-600.

5. Elizabeth Half , Dani Bercovich, Paul Rozen;

Review of Familial adenomatous polyposis.

Orphanet Journal of Rare Diseases.

2009, 4:22

6. Polymnia Galiatsatos, William D. Foulkes;

Familial Adenomatous Polyposis, American

Journal of Gastroenterology. 2006;101:385 –

98

7. Familial Adenomatous Polyposis (FAP)

2002, 2008 The University of Texas MD

Anderson Cancer Center 10/01/08

8. Ambroze WL, Dozois RR, Pemberton JH.

Familial adenomatous polyposis: resultsfollowing ileal pouch-anal anastomosis and

ileorectostomy. Dis Colon

Rectum.1992;35:12-15

9. Giardello FM, Hamilton SR, Krush AJ.

Treatment of colonic and rectal adenomas

with sulindac in familial adenomatous

polyposis. N Engl J Med. 1993;328:1313-16.



1009

Santosh et al., Int J Med Res Health Sci. 2013;2(4):1009-1012


&

Health Scienceswww.ijmrhs.com Volume 2 Issue4 Oct - Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886

Received: 24th


Sep 2013 Accepted: 28th

Sep 2013

Case report

KETOTIC HYPOGLYCEMIA IN CHILDREN “NOT AN UNCOMMON ENTITY BUT IS

RARELY THOUGHT OF”: CASE SERIES

*Santosh Yadav1, Prashant Nigwekar

2, Dhananjay Y Shrikhande

3, Amit Patil

1, Amit Yadav

1, Nilesh

Maniya1

1Resident,

2Assoc. Professor,

3Professor and Head, Department of Pediatrics, Rural Medical College,

Paravara Institute of Medical Sciences, Loni, Maharashtra.


ABSTRACT

Ketotic hypoglycemia is the most common form of childhood hypoglycemia. Periods of Hypoglycemic

episodes typically occur during early morning, especially during intercurrent illness when food intake is

limited. The symptoms and signs of hypoglycemia are often overlooked .Because hypoglycemia is a life

threatening event can lead to severe neurological sequel, intravenous administration of glucose is

necessary. These children respond promptly to glucose. We share our experience of four cases of

Ketotic hypoglycemia admitted during last 2 years.

Key words: Hypoglycemia, Ketosis, Ketotic hypoglycemia, Methylcrotonyl-CoAcarboxylase.

INTRODUCTION

Ketotic hypoglycemia (KH) is a good example of

‘what eyes don’t see that mind doesn’t know’.

KH should be suspected in every child who

present with early morning drowsiness and/ or

convulsions especially after poor intake on theprevious day. So any child presenting with such

symptoms and hypoglycemia proved by

glucometer, urine should be immediately sent for

ketone bodies. If urine ketones are positive the

most likely cause is KH.1

With such an approach we were able to detect

more cases of Ketotic hypoglycemia during the

last few months. This has now become a routine

PICU protocol for children presenting withmorning seizures, drowsiness altered sensorium.

Blood glucose estimation and urine for ketone

bodies as a bedside test are done and confirmed

by laboratory. It is considered as a benign

condition as neurological damage and other

sequels are rare2. The inform consent taken from

parents in the study.

CASE SERIES

Case1. A 6 years old female presented with

complaints of early morning generalized tonic-

clonic convulsions. She had similar episodes 6

times in the past; all occurred early in the

morning. She had been diagnosed as epilepsy

and had been put on anticonvulsants. Seizure

episodes continued. Each episode was associatedwith skipping dinner the previous night.

DOI:10.5958/j.2319-5886.2.4.167



1010


Case2. A 7 years old female presented with

drowsiness since morning, difficulty in arousing

her from sleep and mild grade fever since one

day. History of skipped dinner the previous

night. There was a past history of similar episode

3 months ago. She had been admitted in private

hospital we had low blood sugar was

documented. She improved with IV dextrose and

was discharged. Ketotic hypoglycemia was

neither thought of nor investigated during the

previous episode. We also documented marked

hypoglycemia during this episode.

Case 3. A 4 years male came with the history of

loose motions since previous evening and history

of poor oral intake since previous afternoon. The

child has been drowsy since morning. Therewere no signs of dehydration. No history of

convulsions.

Case 4. A 2 ½ years old female admitted with

altered sensorium and generalized tonic-clonic

convulsions early in the morning. There was no

history of fever.

As per protocols blood sugar was obtained in all

the patients, who showed severe hypoglycemia in

the range of 20- 35mg/dl on glucometer (Modelno.Abbott 0088,Abbott Diabetes care ltd, ART

16648,Rev.B05/10) Hypoglycemia was

confirmed by laboratory method (Glucose

Oxidase Peroxidase) also. Urine ketones were

positive in all patients 3+ to 4+,

Anthropometry, general and systemic

examination was normal in all cases.

Biochemical parameters like serum calcium,

serum magnesium, Liver function test, Renal

function test, Ceribro spinal fluid, CT scan head

and EEG done in all patients, were within normal

limits.

All the four cases were managed according to

routine emergency management. IV 10 %

dextrose bolus was given, followed by

appropriate IV fluid infusion. Blood glucose

level was monitored until condition was

stabilized.

Out of four, only three patients case 1,2,3 wereinvestigated for metabolic disorders by tandem

mass spectrometry (TMS) due to financial

constraints these could not be done in case 4.

Reports of case1,3 patients were within normal

limits.

TMS report of one patient case 2 came positive

for acylcarnitine profile showing increased levels

of 3-OH isovalerylcarnitine (C5OH). Urinary

organic acid profile showed increased levels of

3-methylcrotonyl glycine. Above findings were

suggestive of inborn error of metabolism of

leucine metabolism due to deficiency of enzyme

3-methylcrotonyl-CoA carboxylase (MCC)3.

This child was kept on oral carnitine, restricted

protein diet and asked for regular follow-up.

All patients were discharged with an advice of

frequent feedings of a high-carbohydrate,

balance protein diet and no skipping dinner atnight especially during intercurrent illnesses.

Parents were asked to monitor urine ketones

during intercurrent illness by ketosticks. They

were also told that an improvement and a marked

reduction in the occurrence of these episodes can

be expected as the child grows and attains

puberty and adolescence, with an increase in

muscle mass.

DISCUSSION

KH is most commonly seen in early childhood

between 1.5-5years of age. Condition remits

spontaneously by the age of 8 – 9 years.

Hypoglycemic episodes typically occur during

periods of intercurrent illness when food intake is

limited. The classic history is of a child, who eats

poorly or completely avoids the evening meal,

who is difficult to arouse from sleep the

following morning, and may have a seizure or be

comatose by early or mid morning. Infants with

this condition do not manifest hypoglycemia due

to frequent breastfeeding.

The etiology of ketotic hypoglycemia may be a

defect in any of the complex steps involved in

protein catabolism, oxidative deamination of

amino acids, transamination, alanine synthesis,

or alanine efflux from muscle. Rarely, inbornerrors of fatty acid metabolism present as ketotic

hypoglycemia, although, typically, fatty acid



1011


oxidation defects produce hypoketotic

hypoglycemia1. Diet rich in Carbohydrates and

Protein with more frequent feeding is the

recommended treatment for ketotic

hypoglycemia. The appearance of ketone in

urine precedes hypoglycemia by several hours.

Parents are advised to test the child's urine for the

presence of ketones. In the presence of ketonuria,

liquids of high carbohydrate content should be

given. Patient requires hospitalization in case if

oral feeding is not tolerated. During the

intercurrent illness, if frequent estimations and

early detection of urinary ketones done at home,

hypoglycemia can be prevented (as ketones are

detected in urine much before hypoglycemia).

Other causes of hypoglycemia with ketosis –

Adrenal insufficiency, Hypopituitarism, Glucose-

6-phosphatase debrancher defect, Fructose-1, 6-

diphosphatase defect, Galactosemia, glycogen

storage disease, fatty acid oxidation defects.

Adrenal insufficiency, Hypopituitarism,

glycogen storage disease, galactosemia could be

the other cause in children and infants with

seizures, drowinessor coma in the morning.

Glucose-6-phosphatase debrancher defect,Fructose-1,6-diphosphatase defect have moderate

hepatomegaly. Fatty acid oxidation defects

usually do not manifest as ketosis. More

advanced investigations like estimation serum

levels of alanine, insulin, and lactate before and

after deliberate fasting for 24-36 hours are not

done in our cases due to non availability and

economic reasons.

3-Methylcrotonyl-CoA Carboxylase (3-MCC)

Deficiency: 3-Methylcrotonyl-CoA Carboxylase

(3-MCC) deficiency has been recognized since

19847.It is a defect in the degradation of the

amino acid leucine which is

glucogenicaminoacid7. The clinical presentations

of 3-MCC deficiency range from mild to severe

illness. The age of onset of 3-Methylcrotonyl-

CoA Carboxylase (3-MCC) deficiency

symptoms is between 1-5 years. Clinical

presentation is often with infection, illness, orafter fasting. Most common symptoms are

vomiting, lethargy, hypotonia, apnea, or

hyperreflexia and seizures8. Patients may have

profound hypoglycemia, mild metabolic acidosis,

hyperammonemia, elevated liver transaminases,

and ketonuria8. Plasma free carnitine may be

low. Newborn Screening using tandem mass

spectrometry reveals an elevation of C5-hydroxy

acylcarnitine from the dried blood spot of an

affected patient. Diagnosis of 3-MCC deficiency

then requires further testing. Urine organic acid

analysis finds elevation of 3- hydroxyisovaleric

acid and usually 3-methylcrotonylglycine3.

The condition is inherited as an autosomal

recessive trait. The gene for α subunit ( MCC1) is

located on chromosome 3q25 – 27 and that for the

β subunit ( MCC2) is mapped to chromosome

5q12 – 13. Mutation in either of these genes mayresult in the deficiency of the enzyme activity

5.

Tandem mass spectrometry have identified an

unexpectedly high number of infants with 3-

methylcrotonyl CoA carboxylase deficiency

(1:50,000), suggesting that this condition may be

one of the most common organic acidemias in

certain populations4.

Assay of 3-MCC in fibroblasts or leukocytes can

be used for confirmation of deficiency, alongwith at least one other carboxylase having

normal enzyme activity must also be

assayed.3This assay was not possible in our case.

CONCLUSION

KH though not uncommon, require a high index

of suspicion and should be suspected in any child

with early morning seizure, drowsiness and / or

altered sensorium and confirmed by glucometer.Urinary ketones should be done routinely in such

patients. Further metabolic screening and other

advanced investigations may be done after

inquiry of consanguinity, proper history and

clinical examination. Early recognition of the

condition will prevent further hypoglycemic

episodes and unnecessary anticonvulsants. TMS

should be done in every patient to find a rare

metabolic disorder.



