Journal of Paediatric Pulmonology and Critical Care

VOL-2 ISSUE-1

JOPPCC-2016

ISSN PRINT : 2454-373X

ISSN ONLINE : 2454-2873

Journal of

Paediatric

Pulmonology and

Critical Care Dr. N.K. Kalappanavar

Editor-in-Chief

Index :

Official Journal of

S.S. Institute of Medical Sciences and Research Centre,

Davangere - 577005, Karnataka, India

www.joppcc.org

http://www.joppcc.org/

Vol-2, Issue-1, JPPCC

(Official Journal of S.S.Institute of Medical Sciences and Research Centre, Davangere-577005, Karnataka, India)

oppcc

Sri S S Mallikarjun Chairman, SSIMS&RC

Patron

Dr. B.S. Prasad Principal, SSIMS&RC

Editor-in-Chief

Dr. N.K. Kalappanavar Medical Director, Professor & Head, Department of Paediatric

S. S. Institute of Medical Sciences & Research Centre Davangere 577005. Karnataka, India. Email: [email protected]

Section Editors

Dr. Somashekar A R Dr. Devaraj Raichur Dr. Chandrashekar Gouli Dr. Latha G S

Dr. Basanthkumar G R Dr. Subramanya N K Dr. Mohammed Haseen Basha Dr. Sanjay D

Dr. V D Patil

National Editorial Advisory Board

Dr. H Paramesh Registrar, KLE University

Formal Principal, JNMC, Belgaum Medical Director, Paediatric pulmonology

Lake side Medical centre, B'lore

Dr. Vijayshekaran D Asso. Prof, Dept of Paediatrics & Resp diseases

Madras Medical College, ICH&HC Chennai

Dr. Varinder Singh Prof of Paediatrics, Lady Hardinge Medical College &

Associated Kalavati Children Hospital, New Delhi

Dr. J. Mangalore Devadas Dept. of Paediatrics, Father Muller Medical college, Mangalore India, Email: [email protected]

T U Sukumaran President, IAP-2011, Prof, Dept. of Paediatrics

Pushpagiri Institute of Medical Sciences, Thiruvalla, Kerala

Dr. S Nagabhushana Clinical Asso., CSI Hospital

Consultant Paediatric Pulmonologist, Bangalore

Dr. Pallab Chattarjee Paediatric Pulmonologist RTIICS NH, Kolkata

Dr. C R Banapurmath Director BCHI&RC

Dept of Paediatrics, JJMMC, Davangere

Dr. Suresh Babu P S Prof. Emeritus, Consultant Pulmonologist Dept of Paediatrics, JJMMC, Davangere

Dr. Santhosh Soans Prof & Head, Dept of Paediatrics,

AJ Institute of Medical Science, Mangaluru

International Editorial Advisory Board

Dr. Kallesh Hebbal Senior Consultant, Sohar Hospital,

Oman Medical College, Oman

Dr. Christopher O'Brain Consultant Peadiatric Pulmonologist,

Great North Children's Hospital, Newcastle UK

Dr. Prashanth Kumar Consultant in Paediatrics and Pulmonologist

Sunderland Royal Hospital, UK

Dr. Kiran Kumar B V Consultant in Neonatology Sydney Children Hospital

Sydney Australia

Editorial Board

Journal of Paediatric Pulmonology and Critical Care

mailto:[email protected]


Journal of

Paediatric

Pulmonology and

Critical Care

July 2016 / Vol 2 / Issue 1

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Bapuji Educational Association(R.), Davangere

S.S. Institute of Medical Sciences & Research Centre,

Chairman : Sri S.S. Mallikarjun

Joint Secretary, Bapuji Educational Association Davangere, Karnataka, India

NH-4, Bypass Road, Davangere 577 005,

Karnataka, India.

Vol-2, Issue-1, JOPPCC 2016

International Standard Serial Number:

Print ISSN : 2454-373X

Electronic ISSN : 2454-2873

Correspondence

Address all correspondence regarding submission of articles to:

Dr. N.K. Kalappanavar

Medical Director, Professor & Head, Department of Paediatric

S. S. Institute of Medical Sciences & Research Centre

Davangere 577005. Karnataka, India. Email: [email protected]

Website: www.joppcc.org

© All rights reserved

Disclaimer

Views expressed by authors are not those of the Journal of Educational Research and Medical Teacher.

All statements, opinions expressed in the manuscript are those of the authors and not of the editor(s) or

publishers. The editor(s) and publishers disclaim any responsibility for such material.

JOURNAL OF PAEDIATRIC PULMONOLOGY AND CRITICAL CARE


http://www.joppcc.org/

Scope:

Welcome to the Indexed “Journal of Paediatric Pulmonology and Critical Care”

that publishes high quality scientific research work in basic and advanced

paediatric pulmonary medicine. JOPPCC is a peer reviewed journal, with

renewed pulmonologist and pediatrician on the advisory board. The journal

has a special focus on new developments in pulmonary physiology, clinical

pulmonology, natal and post natal pulmonary issues and effects of

environment on respiratory system issues are published twice a year in the

month of June and December. This is a scientific journal of SSIMS&RC to

promote new generation scientists and perculate the knowledge of advanced

and scientific current issues in respiratory medicine. The journal accepts articles

on current issues of pulmonology, new studies on peadiatric respiratory

diseases including basic to advanced therapeutic modalities which are helpful

to persons involved in child health care.

JOURNAL OF PAEDIATRIC PULMONOLOGY AND CRITICAL CARE oppcc

CONTENTS

EDITORIAL

Recent Trends In Paediatric Pulmonology 1

N.K. Kalappanavar

REVIEW ARTICLE

Continuous Positive Airway Pressure in Newborn 8

Kiran Kumar Balegar V

Cough in Children 18 Subramanya N.K.

ORIGINAL ARTICLE

Neonatal hypernatremic dehydration : Can we prevent it.

Srikanth S, Mallikarjun G.P, Prashanth S.V, Channabasavaraj H 23

Clinical Profile and Outcome of Hospitalized Children with 26 Empyema Thoracis At A Tertiary Care Level Teaching Hospital Vijay Kulkarni, Pranab J., Poornima Kulkarni

CASE REPORT

Joult of Acute Flaccid Paralysis following symptomatic treatment 30

Srikanth S.

Miliary Tuberculosis with Scoliosis : A Case Report 35

Madhu G.N., Siva Saranappa S.B., Saipraneeth Reddy

A Term Neonate with Congenital Pulmonary Airway Malformation 38

Nitin M., Sudha Rudrappa, Girish G.

INSTRUCTION TO AUTHORS 40

Vol-2, Issue-1, JOPPCC 2016

Journal of Paediatric Pulmonology & Critical Care 1 2016;1(1):1-7

Recent Trends In Paediatric Pulmonology

Dr. N.K. Kalappanavar M.D.,DNB (Paed). , MNAMS. FIAP, FRCPCH(UK)

Fellowship in Pediatric Pulmonology, Medical Director

Prof & Head, Consultant Paediatric Pulmonologist, Dept of Paediatrics SSIMS&RC. Davangere-577 005

Correspondence : Dr. N.K. Kalappanavar Medical Director, Prof & Head, Department of Paediatrics, SSIMS & RC, Davangere.

email : [email protected]

The pulmonary function lab of today is heavily

focused on describing pathophysiology and quantifying

the extent of disease. As we move forward, it is important

that the results of pulmonary function tests go beyond

this and be linked to important outcomes that truly affect

clinical decision making. To get there, improvements in

device performance are required, high quality

technicians are critical, and properly trained interpreting

clinicians with good reference standards are mandatory.

Moreover, as accessibility to these tests is increased, it is

important that quality metrics remain intact.

There is a wide array of novel tests that might be

performed by pulmonary function labs in the future.

These range from modification of current technologies

to brand new technologies that are still in early

development. Examples include exhaled breath analysis,

sophisticated analyses of lung mechanics and gas

exchange, cardiac and tissue oxygenation assessments,

and imaging technologies. Adoption of any new

technology will require, even more than today, clear

evidence that the new technology is a real adjunct to

clinical decision making

Pulmonary function testing, however, should not

be limited to just defining buckets and quantifying

descriptive functions. The ultimate goal would be to use

these tests to predict important outcomes. Examples

include assessing and predicting quality of life,

functional capabilities, future morbidity/ mortality, and

the risk/benefit of an intervention. Unfortunately, at the

present time the role of pulmonary function testing

remains heavily focused on “buckets” and arbitrary

severity grading systems. The future pulmonary

function laboratory and the development of future

pulmonary function tests need to be developed with a

focus on integrating test results into the clinical decision

making process future of the pulmonary function

laboratory is bright. Nev- ertheless, a constant striving

for technical and interpretive excellence along with

careful evidence-based studies linking these tests to

outcomes is going to be critical to maintain this

brightness.

Goals of PFT'S

• To predict the presence of pulmonary dysfunction

• To know the functional nature of disease (obstructive or restrictive).

• To assess the severity of disease

• To assess the progression of disease

severity of the derangement. Those are simply • To assess the response to treatment

• To identify patients at increased risk of

Abstract : Pulmonary function testing, however, should not be limited to just defining buckets and

quantifying severity of the . Those are simply descriptive functions. The ultimate goal would be to use these tests

to predict important outcomes. Examples include assessing and predicting quality of life, functional capabilities,

future morbidity/ mortality, and derangement. Unfortunately, at the present time the role of pulmonary

function testing remains heavily focused on “buckets” and arbitrary severity grading systems. The future

pulmonary function laboratory and the development of future pulmonary function tests need to be developed

with a focus on integrating test results into the clinical decision making process future of the pulmonary function

laboratory is bright. Nev- ertheless, a constant striving for technical and interpretive excellence along with

careful evidence-based studies linking these tests to outcomes is going to be critical to maintain this

brightnessThe future of the pulmonary function laboratory is bright. Nev- ertheless, a constant striving for

technical and interpretive excellence along with careful evidence-based studies linking these tests to outcomes

is going to be critical to maintain this brightness.

Key words : PFT. Spirometry,Carban monoxide,

ED

ITO

RIA

L



morbidity and mortality, undergoing pulmonary resection

• To wean patient from ventilator in icu.

• Medicolegal- to assess lung impairment as a result of occupational hazard.

• Epidemiological surveys- to assess the hazards to document incidence of disease

• To identify patients at perioperative risk of pulmonary complications

BED SIDE PFT'S

1) Sabrasez breath holding test:

• Ask the patient to take a full but not too deep

breath & hold it as long as possible.

>25SEC. -NORMAL Cardiopulmonary

Reserve (CPR)

15-25 SEC- LIMITED CPR

<15 SEC- VERY POOR CPR

(Contraindication for elective surgery)

25- 30 SEC - 3500 ml VC

20 – 25 SEC - 3000 ml VC

15 - 20 SEC - 2500 ml VC

10 - 15 SEC - 2000 ml VC

5 - 10 SEC - 1500 ml VC

2) Single breath count :

After deep breath, hold it and start counting till

the next breath.

o N- 30-40 COUNT

o Indicates vital capacity

3) SCHNEIDER'S MATCH BLOWING TEST:

MEASURES Maximum Breathing Capacity.

Ask to blow a match stick from a distance of 6” (15

cms) with-

▪ Mouth wide open

▪ Chin rested/supported

▪ No purse lipping

▪ No head movement

▪ No air movement in the room

▪ Mouth and match at the same level

▪ Can not blow out a match

▪ MBC < 60 L/min

▪ FEV1 < 1.6L

▪ Able to blow out a match

▪ MBC > 60 L/min

▪ FEV1 > 1.6L

▪ MODIFIED MATCH TEST :

DISTANCE MBC

9” >150 L/min.

6” >60 L/ min.

3” > 40 L/ min.

4) Cough Test: Deep breath followed by cough

❖ Ability to cough

❖ Strength

❖ Effectiveness

Inadequate cough If : FVC<20 ml/Kg

FEV1 < 15 ml/Kg

PEFR < 200 L/min.

VC ~ 3 Times TV for effective cough.

A wet productive cough / self propagated

paraoxysms of coughing – patient susceptible for

pulmonary Complication.

5) FORCED EXPIRATORYTIME :

After deep breath, exhale maximally and forcefully

& keep stethoscope over trachea & listen.

N FET – 3-5 SECS.

OBS.LUNG DIS. - > 6 SEC

RES. LUNG DIS.- < 3 SEC

6) WRIGHT PEAK FLOW METER: Measures

PEFR (Peak Expiratory Flow Rate)

N – MALES- 450-700 L/MIN.

FEMALES- 350-500 L/MIN.

<200 L/ MIN. – INADEQUATE COUGH

EFFICIENCY.

7) DEBONO WHISTLE BLOWING TEST:

MEASURES PEFR:

Patient blows down a wide bore tube at the end of

which is a whistle, on the side is a hole with adjustable

knob.

As subject blows → whistle blows, leak hole is

gradually increased till the intensity of whistle

disappears.

At the last position at which the whistle can be

blown , the PEFR can be read off the scale.

8) WRIGHT REPIROMETER: measures tv, mv.