1012


REFERENCES

1. Mark A.Sperling. Nelson text book of

pediatrics, Elsevier, 19th

edition 2012 ; 528-

30.

2. Mitchell GA, Fu Kao T. Inborn error of

ketone metabolism.In: Scriver CR, Baudet

AL. The Metabolic and Molecular Bases of

Inherited Disease..New York: McGraw-hill

Co. Inc.;2001;2(Chap. 102):2327-35

3. http://www.perkinelmer.com/Industries/Healt

hcare/NewbornTestingServices/Clinician-

Information /3-Methylcrotonyl-CoA-

Carboxylase-Deficiency-(3MCC-

Deficiency).xhtml

4. Koeberl DD, Millington DS, Smith WE.Evaluation of 3- methylcrotonyl-CoA

carboxylase deficiency detected by tandem

mass spectrometry newborn screening. J

Inherit Metab Dis 2003; 26:25-35.

5. Baumgatner, Baumgatner MR. Molecular

mechanism of dominant expression in 3-

methylcrotonyl CoA carboxylase deficiency.

J Inherit Metab Dis 2005; 28:301-09

6. Dantas, Dantas MF, Suormala T, Randolph

A. 3-Methylcrotonyl-CoA carboxylase

deficiency: Mutation analysis in 28 probands,

9 symptomatic and 19 detected by newborn

screening. Hum Mutat 2005; 26:164.

7. Satyanarayan U. Metabolism of amnoacids.

Biochemistry. 2010;15;364-66.

8. William L Nyhan. Abnormalities in

aminoacid metabolism in clinical medicine ;

Appleton-Century-Crofts 1984;chapter 5; 65-

78



1013

Saleem et al., Int J Med Res Health Sci. 2013;2(4):1013-1016


&

Health Sciences




thSep 2013

Case report

KIKUCHI-FUJIMOTO DISEASE (HISTIOCYTIC NECROTIZING LYMPHADENITIS): A

CASE REPORT

*Saleem Nasir

1, Mubbasher Ameer Syed

2

1Training Medical officer (Resident), Medicine, Hayatabad Medical Complex, Peshawar, Pakistan

2Medical officer, Peshawar Health Clinic, Peshawar, Pakistan


ABSTRACT

Kikuchi-Fujimoto disease (KFD) is a self-limited pathological entity that is benign in its course. The

main features of this disease are tender regional cervical lymphadenopathy, usually accompanied by

low-grade fever and night sweats. Less frequently patients may report weight loss, nausea, vomiting, and

sore throat. Often referred to as KFD; Kikuchi-Fujimoto disease has a global prevalence with high report

rates from Japan and other Asian regions. That said, it is a very uncommon case to encounter due to its

rare occurrence. A viral causation is suggested keeping in view the clinical presentation, the histologyand immunohistochemical pattern. The recommended procedure to diagnose this disease is an excisional

biopsy of an affected lymph node. This histopathologic analysis is essential for the clinician to

differentiate it from similarly presenting conditions like tuberculous lymphadenitis (scrofula), lupus

(SLE) or malignant lymphoma to state a few. This is especially pertinent in regions where there is a high

index of suspicion for tuberculosis given its high prevalence, like Pakistan and India for example. It is

also essential to inculcate an understanding of this clinically and histopathologically challenging disease

amongst physicians and pathologists alike to decrease the risk of misdiagnosis. Steps to increase

awareness will also help curb the excessive costs and unnecessary interventions that go with wrong

diagnoses. In young patients who present with lymph node enlargement in the posterior cervical chain; abiopsied node showing cellular and nuclear fragmentation along with features of necrosis should incite

the consideration of KFD amongst other differentials. Once diagnosed; symptomatic treatment with

NSAIDs, analgesics, antipyretics and in some cases corticosteroids is sufficient as the self limited

disease resolves by itself within a period of 1 month in most cases. It is unlikely to stretch beyond 4

months. Patients with KFD are followed for many years nonetheless, since these patients are at a slightly

increased risk of developing systemic lupus erythmatosus later in life than the general population.

The case we report is that of an 18 year old female patient who presented with a month history of low

grade fever, night sweats and cervical lymphadenopathy, which was minimally tender. She was initially

labeled as a case of tuberculous lymphadenitis and put on antituberculous therapy. However, she did not

respond and further diagnostic studies revealed the presence of KFD.

Keywords: Cervical lymphadenopathy, Kikuchi-Fujimoto disease, Self-limiting

DOI:10.5958/j.2319-5886.2.4.168



1014


CASE REPORT

An 18 year old female college student presented

to the outpatient department of Medical B unit of

Hayatabad Medical Complex, Peshawar,

Pakistan, in February of 2012, with a one month

history of low grade fever, spiking mostly in the

evening and night, and associated with nausea,

malaise and sweating. The fever was intermittent

in character. There were no aggravating factors,

however it was relieved to some extent with

Mefenamic acid but not with Paracetamol. She

also complained of a few lumps in the cervical

and left axillary area for the same duration. There

was no history of any chronic medical illness inthe past. She had no family history of

tuberculosis, no contact history to an active case

of TB, no family history of rheumatological

disorders like rheumatoid arthritis or systemic

lupus erythematosus and no family history of any

blood disorders. Her vitals on presentation were,

Pulse: 105/min, BP: 130/80, and temperature of

100.5oF. On examination she had pale

conjunctivae, and had left cervical and axillary

lymphadenopathy. The rest of her general

physical and systemic examinations were

unremarkable with no pertinent positive findings.

Notably she had no visceromegaly on abdominal

examination.

Lab Investigations:

CBC: Hb: 9.6mg/dl, TLC: 3600/cmm, Plt:

305000/cmm, ESR: 12mm/1st

hr, LDH:

625U/L, RFTs: Urea: 20mg/dl, S.Creat: 0.7

mg/dl, LFTs: Serum total bilirubin: 0.7 mg/dl,ALT: 64U/L, ANA and anti-dsDNA: Negative,

Mantoux showed an induration of 6mm, which

was reported as borderline positive, HBsAg by

ELISA: non-reactive, Anti-HCV antibodies by

ELISA: non-reactive, Monospot Test: Negative,

Urine R/E: Normal, Chest X-ray: Normal, U/S

of the neck showed cervical lymphadenopathy

involving the left mid cervical nodes, U/S

Abdomen: Normal Study, with no evidence of hepatosplenomegaly.

During a previous admission in another medical

unit two weeks back an FNAC from a lymph

node is the left cervical region was done with an

impression of "chronic granulomatous

inflamation most likely due to Tuberculosis”. As

the FNAC report was inconclusive, a excisional

lymph node biopsy was taken and the patient was

empirically started on anti-tuberculous therapy

while awaiting the biopsy result. She was asked

to report back with the same. The biopsy report

confirmed findings consistent with "Kikuchi

Fujimoto Lympahadenitis."

Treatment: Following the biopsy report the anti-tuberculous medications were stopped. She was

started on oral Prednisone (1mg/kg/day), for a

period of 06 weeks followed by a rapid taper.

She responded dramatically to this treatment and

became asymptomatic over the next 4-5 days.

She was counseled about the benign nature of

this disease and advised a 6 week follow-up in

the OPD. On follow up in the OPD six weeks

later she was asymptomatic with complete

regression of her lymph nodes and abatement of

her symptoms. She has remained in remission

after one and a half years of follow up.

DISCUSSION

A disease that most often presents with cervical

lymphadenopathy in young women; histiocytic

Necrotizing Lymphadenitis or more frequently

known as KFD, has now been established as apathologic entity with global prevalence. It was

an entity unheard of until the first case was

reported and recorded in 1972 from Japan.1,2

In

as much as half the patients, the clinical picture

includes fever and low leucocyte counts.3

When a clinician has the job to draw differentials

for a patient presenting with cervical

lymphadenopathy and fever; he has a lot on his

plate all the way from the most obvious entities

like infectious mononucleosis and bacterial

pharyngitis to the more ominous ones like



1015


tuberculosis and lymphoma. Other considerations

might be cytomegalovirus infection,

toxoplasmosis, syphilis and even HIV. With so

much to work out, it is often a taxing diagnostic

workup that ensues. If the culture and stains for

the various organisms are negative and the

presence of unifocal or multifocal necrosis and

histiocytic infiltrate in the backdrop of capsular

invasion and inflammation around the nodes4

is

detected under a microscope; it is strongly

suggestive of KFD.

Some authors have described an association

between systemic lupus erythmatosus and

histiocytic necrotizing lymphadenitis (KFD).5

Others have even gone on to propose the notion

that KFD is merely an unusual presentation of SLE itself. In 2003 a Medline/LILACS (Latin

American and Caribbean Health Sciences) search

was performed by Santana et al.; that discovered

35 instances where KFD and SLE were reported

in the same patients. As per their findings; most

of the cases of SLE were either found after the

diagnosis of KFD or at the time of labeling.6

Our

patient was tested serologically for SLE but all

her results returned negative.

Since KFD is a disease that has a self-limited

course and is deemed benign to add to its rarity

in presentation; not much has been achieved in

the way of creating a targeted treatment for it. It

is recommended that symptomatic measures to

relieve localized and systemic distress associated

with the disease be employed. To counter

tenderness in the enlarged lymph nodes and the

fever that accompanies it; most clinicians rely on

NSAIDs, analgesics and antipyretics. Although

the efficacy of their use is not established

epidemiologically, corticosteroids have been

prescribed in cases with systemic involvement

outside the nodal region or a more severe

presentation of KFD. Neurological involvement

that often presents with aseptic meningitis or

cerebellar ataxia and/or a fulminant lupus like

presentation with positive serologic titers for

ANA have been cited by some authors asindications for steroid use in KFD patients.

Another similar indication for steroid use is

involvement of the liver with high LDH levels.

This latter finding was positive in our patient.

Although the evidence for these widely accepted

indications for steroid use is insufficient itself;

some have gone on to suggest inclusion of a less

severe presentation amongst the indication for

steroid usage. Jang and colleagues suggested

Prednisolone prescription in patients with

recurrent disease, refractory patients who remain

symptomatic despite two weeks or more of

treatment with NSAIDs and for those who desire

a quicker recovery. The monitoring must not be

ignored though since there is always a risk of

developing SLE and/or, much rarely, a

recurrence of KFD later in life.7

Kikuchi's disease is an entity with an unclearetiology. However, several hypotheses have been

put forth with regards to its etiology and

pathogenesis. A number of organisms like human

herpes virus 6, Epstein-Barr virus, HTLV-1

(human T-cell leukemia virus type 1),

cytomegalovirus, parvovirus B19, Yersinia

enterocolitica and parainfluenza virus have been

suggested as organisms that might be implicated

in the etiology of KFD.8

Since it has been observed and reported in

association with SLE; autoimmune processes

contributing to the etiological picture of KFD

have also been suggested. One of the theories in

regards to its causation cites the concept of

molecular mimicry. It proposes that an antigen of

an infectious agent that is similar to a self-

antigen leads to an attack against self by the

activated T-cells.9

This concept can be

exemplified by quoting Lyme disease where such

cross-reaction between LFA-1 (human leucocyte

function associated antigen type 1) and Borrelia

burgdorferi antigen results in chronically

inflamed joints.10

Yet another proposal puts forth

a theory based on apoptotic cells that express

nuclear antigens on their surface, a process very

strongly implicated in the pathogenesis of SLE.

If such apoptotic cells are not adequately and

promptly cleared (i.e. due to complementdeficiency), these can act as a nidus for an



1016


autoimmune process culminating in severe

damage to self tissues.11

CONCLUSION

In view of the lingering fever and fatigue that

often accompany Kilkuchi’s disease, it can

become quite distressing and frustrating for both

the patient and caring physician whilst running

its course. Stating that observation, we are of the

opinion that clinicians should be reminded to

always consider it on the list of differentials for

young patients who present with cervical

lymphadenopathy. We also suggest an effort to

inculcate awareness amongst the pathologists to

look for the characteristic histopathologic

findings of KFD when deciding on specimenfrom patients with the aforementioned features.

These steps are bound to culminate in a decrease

in the number of opinions sought, unrequired

interventions performed and valuable resources

expended. It deserves mention here that in our

review of literature of the disease, we concluded

that whilst associations of KFD with systemic

lupus erythmatosus and other autoimmune

diseases are cited

12,13

; these claims are yet to beadequately verified.

REFERENCES

1. Lopez C, Oliver M, Olavarria R, Sarabia

MA, Chopite M. Kikuchi-Fujimoto

necrotizing lymphadenitis associated with

cutaneous lupus erythematosus: a case

report. Am J Dermatopathol. 2000;22

(4):328 – 332. Kaur S, Thami GP, Kanwar AJ. Kikuchi's

disease, skin and systemic lupus

erythematosus. Br J Dermatol. 2002;146(1):

167 – 68

3. Norris AH, Krasinskas AM, Salhany KE,

Gluckman SJ. Kikuchi-Fujimoto disease: a

benign cause of fever and lymphadenopathy.

Am J Med. 1996;101(4):401 – 05

4. Loachim HL, Ratech H. Loachim's Lymph

Node Pathology. 3rd ed. New York:

Lippincott Williams & Wilkins; 2002.

5. Mahajan T, Merriman RC, Stone MJ.

Kikuchi-Fujimoto disease (histiocytic

necrotizing lymphadenitis): report of a case

with other autoimmune manifestations .Proc

(Bayl Univ Med Cent). 2007 April; 20(2):

149 – 51

6. Santana A, Lessa B, Galrao L, Lima I,

Santiago M. Kikuchi-Fujimoto's disease

associated with systemic lupus

erythematosus: case report and review of the

literature. Clin Rheumatol. 2005;24(1):60 –

63

7. Litwin MD, Kirkham B, Henderson DR,

Milazzo SC. Histiocytic necrotising

lymphadenitis in systemic lupus

erythematosus. Ann Rheum Dis.1992;51(6):805 – 07

8. Menasce LP, Banerjee SS, Edmondson D,

Harris M. Histiocytic necrotizing

lymphadenitis (Kikuchi-Fujimoto disease):

continuing diagnostic difficulties.

Histopathology. 1998;33(3):248 – 54

9. Marrack P, Kappler J, Kotzin BL.

Autoimmune disease: why and where it

occurs. Nat Med. 2001;7(8):899 – 05

10. Gross DM, Forsthuber T, Tary-Lehmann M,

Etling C, Ito K, Nagy ZA, Field JA, Steere

AC, Huber BT. Identification of LFA-1 as a

candidate auto-antigen in treatment-resistant

Lyme arthritis. Science.

1998;281(5377):703 – 06.

11. Botto M. Links between complement

deficiency and apoptosis. Arthritis Res.

2001;3(4):207 – 10.

12. Bosch X, Guilabert A, Miquel R, Campo E.

Enigmatic Kikuchi-Fujimoto disease: a

comprehensive review. Am J Clin Pathol.

2004;122:141 – 52.

13. 13.Martinez-Vazquez C, Hughes G, Bordon

J, Alonso-Alonso J, Anibarro-Garcia A,

Redondo-Martinez E, Touza-Rey F.

Histiocytic necrotizing lymphadenitis,

Kikuchi-Fujimoto's disease, associated with

systemic lupus erythemotosus. QJM.1997;90:531 – 33.



1017

Meena H et al., Int J Med Res Health Sci. 2013;2(4):1017-1020


&

Health Sciences

www.ijmrhs.com Volume 2 Issue 4 Oct - Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886

Received: 24th


Sep 2013 Accepted: 27th

Sep 2013

Case report

MECKEL'S DIVERTICULUM SIX CASE REPORTS OUR EXPERIENCE AND REVIEW OF

LITERATURE

*Meena H. Shaikh, Khilchand Bhangale, Swapnil Kadam, Shantanu Pawar, Tanmay Bhavthankar

Department of General Surgery, Rural Medical College, Pravara Institute of Medical Sciences (DU),

Loni, Ahmednagar, Maharashtra, India


ABSTRACT

A Meckel's diverticulum, a true congenital diverticulum, a vestigial remnant .It connects the yolk sac to

the small intestine in the early embryonic life. It remains without symptoms. In the children symptoms

occur below 2 years. It may contain heterotopic gastric, pancreatic tissue. Presentation can include

gastrointestinal bleeding, obstruction, perforation, and volvulus. Because of this wide range of clinical

scenarios it is important for a clinician to have a high index of suspicion to prevent significant

complications. Investigations like Ultrasonography, Computed tomography (CT scans) and Technetium

99m pertechnate scan helps in diagnosis Treatment is surgical. We are presenting the management of the

six cases supported by a review of the literature. The five patients presented with complications and

needed emergency operation. This is from the rural set up where the advance facilities are limited. The

knowledge of its anatomical and patho-physiological properties is essential to deal with such

complications.

Keywords: Meckel's Diverticulum, Volvulus, Perforation, Gangreen.

INTRODUCTION

According to Dr Charles Mayo, a Meckel's

diverticulum is frequently suspected, often

sought for and seldom found.1

An accepted

incident of Meckel’s diverticulum is 1 to 3

percent. There are many complications related to

Meckel's diverticula . It is difficult to diagnose

Meckel’s diverticulum clinically and by modern

imaging technique. Depending on the type of the

anomaly patients may be completely symptomfree or may present with the complications with

the chronic abdominal pain. The presentation in

six patients in the present case report is different

and created diagnostic dilemma. Meckel’s

diverticulum have no specific signs so difficult to

diagnose High index of possibility of the

Meckel’s diverticulum is essential to manage it

properly. The aim of presenting these case

reports is to share our experience in these cases

and to make clinicians aware of the Meckel's

diverticulum.

DOI:10.5958/j.2319-5886.2.4.169



1018


Case report

Case 1: A five year old boy diagnosed as acute

appendicitis. He was taken for emergency

operation. Laparotomy reveled inflamed and

obstructed Meckel's diverticulum. The obstructed

part resected and ileoileal anastomosis was

done. Histopathology confirmed the diagnosis.

Case 2: A 6 years old boy Presented with

chronic pain in abdomen. His ultrasonography

showed inflamed Meckel's diverticulum. He

underwent elective laparotomy. There was a

band extending from the ileum to the umbilicus.

At the umbilicus there was cystic swelling. (Fig.

1) There was no communication between the cyst

and the umbilicus. Resection and anastomosis

with excision of the band and cyst was done. Thepostoperative course was uneventful.

Histopathology confirmed the diagnosis.

Case 3: Ten years old boy presented in the

emergency with the signs suggestive peritonitis.

He underwent emergency laparotomy. There was

perforation of Meckel's diverticulum at its base.

(Image no2) .Resection and anastomosis was

done. The postoperative course was uneventful.

Histopathology confirmed the diagnosis. [Fig 2]

Case 4: Thirteen-year-old boy was presented

with intestinal obstruction. Plain x-ray abdomen-

erect and USG abdomen confirmed the

diagnosis. Except leucocytosis all other blood

report were normal.

The laparotomy showed gangrenous small

bowel around the constricting band of Meckel's

diverticulum. The affected part excised and

anastomosis was done. Histopathology

confirmed the diagnosis.Case 5: Eighteen year-old boy was presented

with signs and symptoms of intestinal

obstruction in shock. He was operated for acute

appendicitis six months back by the Mac

Burneys incision. He had leucocytosis, decreased

platelet count, Raised blood urea and creatinine.

He was taken for emergency surgery. On

exploring the abdomen, we found the small

bowel volvulus with extensive gangrene due theband extending from small intestine to the

umbilicus. Resection and anastomosis was

performed. Postoperatively the patient went into

the renal failure. He received two hemodialysis.

He expired, gave the message that every effort

must be taken to exclude the Meckel's

diverticulum and to treat it properly.

Histopathology confirmed the diagnosis.

Case 6- Seventy five year-old male patient

admitted with generalized abdominal pain,

vomiting and absolute constipation since two

days before admission. He gave the history of

operation two years back for blunt abdominal

trauma. He was taken for emergency laparotomy

for intestinal obstruction. On exploration, a

Meckel's diverticulum with a length of seventeen

cm was found, with adhesions extending from

Meckel's diverticulum to the umbilicus. Meckel'sdiverticulum showed gangrene. (Fig 3).

Adhesinolysis and resection- anastomosis was

performed. The post-operative course was

unremarkable. Histopathology confirmed the

diagnosis.

Fig.1: Resceted small intestine with Meckel’s

diverticulum and cyst.

Fig.2: Arrow shows perforation of Meckel’sdiverticulum at its base.



1019


Fig.3: Arrow shows gangrene of meckel

sdiverticulum

DISCUSSION

German surgeon Wilhelm Fabricius Hildanus

was first described the diverticulum in 1598, theentity was not named until 1809, when Johann

Friedrich Meckel reported diverticulum's

anatomy and embryology in his research.2,3

Furthermore, Meckel also showed that the

incomplete obliteration of the vitelline duct can

result in not only Meckel diverticulum but also

enterocysts, mesodiverticular bands and

intestinal-umbilical fistulas. Salzer became the

first to identify ectopic mucosa within thediverticulum in 1904.4 Meckel’s diverticulum is

located on the antimesentric border of ileum

around 45 to 60 cm proximal to ileocecal valve.

It is usually 3-5 cm 2% are in length.Its walls

are made up of three layers and are similar to the

intestinal wall.It derives its arterial blood supply

from superior mesenteric artery.5-7

It is present in

2% of population. 2 feet from the ileocecal valve.