▪ Simple and rapid

▪ Instrument- compact, light and portable.

▪ Disadvantage: It under- reads at low flow rates

and over- reads at high flow rates.

▪ Can be connected to endotracheal tube or face

mask

▪ Prior explanation to patients needed.

▪ Ideally done in sitting position.

▪ MV- instrument record for 1 min. And read


directly

• TV-calculated and dividing MV by counting

Respiratory Rate.

USES: 1)BED SIDE PFT

2) ICU – Weaing Pts from Ventilation.

9) MICROSPIROMETERS – MEASURE VC.

10) BED SIDE PULSE OXIMETRY

11) ABG.

Categorization of PFT

1) Mechanical Ventilatory Functions of Lung / Chest

wall:

A) Static Lung volumes & capacities – VC, IC, IRV,

ERV, RV, FRC.

B) Dynamic Lung volumes – FVC, FEV1,

FEF 25-75%, PEFR, MVV, Resp. muscle

strength.

C) Ventilation tests – TV, MV, RR.

2) GAS- EXCHANGE TESTS:

A) Alveolar-arterial po2 gradient

B) Diffusion capacity

C) Gas distribution tests- single breath

- N2 test.

-Multiple Breath N2 test

- Helium dilution method.

- Radio Xe scinitigram.

D) ventilation – perfusion tests

A) ABG

B) single breath CO2 elimination test

C) Shunt equation

3) CARDIOPULMONARY INTERACTION:

A) Qualitative tests:

- History , examination

- Abg

- Stair climbing test

B) Quantitative tests

-6 min. Walk test (gold standard)

What these tests really asses

l First : Clinical and physiological functions

Fig. 1. The concept of using pulmonary function tests to place subjects into

physiologic “buckets” using the interpretation algo- rithm of the American

Thoracic Society/European Respiratory So- ciety task force. VC vital capacity.

LLN lower limit of normal. PV pulmonary vascular. CW chest wall. NM

neuromuscular. CB chronic bronchitis

LLN - Lowerlimit of normal

➢ Second: pulmonary function testing is to

quantify the severity of a physiologic

derangement

➢ Usually this requires comparing the measured

value to a predicted or reference value, but the

actual quantification is often done in a

somewhat arbitrary fashion for FEV1 (ie,

80%, 50 –79%, 30 – 49%, and 30%)

➢ Pulmonary function testing, however, should

not be limited to just defining buckets and

quantifying severity of the derangement

➢ Because those are descriptive functions

Problems with current PFT'S

➢ At present these pulmonary function test

results often lack sufficient discriminatory

power to be really helpful in individual patient

decision making.

➢ False positive and false negative reports

➢ Finally, not accessible to those who need it

What future needs

➢ Assessing and predicting outcomes

➢ Quality of life

➢ Functional capabilities

➢ Future morbidity/ mortality

➢ The risk/benefit of an intervention focus on


Pneumotachometer

integrating test results into the clinical decision

making process

What New Procedures Available Today

• Respiratory system mechanics

• Pulmonary gas exchange

• Non invasive cardiac output

• Analysis of exhaled biomarker

Respiratory system mechanics

Forced pressure oscillations

➢ Sophisticated analyses of the pressure and flow

signal as the oscillations are delivered and

reflected back to the device can give unique

insight into airway resistance and reactance.

➢ Large airway and small airway function can be

separated during rest, exercise, and after

exposure to an airway challenge

➢ It may also help in evaluating the interactions

of applied PEEP and intrinsic PEEP in

subjects with airway obstruction.

Offers advantages in patients unable to cooperate

with spirometry. (Eg: young children)

Esophageal balloon to estimate pleural pressures

• This technique requires insertion of an air-

filled balloon into the mid-esophagus and then

measuring pressures during various breathing

maneuvers

• Measurement of esophageal pressure

permits the separation of chest

wall/abdominal compliance properties

from actual lung compliance.

This can be helpful especially in patients with

such things as ascites, obesity, chest wall deformities,

and anasarca, which can have profound effects on

the work of breathing. Respiratory muscle strength

capabilities

Infant lung function tests using a facemask and a

pneumotachometer

Assessment of tidal breathing using structured

lightplethysmography (SLP).


Quantitative assessments of tidal breathingduring quiet

sleep using SLP

Pulmonary gas exchange

• Pulseoximetry

• Expanded pulse oximetry (capabilities now

include carboxyhemoglobin and total

hemoglobin)

• Carban monoxide uptake( DLCO) with real

time gas analyser: Reflects the

capillary “recruitability”

• Nitric oxide uptake: complimentary to

DLCO.

Expanded pulse oximetry

Transcutaneous technology. ( measure the partial pressure of oxygen or carbon dioxide)

Pulmonary Gas Exchange

(Ventilation-Perfusion Matching)

• Interesting technique describes

ventilation- perfusion relationships

throughout the lungs. Known as the

multiple inert gas elimination technique

(MIGET)


The procedure involves infusing a solution

containing 6 gases of different solubilities and then

measuring their elimination in alveolar gas

Conceptually, this has the potential to characterize

all lung diseases into important physiologic pheno-

types.

Tissue Oxygen Delivery

▪ Near infrared spectroscopy

▪ To assess tissue cytochrome

reduction/oxygenation status

Near infrared spectroscopy

❖ This approach conceptually measures the

“bottom line” the actual entry of oxygen into the

cytochrome system to generate ATP in

important organs such as the brain

❖ Reliable, reproducible signal processing with

minimal artifact interference is still a challenge,

and the expense can be considerable

M.J.T. Van de Ven et al. Eur Respir J 2001;18:61-68

❖ Barriers to Implementation of New Technologies

❖ Barriers to implementation of new techniques

are many. First, reliable devices have to be built

that are inexpensive

Fig. 5. Current status of exhaled biomarkers. EBC exhaled breath condensate. GP general practice. FENO fraction of exhaled

nitric oxide. MEFENO multiple exhalation flow NO. VOC volatile organic compounds. E-BreathT exhaled breath temperature. E-

Nose electronic nose type of breath analysis. BBF bronchial blood flow. (From Reference 35, with permission.)


and relatively easy to use. Good technical training is going to be

critical to assure accurate and reliable results. As noted above,

before these devices are adapted clinically it is going to be

critically important to prove that they are related to important

outcomes and that they truly affect decision making on the part of

clinicians. And of course, getting it paid for is a major hurdle for

any new technique to overcome. This will require getting Current

Procedural Terminology (CPT) codes with clear indications and

clinical scenarios. The next step is convincing clinicians that

data exist showing that this test is linked to outcomes and thus

should impact decision making. Finally third-party payers must

be convinced of a favorable cost/benefit ratio (ie, the improved

outcomes are worth the cost).

Summary

The pulmonary function lab of the future needs to go beyond

simply describing physiologic buckets and quantifying the

extent of disease. It is absolutely critical that the results of

pulmonary function tests be linked to important outcomes and

truly affect clinical decision making. To get there, current labs

need to have maximum accuracy and reliability of their devices,

high quality technicians per- forming these tests, and high

quality clinicians interpreting the tests using appropriate

reference standards. As accessibility to these tests is increased,

it is important that these quality metrics remain intact. There is a

wide array of future tests that might be performed by pulmonary

function labs in the future. These range from modification of

current technologies to brand new technologies such as exhaled

breath analysis, sophisticated analyses of lung mechanics and

gas exchange, cardiac and tissue oxygenation assessments,

imaging technologies, as well as others. The future of the

pulmonary function laboratory is bright. Nev- ertheless, a

constant striving for technical and interpretive excellence

along with careful evidence-based studies linking these

tests to outcomes is going to be critical to maintain this

brightness.

REFERENCES

1. Pellegrino R, Viegi G, Brusasco V, Crapo RO, Burgos F, Casaburi

R, Coates A, et al. Interpretative strategies for lung function tests.

Eur Respir J 2005;26(5):948-968.

2. Miller MR, Crapo R, Hankinson J, Brusasco V, Burgos F, Casaburi

R, Coates A, et al; ATS/ERS Task Force. General considerations for

lung function testing. Eur Respir J 2005;26(1):153-161.

3. American Thoracic Society. Evaluation of impairment/disability

secondary to respiratory disorders. Am Rev Respir Dis

1986;133:1205-1209.

4. Global Initiative for Chronic Obstructive Lung Disease. Guidelines

and resources. http://www.goldcopd.org/Guidelines/guidelines-

resources.html. Accessed November 2, 2011.

5. Mannino DM, Buist AS, Petty TL, Enright PL, Redd SC. Lung

function and mortality in the United States: data from the first Na-

tional Health and Nutrition Examination Survey follow-up. Thorax

2003;58(5):388-393.

6. Celli BR. Predictors of mortality in COPD. Respir Med

2010;104(6) : 773-779.

7. Neas LM, Schwartz J. Pulmonary function levels as predictors of

mortality in a national sample of US adults. Am J Epidemiol 1998;

147(11):1011-1018.

8. Smetana GW, Lawrence VA, Cornell JE. Preoperative pulmonary

risk stratification for noncardiothoracic surgery: systematic review

for the American College of Physicians. Ann Int Med 2006;144(8):

581-595.

9. Miller JI. Physiologic evaluation of pulmonary function in the can-

didate for lung resection. J Thorac Cardiovasc Surg 1993;105(2):

347-351.

10. Collard HR, King TE Jr, Bartelson BB, Vourlekis JS, Schwarz MI,

Brown KK. Changes in clinical and physiological variables predict

survival in pulmonary fibrosis. Am J Respir Crit Care Med 2003;

168(5):538-542.

http://www.goldcopd.org/Guidelines/guidelines-


Continuous Positive Airway Pressure in Newborn

Kiran Kumar Balegar V Consultant Neonatologist

Nepean Hospital and University of Sydney, Sydney, AUSTRALIA Correspondence: [email protected]

Correspondence : Dr. Kiran Kumar Neonatologist, Nepean Hospital, Sydney, Australia

Affiliation: University of Sydney. E mail: [email protected]

What is Continuous Distending Pressure?1

Continuous distending pressure (CDP) is a method

of delivering low pressure distension to the lungs during

both inspiratory and expiratory phases of the respiratory

cycle. Methods of achieving this include positive end

expiratory pressure (PEEP) during mechanical

ventilation, continuous positive airways pressure

(CPAP) applied to the upper airway (usually nose) and

continuous negative expiratory pressure (CNEP). In

preterm infants with respiratory distress, use of CDP as

compared to head box oxygen has been shown to reduce

the rate of the combined outcome of death or assisted

ventilation [RR 0.65 (95% CI 0.52, 0.81, NNT 5 (4, 10)].

NCPAPvs BiPAP

CPAP machines deliver pressurised air/oxygen to

upper airways. There are 2 types of CPAP machines:

Nasal CPAP (NCPAP) provide the same level of pressure

during both inspiration and expiration. Bilevel CPAP

(BiPAP) or Synchronised Positive Airway Pressure

(SiPAPTM

– manufacturer's trademark) machines try to

more closely match normal breathing by providing

different pressure levels during inspiration and

expiration (higher pressure during inspiration and lower

pressure during expiration). NCPAP is more commonly

used than BiPAP in neonates and is commonly referred to

in this document as CPAP.

What are the Physiological Effects of CPAP?2-9

1. Increases functional residual capacity. This helps

to prevent alveolar collapse, reduce the work of

breathing and improve gas exchange.

2. Reduces intrapulmonary right to left shunting by

reducing the ventilation: perfusion mismatch.

3. Decreases airway resistance by increasing

pharyngeal cross-sectional area.

4. Improves lung compliance.

5. Reduces obstructive apnoea by splinting airways,

chest wall and diaphragm.

6. Reduces the severity of central apnoea by

stimulating J receptors and improving respiratory

drive.

7. Conserves surfactant.

8. Decreases alveolar oedema by increasing trans-

pulmonary pressure.

9. Stimulates lung growth.

Indications for using CPAP

Parenchymal lung disease (Eg. RDS, pneumonia,

meconium aspiration, chronic lung disease etc.)

In our Unit, CPAP is the initial mode of breathing support

in infants admitted with

• Signs of respiratory distress

• Oxygen requirement (generally 30% or more)

Early vs late CPAPin RDS

CPAP when applied early before atelectasis occurs

may better conserve an infant's own surfactant stores and

consequently be more effective than CPAP applied later

in the course of RDS.

Abstract : CPAP machines deliver pressurised air/oxygen to upper airways. There are 2 types of CPAP

machines: Nasal CPAP(NCPAP) provide the same level of pressure during both inspiration and expiration. Bilevel

CPAP (BiPAP) or Synchronised Positive Airway Pressure TM (SiPAP – manufacturer's trademark). CPAP when

applied early before atelectasis occurs may better conserve an infant's own surfactant stores and consequently

be more effective than CPAP applied later in the course of RDS. There is a paucity of data in the literature

regarding the use of CPAP for respiratory distress in term infants. CPAP has been shown to reduce the risk of

death and mechanical ventilation in preterm infants with respiratory distress. · CPAP provides benefit by

multitude of mechanisms and is most effective when commenced as early as possible in the disease course.