2 inches in length.symptomatic. 2 types of

common ectopic tissues are present. 2 times

more boys are affected. In the present case report

all the patients are male. Furthermore, it can be

attached to the umbilical region by the vitelline

ligament, with the possibility of vitelline cysts, or

even a patent vitelline canal forming a vitelline

fistula when the umbilical cord is cut. Torsions

of intestine around the intestinal stalk may also

occur, leading to obstruction, ischemia, and

necrosis. A six years old boy in the case reportfive presented with cyst at the umbilical side.

The male patient in the case reports one, two,

three, four and five were asymptomatic and

presented as intestinal obstruction with gangrene.

One patient expired in the immediate

postoperative period.7

The majority of people

with Meckel's diverticulum are asymptomatic. If

symptoms occur, they typically appear before

two years of age. Meckel's diverticulitis

occasionally may present with all the features of

acute appendicitis .The presence of ectopic

gastric cells lead to acid-peptic disease .

Bleeding, strangulation of bowel, bowel

perforation or bowel obstruction are known

complications, treatment involves surgical

resection of the Meckel's diverticulum itself

along with the adjacent bowel segment. In

patients without any complications, treatmentinvolves surgical resection of the Meckel's

diverticulum only.8

In every case of

appendicectomy / laparotomy a search for

Meckel's diverticulum must be done and if

found Meckel's diverticulectomy or resection

should be performed to avoid secondary

complications arising from it

CONCLUSION

Meckel’s diverticulum is a rare entity. It may

remain asymptomatic. It may present with life

threatening complications. Every effort should be

taken to exclude Meckel's diverticulum in every

case of abdominal pain.

ACKNOWLEDGEMENT

The authors gratefully acknowledge the support

from the management of Pravara Medical Trust,PIMS and Principal Rural Medical College,

Loni. We appreciate the help of colleagues in the

surgery department. We are grateful to the

patients for their cooperation consent.

REFERENCES

1. Neil J. McC, Mortensen. The small and large

intestines.IN Bailey & Love’s short practice

of surgery. 23rd

Edition. chapter 57, 1033.



1020


2. Jay GD III, Margulis RR, McGraw AB.

Meckel's diverticulum: a survey of 103 cases.

Arch Surg. 1950;61:158 – 169

3. Haber JJ. Meckel's diverticulum: review of

literature and analytical study of 23 cases

with particular emphasis on bowel

obstruction. Am J Surg. 1947;73:468 – 85.

4. Mortensen NJ, Jones O. The Small and Large

Intestines. In Bailey & Love's Short Practice

of Surgery 24th edition. Edited by Russell

RCG, Williams NS, Bulstrode CJK Arnold.

2004, 1159-60.

5. Evers BM. Small Intestine. In Sabiston

Textbook of Surgery. 17th edition. Edited by

Townsend CM. Elsevier; 2004:1366-1368.

6. Whang EE, Ashley SW, Zinner MJ. Smallintestine. In Schwartz's Principles of Surgery.

Eighth edition. Edited by Brunicardi FC.

McGraw-Hill; 2005:1043-1044.

7. Yamaguchi M, Takeuchi S, Awazu S:

Meckel's diverticulum: investigation of 600

patients in Japanese literature. Am J Surg

1978, 136:247-49.

8. Horn F, Trnka J, Simickova M, Duchaj B,

Makaiova I. Symptomatic Meckel's

diverticulum in children. Rozhl Chir 2007,

86(9):480-2



1021

AmitYadav et al., Int J Med Res Health Sci. 2013;2(4):1021-1023


&

Health Sciences




thSep 2013

Case report

LATE ONSET HEMORRHAGIC DISEASE OF NEWBORN DUE TO CMV HEPATITIS

PRESENTING AS SCALP HEMATOMA

*Amit Yadav1,Shrikhande DY

2, Rajib Chatterjee

3, Amit Narkhede

1, Amol pokharkar

1, Santosh Yadav

1

1PG student,

2Professor & Head,

3Professor, Department of Pediatrics, Rural Medical College, PIMS,

Loni, Maharashtra


ABSTRACT

Vitamin K deficiency bleeding (VKDB) according to recent studies is the preferred term for

hemorrhagic disease of the newborn (HDN). This is due to deficiency of clotting factors as a result of

vitamin K deficiency. VKDB was first described over a hundred years ago but its relationship to vitamin

K was not released until 40 years later. Vitamin K is required for the production of clotting factors II,

VII, IX and X. It is involved in the normal clotting of blood, is present in some plants and is also

synthesized by some E. coli in the gut. Due to low levels of vitamin K all newborn infants are at risk of developing hemorrhagic disease of the newborn. The body has very limited ability to store the vitamin.

We present an unusual case of Neonatal Hepatitis due to CMV as a rare cause of late onset vitamin k-

deficiency bleeding.

Keywords: Cholestatic liver disease, Vitamin K, Vitamin K deficiency bleeding.

INTRODUCTION

Hemorrhagic disease of the newborn (HDN) is a

coagulation disturbance in newborns due toVitamin K deficiency. As a consequence of

vitamin K deficiency there is an impaired

production of coagulation factors II, VII, IX, X

by the liver.1,2

Newborns are relatively vitamin K

deficient for a variety of reasons. They have low

vitamin K stores at birth, Vitamin K passes the

placenta poorly, the levels of vitamin K in breast

milk are low and the gut flora have not yet been

developed (Vitamin K is normally produced by

bacteria in the intestines). HDN causes an

increased risk of bleeding. The common sites of

bleeding are the gastrointestinal tract, Mucous

membranes, umbilicus, injection sites and

circumcision.3

A number of review articles provide useful

overviews of vitamin K and its importance to

human beings. Bleeding disorders in newly born

infants were first described over 100 years ago

when Townsend reported 50 cases in 1894.1

Vitamin K, however, was only discussed about

40 years later, by Dam, in a study of bleeding

disorder in chickens.1

CASE REPORTA term male baby appropriate for gestational age

(AGA) with birth weight 2400grms was

DOI:10.5958/j.2319-5886.2.4.170



1022


delivered vaginally to a primigravida mother at a

private hospital without any antenatal or

postnatal complications, baby was discharged on

breast feeding on 3rd

day of life. The baby was

asymptomatic till 1month 5days and was on

exclusive breast feeding brought to our hospital

with c/o convulsion and swelling over scalp on

left side (7 x 8 cm), there being no h/o drug

intake during pregnancy.

On physical examination baby had severe pallor,

icterus, hepatomegaly, one oval shaped (7x8cm)

swelling present over left fronto-temporo-

parietal region, admission weight was 3400grms,

head circumference was 34.5cm.

Investigations revealed Hb 5.9 %, TLC

18400/cumm, DLC (N 56%, L40%,M4%),

platelet count 4.9 Lacks/cumm, prothrombin

time(PT)>2 min, partial thromboplastintime

(APTT)>2 min, LFT (Total Bilirubin 9.3gm/dl,

Direct Bilirubin 5.6gm/dl, SGOT 290IU/L,

SGPT235IU/L) , CSF study reaveled 2 cells, all

lymphocytes with normal protein and sugar, CT

scan suggestive of hemorrhagic contusions in

left temporal-parietal region, generalized cerebral

oedema, scalp hematoma ,USG abdomenshowed Liver parenchymal disease. Torch study

of baby CMV (cytomegalovirus) IgG & IgM

Both positive also mother CMV reports shows

IgG +ve, IgM -ve

Fig 1: Plain CT scan of brain

Respectively showing hemorrhagic contusion in

left temero-perital region, generalized cerebral

oedema, scalp hematoma

Fig 2: Contrast CT of brain

In treatment IV vit k 1mg, inj phenobarbitone,

inj Gancyclovir (6mg/kg/day, 12 hrly) for 21

days with monitoring complete blood count

every alternative day. Patient recovered

completely.

On follow up patient showed complete recovery

with normal hematological parameter and with

normal growth and development.

DISCUSSION

In 1894, Townsend described a self-limited

bleeding condition that usually occurs 1-5 days

after birth in patients with nonclassic

hemophilia.1,4,5The term vitamin K originatedfrom coagulations-vitamin in German.

5Henrik

Dam and Edward Doisy won the 1943 Nobel

Prize for the discovery and functions of vitamin

K. Subsequent research has provided significant

contributions to current knowledge of vitamin K

and its association with coagulation factors,

namely the vitamin K – dependent coagulation

factors VII, IX, and X.6

• Early VKDB occurs within 24 hours of

birth.

• Classic VKDB happens between day 1 and

day 7 of life.

• Late VKDB occurs between week 2 and

week 12 of life.

Late VKDB can result in significant morbidity

and mortality due to intracranial hemorrhage and

has resulted in most developed countries having

in place a protocol for giving supplemental

vitamin K to all newborn babies.



1023


Late VKDB most commonly occurs at 2-12 week

of age, although cases can occur up to 6 months

after birth. All cases are in breast-fed infants due

to low vitamin k content of breast milk. An

additional risk factors are occult malabsorption

of vitamin k (cystic fibrosis), cholestatic liver

disease, pancreatic disease, intestinal disorders

(celiac sprue, inflammatory bowel disease, short

bowel syndrome). Cholestatasis in newborns can

be due to infectious, genetic, metabolic or

abnormalities giving rise to mechanical

obstruction of bile flow or to functional

impairment of hepatic excretion function and bile

secretion3

Human cytomegalovirus (CMV) is widely

distributed. Most CMV infections inapparent, but

virus can cause a variety of clinical illness that

range from mild to fatal. The incidence of

congenital CMV infection ranges from 0.2% to

2.2% (average 1%) of all live births, with the

higher rates among populations with a lower

economic standard of living. The risk for fetal

infection is greatest with maternal primary CMV

infection (30%) and much less likely with

recurrent infection (<1%).In infants and youngchildren, primary CMV infection occasionally

causes pneumonitis, hepatomegaly, hepatitis

(cholestatic liver disease) and petechial rashes.3

In our case, patient had swelling over scalp with

convulsion due to intra-cerebral contusion which

was present with late VKDB due to unusual

causes of hepatitis due to CMV infection.A

randomized controlled study with ganciclovir (6

mg/kg/dose every 12 hrly for 2-4 weeks)

concluded as a treatment for hepatitis due to

CMV infection.

CONCLUSION

We suspected late VKDB due to its presentation

at age of 4 weeks, PT/APTT had been improved

after giving single dose vitamin k, reduction in

swelling over scalp and also recovered from

neonatal cholestasis(hepatitis) after giving inj

Gancyclovir. CMV induced hepatitis is an

unusual presentation of late VKDB. On follow

up patient showed complete recovery with

normal hematological parameter and with normal

growth and development.

REFERENCES

1. Townsend CV. The Hemorrhagic Disease of

the Newborn. Arch Pediatr. 1894, 11:559-62.2. Hubbard D, Tobias JD. Intracerebral

hemorrhage due to hemorrhagic disease of

the newborn and failure to administer vitamin

K at birth. South Med J 1999; 11: 1216-20.

3. Stoll BJ, Kliegman RM, Behrmann RE,

Kliegman RIV, Jenson HB. Nelson’s

Textbook ofPediatrics. 18th Ed. Philadelphia:

W.B Saunders; 2007. p. 773-5.

4. McNinch AW, Tripp JH. Hemorrhagicdisease of the newborn in the British Isles:

two year prospective study. BMJ.

1991;303(6810):1105-9.

5. Chaou WT, Chou ML, Eitzman DV.

Intracranial hemorrhage and vitamin K

deficiency in early infancy. J Pediatr.

1984;105(6):880-4.

6. Van Winckel M, De Bruyne R, Van De

Velde S. Vitamin K, an update for the

pediatrician. Eur J Pediatr. 2009;168(2):127-

34.

7. Puckett RM, Offringa M. Prophylactic

vitamin K for vitamin K deficiency bleeding

in neonates. Cochrane Database Syst Rev.

2000;Issue4. Art. No.:CD002776.

8. Costakos DT, Greer FR, Love LA. Vitamin

K prophylaxis for premature infants: 1 mg

versus 0.5 mg. Am J Perinatal.

2003;20(8):485-90.9. Loughnan PM, McDougall PN.

Epidemiology of late onset hemorrhagic

disease: a pooled data analysis. J Pediatric

Child Health. 1993;29(3):177-81.

10. No authors listed; Controversies concerning

vitamin K and the newborn. American

Academy of Pediatrics Committee on Fetus

and Newborn. Pediatrics. 2003;112(1 Pt

1):191-2.

11. Zipursky A. Prevention of vitamin K

deficiency bleeding in newborns. Br J

Haematol. 1999;104(3):430-7.



1024

Vandana et al., Int J Med Res Health Sci. 2013;2(4):1024-1026


&

Health Sciences




thSep 2013

Case report

AN UNUSUAL FINDING OF EPIDIDYMAL SPERM GRANULOMA IN AN

ORCHIDECTOMY SPECIMEN: A CASE REPORT

*Vandana Gangadharan1, Geetha Prakash

2, Hema Maheshwari

3, Shaffy Tukkral

4, Archana S

4

1&3Assistant Professor,

2Professor& HOD,

4Post Graduates, Department of Pathology, Meenakshi

Medical College & Research Institute, Enathur , Tamilnadu, India


ABSTRACT

Epididymal sperm granuloma as a cause of granulomatous epididymitis is rare. Most of the cases are

found post vasectomy as part of the late vasectomy syndrome. These lesions are known to mimic other

conditions including testicular malignancies. We report this interesting case of an epididymal sperm

granuloma which was not only an incidental finding in an orchidectomy specimen of a 55 year old male

with no antecedent history of surgery, trauma or clinical infection but also mimicked a testicular tumor.

Keywords Epididymitis, Sperm granuloma,Vasectomy

INTRODUCTION

Epididymitis is defined as the inflammatory

condition of the epididymis. It may be acute or

chronic depending on the inciting agent as well

as the duration. Specific causes of chronic

epididymitis include a) Tuberculosis b) Leprosy

c) sarcoidosis and d) Sperm granuloma

1

.Sperm granuloma is an exuberant foreign body

reaction to extravasated sperm and occurs in 42%

of patients after vasectomy2

and 2.5% of routine

autopsies1

.This lesion is thought to result from

damage to the epithelium and basement

membrane of epididymal ducts by inflammation

or trauma3

with subsequent spillage of sperm

into interstitium. The granulomatous reaction is

probably induced by an acid fast fraction of lipid

from the sperm; a hypothesis supported by the

fact that this material has been found to provoke

a granulomatous reaction when injected

subcutaneously in hamsters4. Epididymal sperm

granuloma may account for ‘late vasectomy

syndrome’ in which patients complain of pain

many months or years after vasectomy. Ligation

vasectomy accounts for most cases whereascauterization vasectomy rarely results in

granuloma1.

CASE REPORT

55 year old male reported with h/o pain abdomen

since 10 days with inguinoscrotal swelling on left

side since 1 month. He also complained of pain

in the scrotal region on and off since 10 days. No

other positive history or co morbidities noted. On

examination vitals were normal and a left direct

inguinal hernia with scrotal swelling measuring

DOI:10.5958/j.2319-5886.2.4.171



1025


2x1 cm was felt. On ultra sound the inguinal

hernia was confirmed and the scrotal swelling

was hypoechoic with calcification of testis. With

a suspicion of carcinoma testis (L) meshplasty

with (L) orchidectomy was planned.

For histopathological examination we receivedan orchidectomy specimen measuring 6x4x3cm

with spermatic cord measuring 9cm. A nodule

measuring 2 cmx1cm was felt in the epididymal

area. On microscopic examination testicular

tubules with both normal and arrested

spermatogenesis were seen. The epididymal

tubules showed extravasated sperms along with a

granulomatous reaction composed of

lymphocytes, lipid laden and sperm ladenmacrophages (Spermiophages). Some of the

epididymal tubules showed haemorrhage,

necrosis and cholesterol clefts. Focal areas of

calcification were also seen. A diagnosis of

Epididymal Sperm granuloma was given.

Fig 1: Focal areas of calcification. H & E 10x

Fig 2: Sperm granuloma H & E 40x

Fig 3: Sperm granuloma with spermiophages. H &

E 40x

DISCUSSION

Sperm granuloma was first described byGrunberg in 1926

5. They have been reported in

upto 42% of men who have undergone

vasectomy and 2.5% of general population1.

They can range in size from microscopic upto

4cm but most are less than 1 cm1. Although

most sperm granulomas are asymptomatic, some

manifest as painful nodules. They are generally

well defined, hypoechoic, solid masses at ultra

sonography. On histopathology foreign body

granulomas may be present with necrosis and

later progressive fibrosis. Extravasated sperms

are plenty with many engulfed by macrophages

(referred to as spermiophages).Yellow brown

ceroid pigment; a lipid degradation product of

sperm may persist. Vasitis nodosa occurs in

about one third of cases of sperm granuloma1.Although they can occur anywhere in the ductal

system, they are most common at the cut ends of

the vas deferens and can be multiple 6. It is alsoknown to occur in the epididymis. However the

incidence in the testis is exceptional. It is

probably the microenvironment of the testicular

interstitium rather than the extravasated

components from the ruptured seminiferous

tubules, which is the main factor determining the

limited formation of spermatic granuloma in the

testis7.The incidence of sperm granuloma in our

knowledge is limited. In his study of 228 cases of epididymal nodule in india Gupta et al found an

incidence of 5.3%8.In another study by Shah et



1026


al the incidence was found to be 7.5%9.

Commonest cause of these granulomas is thought

to be vasectomy. However, trauma , epididymitis

and orchitis have also been described1, 8

. Silch et

al describes sperm granuloma in a patient 4 years

after inguinal hernia repair 10 and Deane et aldescribes sperm granuloma presenting as a

recurrent inguinal hernia11

. However as in our

patient, case reports without any antecedent

history of surgery trauma or clinical infection

have been seen3, 8

. Another important feature is

the rare confusion it can cause with testicular

tumor12, 13

. As seen in our case the testicular

tumor is thought of because of proximity to the

testes, solid nature and calcification.

CONCLUSION

We present this rare case of sperm granuloma

which was an incidental finding with no

antecedent history of vasectomy, trauma or

clinical infection and mimicked a testicular

tumor. The patient also had a concurrent direct

inguinal hernia on the same side. The possible

etiology of sperm granuloma in our patient may

be an unnoticed trauma or subclinical epididymal

infection.

REFERENCES

1. Bostwick DG, Eble JN .Urologic surgical

pathology. St Louis Mosby 2000.

2. Mc Donald SW. Cellular responses to

vasectomy. Int Rev Cytol 2000; 199:295-339.

3. Glassy FJ, Mostofi FK. Spermatic

granulomas of the epididymis. Am J Clin

Pathol 1956; 26:1303-13.

4. Berg JW. An acid fast lipid from

spermatozoa. Arch Pathol. 1954; 57; 115-20.

5. JBL Taylor. Spermatic granuloma. British

Journal of Urology 1959; 31 (2):196-200.

6. Holden A, List A.Extratesticular lesions: A

radiological and pathological correlation.

Australas Radiol 1994; 38:99-105.

7. Itoh M, Xieq, Miyamoto K. Major

differences between the testis and epididymis

in the induction of granulomas in response toextravasated germ cells. A light

microscopical study in mice. Int J Androl

1999;22(5):316-23.

8. Gupta N, Rajwanshi A, Srinivasan . Fine

needle aspiration of epididymal nodules in

Chandigarh, North India : An audit of 228

cases. Cytopathology 2006;17(4):195-8.

9. Shah VB, Shet MT, Lad KS. Fine needle

aspiration cytology of epididymal nodule. Jcytol 2011; 28(3) : 103-07.

10. Silch RC, McSherry CK. Spermatic

granuloma an uncommon complication of

tension free hernia repair. Surgical

endoscopy.1996;10(5):537-39.

11. Deane LA, Suding PN, Lekawa ME, Narula

N, McDougall EM. Sperm granuloma of the

inguinal vas deferens mimicking recurrent

incarcerated inguinal hernia. Urology.

2007;69(6):1-3.

12. Oliva E, Young RH. Paratesticular tumor-

like lesions. Semin Diagn Pathol

2000;17(4):340-58.

13. Wada N, Kato Y, Iwats T. A case of

spermatic granuloma difficult to differentiate

from malignant tumour. Hinyokika Kiyo

2002;48(9):549-5



1027

Koushik et al., Int J Med Res Health Sci. 2013;2(4):1027- 1031


&

Health Sciences




thSep 2013

Case report

CASE OF KIKUCHI’ S DISEASE AND SYSTEMIC LUPUS ERYTHEMATOSUS ASSOCIATED

WITH ANTIPHOSPHOLIPID ANTIBODY SYNDROME AND COMPLICATED BY

HEMOPHAGOCYTIC SYNDROME (HPS)

*Koushik Pan, Subrata Chakrabarti, Rajdip Choudhury, Anup Sarkar

Department of General Medicine, SSKM, IPGME& R, Kolkata, West Bengal, India


ABSTRACT

Kikuchi disease is a rare benign self limited lymphadenopathy. It is often associated with Systemic

Lupus Erythematosus which can be diagnosed before; at the same time or after a diagnosis of Kikuchi

disease is made. Again SLE is usually associated with APLA syndrome. Furthermore both SLE and

Kikuchi disease can be complicated by HPS. We present a unique case in which Kikuchi disease and

SLE were diagnosed together and disease course was complicated by Hemophagocytic syndrome (HPS).

SLE was also associated with Anti Phospholipid Antibody Syndrome (APS) in this patient.