Babies on CPAP need very close and vigilant monitoring so as to provide effective CPAP and avoid CPAP related

complications such as pneumothorax, nasal septal injury, abdominal distension etc.

Key words : CPAP, Non invasive ventilation

RE

VIE

W A

RT

ICL

E




A Cochrane review10

demonstrated that in preterm

infants with RDS early (starting CPAP at randomisation)

as compared to late CPAP (starting CPAP late in the

course of RDS, when FiO2 is >60%) was associated with

a significant reduction in the use of intermittent positive

pressure ventilation (RR 0.55, 95% CI 0.32, 0.96, NNT

6) although there was no difference in mortality; rate of

pneumothorax or BPD.

In extremely premature infants (<28 weeks) meta-

analysis11

has shown that prophylactic administration of

surfactant results in increased risk of chronic lung

disease or death as compared to early stabilization on

CPAP with selective surfactant administration. [RR

1.12, 95% CI 1.02, 1.24]. However, it is important to note

that many of these trials involved extremely preterm

neonates (<28 weeks) where the use of antenatal steroid

coverage was very high (>90%) and may not be

applicable to developing countries.

At Nepean Hospital, it is a routine practice to

stabilise preterm infants on CPAP in the delivery room,

transfer on CPAP in heated, humidified blended

air/oxygen and continue on CPAP. If there is persistent

respiratory distress, increasing FiO2 requirement

(generally >30%) and /or lack of adequate spontaneous

breathing the baby will then be intubated and given

surfactant. There is a paucity of data in the literature

regarding the use of CPAP for respiratory distress in term

infants. Our clinical experience suggests that term

infants do not tolerate the application of the CPAP

devices well, resulting in restlessness and labile

oxygenation. In such situation we trial them on HHFNC

or ventilate them.

Weaning from ventilation (Post-Extubation)

A meta-analysis12

of nine trials showed that

premature infants extubated to CPAP as compared to

head box oxygen had less incidence of respiratory failure

(apnea, respiratory acidosis and increased oxygen

requirements).

Apnoea of prematurity

CPAP with caffeine is commonly used in apnea of

prematurity. The use is so widely established that it is

ethically impossible to perform RCTs using CPAP vs no

CPAP in apnea of prematurity. Observational studies8

done many years ago suggested that apnoea of

prematurity is improved by the use of CPAP.

Anatomical Abnormalities / Obstructive apnoea

Airway abnormalities that predispose to airway

collapse and those that need splinting (Laryngo-tracheo-

bronchomalacia, phrenic nerve palsy) may benefit from

the application of CPAP. Distending pressure prevents

pharyngeal collapse and increases the cross-sectional

area of the upper airways thereby decreasing the risk of

obstruction.

Are there any contra-Indications to CPAP?

• Poor respiratory effort (eg: extreme prematurity,

severe encephalopathy).

• Bilateral choanal atresia (pressure cannot be

delivered)

• Tracheo-oesphageal fistula (potential rupture of

blind end of oesophagus)

• Diaphragmatic hernia (worsening of respiratory

distress due to distension of GI tract in thorax)

• Unrepaired gastroschisis/omphalocele (distension of

exposed GI tract)

• Severe nasal trauma/severe deformity that might be

exacerbated by use of nasal prongs and masks.

(Relative contraindication)

• Gastro-intestinal perforation

• Cardiovascular instability - These infants may be

better stabilised by intubation and ventilation.

• Necrotising enterocolitis - These infants may also

have secondary apnea, cardiovascular instability etc.

and are hence better stabilised by ventilation.

Essentials of CPAPdelivery system :

The system has 4 components:

• CPAP pressure generator

• Gas flow system – warmth, humidification and

oxygen blending

• Patient interface (device to connect the circuit to the

neonate's airway

• Accessories: hats, straps, Velcro etc. to secure the

interface

CPAPpressure generator

Pressure is generated by flow of gas through an

exhalation port which is either controlled by a valve or

underwater pressure. There are 2 types of CPAP

generators :

• Continuous flow CPAP–e.g.: Ventilator derived

CPAP and Bubble CPAP.

• Variable flow CPAP - e.g.: Infant Flow Driver (IFD)

Ventilator derived CPAP

The same ventilator that is used for mechanical

ventilation can also be used to deliver CPAP. By using

the PEEP knob (controlling the exhalation valve, as

shown in Fig 1) a specific CPAP pressure can be

prescribed.


Bubble CPAP

Fig 2: Principles of bubble CPAP

Fig 3: Fisher and Paykel bubble CPAP system

CPAP is generated by placing the expiratory limb

under water as shown in Fig 2. Greater the depth of

insertion, higher is the pressure generated. Bubble CPAP

is simple, easy to prepare and cost-effective. As a rule of

thumb, at a flow rate of 4-8 L/min, pressure generated

(cm of water) is at least equal to (more often slightly

higher but not more than the next number) the depth of

insertion (cm) of expiratory limb under water. Flow of

air bubbles under water also produces oscillations

(similar to high frequency). The noisy pressure

waveform superimposed over pressure fluctuations

(stochastic resonance effect) promotes alveolar

recruitment13. As a result bubble CPAP is perceived to be

more effective than ventilator CPAP. Bubbling indicates

that the desired CPAP pressure is being generated.

Absence of bubbling generally indicated a leak in the

system. Gentle bubbling is shown to be as effective as

vigorous bubbling. In Australia Fisher and Paykel

bubble CPAP system is widely used.

Infant Flow Driver (IFD)

With continuous flow CPAP, baby has to breathe out

against gas flow thereby potentially increasing work of

breathing. This is alleviated by variable Flow CPAP

system wherein the flow of gas flips away from the baby

during expiration. Theoretically, variable Flow CPAP

provides more effective CPAP with less work of

breathing compared to continuous flow CPAP.

Mechanism of action - Coanda effect

When a jet of air passes through a narrow nozzle, a

low pressure is created around the jet. As a result, the jet

entrains (sucks in) air from the surrounding and carries

along with it as it flows towards the baby, as shown in Fig

4. Thus during inspiration, there is an accelerated flow

thereby reducing the work of breathing.

Fig 4: Mechanism of action of IFD: Inspiration

When the infant makes spontaneous expiratory

breathing effort, there is a slight increase in pressure at

the site of nasal connection. As a result, the jet flips away

towards the lower pressure area (expiratory limb) as

shown in Fig 5. Due to fluid flip the patient does not

have to breathe out against flow, thus reducing the work

of breathing.

Exhalation

valve

Fig 1: Principles of Ventilator CPAP


Fig 4: Mechanism of action of IFD:

Fluidic flip during expiration

At Nepean Hospital Infant flow driver (VIASYS SIPAP

DRIVER) is used as the primary mode of CPAP and

BiPAP.

Fig 5: VIASYS Infant Flow

® SiPAP

TM

Though, there is some evidence for the superiority

of IFD and bubble CPAP over ventilator CPAP, the

differences in study design, indications, short study

epochs and insufficient relevant clinical outcomes

necessitate the need for further studies on this issue. At

present there is no evidence to support or refute the use of

one CPAP generator over other.

Gas flow system - CPAPcircuit

Higher flow results in higher CPAP pressure. Very

high flow rate results in undesirable side effects such

as abdominal distension. Optimum flow is the lowest

flow rate that achieves desired CPAP pressure. A

flow rate of 6-8 L/min is commonly used.

Gas contains oxygen blended with air (21-100%).

CPAPHumidity

During normal inspiration the human airway

conditions inspired gases with heat and humidity to body

temperature (100% Relative Humidity with 44 mg/L of

Absolute Humidity). The lungs rely on these conditions

to maintain the physiological balance of heat and

moisture necessary for optimized airway defence and gas

exchange while maintaining infant comfort. When

delivering respiratory support to infants, aim is to deliver

gas (air/oxygen) at the nose at or near body temperature

with optimal humidity (100% relative humidity at 370C).

Optimal humidity prevents14

(1) airway cooling, which is

a primary cause of pain and discomfort, (2) airway

drying and water loss, which will lead to thickened

secretions, (3) airway inflammation and constriction (4)

slowing of mucociliary clearance.

In our NICU, we use F&P MR850 humidifiers for

all respiratory devices with pre-set temperature. An

adequate water level is required to maintain inspired gas

humidity. Condensation will cause water to accumulate

in tubing. This needs to be regularly removed in order to

prevent water from reaching the infant.

Fig 6: F & P MR850 humidifier

Patient interface –Nasal prongs

Short (6-15 mm) vs long (40-90 mm)

Long nasal prongs (nasopharyngeal prongs) have the

advantage that they consistently deliver pressure into

upper airways. Disadvantages include greater

discomfort, higher resistance, kinking, blockage by

secretions and difficulty in monitoring local side-

effects. Short nasal prongs overcome these

disadvantages but tend to dislodge more often and

hence need to be closely monitored to keep them in

situ.

Single vs binasal

Binasal prongs are more effective than single nasal

prongs for obvious reasons. Single nasal prongs

(usually a short endotracheal tube) situated in the

nasopharynx may be considered in infants where

facial anomalies such as bilateral cleft lip / palate

preclude the use of short prongs. Various types are

available for different CPAP circuits as shown in

Fig 7.


Bubble CPAP prongs

F & P prongs

Argyle prongs

IFD prongs

Fig 7: Different types of short binasal prongs

available in the market:

Nasal masks

Masks are generally considered to be less effective in

providing appropriate seal and hence result in pressure

leak. They are usually used when prongs do not

provide an adequate seal in a given baby; baby's

nostrils are too narrow to fit into prongs (e.g.

extremely premature babies) or the nares are in need of

a rest (e.g. nasal septal trauma due to prongs).

Fig 8: Nasal masks

CPAP delivered by short binasal prongs have been

shown to be more effective at preventing re-intubation

than single nasal or nasopharyngeal prongs [RR 0.59;

95% CI: 0.41, 0.85; NNT 5 (CI: 3, 14)] in preterm

neonates15and are shown to lower oxygen requirement

and respiratory rate when compared to nasopharyngeal

prongs16. Evidence is conflicting in terms of superiority

of prongs over masks. Contrary to the popular belief,

masks are shown to be superior to prongs in a more recent

trial17. In this RCT involving 149 newborns, frequency of

CPAP failure within 24 h of life was higher; duration of

CPAP was longer and the rate of moderate and severe

BPD was significantly greater in the nasal prong group

when compared with the nasal mask group. Further

studies are required to resolve this issue.


Presently, use of short binasal prongs has become

the standard of practice in neonates requiring CPAP

except in those with facial anomalies. Nasal masks are

used when prongs are ineffective or contraindicated. At

Nepean Hospital, we alternate prongs and mask every 6-

8 hourly especially in extremely premature babies

needing long duration of CPAP, unless either of them is

ineffective or contra-indicated in a given baby.

What level of CPAPpressure to use?

There is paucity of data regarding the ideal range of

CPAP pressures in neonates. Following are the general

principles

Minimum CPAP pressure should not be less than the

normal physiologic PEEP of 2-3 cm water. A level of

5cms of water (3-5 cm) is generally the lower limit

used in our nursery.

In selecting the ideal CPAP consider the condition

that is being targeted. For example one may use

higher CPAP (e.g.: 8 cm water) in infant with acute

phase of Respiratory Distress Syndrome while use

minimal CPAP in babies with apnea of prematurity

and normal lungs. In babies weaned from ventilator

to CPAP, it makes logical sense to commence CPAP

pressure equivalent to the mean airway pressure on

ventilator. (Generally 6-8 cm water).

• Once a certain pressure is selected one should closely

monitor clinical signs, oxygenation (FiO2

requirement), blood gas parameters ± chest X-ray.

Improvement in these parameters (especially

oxygenation and clinical parameters) indicates that

ideal CPAP pressure has been selected. If there is no

improvement, increase CPAP pressure in steps of 1-2

cm water up to 10 cm water. Oxygenation has been

shown to improve with each centimetre of water

increase in distending pressure applied18. However at

a certain point, over-distension of the alveoli will

occur and oxygenation may fall. This may be due to

capillary compression by the distended alveoli and

subsequent shunting of the blood to an area of the

lung with decreased ventilation: perfusion ratio4.If

moderate to high levels of positive airways pressure

(up to 10 cms of water) are being used and

oxygenation deteriorates, or carbon dioxide levels

rise then the distending pressure should be reduced.

Chest X-ray also helps to ascertain the degree of lung

distension.

Nursing monitoring of a baby on CPAP

Ababy on CPAP needs to be monitored continuously

with cardiorespiratory and saturation monitor. Bedside

nurse needs to monitor the baby vigilantly and record the

parameters on hourly chart:

Hourly chart:

Vital signs - including the work of breathing

Oxygen saturation

Fraction of Inspired Oxygen concentration(FiO2)

CPAP settings

• If on ventilator CPAP or Infant Flow Driver -

CPAP pressure

• If on bubble CPAP - Gentle bubbling (no

bubbling indicates suboptimal pressure)

• Gas flow

• Humidifier and circuit temperature

• Water level in humidifier

Things to consider if there is failure to achieve

desired pressure or wide fluctuation in pressure:

leak in the circuit, baby's mouth wide open, wrong

size prongs/mask or hat; problems with gas flow;

secretion; condensation inside tubings etc.