Keywords: Kikuchi, SLE, APLA, Hemophagocytic syndrome

INTRODUCTION

Kikuchi disease or histiocytic necrotizing

lymphadenitis a rare, benign, self limiting

cervical lymphadenitis of unknown etiology1

mainly affecting young adults with females

outnumbering males.2

Sometimes association

with SLE has led to the probability of

autoimmune etiology being one of factors

leading to Kikuchi disease. SLE is probably the

most common underlying diseases of APLA

syndrome.3

Hemophagocytic syndrome is a rare

but potentially fatal disease of normal but

overactive histiocytes and lymphocytes often

complicating connective tissue disorder &

haematological malignancies. Kikuchi disease

can independently lead to hemophagocyticsyndrome in rare instances. Kikuchi disease and

SLE with APLA syndrome can coexist rarely &

may be complicated by hemophagocytic

syndrome.

CASE REPORT

A 16 year Hindu Male from rural Bengal, student

by profession, presented with fever, joint pain

and glandular swelling in neck and axilla for last

1 month. Fever was high grade reaching upto

104˚F; continuous; chill and rigor; intense

constitutional symptoms, no localising

symptoms; relieved partly on medications. Joint

pain involved mainly small joints of both upper

limb and lower limbs [metacarpophalangeal joint

(MCP), Proximal interphalangeal joint (PIP),

distal interphalangeal joint(DIP),

metatarsophalangeal joint (MTP),

Interphalangeal joints (IP)] ; simultaneous onset;

DOI:10.5958/j.2319-5886.2.4.172



1028


additive; pain, Restriction of movement present

but no swelling or redness. Painless glandular

swelling in the neck and axilla started for last 15

days; gradually increasing in size but no

discharge. No history of bleeding manifestations,

purpuric rash, bone pain. No history of morningstiffness, pain in large joints or spine, oral or

genital ulcers, facial rash, erythematous,

evanescent rash over the trunk during spikes of

fever. No history of prior tuberculosis, malaria,

kalaazar. No history of chronic intake of any

drug or any family history of arthritis. A

significant history of spontaneous development

of painful swelling in Right thigh 1 year ago

which was documented as deep vein thrombosisinvolving iliofemoral veins. On clinical

examination, patient had significant pallor, mild

icterus. Lymph nodes palpable in right

supraclavicular middle group, bilateral axillary

central group and posterior triangle; all were soft,

mobile, nontender with no fixity; mediastinal

percussion resonant. No sternal tenderness. Chest

-Bilateral Vesicular breath sounds heard normally

with normal S1, S2. Abdomen was soft,

nontender; spleen palpable 2cm below Left

costal margin, nontender, no rub; liver not

palpable; no free fluid. Musculoskeletal exam

reveals pain, slight swelling, range of movement

restricted in bilateral MCP, PIP, DIP joints in

upper limb; MTP, IP joints in lower limb;

tenderness at bilateral Achilles tendon insertion;

Axial system uninvolved. Routine blood tests

show Hb-7.2 gm/dl, PCV-22.3%, TLC-

2300/cmm; N-69%; L-25%; M-5% ; E-1% ,Platelet-41000/cmm , Reticulocyte-2%, MCV-

72.4fl; MCH-23.3pg; MCHC-32.2%, RDW-

16%; Peripheral blood smear shows

hypochromic, microcytic RBCs; anisocytosis,

elliptocytes, tear drop cells but no abnormal

cells, ESR- 84mm/1st

hr, Ur-19mg/dl; Cr-

1mg/dl; LDH-1890U/L, Bil-0.7mg/dl; SGOT-

39U/L; SGPT-56U/L; Alkaline phosphatase-112;

Albumin-3.2gm/dl; Gloulinb-2.8gm/dl; A:Gratio:1.1, Na+-137.3meq/l; K

+-3.89meq/l; Ca

++-

8.9mg/dl; TG-360mg/dl, PT-13s; INR-1.03;

APTT-70s

HBsAg, Anti HCV, ICTC were all negative;

Chest X Ray-within normal limit; USG Whole

abdomen showed mild splenomegaly; ECHO

Cardiography: Normal; Malaria parasite DualAntigen-Negative; Malaria Parasite on slide-not

found. Dengue serology was Negative. Blood

and urine Cultures were sent on day of

admission; Sputum AFB-Not found; Mantoux-

negative; urine routine & microscopic

examination -normal. Patient was started on

empirical IV antibiotics after sending blood and

urine cultures; Bone marrow aspiration and

Lymph node excision biopsy done. In thebackground of history of spontaneous DVT and

isolated APTT rise, testing for Antiphospholipid

antibody syndrome was done. PTT-A(test)-

161.3s( N--35-42s)

• PTT-A(control)-39s(N — 35-42s)

• PTT-A1:1 Mixing test-108.9s

• Interpretation- NOT CORRECTED

• DRVV(diluted russel viper venom)(test)-

155.2s (N — 35-42s)

• DRVV(control)-38.3s (N — 35-42s)

DRVV ratio: 4.05 (N-0.85-1.12), Cardiolipin Ab-

IgG-Positive 57.53 GPL U/ml (N<10 U/ml)

antiphospholipid Ab IgG-POSITIVE 35.11

GPL U/ml (N<10 U/ml); lupus anticoagulant was

positive. A diagnosis of possible APLA syndrome

was made based on the presence of 1 episode of

venous thrombosis; anticardiolipin Ab >40 GPL

U/ml and lupus anticoagulant positivity. Patient

was started on inj.LMWH (given for 5 days withtarget INR 2-3) with oral Warfarin to be given

lifelong.Blood culture & sensitivity, Urine

culture & sensitivity reports reached our hands

which revealed no growth; Bone marrow

aspiration showed reactive hyperplasia; no

leukemic cells; Hemophagocytosis noted;

Ferritin -1480mcg/l ; serum Fe-28mg/dl;

Transferrinsaturation36%.



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Fig 1: Bone marrow showing hemophagocytosis

(40 x)

X ray both hands- No erosive features. A

diagnosis of HPS was made due to presence of fever, pancytopenia, splenomegaly, raised ferritin

(>500ng/ml), raised Triglyceride (>250mg/dl)

and evidence of hemophagocytosis on

BMAspiration. Patient continued to have high

fever and on 11th

day of admission became

disoriented with irrelevant words. CT brain was

normal; CSF Study revealed no features of acute

CNS infection. Psychiatry referral done; a

diagnosis of psychosis was made. Now workup

for collagen vascular diseases was done- ANA-

2+ homogeneously at 1:200 dil; C3 —

50.9mg/dl(N — 90-180mg/dl) C4 — 7.3mg/dl (N-

10-40mg/dl). Anti ds-DNA-negative; A diagnosis

of SLE was made based on the presence of

clinical features (non erosive arthritis involving

more than 2 peripheral joints with

tenderness,swelling; psychosis without other

causes)and lab features (an abnormal titre of

ANA in the absence of drugs known to induceANAs and leucopenia (<4000/cmm),

lymphopenia(<1500/cmm), thrombocytopenia(

<100000/cmm)in the absence of offending

drugs). Patient was treated accordingly. Fever

gradually abated and patient became conscious

and responsive. He was put on oral steroids

1mg/kg/day with gradual tapering. LN HPE

report reached our hands which revealed

Necrotizing Histiocytic Lymphadenitiscompatible with Kikuchi”s disease. Patient was

followed up at 6 weeks & repeat anti

phospholipid antibody and anti cardiolipin

antibody was positive in significant titre.

Fig 2: Lymph node histopathology (40X)

CT thorax and abdomen was done which

revealed no malignancy. So the complete

diagnosis was SLE associated with Kikuchi

disease and APLA syndrome and

hemophagocytic syndrome.

DISCUSSION

Kikuchi-Fujimoto disease (KFD) is a unique

disease which was first described in 1972 in

Japan. KFD is a very rare disease and mainly

seen in Japan although occasional cases arereported in America and Europe. It is also known

as Kikuchi disease1, histiocytic necrotizing

lymphadenitis, phagocytic necrotizing

lymphadenitis, subacute necrotizing

lymphadenitis.KFD generally affects the cervical

lymph nodes. Cause of disease is unknown

although infectious and autoimmune etiologies

have been discussed as probable etiologies. A

genetic predisposition to the proposedautoimmune response cannot be ruled out.

Several infectious candidates have been proposed

like Mycobacterium szulgai, Yersinia and

Toxoplasma. Role of Epstein-Barr virus, as well

as other viruses (HHV6, HHV8, Parvovirus B19,

HIV- and HTLV-1) in the pathogenesis cannot

be ruled out. Serologic tests including antibodies

to viruses have not been proven fruitful and viral

particles cannot be identified in electron

microscopy. KFD generally affects the cervical

lymph nodes. It can be confused with

Area of necrosis surrounded

by infiltrated histiocytes



1030


tuberculosis, lymphoma which can have similar

presentation it mainly affects young adults (20 –

30 years), with females outnumbering males2.

Course of the disease is generally benign and

self-limiting. Lymphadenopathy usually resolves

within several weeks to months. Recurrence rateis about 4-5%. Mortality is very rare and usually

results from hepatic, respiratory, or cardiac

failure. SLE is the single most disease associated

with this disorder.3,4

Similar autoimmune states

such as polymyositis, juvenile idiopathic

arthritis, antiphospholipid syndrome can be

associated with KFD. KFD may be an aberrant

T-cell mediated immune disoeder in a genetically

susceptible individual in response to appropriatestimuli. The exact relationships between SLE and

KFD are not known as SLE can coincide,

proceed, or follow KFD. Clinical features of

SLE and KFD can be identical; fever,

lymphadenopathy, fatigue, and joint pain are

noted in both. These two diseases are separated

by histopathological features; the presence of

hematoxylin, plasma cells, and deposition of

DNA is seen in SLE only.SLE is probably the

most common underlying diseases of APLA

syndrome. Kikuchi disease and SLE with APLA

syndrome can coexist as documented in

literature.5

SLE is often complicated by hemphagocytosis

syndrome6

which is also called as Macrophage

Activation Syndrome (MAS). Now MAS is

called hemophagocytic lymphohistiocytosis

(HLH).Criteria for hemophagocytic

lymphohistiocytosis (HLH) , which includefever, splenomegaly, cytopenias affecting at least

two of three lineages in the peripheral blood,

hypertriglyceridemia and/or hypofibrinogenemia,

hemophagocytosis in bone marrow, spleen or

lymph nodes, low or absent natural killer cell

activity, hyperferritinemia, and high levels of

sIL-2 receptor. Five of the eight criteria should

be fulfilled to make this diagnosis. Patients with

a molecular diagnosis of HLH are exemptedfrom fulfilling all the diagnostic criteria. The

prevalence of HPS among patients with

autoimmune diseases varies but around

3%4.Incidence is highest in patients with adult

onset Still’s disease, followed by Sjogren’s

Syndrome and SLE. Increased mortality is noted

in age above 50 years, the presence of coexistent

infection, leucocyte count < 5000/mcl, plateletcount < 50000/mcl and CRP level < 50 mg/L at

the onset of HPS5

.Current treatment strategy is

induction therapy over an eight-week period with

dexamethasone, etoposide (VP-16), and

intrathecal methotrexate, followed by

cyclosporine started at 9 th week . Pulses of

dexamethasone and etoposide to be given for one

year.7

This case presents an extremely rare

coexistence of SLE, Kikuchi disease, APLAsyndrome and finally HPS & highlights the fact

that patient may manifest with APLA at earlier

stage & later turn into florid SLE in the

subsequent disease course, even after years.