CPAP interface is positioned correctly (not

distorting features or pushing nasal structures

upwards)

• Inspect circuit and patient interface for any

accumulated condensation – empty as required to

prevent aspiration

Septal columellar integrity

Eyes are clearly visible

Securing devices are not causing indentation,

pitting or periorbital oedema

Orogastric tube positioned at correct length

Abdominal distension

Supportive care

• Perform cares as indicated by the neonate's

clinical condition - usually 4–6 hourly.

• Position the neonate to avoid inadvertent tension

to the interface and/or accumulation of

condensate at the nares (e.g. cot propping).

• Insert CPAP circuit through lowest insertion port

of incubator to promote drainage of

condensation away from neonate.

• Check straps are not too tight.

• Inspect nose, periorbital region, ears and head.

Massage nares using a small amount of soft

white petroleum jelly applied to gloved finger.


• Gentle nasal suction as required; oral suctioning

usually more frequently required. Perform

suction if there is visible secretion; audible

course, wet breath sounds; alteration in vital

signs or oxygen saturation; increasing

respiratory distress; agitation etc.

• Insert an Oro Gastric Tube (OGT) to minimise

abdominal distension and leave on free drainage.

Aspirate 4–6 hourly.

• Optimal CPAP is achieved when mouth is closed

(e.g. use pacifier, chin strap).

• Incorporate principles of developmental care

individualised to the needs of the neonate.

• Incorporate a family centred approach to care

and parental involvement.

• Encourage Kangaroo cuddle once the baby is

stable.

• Provide information/education to parents

regarding disease process/treatment as

required.

• Complete circuit, including hat, is to be

changed weekly. Use correct size prongs and

hat each time.

Signs of improvement

• Clinical improvement: Reduction in the work

of breathing as indicated by decreased

Respiratory rate, Grunting, Sternal/intercostal

recession, Nasal flaring.

• Stabilization or reduction in Oxygen

requirement

• Improving blood gas parameters

• Improvement in lung volumes and chest x-ray

appearance

• Increased patient comfort as assessed by bed-

side nurse

Improvement in clinical status (baby looking

comfortable without respiratory distress) and

oxygenation are the 2 most important parameters

that indicate stability on CPAP.

Weaning CPAP

Consider weaning when the baby shows signs of

stability (improvement in respiratory distress, blood

gases and chest X-ray findings) and has good

spontaneous breathing. Other things to consider before

weaning:

• gestation

• Chronological age

• Cardiac status

• Metabolic status

• Sepsis

• 24- hour oxygen download (proportion of time

a baby desaturates in 24 hours)

Principles of weaning

Rate of weaning is dependent on the baby. Wean

slowly, in steps and as tolerated by the baby.

Wean when the baby is holistically (not just

respiratory status) stable for a reasonable period of

time and has good spontaneous breathing.

Wean oxygen before pressure: It is our usual practice

to wean oxygen until close to 21% (21-25%) based on

SPO2 readings then wean pressure slowly based on

signs of respiratory distress until 3-5 cm water

achieved.

Ceasing CPAP

Consider ceasing CPAP when stable in 21% Oxygen

and CPAP pressure 3-5 cm water.

Methods of ceasing CPAP

• Abrupt cessation: Once the baby reaches

stability, cease CPAP abruptly. If the baby shows

signs of respiratory distress recommence CPAP.

• On and off cycling – Less mature babies (<30

weeks) tend to require distending pressure

without oxygen requirement for longer duration

of time. In such babies some NICUs practice

cycling on and off CPAP (E.g.: 4 hours on and 4

hours off) and progressively extend the duration

of period without CPAP.

A Cochrane review19

of three RCTs concluded

that neonates in whom CPAP pressure was

weaned to a predefinedlevel, and then stopped

completely have less total time on CPAP and

shorter durations of oxygen therapy and hospital

stay compared with those who underwent on and

off cycling.

• Wean to HFNC – In babies <30 weeks who meet

the stability criteria, many units in Australia

including ours practise weaning from CPAP to

HHFNC.

The infant needs to be closely monitored for at

least another 24 hours when CPAP support is ceased

(except when weaned to HHFNC, in which case

ongoing vigilant monitoring is needed). Baby may not

tolerate cessation of CPAP and may need to go back

on CPAP. Some babies may need nasal prong oxygen


for a short while following cessation of CPAP.

Failure of CPAP: when to consider intubation?

Increasing work of breathing (sternal and intercostal

recession, grunting, tachypnoea)

Oxygen requirement greater than 30-50% (threshold

depends on the baby as well the treating clinician!)

Rapid increase in FiO2 (consider pneumothorax)

Unstable respiratory drive with frequent apnoeic

episodes resulting in desaturation and/or bradycardia

Severe cardio-respiratory instability

Respiratory acidosis (e.g. pH less than 7.2 or PaCO2

greater than 60 mmHg

Agitation that cannot be relieved despite

containment, nesting, dummy or sucrose (This

happens especially in full term infants). Narcotics

should not be administered as these drugs cause

respiratory depression.

Evidence of adverse effect (see below) that cannot be

managed with optimising CPAP

Adverse Effects

Air leaks

Air leaks may occur due to a combination of the

disease process (e.g. alveolar over distension with RDS)

and the distending pressure from CPAP (particularly

when the lung compliance is improving).

pain, periorbital oedema, long term functional and/or

cosmetic sequelae.

• Occurs due to incorrect selection of size and/or

device type or over-tightening of the strapping

resulting in the prongs touching the septum. Greatest

risk for nasal trauma is in babies with

• Gestational age less than 32 weeks

• Birth weight less than 1500 g

• Duration of CPAP greater than 5 days

• Pressure injury prevention22-23

• Use appropriate size hat – secure hat so that the rim

covers top of ears and just above eye brows,

preventing excessive pressure

• Use appropriate size prongs as per the

manufacturer's recommendation. Binasal prongs

should fit nares firmly but without blanching skin.

• Position binasal prongs about 2 mm from the

nares and so they are not in contact with the

septal columella

• Regularly inspect:

o Nasal redness, skin breakdown, bruising,

indentation, bleeding, altered nasal shape

o Ears for pressure areas, creases or folds

o Forehead if using midline device (mask or

prongs)

o Nasal bridge mid-facial indentation (mask) Recent Cochrane review

1 suggested that use of

CDP is associated with an increased rate of

pneumothorax [RR 2.36 (95% CI 1.25, 5.54), NNH 7 (4,

24)]although it is associated with reduced respiratory

failure and reduced mortality. The incidence is highest in

babies < 1000g and prophylactic or early surfactant

reduces this risk20-21

.

Abdominal distension

This occurs because the delivered gas also enters

the stomach and gastrointestinal tract resulting in what is

popularly known as "CPAP belly"

This is reduced by

• Use lowest possible flow of gas to achieve desired

pressure.

• Insertion of an orogastric tube (OGT) of size ≥5 FG

on free drainage or regular aspiration (4-6 hrly). If

neonate is receiving OGT feeds, open OGT to free

drainage and suspend above infant in between feeds.

Pressure injury

• Results from local pressure of CPAP devices applied

to the nasal area, ears, forehead and/or other pressure

points. This can cause irritation, necrosis, infection,

o Head by removing hat every 4-6 hrly with

cares

• Alternate prongs and masks every 4-6 hrly

• Prong release – Do a quick prong release with

gentle rubbing of septum, every 2nd

hrly. Apply a

very thin film of soft white petroleum jelly to

nares with gloved finger, every 6 hrly and gently

massage the nares

• Document the presence/absence, location,

nature and extent of pressure injuries

• If septal redness without skin break down, apply

hydrocortisone cream to reduce inflammation.

• There is equivocal evidence about the use of

nasal protection devices in reducing pressure

injury.

• Consider high flow. In desperate situations we

have even had to intubate and ventilate babies to

give rest to nose.

Over distension of lungs

Use of excessive CPAP pressures can:


• Increase the work of breathing - can cause poor

oxygenation and carbon dioxide retention.

• Reduce cardiac output secondary to impeded venous

return

Obstruction of the prongs

Obstruction of the prongs by secretions or other

means will stop delivery of continuous distending

pressure to the lungs and airways. The pressure will be

maintained by theobstruction. Humidification of gases

and selective, gentle suction of the airways are important

strategies to prevent this problem.

Risk of sepsis from contamination of humidifiers

This is a potential problem.

Long-term outcome in babies managed on CPAP

In SUPPORT trial24

that included 1234 infants with

gestation 24 weeks 0 days and 27 weeks 6 days, there was

no difference in the composite outcome of

death/neurodevelopmental outcome at 18-22 months

corrected age [RR 0.93; 95% CI 0.78-1.10; P=0.38]

between the group that received CPAP and the group that

received mechanical ventilation and surfactant. Further

studies are needed to evaluate long-term impact of

CPAP.

Key Points

CPAP has emerged as the initial mode of breathing

support in an infant admitted with respiratory

distress or oxygen requirement. Mechanical

ventilation should only be considered in babies who

do not respond to CPAP or where there are

contraindications to its use.

CPAP has been shown to reduce the risk of death and

mechanical ventilation in preterm infants with

respiratory distress.

CPAP provides benefit by multitude of mechanisms

and is most effective when commenced as early as

possible in the disease course.

Different types of CPAP devices are available in the

market. There is no convincing evidence to suggest

that one is better than the other. Bubble CPAP can be

indigenously prepared and may prove cost-

effective25.Each unit should develop expertise using

a particular type of CPAP system and should stick to

the same system.

Short binasal prongs are superior to nasopharyngeal

or single nasal prongs and have become the standard

of practice in neonates requiring CPAP. Nasal masks

are usually used when prongs are ineffective or

contraindicated.

Initial CPAP pressure should be selected according

to the condition that is being targeted. Based on a

combination of clinical signs, oxygenation (FiO2

requirement), blood gas parameters and chest X-ray,

one should gradually increase (maximum 10 cm

water) or decrease CPAP pressure (minimum 3-5 cm

water). Flow rate is generally selected at 6-8 L/min

and FiO2 requirement should be altered to target

Oxygen saturation levels. Once stability criteria is

reached, CPAP needs to be weaned slowly (wean

FiO2 first and pressure later) with a view to cease

CPAP. Babies need to be closely monitored for at

least another 24 hours following CPAP cessation.

Babies on CPAP need very close and vigilant

monitoring so as to provide effective CPAP and

avoid CPAP related complications such as

pneumothorax, nasal septal injury, abdominal

distension etc.

References :

1. Ho JJ, Subramaniam P, Henderson-Smart DJ, Davis PG. Continuous

distending pressure for respiratory distress syndrome in preterm

infants (Cochrane review). The Cochrane Library, 2015.

2. Gregory GA, Kitterman JA, Phibbs RH et al: Treatment of

idiopathic respiratory distress syndrome with continuous positive

airway pressure. New England Journal of Medicine 1971; 284(24):

1333-40.

3. Haman S, Reynolds EO: Methods for improving oxygenation in

infants mechanically ventilated for severe hyaline membrane

disease. Archives of Diseases in Childhood 1973; 48(8): 612-7.

4. Goldsmith JP, Karotkin EH: Assisted ventilation of the neonate:

Saunders, 5th

Edition, 2014.

5. Alex AG, Aronson RM, Onal E, Lopata M. Effects of positive

airway pressure on upper airway and respiratory muscle activity.

Journal of Applied Physiology. 1987; 62(5): 2026-30.

6. Cotton RB, Lindstrom DP, Kanarek KS, Sundell H, Stahlman MT.

Effect of positive-end-expiratory-pressure on right ventricular

output in lambs with hyaline membrane disease. Acta Paediatrica

Scandinavica. 1980; 69(5): 603-6.

7. Miller MJ, Carlo WA, Martin RJ. Continuous positive airway

pressure selectively reduces obstructive apnea in preterm infants.

Journal of Pediatrics 1985; 106(1): 91-4.

8. Speidel BD, Dunn PM. Effect of continuous positive airway

pressure on breathing pattern of infants with respiratory-distress

syndrome. Lancet. 1975; 1(7902):302-4.

9. Speidel BD, Dunn PM. Use of nasal continuous positive airway

pressure to treat severe recurrent apnoea in very preterm infants.

Lancet 1976; 2(7987): 658-60.

10. Ho JJ, Henderson-Smart DJ, Davis PG. Early versus delayed

initiation of continuous distending pressure for respiratory distress

syndrome in preterm infants. Cochrane Database Syst Rev.

2002;2:CD002975.

11. Rojas-Reyes MX, Morley CJ, Soll R. Prophylactic versus selective

use of surfactant in preventing morbidity and mortality in preterm

infants. Cochrane Database Syst Rev.2012;3:CD000510.

12. Davis PG, Henderson-Smart DJ. Nasal continuous positive airways

pressure immediately after extubation for preventing morbidity in

preterm infants. Cochrane Database Syst Rev. 2007.