Whether the HPS in this case was a complication

of kikuchi’s disease or SLE per se cannot be

determined with certainty as both of them are

established predisposing factor for HPS.

REFERENCES

1. Kikuchi M. Lymphadenitis showing focal

reticulum cell hyperplasia with nuclear debris

and phagocytes. Acta haematologica

Japonica. 1972;35:379 – 80.

2. Fujimoto Y, Kojima Y,. Yamaguchi K.

Cervical Subacute necrotizing

lymphadenitits. Naika.1972, 20:920 – 27.

3. Khanna D, Shrivastava A, Malur PR, KangleR. Necrotizing lymphadenitis in systemic

lupus erythematosus: is it kikuchi-fujimoto

disease? Journal of Clinical Rheumatology.

2010;16(3):123 – 24

4. Londhey VA, Buche AS, Kini SH,

Rajadhyaksha GC. Kikuchi fujimoto disease

and systemic lupus erythematosus — a rare

association,” Journal of Association of

Physicians of India. 2010;58(10):642 – 43.

5. Chen HC, Lai JH, Huang GS. Systemic lupus

erythematosus with simultaneous onset of



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Kikuchi-Fujimoto's disease complicated with

antiphospholipid antibody syndrome: a case

report and review of the literature.

Rheumatology International. 2005;25(4): 303

– 06.

6. Kampitak T. Fatal Kikuchi-Fujimoto diseaseassociated with SLE and hemophagocytic

syndrome: a case report,” Clinical

Rheumatology. 2008;27(8):1073

7. Fukaya S, Yasuda S, Hashimoto T, Oku K,

Kataoka H, Horita T, Atsumi T, et al.

Clinical features of haemophagocytic

syndrome in patients with systemic

autoimmune diseases: analysis of 30 cases.

Rheumatology (Oxford). 2008;47(11):1686-91



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Radha Bai et al., Int J Med Res Health Sci. 2013;2(4):1032-1035


&

Health Sciences




thSep 2013

Case report

URINARY TRACT ENDOMETRIOSIS: A CASE REPORT

*Radha Bai Prabhu T, Velayudam DA, Manjula P, Niharika S, Cynthia S

Department of Obstetrics & Gynaecology, Meenakshi Medical college and Research Institute,

Kancheepuram, Tamilnadu, India

*Corresponding author email: [email protected].

ABSTRACT

Endometriosis affecting the urinary tract is rare and when involved it predominantly affects the bladder,

followed by the ureter. The diagnosis of bladder endometriosis is difficult because of its varied clinical

presentation. Here we report a case of bladder endometriosis, which was suspected pre-operatively and

was confirmed after the histo pathological examination of the excised tissue.

Key words: Extra genital Endometriosis, Bladder Endometriosis, Vesical Endometriosis

INTRODUCTION

Endometriosis is the presence of functioning

endometrial glands and stroma outside the

uterine cavity and musculature. It is a well

recognised gynaecological condition affecting 5-

10% of women of reproductive age and up to

50% of infertile women. Though endometriosis

is a disease of the genital tract, literature review

shows that endometriosis can be found in almost

any tissue in the body1. Here we describe a case

of bladder endometriosis, its clinical

presentation, diagnosis and management.

CASE REPORT

44 years old, Para 2, presented to the

Gynaecological outpatient department with a

history of constant lower abdominal pain for 8

years and cyclical heavy periods of six months

duration. In detailed questioning, she described

the pain to be worse during the premenstrual and

menstrual period. She also complained of urinary

symptoms such as increased frequency and

painful micturition for the last four years which

was worse during the premenstrual period. There

was no history of haematuria. She was married

for 25 years, delivered two children by caesarean

section and the last childbirth was 21 years ago.

In the past, she has had regular menstrual cycles

lasting for 3-4 days. However, in the last six

months her periods became very heavy and

prolonged, occurring once in 30 days, lasting for

10-15 days and changing 10-15 pads per day.

She also complained of congestive

dysmenorrhoea and deep dyspareunia. There was

no history suggestive of pelvic inflammatory

disease (PID) and her bowel habits were normal.

In her past history she was treated by many

doctors for PID and was not relieved of her

symptoms. Because of her recurrent urinary

DOI:10.5958/j.2319-5886.2.4.173



1033


symptoms, she was also evaluated and treated by

Urologists many times. In the last four years only

once her urine culture showed evidence of

infection and was treated. She has had a

cystoscopy two years ago which showed a raised

lesion in the trigone close to the left uretericorifice. The biopsy of the lesion was reported as

inflammatory lesion.

On examination, the patient was thin made, very

pale, thyroid and breasts were normal. She had

two vertical scars in the abdomen, there was

suprapubic tenderness and the uterus was

palpable 3 centimeters above the symphysis

pubis. By speculum examination, the cervix was

eroded. Bimanual pelvic examination showed theuterus to be uniformly enlarged to 16 weeks size

and was tender. There was also tender nodularity

in the midvaginal region in the anterior fornix.

Rectal examination did not reveal any nodules in

the pouch of douglas. Her investigation results

were as follows: Haemoglobin – 6.1gms. %,

PCV – 18, bleeding time, clotting time were

normal, TSH – 2.1, and other investigations were

within normal limits. Pap smear was negative for

intra epithelial lesion. Combined transvaginal

and transabdominal ultrasound of the pelvis

showed an enlarged uterus with asymmetrically

thickened myometrium with heterogenous echo

texture. The endometrial thickness was 18 mm.

The left ovary showed a clear cyst measuring

6cm. in size. Some irregularity was noted near

the bladder base. Because of the long duration of

her symptoms, MRI of the pelvis was also taken.

MRI confirmed the USG findings and showedthe bladder wall to be thickened to 8mms. near

the trigone.

Her anaemia was corrected with three units of

packed cells and she was taken up for a

diagnostic curettage. Under anaesthesia, the

irregularity in the anterior fornix was well

appreciated. The HPE of the endometrial

curetting showed severe complex hyperplasia

without atypia.With her history, examination findings and the

results of imaging studies, a diagnosis of

adenomyosis with endometrial hyperplasia was

made and the possibility of endometriosis of

bladder was strongly suspected.

She was prepared for Total abdominal

hysterectomy with bilateral salpingo-

oophorectomy (TAH with BSO). Because of herprevious two caesarean sections and the strong

possibility of bladder endometriosis, it was

decided to proceed with the surgery with a

preliminary cystoscopy. The patient was

adequately counselled as to the possibility of

opening into the bladder and extensive bladder

surgery may be required.

At cystoscopy, there were bluish nodules bulging

into but not eroding through the mucosa aroundthe left ureteric orifice. (Fig. 1) Other areas of the

bladder mucosa were normal. Ureteric stenting

was done on the left side and was not possible on

the right side. On opening the abdomen, there

were dense omental adhesions and were released.

The bladder was densely adherent to the cervix

and was freed by sharp dissection. On the left

side there was a firm bluish nodule between the

bladder and the cervix. (Fig.2) In order to avoid

injury to the bladder, sharp dissection was

carried out close to the cervix and a wedge of

tissue was excised from the nodular area for

HPE. The remaining nodular area over the

bladder was ablated with bipolar diathermy and

TAH with BSO was carried out. Her

postoperative period was uneventful except for

the haematuria which cleared after one week.

She was kept on continuous bladder drainage for

10 days and the ureteric stent was removed after15 days.

The HPE was reported as follows:

Endometrium showing complex cystoglandular

hyperplasia without atypia, and the myometrium

showing adenomyosis with marked

myohyperplasia. The left ovary showed a simple

ovarian cyst and the excised nodule was reported

as endometriosis.

At one year follow up, patient did not have anyurinary symptoms or lower abdominal pain. On



1034


examination, the anterior vaginal fornix was

smooth without any nodularity.

Fig1: Picture showing bluish nodules around the

ureteric orifice at cystoscopy

Fig 2: Picture showing bluish area between the

bladder and the cervix

DISCUSSION

Involvement of the urinary tract by

endometriosis is rare, and it predominantly

affects the bladder, followed by the ureter and

the kidney in a ratio of 40:5:1.2

Endometriosis affecting the bladder could be

primary or secondary. The primary form is a

spontaneous disease. The secondary

manifestation results following pelvic surgery

such as caesarean section.3

The primary form is

commonly seen in association with severe pelvic

endometriosis. Tohic et al reported that in a

series of 24 patients with bladder endometriosis

concomitant deep nodules were seen in the

rectovaginal septum and uterosacral ligaments in

66% of patients.4

Bladder endometriosis can be

intrinsic or extrinsic and the extrinsic disease is

more common, where the disease involves the

serosa and the peritoneal surface. The lesions are

generally found in the trigone, dorsal wall or at

the ureterovesical junction.

In nearly 50% of cases, there are catamenialfrequency, urgency and dysuria. (Symptoms

presenting around the time of menstruation).

Most of them present with features of recurrent

cystitis but, without evidence of bacteriuria.

They can also present with dyspareunia with the

involvement of the anterior vaginal wall.

Occasionally gross haematuria is encountered

where there is an intrinsic bladder disease.5

Our case was more of an extrinsic disease,because, though she had suffered from

catamenial urinary symptoms for many years,

she has never had haematuria. As well as at

cystoscopy , endometriotic implants were not

eroding through the bladder mucosa.

Endometriosis of the bladder, especially the

extrinsic type is very difficult to diagnose and

relies heavily on clinical suspicion. When young

women present with urinary symptoms around

the time of menstruation, with or without a

possible diagnosis of pelvic endometriosis one

should suspect bladder involvement and

investigations should be initiated. In our case,

endometriosis of the bladder was suspected pre-

operatively as the patient presented with

catamenial urinary symptoms and the presence of

nodularity in the anterior vaginal fornix.

The occurrence of bladder endometriosis has

been explained by various theories such as adevelopment from the Mullerian remnants in the

vesico-uterine/ vesico- vaginal septum, extension

of an adenomyotic nodule of the anterior uterine

wall or it results from implantation of

regurgitated endometrium. Vercellini et al has

looked at the association between the bladder

endometriosis and adenomyosis and they have

concluded that vesical endometriosis seems to

originate from the implantation of regurgitatedendometrial cells in the anterior cul-de-sac and

not to be associated with uterine adenomyosis.6

Bluish area between the bladder andthe cervix

Ureteric orifice



1035


In our case the involvement of bladder with

endometriosis could be due to the direct

implantation of the endometrial cells on to the

bladder because of the previous two uterine

surgeries.