13. Pillow JJ, Hillman N, Moss TJ, Polglase G, Bold G,Beaumont C, et

al. Bubble continuous positive airway pressure enhances lung


volume and gas exchange in preterm lambs. Am J Respir Crit Care

Med. 2007;176(1):63-9.

14. Williams R, Rankin N, Smith T, Galler D, Seakins P. Relationship

between the humidity and temperature of inspired gas and the

function of the airway mucosa. Crit Care Med.1996;24(11):1920-9.

15. De Paoli AG, Davis PG, Faber B, Morley CJ. Devices and pressure

sources for administration of nasal continuous positive airway

pressure (NCPAP) in preterm neonates. Cochrane Database Syst

Rev. 2008;1:CD002977.

16. Mazzella M, Bellini C, Calevo MG, Campone F, Massocco D,

Mezzano P, et al. A randomised control study comparing the Infant

Flow Driver with nasal continuous positive airway pressure in

preterm infants. Arch Dis Child Fetal Neonatal Ed. 2001;85(2):F86-

90.

17. Say B, Kanmaz Kutman HG, Oguz SS, Oncel MY, Arayici S,

Canpolat FE et al. Binasal Prong versus Nasal Mask for Applying

CPAP to Preterm Infants: A Randomized Controlled Trial.

Neonatology. 2016;109(4):258-64.

18. Fox WW, Gewitz MH, Berman LS, Peckham GJ, Downes JJ. The

PaO2 response to changes in end-expiratory pressure in the newborn

respiratory distress syndrome. Critical Care Medicine 1977; 5(5):

226-9.

19. Jardine LA, Inglis GD, Davies MW. Strategies for the withdrawal of

nasal continuous positive airway pressure (NCPAP) in preterm

infants. Cochrane Database Syst Rev.2011;2:CD006979

20. Soll RF, Morley CJ. Prophylactic versus selective use of surfactant

in preventing morbidity and mortality in preterm infants. The

Cochrane Library, 2001.

21. Klinger G, Ish- Hurwitz S, Osovsky M et al. Risk factors for

pneumothorax in very low birth weight infants. Pediatr Crit Care

Med. 2008;9(4):398-402.

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2008;8(2):116-24.

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2009;28(1):13-27.

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Cough in Children

Subramanya N.K. Department of Pediatrics, Vydehi Institute of Medical Sciences, Whitefield, Bangalore.

Correspondence :Proff Dr. Subramanya N K, Professor, Department of Paediatrics,

Vydehi institute of medical sciences, whitefield, Bangalore-560066. [email protected]

Cough is a frequent presenting symptom and an

important protective reflex that allows clearance of

secretions and particulates from the airways, so as to

keep the airway clean and healthy. Cough is not a disease

by itself, but, a symptom of underlying disease ranging

from benign self-limiting upper respiratory tract

infection to severe life threatening airway disease.

Cough in children causes significant anxiety to parents.

Drugs prescribed for treatment of cough and the

available over the counter sales account for huge revenue

sales and it is important to note that majority of

medications are unnecessary, irrationally prescribed or

administered by parents.

Cough can be the symptom of underlying

respiratory disease or a non-respiratory illness such as

cardiac diseases. When cough presents with other

symptoms that gives clue to the causative factors like

fever, dyspnea, hemoptysis etc. the diagnosis depends on

the clinical manifestations. Any respiratory disease can

manifest cough and discussing all the causes of cough is

beyond the scope of this article and the readers can refer

to the respective chapters. It is therefore reasonable to

focus more on diseases where cough is the 'sole

manifestation'. The other causes of cough are also

described in brief as and when required.

Basics :

Cough receptors are present in airways, sinuses,

middle ear, pleura, diaphragm, but the distribution of

receptors is non-uniform. The intensity of cough is

maximum when it is laryngeal(vocal cords) as those are

the most sensitive and the cough becomes less explosive

as we move proximal or distal to vocal cords in the

airways. Vagal afferent nerves regulate involuntary

coughing. There is higher cortical control that regulates

voluntary coughing. The implication of cortical

regulation is evident from the fact that the placebos can

have profound effect on coughing. The psychological

issues can be considered either cause or effect of

coughing. Cough center is situated in the medulla

oblongata, which will be suppressed by cough

suppressants. The defensive nature of the cough reflex

can be sub optimal in neuromuscular weakness of

breathing. Violent bouts of cough can cause syncope, rib

fractures, sub-conjuctival hemorrhage, prolapse, hernia

and alterations in intracranial pressures.

Cough can be categorized based on duration (i.e.

acute or chronic), quality (dry or wet, brassy or staccato)

or etiology (specific or nonspecific)

Acute cough :

Acute cough is generally defined as the cough of

less than 4 weeks duration. The pediatric definition of

acute or chronic cough is based on the natural history of

acute URTIs in children, where in usually the cough

resolves within 1 to 3 weeks. Hence it is logical to define

chronic cough as daily cough lasting more than 4 weeks.

Published definitions of chronic cough in children have

varied duration from 3 to 12 weeks. In contrast, the

current definition of duration of chronic cough in adults

is 8 weeks. The cough between 4to 12 weeks in adults is

called sub-acute cough, the relevance of this definition in

children is not clear.

The cause of acute cough in children is usually

obvious by clinical evaluation. The infections of upper

and lower respiratory tracts account for majority of

cases. Nose block, mouth breathing, post nasal

discharge, soreness of pharyngeal mucosa exposing

cough receptors to be stimulated believed to be

responsible for cough.

Abstract : The aetiology and management approach for cough in children differs greatly to that in adults, so the

empirical approach commonly used in adults is unsuitable for children. Clinical evaluation of cough in children

should include an assessment of environmental factors, particularly tobacco smoke, parental concerns and

expectations. Most children with acute cough are likely to have an uncomplicated viral acute respiratory tract

infection, but the possibility of a more serious problem, especially aspiration of foreign material, should always be

considered. Over-the-counter and prescription medications are ineffective for the symptomatic relief of acute

cough. Chronic cough i.e cough for more than 4 weeks will have specific lung conditions which are evaluated

based on the nature, duration and timing of cough. Treatment for chronic cough should be based on aetiology.

Children should be reassessed within the expected timeframe of response to therapy.

Key words : Cough, Acute Cough, Chronic Cough, Cough Syrup

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Three clinical patterns of cough over a period of time:

1.Self limiting 2.Persisting and progressive 3. Recurrent

Post infectious cough :

The post infectious cough can follow an upper or

lower airway infection. The child continues to cough

while other symptom like fever resolve. It is thought to

be due to exhaustive inflammation and disruption of

airway mucosal integrity. In lower respiratory tract

infection this is often associated with excessive

accumulation of mucus and transient airway & cough

receptor hyper responsiveness. This may be clinically

identified as acute or 'sub-acute' cough pattern described

in adults.

Management of acute cough :

The diagnosis of the illness causing acute cough is

essentially clinical such as acute rhino-sinusitis, acute

otitis media, sore throat, acute laryngitis etc. They are

managed as per the standard guidelines. The

accompanying cough resolves with recovery of

underlying cause in most of the children. There is no

need of laboratory investigations in general, unless an

individual case demands work up. Anti-cold

preparations available over the counter and also largely

prescribed by clinicians have largely been criticized for

lack of scientific evidence. The expectorants have

variable response and cough suppressants can be

dangerous in children younger than 6 years of age. The

clinician should weigh the advantages of such

prescription over the benign self-limiting nature of many

infections in day to day practice. The herbal remedy,

honey, and steam inhalation are popular among parents

and pediatricians but lack strong scientific evidence.

Table no 1.Drugs in acute cough

Drugs Mechanism Examples Age Sideeffects Utility

Anti-tussives Suppress cough

center or

receptors in

airways

Dextromethorphan

Codeine

> 6 years Confusion

Sensorial

disturbances

Muscle

weakness

Not to be

used for

acute

cough

Expectorants Increase he

amount of

secretions or

hydration of

airways

Guafenasin

Bromhexine

>2 years Palpitations

Paradoxical

excitability

Start

their

action

after 5-7

days

Antihistamines Dry airways Chlorphenaramine

Maleate

>6 month Restlessness

Sedation

Mucolytics Dissolve the

thick mucus by

breaking bonds

Ambroxol

Acetyl cysteine

>2years Alterations in

liver

functions

Start

their

action

after 5-7

days

Please note that all the above drugs neither

hasten the recovery nor modify the course of disease in

acute self limiting cough commonly seen in practice.

Recurrence of acute cough

Upper respiratory tract infections are common in

early life and on an average 6-8 episodes occur in

infancy. The frequency of these episodes decrease

with increasing age and reassurance to the anxious

parents may avoid unnecessary investigations.

However, malnutrition, bottle feeding, day care

admissions, exposure to environmental factors like

parental smoking, pollution is responsible for

'recurrent episodes' of acute cough. Exacerbations of

asthma as a cause of recurrent cough is common and

associated history should be elicited to make the

diagnosis.


Chronic cough

Chronic cough is defined as cough lasting

more than 4 weeks. Chronic cough in children is

evaluated and managed differently than in adults.

Unlike in adults, the relationship between chronic

cough and upper airway disorders, asthma, and GERD

is less convincing in children. Pediatric cough can be

classified in several ways, including those based on

the etiology, time frame, characteristics and specific/

nonspecific cough.

Cough is categorized as 'expected', 'specific' and

'nonspecific'. In expected cough, the presence of

cough is expected (e.g., after an acute respiratory tract

infection). In specific cough, the etiology and

necessity for further investigations is usually evident

from the presence of coexisting symptoms or signs

(e.g. suppurative lung disease, immunodeficiency

etc.). The presence of any of these symptoms or signs

suggests that the cough is likely to be associated with

an underlying specific etiology. The clinical

evaluation and investigation depend upon the

suspected specific diagnosis. The standard guidelines

for the diagnosis should be followed e.g., work up of a

child with suspicion of tuberculosis. The readers are

referred Table no.2 for these 'specific' pointers.

Table No 2. 'Specific' pointers of cough

[CF-Cystic fibrosis, PCD-Primary ciliary dyskinesia,ID-immunodeficiency,FB-foreign body,TEF-Tracheo esophageal fistula]

The diagnosis can be based on the characteristics

of cough such as age at the onset of cough (Table No

3), nature of cough (Table no 4), and the timing of the

cough in the day (Table no 5). A detailed history,

repeated questions and clinical examination (Table no

5) are needed to find out etiology.

The following tables guide us to evaluate the

cough.

Table No. 3. Age and onsetof cough

Age Acute Recurrent Persistent

Infancy Viral infection GERD Congenitalanomalies.

Earlychildhood Foreignbody Asthma RetainedFB Tuberculosis

Olderchildren Asthma Rhino-sinusitis Psychogenic

Bronchiectasis (CF/ Non-CF/ immuno-deficiency),ILD

[GERD-Gastro esophageal reflux disease, ILD- Interstitial lung Disease]

Table No 4. The Nature of cough

Nature of cough Probable cause

Throat clearing Post nasal drip

Dry, irritating Post viral

Barking cough Laryngitis.

Brassy Tracheitis /Mediastinal mass or nodes

Paroxysmal Pertussis, Asthma

Staccato cough Chlamydial infection

Nocturnal Asthma

Wet, rattling Suppurative lung diseases

Asthm Seasonal, trigger induced, atopic, nocturnal, Responding to salbutamol/steroids.

Bronchiectasis or recurrent pneumonia

CF, PCD, ID, Congenital airway lesions, FB, TEF.

Aspiration Neurologicallyabnormal, TEF, GERD, Cleft palate

Chronicinfections TB,Nontubercularmycobacteria,fungaldiseases,parasites Interstitiallungdisease Drugs,radiation,autoimmunediseases Airwayabnormality Tracheomalacia,airwaycompressions Cardiacdiseases Murmurs, Pulmonaryhypertension. Misc.pulmonaryconditions Tumors


Table No. 5 Timing of cough

Time of cough Probable cause Early morning Dry cough: Asthma

Wet Cough: Bronchitis

Worsen in evening Pollution Worse in night Asthma, Post nasal drip After feeds, lying down GERD

Soon after exercise Asthma Loud, bizarre, absent during sleep Psychogenic

Table no 6. Cough and clinical features

Clinical finding Cause Wheeze, atopy, Rhinitis Asthma Cold, fever, rashes Viral infections

Excessive regurgitation GERD

Multiple multifocal infections Immunodeficiency

Clubbing Suppurative lung diseases, ILD

Mal-absorption, Failure to Thrive Cystic fibrosis

Some special situations with chronic cough

Upper airway cough syndrome (UACS)

UACS, also referred to as post nasal drip,

characterized by dry cough with throat clearing

associated with upper airway problems such as rhino-

sinusitis of infective or allergic origin. Some of the

children also have GERD as the comorbid condition

aggravating the cough.

Aspiration syndrome :

Micro or macro aspiration of contents of upper GIT

can occur from lower esophagus (GERD), mid

esophagus (Tracheo esophageal fistula) or at higher level

(palate-pharyngeal in coordination, cleft palate, etc.).

The relationship of the cough aggravated by supine

posture or after feeds makes the diagnosis clinically

possible. Barium studies clinch the diagnosis in TEF and

diaphragmatic hernia. Gastro esophageal reflux disease

requires 24hour PH monitoring of esophagus, and

responds to thickening of feeds with anti-reflux therapy

(PPI).

Asthma

Asthma is a clinical diagnosis. Cough in asthma is

recurrent, episodic, seasonal, trigger induced, nocturnal

and occasionally paroxysmal resulting in vomiting. The

accompanying breathlessness and wheeze help in the

diagnosis. Cough responds typically to bronchodilators

and steroids. Isolated cough in the absence of wheezing,

responding to bronchodilators is called cough variant

asthma.

Pertussis

Pertussis is often under diagnosed. The typical

paroxysmal cough with or without whoop, with

laboratory evidence of lymphocytosis ishallmark of the

disease. The diagnosis should be considered even in

immunized children. Cough does not respond to

bronchodilators or cough suppressants. Cough is very

distressing and macrolides (azithromycin) given early in

the first week of illness reduces morbidity.

Tuberculosis

Cough of more than two weeks with history of

contact in developing country should be evaluated

for tuberculosis. Parenchymal involvement, extrinsic

compression of airways by lymph nodes, endo-bronchial

spread, cavitation, and bronchiectasis can cause chronic

cough. The attempt should always be made to isolate

AFB.

Foreign body in airway

In acute cases, history of sudden onset of cough

with choking in a toddler should rise the suspicion of FB.

In chronic cases the ingestion of FB may be 'forgotten'

and high index of suspicion is needed. When in doubt,

rigid bronchoscopy should be done even in the 'absence'

of history. X ray chest can show air trapping, localized

emphysema, mediastinal shift depending on the sight of

FB in airways. Normal x ray does not exclude the

presence of foreign body.

Psychogenic cough

It is also referred to as habit cough typically seen

young adolescents and cough is explosive, attention

seeking and disappears in sleep. Counseling and referral


to psychiatrist, multi-disciplinary approach is required.

Protracted Bacterial Bronchitis

Prolonged 'wet' cough of more than 2 weeks

duration is usually due to the formation 'biofilms' due to

microbial colonization in the airway mucosa making it

difficult to treat. Antibiotics (Amoxy-clav) for two

weeks will result in clinical improvement.

Evaluation and approach to chronic cough.

Every effort should be made by the clinician to

arrive at specific diagnosis of cough. If specific

diagnosis is not possible at the point of evaluation, a

diagnosis of non-specific cough is made. Non-specific

cough has been defined as usually dry cough in the

absence of identifiable respiratory disease or known

etiology. The categorization is overlapping and is not

very well demarcated. Cough is subjected to period

effect (i.e., spontaneous resolution of cough). The

therapeutic benefit of placebo treatment for cough has

been reported to be as high as 85%. This forms the basis

for “wait and watch, and review approach in many

children with non-specific cough. It can also be noted

that in some children the specific pointers to diagnosis

evolves over a period of time.

Chest x-ray should be done in all cases of chronic

cough except in asthma, as asthma is essentially clinical

diagnosis.

Table no.7 Chest x-ray in chronic cough

x-ray findings Probable causes

Normal Asthma, Postnasaldrip,

Aspiration syndromes,

Habitcough, FB, Drugs,

Vascular compression

Persistent shadow FB, TB, Congenital

anomalies.

Multifocallesions Aspiration, Asthma, CF,

Immunodeficiency, CHD.

Focal shadows Nodes, tumors, cysts

Interstitial pattern Infections, ILD.

Table no.8 Investigations in chronic cough

Asimplified approach to chronic cough

1. If specific pointers are present, evaluate as per

standard guidelines.

2. If not, do chest x-ray and spirometry (if >6years,

based on the availability)

3. Is cough characteristic? If yes, refer to tables no 2, 3

and 4.

4. If not it is non-specific cough, follow “wait, watch

and review”

5. Evaluate for environment, child's activity and review

in 1-2 weeks.

6. If not resolving, discuss with parents for' trial of

therapy'

7. Trail of therapy for 'wet cough' is antimicrobial

therapy.

8. Trail of therapy for 'dry cough' is inhalational

corticosteroids (Budesonide 400 mcg daily).

9. If responding to ICS by 2-3 weeks, consider asthma,

if not stop ICS and investigate further.

Points to remember :

1. Acute cough is commonly due to URTI, self-

limiting, and unnecessary investigations and

indiscriminate use of drugs should be avoided.

2. Chronic specific cough should be evaluated based

on clinical clues/ pointers, individualized in

approach, and treated.

3. Chronic nonspecific cough should be evaluated

over the period of time: wait and watch policy

adopted. Re-evaluated for appearance of specific

pointers; consider trial of antibiotics (infective) or

ICS (Allergic). Parents should be involved in

decision making.

Further reading :

1. Chang AB. Diagnosis and management of cough.

ACCPguidelines.Chest.2006:129:260s-283s,

Availablefrom:URL:http://journal.publication.chest

net.org

2. Subramanyam L, Balachndran A, Management of

cough, IJPP 2010:12.P.17-22.

3. Patricia Kritek, Christopher Fanta. Cough and

hemoptysis. In: Harrison's principles of Internal

m e d i c i n e , 1 8 t h e d n / e d i t o r s , D a n L

Longo...[et.al].p282-84.

4. British Thoracic Society Guidelines2008.

Recommendations for the assessment and

management of cough in children.Available

from:URL:http://thorax.bmj.com/cgi/content/full/6

3/supl_3/iii1.

X-raychest Allcases

Sputumexamination AFB,fungalstudies

Barium study Aspiration syndromes

2D-Echo CHD,Pulmonary

Hypertension

Pulmonary function tests Asthma

HRCT Suppurative lung disease

ILD

http://journal.publication.chest/

http://thorax.bmj.com/cgi/content/full/6


Neonatal hypernatremic dehydration : Can we prevent it

Srikanth S, Mallikarjun G. P, Prashanth S. V, Channabasavaraj H, Kalappanavar N. K Dept of Pediatrics, S S Institute of Medical Science and Research Center, Davangere.

Correspondence : Dr. Srikanth S. Dept of Pediatrics, S S Institute of Medical Science and Research Center, Davangere.

Mob. : 9845299048

Introduction

The benefits of breastfeeding is well established in

children and include improved neurodevelopmental

outcomes and decreased incidence of acute infections

and chronic diseases 1,2

.

Hypernatremic dehydration is assumed to be a rare

complication of breastfeeding3, but recent reports are

suggesting that the incidence is increasing4–7

. Neonatal

hypernatremic dehydration results from inadequate

transfer of breast milk from mother to infant. The infant's

plasma sodium concentration is elevated predominantly

due to loss of extracellular water. In the past,

hypernatraemia most frequently occurred when artificial

feeds with high sodium concentration were fed to

babies8.

Depending on amount of deficit in total body fluids,

hypernatremia is described as either hypovolemic,

euvolemic or hypervolemic. Infants are worst affected,

because of (a) immaturity of the kidney that hinders its

ability to excrete an excess sodium load (b) babies have

limited or no ability to express thirst and (c) infants can't

feed themselves and depend on caregivers to provide

adequate and appropriate fluids and feeds9.

In 1949 Macy 10

established that the sodium content of

colostrum in the first five days is (22±12) mmol/ L, and

of transitional milk from day five to ten is (13±3)

mmol/L, and of mature milk after 15 d is (7±2) mmol/ L.

Morton 11

studied the breast milk of 130 women as they

began to breast-feed. Women who failed to establish

good breast-feeding did not experience the normal

physiological drop in breast milk sodium concentration

compared to those who had little difficulty in

establishing a good milk flow.

Brain is the most vulnerable organ from

hypernatremia. Plasma hypertonicity and the subsequent

intracellular water loss causes the brain cells to shrink,

leading to rupture of bridging vessels with hemorrhages

in subarachnoid and brain parenchyma and thrombosis 12.

Parents may fail to identify that the infant is ill, and

professionals may also falsely reassure about infant's

apparent well-being. Signs may be non-specific,

including lethargy and irritability. Occasionally there is

an acute deterioration which precipitates the infant's

emergency admission to hospital. During acute

isonatremic or hyponatremic dehydration clinicians may

rely on sunken eyes and depressed anterior fontanelle as

signs of total body water loss. In hypernatremic

dehydration however there may be changes in brain cell

osmolality and cerebral oedema, and the resultant

fullness of the anterior fontanelle may mislead the

underlying dehydration. Clinical examination of these

infants at presentation is variable. Some present with

lethargy; others may be alert, hungry and clinically

dehydrated 13.

In this study we are trying to see for the probable

causes of hypernatremia in babies admitted to our NICU

and if it was preventable.

Aims & Objectives:

1. Ascess the degree of dehydration in hypernatremic

neonates

2. Factors leading to hypernatremia

Study design

This is a cross section observational study conducted

in NICU, Department of Pediatrics, SSIMS-RC,

Davangere, Karnataka.

It is an observational study done in hypernatremic

neonates admitted to NICU between march 2016 to april

2016.

Materials and Methods :

Infants admitted to NICU SSIMS-RC, Davangere

between march and april 2016 was observed and those

with hypernatremia (Serum Sodium >145mEq/L) at

admission was taken for study and analysed. Details of

the birth like mode of delivery, birth weight, date of birth,

date of admission, weight at admission, symptoms,

mode of feeding and lab details were collected. All the

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babies where on exclusive breast feeding. The details

collected were entered in the excel sheet and analysed.

Data was analysed by chisquare test and p value <0.05

was taken as significant.

Results :

14 neonates where analysed out of 123 (61+62)

admissions to NICU in march and april 2016. Table 1

shows the details of the neonates with hypernatremia

with the day of life at admission, birth and admission

weight and initial investigation. Septic workup done was

negative. Majority of neonates had elevated urea and

creatinine. Dehydration correction was started as per

protocol and electrolytes were repeated regularly. Urine

output was monitored. Feeds were started after

correction of dehydration and babies tolerated well.

Table 1

Sl No 1 2 3 4 5 6 7 8 9 10 11 12 13 14

Day of Life at admission

3 13 3 3 6 4 3 6 3 3 4 6 4 6

Sex F M M F M M F F M M M M M M

birth weight 3600 3500 3700 3300 2750 2400 2800 2300 3000 3000 2550 2450 3000 3000

admission weight 2900 2850 3400 2600 2550 2060 2600 1910 2600 2600 2400 2050 2800 2410

Investigation

Complete Blood Count

Hemoglobin

16.6

10.1

15.60

17.9

22

17.2

17.7

15.4

20.4

18.8

9.8

15.6

16.4

17.6

Total WBC count 10900 7700 11700 22100 20900 10200 16000 5000 9700 14500 3300 8700 10300 8800

Hematocrit 52.4 30.8 46.3 59.1 67.9 51.6 56 46.2 57.2 52.4 27.4 50.8 49.2 52.8

Platelet count 3.37 3.3 3.61 4.43 2.5 3.03 3.2 0.92 2.4 2.84 2.53 4.6 2.57 3.85

Urea 45.9 403 43.3 139 111.2 72 74.9 311 32 36 22 63.2 31.1 112

Creat 1.03 6.5 1.26 2.9 1.29 1.2 0.8 3.5 1.1 0.7 0.6 1.6 1.05 1.2

Sodium (mEq/L) 158 199 158 175 196 158.8 163 176 161 157 151 158.9 153 157

Potasium (mEq/L) 4.7 4.4 4.8 7 5.2 4.02 5 5 3.7 4.1 6.4 4.5 4.2 4

Chloride (mEq/L) 118 150 114 127 143 117.4 120 134 111 114 111 115.3 111 106

Table 2 shows the details of weight loss with percentage of dehydration at admission. Accordingly weight loss

per day and percentage of weight loss per day was calculated. Chisquare test done to see for association.

Table 2

Sl No 1 2 3 4 5 6 7 8 9 10 11 12 13 14

Weight loss (g) 700 650 300 700 200 340 200 390 400 400 150 400 200 590

Dehydration persentage (%)

19.44 18.57 8.11 21.21 7.27 14.16 7.14 16.95 13.33 13.33 5.88 16.32 6.66 19.66

Fluid deficit (ml)

700 650 300 700 200 340 200 390 400 400 150 400 200 590

wt loss per day (g)

233.3 50 100 233.3 33.33 85 66.66 65 133.3 133.3 37.5 66.66 50 98.33

% of wt loss/day (%)

6.48 1.43 2.7 7.07 1.21 3.54 2.38 2.82 4.44 4.44 1.47 2.72 1.66 3.277

Table 3

Table 3 & 4 tells us the association of percentage of

dehydration and hypernatremia. Daily weight loss of

more than 3% per day or overall dehydration more than

10% is better predictor of hypernatremia that more than

2% weight loss per day.

Dehydration <10%

Dehydration >10%

P value

% of wt loss/day

<3

5

3

0.0157

>3 0 6


Conclusion :

Table 4 5. Oddie S, Richmond S, Coulthard M. Hypernatraemic dehydration

and breast feeding: a population study. Arch Dis Child.