Imaging modalities such as USG, CT and MRImay facilitate diagnosis.. Cystoscopy is able to

visualize the endometriosis foci only when

present on bladder mucosal surface.7

In our case,

cystoscopy which was done 2 years ago was

reported normal. However, with increasing

severity of the symptoms and further progression

of the disease, repeat cystoscopy revealed the

presence of endometriotic areas around the left

ureteric orifice in the trigone.Majority of bladder lesions are superficial and

can be vaporized or ablated with bipolar or co2

laser. In our case, after the bladder was

separated from the cervix, the bladder lesion was

fulgurated with bipolar diathermy. When

endometriosis invades the mucosa of the bladder,

segmental resection of the bladder is the

treatment of choice.8

Some authors have suggested hysterectomy with

bilateral salpingo-oophorectomy to prevent

relapses. Namnoum et al9

concluded that

compared with women who had oophorectomy

for endometriosis, patients who underwent

hysterectomy with ovarian conservation had 6.1

times greater risk of developing recurrent pain

and 8.1 times greater risk of reoperation.9

Others

claim no specific advantages and suggest that

hysterectomy with BSO should not be carried out

for the sole purposes of prevention of relapses.5

In our case, we had to proceed with TAH with

BSO because of the adenomyosis of the uterus

and the complex hyperplasia of the endometrium.

CONCLUSION

Endometriosis involving the bladder is rare. One

should have a high degree of clinical suspicion to

diagnose the condition. Urinary tract

involvement with endometriosis should be

considered in all women who present with

recurrent urinary symptoms not responding to

medical management, especially in those who

have undergone caesarean deliveries or other

pelvic surgeries.

REFERENCES

1. Douglas C, Rotimi O. Extragenital

endometriosis: a clinicopathological review

of a Glasgow hospital experience with case

illustrations. J Obstet Gynaecol. 2004; 24:

804-08.

2. Nezhat CH, Malik S, Osias J, Nezhat F,

Nezhat C. Laparoscopic management of 15

patients with infiltrating endometriosis of the

bladder and a case of primary intravesical

endometroid adenosarcoma. Fertil steril.2002; 78:872-75.

3. Agarwal N, Kriplani A, Parul, Nabi G.

Intramural bladder endometriosis after

caesarean section: diagnostic and therapeutic

aspects. J Gynecol Sur. 2002; 18: 69-73

4. Le Tohic A, Chis C, Yazbeck C, Koskas M,

Madelenat P, Panel P. Bladder endometriosis:

diagnosis and treatment: A series of 24

patients. Gynecologie, Obstetrique & FertiliteDOI: 10.1016/j.gyobfe. 2009.01.018.

5. Veeraswamy A, Lewis M, Mann A, Kotikela

S. Extra genital endometriosis: In clinical

obstetrics and gynecology. Lippincott

Williams and Wilkins. 2010;53:449-66

6. Vercellini P, Frontino G, Pisacreta A, De

Giorgio, Cattaneo M, Crosignani PG. The

pathogenesis of bladder endometriosis. Am J

Obstet Gynecol. 2002; 187: 538-42.

7. Liselotte Mettler, Vidya Gaikwad, Bastian

Riebe and Thoralf Schollmeyer. Bladder

endometriosis: Possibility of treatment by

Laparoscopy. JSLS. 2008; 12 (2): 162-65.

8. Nezhat CR, Nezhat FR. Laparoscopic

segmental bladder resection for

endometriosis: a report of two cases. Obstet

Gynecol , 1993;81: 882-84.

9. Namnoum AB, Hickman TN, Goodman SB,

Gehlbach DL, Rock GA. Incidence of symptom recurrence after hysterectomy for

endometriosis. Fertil Steril.1995;64:898 -902.



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Ravishanker etal., Int J Med Res Health Sci. 2013;2(4):1036-1039


&

Health Scienceswww.ijmrhs.com Volume 2Issue4 Oct - Dec Coden: IJMRHS Copyright @2013 ISSN:2319-5886Received: 24th Aug 2013 Revised: 16th Sep 2013 Accepted: 28th Sep 2013

Case report

LIMB SALVAGE IN RECURRENT GIANT CELL TUMOUR PROXIMAL END RADIUS

*Ravishanker R

Professor, Reconstructive & Burns Unit, Rural Medical College, Pravara Institute of Medical Sciences,

Loni, Maharashtra, India


ABSTRACT

An 18years old male patient had undergone surgery for a giant cell tumour upper end of the right radius

in Jan 2007. The tumour recurred within two months. Patient took alternative methods of treatment

including indigenous medicines for the condition; all these failed and the patient was advised an above

elbow amputation. By Sep 2008 the tumour had grown to a 14”x11”x11” swelling in the forearm

extending to the distal arm with neurovascular involvement. A total resection of the tumour was done;

vascular continuity of the brachial to the ulnar artery was done with a vein graft to salvage the limb. In

2012 tendon transfer was done to restore function to the wrist. Now there is no recurrence of the tumour

and the patient has a fully functional limb.

Keywords: Giant cell tumour; proximal end radius; recurrent; salvage of limb; functional limb

INTRODUCTION

Giant cell tumours represent 5% of all bone

neoplasm’s.1,2

A benign but locally aggressive

tumour it typically occurs in patients between 30

to 40 years, with a female predominance. 75% to

90% of all tumours are found in the long tubular

bones especially the distal femur (30%),

proximal tibia (25%), distal radius (10%) and the

humerus (6%). The spine in 7% and the

inominate bone in 4% cases are other common

sites.3

The upper end of the radius is very rarely

involved and in literature there are just about a

dozen cases reported.4,5

This case report is not only a giant cell tumour in

the upper end of the radius, but one which hasoccurred in a young adolescent male. The tumour

was surgically removed after a local recurrence;

vascular continuity of the brachial artery to the

ulnar artery with a vein graft restored viability to

the limb. Tendon transfers have given a good

functional recovery. There is no recurrence after

five years of follow up.

The case is unusual in the rarity of the lesion; a

recurrence which occurred within months of the

original resection; and the fact that the limb

could not only be saved but also made fully

functional; there is no evidence of recurrence

five years post surgery.

CASE HISTORY

An 18y old male patient had reported to a

surgeon with a painful swelling upper end of the

right forearm in Jan 2007. He was diagnosed as a

case of a Giant Cell Tumour and resection of the



1037


upper end of the radius was done in Feb 2007.

The patient however noticed a recurrence of

swelling at the same site in the forearm within

two months of the surgery. For reasons

unexplained he did not go in for a redo surgery,

but took a series of treatment of indigenousmedicine including Ayurveda, Homeopathy etc.

After all these failed he was advised an above

elbow amputation of the limb.

By Sep 2008 the tumour had grown to a

14”x11”x11” painful lobulated swelling at the

site of the previous surgical scar. (Fig 1, 2).

Fig: 1: Recurrent giant cell tumour upper end radius

Fig 2 : Lobulated swelling with the scar of previoussurgery

The tumour had extended into the distal arm. The

skin over the swelling was warm, adherent to the

growth over the scar. There were dilated veins

over the swelling. There was evidence of radial

palsy and the distal radial pulsation was not

palpable. An MRI scan revealed a soft tissue

recurrence of the GCT encompassing the radio-

ulnar neurovascular bundle, the brachial artery

and the muscles in the proximal forearm.

In view of the young age of the patient and the

limb being a dominant one, a calculated risk was

taken to salvage the limb by an enbloc resection

and necessary reconstruction.

The patient and relatives were however

explained about the real possibility of having to

do an above elbow amputation and a pre-

operative consent for the same was taken.The patient was operated on 6 Sep 2008. During

surgery an enbloc removal of the recurrence

along with the tissues enveloped by the tumour

along with the scar over the tumour was done.

The resection included the encompassed radial,

ulnar and brachial arteries, the radial nerve, and

involved muscles with a 2 inch segment of the

radius and the previous scar. (Fig 3,4).

Fig 3: Resected tumour with 2 inches of radius

Fig 4: Bridging of brachial artery to ulnar artery

with a vein graft

Further specimens were taken from deeper

tissues including the joint capsule, forearm soft

tissue, from over the ulna and bone marrow from

the distal radius.

Vascular reconstruction was done by bridging

the brachial and ulnar arteries with a vein graft.(Fig 4).



1038


Fig 5: Well healed transposition flap over vessel

repair

The repaired vessels and exposed joint capsule

were covered with a local transposition flap.

Other raw areas were split skin grafted. All these

healed well. (Fig 5)

The histopathology report confirmed soft tissue

recurrence of the giant cell tumour with all

margins including the bone marrow, and deeper

soft tissues free of tumour.

The patient did well and despite a wrist drop with

the help of a radial palsy splint could carry out

all his normal functions of life.

In August 2011 a tendon transfer to correct the

wrist drop was done. As most of the major flexor

and extensor tendons of the forearm had been

removed at the time of the tumour resection, only

the Flexor Carpi Ulnaris could be spared. (Fig 6).

Fig 6: FCU being tunneled for transfer

The tendon was split into two and used to power

both the Extensor. Digitorum Communis and the

Extensor Pollicis Longus.

The patient has good wrist and thumb extension

following the tendon transfer and is able to carry

out all functions with the hand. (Fig 7)

Fig 7: Return of function in the hand with a good

grip and extension of the thumb, fingers and wrist

A follow up done five years after the recurrence

and resection have shown no evidence of local

recurrence. There are no pulmonary metastases.

DISCUSSION

Though giant cell tumours represent 5% of bone

neoplasms (as reported in a study from the Mayo

clinic)1,2

, the proximal end of the radius is an

extremely uncommon site of the lesion, Lewis et

al having reported only seven cases in their

extensive study.4-7

The lesion mainly affects

patients between the third and fourth decades of

life (60% to 70% of cases) with the frequency

being more in women than men.1- 6

The lesion in

the order of predominance affects the distal

femur (30%) the proximal tibia (25%) and the

distal radius (10%). Other sites affected are the

humerus (6%), the spine (7%) and the inominate

bone (4%). The proximal radius is affected in

only about 0.5% cases.3-6

Treatment ranges from simple curettage for

Stage 1 lesions to resection and reconstruction

for Stage 3 lesions. The recurrence rate after

simple curettage however ranges from 10% to 50

%.1-3,7,10,11

With adjuvant therapy like

radiotherapy, cryosurgery, argon therapy the

recurrence rate can be brought down. However

nearly one third of the long term survivors of

bone tumours require an amputation.6-11

Limb saving surgery after an extensive soft tissue

recurrence has not been reported in literature, themainstay of treatment recommended being in

these cases being an amputation, as the risk of



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