2001;85:318–320

6. Manganaro R, Mami C, Marrone T, Marseglia L, Gemelli M.

Incidence of dehydration and hypernatremia in exclusively breast-

fed infants. J Pediatr. 2001;139:673–675

7. Laing IA, Wong CM. Hypernatraemia in the first few days: is the

incidence rising? Arch Dis Child Fetal Neonatal Ed.

2002;87:F158—F162

8. Chambers TL, Steel AE. Concentrated milk feeds and their relation

1. Daily weight monitoring is a simple and easy tool to asscess dehydration.

2. This helps us to intervene early in case of

hypernatremic dehydration and also helps in

establishing breastfeeding.

3. Hypernatremic dehydration due to faulty feeding can

be completely prevented by this method.

Reference :

1. Scariati PD, Grummer-Strawn LM, Fein SB. A longitudinal analysis

of infant morbidity and the extent of breastfeeding in the United

States. Pediatrics. 1997;99(6). Available at:

www.pediatrics.org/cgi/content/ full/99/6/e5

2. Reynolds A. Breastfeeding and brain development. Pediatr Clin

North Am. 2001;48:159–171

3. Moritz ML, Ayus JC. The changing pattern of hypernatremia in

hospitalized children. Pediatrics. 1999;104:435–439

4. Cooper WO, Atherton HD, Kahana M, Kotagal UR. Increased

incidence of severe breastfeeding malnutrition and hypernatremia in

a metropolitan area. Pediatrics. 1995;96:957–960

to hypernatraemic dehydration in infants. Arch Dis Child 1975; 50:

610-5.

9. Elamin A and Nair P. Case reports: hypernatremic dehydrationin

infancy. Sudanese Journal of Pediartics 2007; 8: 161-170.

10. Macy IG. Composition of human colostrum and milk. Am J Dis Child

1949; 78: 589-603.

11 Morton JA. The clinical usefulness of breast milk sodium in the

assessment of lactogenesis. Pediatrics 1994; 93: 802-6.

12. Hilliard TN, Marsh MJ, Malcolm P, Murdoch lA, Wood BP. Sagittal

smus thrombosis in hypernatremic dehydration. Arch Pediatr

Adolesc Med. 1998; 152:1147-1149.

13. Schwaderer AL and Schwartz GJ. Treating hypernatremic

dehydration. Pediatrics in Review 2005; 26(4): 148-151.

Dehydration <10%

Dehydration >10%

P value

% of wt loss/day <2

3 1 0.052

>2 2 8

http://www.pediatrics.org/cgi/content/


Clinical Profile and Outcome of Hospitalized Children with Empyema Thoracis At A Tertiary Care Level Teaching Hospital

Vijay Kulkarni, Pranab J, Poornima Kulkarni Dept of Pediatrics

SDM Medical College Dharwad Karnataka, India.

Correspondence : Dr. Vijay Kulkarni Professor and unit head ,SDMMCH.

Mob. : 9448862279

Inroduction :

Hippocrates in 600 B.C. defined empyema thoracis as

a collection of pus in the pleural cavity and advocated

open drainage as its treatment.(1) Empyema thoracis, a

common condition in childhood.(2,3) and has significant

morbidity and mortality. Empyema thoracis constitutes

approximately 5- 10% of cases seen by pediatrician in

India.(4,5) Acute respiratory infections are the most

common illness of childhood accounting 50% of all

illness in under-fives and 30% in the 5–12 years age

groups, largely involving the upper respiratory.

However, about 5% involve the lower respiratory tract

resulting in serious diseases, especially the bacterial

pneumonia.(6) Forty percent of bacterial pneumonia are

said to be complicated by parapneumonic effusions, 10%

of whom would evolve into empyema.(7) Possible

reason for this include delay in initiating treatment,

prolonged oral treatment in the community with

antibiotics inadequate drug level in the pleural space and

delayed presentation, or unusual casual organism.(8)

It is a significant cause of pediatric hospital admissions

and morbidity especially in developing countries where

hospital resources are scarce.(9,10,11) The proper

management of empyema thoracis in children continues

to be a source of debate. It continues to have a high

mortality rate 10-16%.(12) Pleural effusion and

empyema are known complications of bacterial

pneumonia. Effusion occur in at least 40% of bacterial

pneumonia with up to 60% of effusions resulting in the

formation of empyema in all age groups.(13,14) The

American Thoracic Society has described three stages of

empyema namely exudative, fibrinopurulent and

organized.(15) It is postulated that most appropriate

therapy depends on stage of disease at presentation.

Staphylococcus aureus is the most common cause of in

the developing world, while streptococcus pneumonia in

the developed world.(16,17,18) The reported rates of

identifying an infectious cause from pleural fluid vary

from between 8% and 16% respectively. Pleural fluid is

sterile due to widespread early use of antibiotics.(19,20)

The aim of therapy is to ensure rapid recovery with a

normal long-term pulmonary outcome. Medical therapy

includes use of antibiotics and chest tube drainage. More

recently, early intervention in the form of

Video–Assisted Thoracoscopic Surgery (VATS) has

been reported.

Abstract : Empyema thoracis remains a common problem in pediatrics age group. We undertook the present

study to outline key aspects of the presentation and management of this condition at our tertiary care hospital

Material &Methods : This is a descriptive retrospective study conducted in PICU of SDM College of Medical

sciences and hospital, Dharwad from March 2012 to 2016 .Presenting complaints, clinical features and laboratory

data of 35 children were analysed from hospital records of all patients with confirmed diagnosis of empyema

thoracis. Patients were subjected to detailed evaluation and management as per standard protocol.. Results :The

mean age of presentation was 1 to 5.out of 35 cases 17 Were boys and 18 were girls. Median day of presentation

was 15 days. Of which PEM status was found in 27 patients (77 %), And most common presenting symptom being

fever (100%) followed by cough(91%) and hurried breathing in (56%). Pus and blood c/s together was positive in

18 (51%) with Staphylococcus Aureus being the most common 8 (44%) followed by streptococci pneumonia

4(22%)Sterile cultures in (49%). x ray done in (100%) and CT scan in 22(62%). Icd was inserted in 24 patients and

mean duration of insertion from admission being 3 days of which about 17 required surgery by decortication or

VATS.

Conclusion : In this study it was found commonest age group affected was 1-5 yrs. Staphylococcus was

commonest organism isolated in cultures from patients of empyema. Association of PEM with empyema. Early

intervention with medical and surgical treatment is associated with decreased mortality and morbidity.

Key words : Empyema thoracis, VATS .decortication, PEM

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We undertook the present study to outline key aspects

of the presentation and management of this condition at

our tertiary care hospital

MATERIALSAND METHODS :

This was a retrospective observational study,

conducted in the Department of Pediatrics, SDMMCH,

Dharwad, from March 2012 to Feb 2016. The study was

approved by the Institute's Ethical Committee and

written informed consent was obtained from all patients.

All children in age group of 0 to 12 years diagnosed

pyogenic empyema during the study period were

included in the present study. Children with empyema

secondary to postsurgical cause or post traumatic cause

were excluded from the study. The diagnostic criteria for

empyema thoracis was presence of pleural effusion,

clinical and radiological examination and aspiration of

pus from the thoracic cavity. Adetailed history was taken

regarding complaints, predisposing factors,

immunization and communications. Detailed general

and systemic examination done. Routine and relevant

specific examinations were done. These include

hemoglobin estimation, total leukocyte count, ESR,

HIV. All patients suspected of pleural effusion clinically

were subjected to chest X-ray, USG and (If required) CT

thorax. Other investigations includes pleural tap fluid

was studied for gram staining, microscopy cytology

biochemical analysis including protein estimation,

pleural culture and antibiotic sensitivity pattern. A chest

radiograph (PA or AP) and a lateral view if indicated

were done after chest tube insertion. Intercostal drainage

with tube thoracostomy was performed in all patients.

The patient requiring prolonged hospitalization and

who did not respond to conventional antibiotics and tube

thoracostomy or developing complications or those not

showing radiological signs of lung expansion were

referred to the pediatric surgeon for thoracoscopic

decortications or VATS. All patients were studied for

complications during hospital stay.

Nutritional status

No Malnutrition 6 18%

Grade 1 10 28.5%

Grade 2 9 25.8%

Grade3 6 18.1%

Grade4 4 11.4%

Symptomatology

symptom number %

Fever 35 100

Cough 31

Breathlessness 15

Chest pain 2

Refusal of feeds 1

Bacteriological profile /pus culture profile:

Mean age of icd insertion :

1 st day of admission 15

2-6 days 11

>1 week 6

Modalities of treatment :

Mean duration of hospital stay:

Sex distribution

Age Number %

Male 17 48.6%

Female 18 51.4%

gram neg organisms

11%

fungal 10%

pseudomonas 6%

staph aureus 42%

streptococci 31%

Antibiotics +icd insertion 15 42.8%

Surgery + icd insertion 17 48.5%

Vats only 3 8%

Age Number %

< 1year 3 8.56%

1-5 year 24 68.1%

5year 8 22.8%

Antibiotics+icd 21

Antibiotics followed by surgery 16

Immediate surgery 14


Empema Right sided: Bilateral empema :

PRE OP POST OP

Results:

1) The mean age of presentation is 1-5 years

2) Out of 35 patients 17 were boys and 18 were girls

3) Median day of presentation is day 15

4) Association of PEM wass found in 27 patients (77%)

5) Most common presenting feature being fever present in 100% patients followed by cough

6) Either pus or blood c/s was positive in 18 patients (51%) with staphylococcus being the most common followed by streptococci

7) X ray as diagnostic modality was done in all patients and usg or ct used as second modality in 22 that is (66%) of patients

8) ICD was inserted in 24 patients and mean duration of insertion is 3 days from admission

9) About 17 patients required treatment by surgery either VATS or open Decortication

10) Mean duration of hospital stay is reduced in patients who are treated early with surgery.

Discussion :

Though the incidence of empyema thoracis has declined in the west due to effective use of broad spectrum antibiotics, but it still remains a significant health problem in developing countries due to low socioeconomic status, malnutrition and delay in diagnosis of pneumonia, delayed referral to higher centre. Therapy for thoracic empyema requires appropriate antibiotics, prompt drainage of the infected pleural space and lung expansion. However there is no clear consensus on the best way to obtain these objectives. (21,22,23).

The age of presentation was consistent with similar other studies.(17,24,25) The higher prevalence in under-fives is in general agreement with the established pattern of acute lower respiratory infections in children. (6) In our study, 77% of the children were malnourished as per IAP classification.(27) Fever, breathlessness and cough were the most common (90%) manifestations found at admission similar to many other studies.(26,24,25) Other associated manifestations were anorexia, malaise and weight loss.

A higher incidence of empyema cases were seen more often in malnourished children as seen in this study, similar to other studies conducted in developing countries.(28,29,31) Predisposition of malnourished children to recurrent , severe and complicated infection is a known factor.

In our study, pleural fluid culture or blood cultures showed bacterial growth in 51% of patients and no growth in 49% of patients.(24) The present study culture reports were similar to other reports. Most common organism isolated was staphylococcus aureus which is comparable to previous studies from other developing countries.(26,24,25,32,33) Other causes are streptococcus pneumoniae, pseudomonas and Klebsiella pneumoniae. The sterile sample might be due to high rate of antibiotics pre- treatment or lack of better facilities for culturing fastidious organism like anaerobes. Pneumococcus is the major pathogen in developed countries.(17,18)

In our study about 20 patients are treated by surgery either VATS or decortication which is high when compared to other studies .This is mainly due to delayed presentation and majority of patients presented with loculated empyema which could not be drained through simple ICD insertion along with antibiotics . All patients have improved with no mortality . Antibiotic duration and hospital stay is reduced in patients manged by surgery when compared to those managed by antibiotics.

This outcome is similar to other studies done where 100% is the survival.(34) Recovery and long-term outcome is good with appropriate treatment. However, in the present study complete pleural recovery could not be documented due to shorter period of followup and was a major limitation. Spirometry could not be done for a majority of the patients because of a younger age and was a limitation Decortication is effective,safe ,curative treatment. Decortication reduced prolong hospital stay,antibiotic theraphy and long term morbitity .95% success rate in 2nd and 3rd stage .


References :

1. Adams F. The genuine works of Hippocrates, Baltimore: William

and Wilkins Company; 1939;51-2.

2. Eastham KM, Freeman R , Kearns AM, Eltringham G, Clark J,

Leeming J, et al. Clinical features, aetiology and outcome of

empyema in children in the North East of England. Thorax.

2004;59:522-5.

3. Roxburg CSD, Young Son GG, Towend JA, et al. Trends in

pneumonia and empyema in Scottish children in the past 25 years.

Arch Dis Child. 2008;93:316-8.

4. YC 5. Jeffery M Bender, Krow Ampofo, Xiaoming Sheng, Andrew

T Pavia, Lisa Cannon-Albright and Carrie L Byington.

Parapneumonic empyema deaths during past century. Utah Emerg

Infect Dis. January 2009;15(1):44-48.

5. Phelan, Landau PC, L. I. and Olensky A. Respiratory illness in

children. Blackwell scientific publications. Second Edition,

1982;29-47.

6. Light, RW. Management of parapneumonic effusions, J Empyema

thoraces during a 10-year period (1952-67). Arch Ins Med

1981;141:1771-1776.

7. Peter Mattei, Julian LAllen. Treatment of empyema in children from

Hippocrates' time to the present and back again. Editorial Am J Res

Crit Care Med 2006;174:110-111.

8. Maziah W, Chook E, Ray JG, et al. Empyema thoracis in

hospitalized children in Kelantan, Malaysia. J Trop Pediatr

1995;41:185-8.

9. Mishra OP, Das BK, Jain AK, Lahiri TK, Sen PC, Bhargara V.

Clinico-bacteriological study of empyema thoracis in children. J

Trop Pediatr 1993;39:380-1.

10. Asendi AA, Estem SE, Asuquo ME. Clinical and bacteriological

study on childhood empyema in South Eastern Nigeria, East Afr

Med J 1992;69:78-82.

11. Anstadt MP, Guill CK, Ferguson ER, Gordon HS, Soltero ER, Beall

AC Jr, et al. Surgical versus no surgical treatment of empyema

thoracis–An outcome analysis. Am J Med Sci 2003;326:9-14.

12. Strange C, Tomlinson JR, Wilson C, Harley R, Miller KS, Sahn SA.

The histology of experimental pleural injury with tetracycline,

empyema and carragunan. Exp Mol Pathol. 1999;51:205-19.

13. Givan DC, Elgen H. Common pleural effusions in children. Clin

Chest Med. 1998;19:363-71.

14. The American Thoracic Society Subcommittee on Surgery.

Management of non-tuberculous empyema. Am Rev Respir Dis.

1962;85:935-6.

15. Narayanappa D, Rashmi N, Prasad NA, et al. Clinicobacteriological

profile and outcome of empyema. Indian Pediatr. 2013;50:783-5.

16. Byington CL, Spencer LY, Johnson TA, Pavia AT, Allen D, Mason

EO, et al. An epidemiological investigation of a sustained high rate

of pediatric parapneumonic empyema: Risk factors and

microbiological associations. Clin Infect Dis. 2002;34:434-40. 17.

Estham KM, Freeman R, Kearns KM, Eltringham G, Clark J,

Leeming J. Clinical features, aetiology of empyema in children in

the North East of England. Thorax. 2004;59:522-5.

18. Dass R, Deka NM, Barman H, Durwarah SG, Khyriem AB, Saikia

MK, et al. Empyema thoracis: analysis of 150 cases from a tertiary

care centre in North East India. Indian J Pediatr. 2011;78:1371-7.

19. Sarihan H, Cay A, Aynaci M, et al. Empyema in children. J

Cardiovasc Surg (Torino). 1998;39:113-6.

20. Strange C, Sahn SA. The clinician's perspective on parapneumonic

effusions and empyema. Chest. 1993;103:259-61.

21. Tiryaki T, Abbasoglu L, Bulut M. Management of thoracis empyema

in childhood: A study of 160 cases. Pediatr Surg Int. 1995;10:534-6.

22. Cham C, Haq SM. Rahamim J Empyema thoracis: a problem

with late referral? Thorax. 1993;48:925-7.

23. Vikas G, Ajay K, Monika G, et al. Empyema thoracis in children:

Still a challenge in developing countries. Afr J pediatr surg.

2014;11:206-210.

24. Zel SK, Kazeza, Kilic M, Koseogullaric AA, Yelmaza, Aygun AD.

Conservative treatment of post parapneumonic thoracic empyema

in children. Surg Today. 2004;34(12):1002-5.

25. Singh V. IAP Textbook of Paediatrics, 5th edn, Jaypee Publishers.

2013;478-80. 26 19

26. Hailu S, MD. Paediatric thoracic empyema in an Ethiopian referral

hospital. East Afr Med J 2000;77:618-621

27. Satpathy SK, Behera CK, Nanda P. Outcome of parapneumonic

empyema. Indian J Pediatr.2005;72:195-9.

28. Yilmaz E, Dugan Y, Aydinoglu AH, et al. Parapneumonic empyema

in children: conservative approach. Turk J Pediatr. 2002;44:134 -8.

29. Menon P, Rao KL, Singh M, Venkatesh MA, Kanojia RP, Samujh R,

et al. Surgical management and outcome analysis of stage III

pediatric empyema thoracis. J Indian Assoc Pediatr Surg.

2010;15:9-14.

30. Ekpee EE, Akpan MU. Poorly treated bronchopneumonia with

progression to empyema thoracis in Nigerian children. TAF Prev

Med Bull. 2010;9:181-6.

31. Shah K, Shaikh F, Poddutoor PK, et al. Clinical profile of empyema

in tertiary health care centre. Indian J Child Health. 2015;2(1):5-8. 32 . Potts DE, Levin DC, Sahn SA. Pleural fluid pH in

parapneumonic effusions. 1976;70(03):328-31. 33. Jigui YU, Douglas Salmon, Mario Marcon, et al. Pneumococcal

serotype causing pneumonia with pleural effusion in pediatric patients. Journal of Clinical Microbiology. J Clin Microbiol. February 2011; vol. 49(2):534-536.

34. Grisario-Soen G, Eisenstadt M, Parit G, Schwartz D, Keller N, Nagar H, et al. Pediatric parapneumonic empyema: risk factors clinical characteristics, microbiology and management. Pediatr Emerg Care.2013 Apr;29(4):425-9.


Joult of Acute Flaccid Paralysis following symptomatic treatment

Srikanth S, Shruthi S. B, Kalappanavar N. K Dept of Pediatrics, S S Institute of Medical Science and Research Center, Davangere.

Correspondence : Dr. Srikanth S. Dept of Pediatrics, S S Institute of Medical Science and Research Center, Davangere.

Mob. : 9845299048

The cation potassium plays a critical role in many

metabolic cell functions; 98% of potassium in the body

is found in intracellular fluid compartments, leaving 2%

in extracellular fluid spaces. This balance is regulated by

the sodium-potassium adenosine triphosphatase

(ATPase) pump, an active transport mechanism that

moves ions across the cell membrane against a

concentration gradient.1–5

An imbalance of potassium

can have significant effects on nerve impulse

transmission, skeletal and cardiac muscle contraction,

and acidbase balances. Certain diseases, injuries, and

specific medications have the potential to affect

potassium homeostasis. As a result, small alterations in

serum potassium levels can lead to detrimental effects

within the body.

Normal serum potassium levels range from 3.5 to

5 mEq/L; however, certain hormones, illnesses, and

dietary deficiencies can lead to imbalances, including

acid-base disturbance, aldosterone, insulin,

catecholamines, and tonicity of body fluids, as well as

gastrointestinal (GI) and renal excretion. Daily intake of

potassium is required because the body does not

routinely conserve this electrolyte. About 80% of

consumed potassium is eliminated in the urine, 15% is

excreted in the feces, and 5% is lost in sweat.3,4

Hypokalemia is defined as a serum potassium

concentration of less than 3.5 mEq/L. This is one of the

most commonly encountered electrolyte abnormalities

in clinical practice. Hypokalemia is further categorized

as mild (serum potassium, greater than 3 to 3.5 mEq/L),

moderate (serum potassium, 2.5 to 3 mEq/L), or severe

(serum potassium, less than 2.5 mEq/L), as noted in

Table 1.3

Hypokalemia results either when there is a

total-body potassium deficit, or when serum potassium

is shifted into the intracellular compartment.1–6

When

hypokalemia is detected, a diagnostic workup that

evaluates the patient's comorbid disease states and

concomitant medications should be completed.

Table 1 reviews the signs and symptoms of

hypokalemia. In mild cases of hypokalemia, patients are

usually asymptomatic and are often diagnosed

incidentally during routine blood testing. Moderate

hypokalemia is often associated with cramping,

weakness, malaise, and myalgias. In severe

hypokalemia, electrocardiogram (ECG) changes often

occur, including ST-segment depression or ST segment

flattening, T-wave inversion, and/or U-wave elevation.

These ECG changes can lead to various arrhythmias,

including heart block, atrial flutter, paroxysmal atrial

t achycardia , and vent r icular f ibr i l la t ion.

Musculoskeletal cramping and impaired muscle

contraction are other common manifestations of severe

hypokalemia.1–4

Hypomagnesemia, which is present in more than

50% of cases of clinically signify cant hypokalemia,

contributes to the development of hypokalemia by

reducing the intracellular potassium concentration and

promoting renal potassium wasting.7

While the exact

mechanism of the accelerated renal loss remains

unclear, it is theorized that the intracellular potassium

concentration may decrease because hypomagnesemia

impairs the function of the sodium-potassium ATPase

Abstract : The cation potassium plays a critical role in many metabolic cell functions; 98% of potassium in

the body is found in intracellular fluid compartments, leaving 2% in extracellular fluid spaces.The absence of

early detection and treatment, hypokalemia can cause serious complications that could be life- threatening.

The vast majority of hypokalemia cases are drug-induced, as was finally evident in this case. Our patient

exhibited profound hypokalemia with significant symptoms. Fortunately, the etiology was identified relatively

early. we can assist in early treatment interventions to improve patient outcomes and decrease lengths of stay

while preventing untoward reactions and associated medical complications.

Key words : Hypokalemia, Flaccid paralysis, Potassium

CA

SE

A

RT

ICL

E


pump, thereby promoting potassium wasting. When

concomitant hypokalemia and hypomagnesemia exist,

the magnesium deficiency should be corrected first;

other wise, full repletion of the potassium deficit is

difficult to achieve.

Total-body potassium deficiencies are either

secondary to inadequate intake or caused by excessive

renal and GI fluid losses from diarrhea or vomiting . In

cases of severe diarrhea and vomiting, metabolic

alkalosis can occur and lead to an intracellular shifting

of potassium, which further decreases the serum

potassium concentration.4

Other potassium losses are

seen in nephritis and renal tubular acidosis, Cushing's

syndrome, and periods of high stress. Additional

disorders that lead to potassium loss include hepatic

disease, hyperaldosteronism, acute alcoholism, heart

failure, Bartter's syndrome, and acute leukemias.1–8

Medications cause hypokalemia through a variety of

mechanisms, including intracellular potassium

shifting, increased renal loss, and/or stool loss. Table 2

highlights selected medications associated with

hypokalemia. Some published cases have reported an

association \ between antidepressant use and the risk for

hypokalemia. This adverse effect may put psychiatric

patients at risk.4,9,10

Further studies are required to

elucidate a possible association between selective

serotonin reuptake inhibitors and hypokalemia.

Additionally, a few case reports have noted a risk for

hypokalemia with the use of iodinated contrast.11

In

t h e s e c a s e s , i o d i n a t e d c o n t r a s t - i n d u c e d

hyperthyroidism leads to thyrotoxic periodic paralysis.

Up to 32% of acute hypokalemia paralysis is thyrotoxic

in nature. The overstimulation of the sodium-potassium

ATPase pump by thyroid hormones during thyrotoxic

paralysis leads to an acute intracellular shift of

potassium into the cells, causing a hypokalemic medical

emergency.

Table 2 Selected Medications Associated With Hypokalemia 1–5,12

Medication Class Examples of Common

Drugs

Mechanism

Antimicrobials Nafcillin Ampicillin

Penicillin

Aminoglycosides*

Amphotericin B*

Foscarnet*

Renal potassium loss

Beta2-receptor agonists • Albuterol

• Ephedrine

• Epinephrine

• Formoterol

• Isoproterenol

• Pseudoephedrine

• Terbutaline

• Salmeterol

Shift of potassium from

extracellular fluid to

intracellular fluid compartment

Table 1 : Severity, Levels, and Symptoms of Hypokalemia1–4

Severity Level Symptoms

Mild > 3.0–3.5 mEq/L Asymptomatic

Moderate 2.5–3.0 mEq/L Cramping, malaise, myalgia, weakness

Severe < 2.5 mEq/L Electrocardiogram changes (including

ST-segment depression, U-wave

elevation, T-wave inversion),

arrhythmias, paralysis


Diuretics • Acetazolamide • Bumetanide

• Chlorthalidone

• Ethacrynic acid

• Furosemide • Indapamide

• Metolazone

• Thiazides

• Torsemide


Insulin High dose (overdose) Shift of potassium from



Mineralocorticoids

and glucocorticoids

• Hydrocortisone† • Fludrocortisone

• Prednisone†


Laxatives • Sodium polystyrene

sulfonate • Phenolphthalein

• Sorbitol

Stool (gastrointestinal)

potassium loss

Xanthines • Theophylline

• Caffeine Shift of potassium from



Other Verapamil (in overdose) Shift of potassium from


intracellular

fluid compartment

* Also associated with magnesium depletion

† Increases potassium excretion nonspecifically through effect on filtration rate and distal

sodium delivery

Case Report

A 11 month old infant presented to us with

complaints of fever, cough and hurried breathing since 4

days and sudden onset of weakness of all four limbs

along with head lag, breathing difficulty and unable to

speak as before since evening. He was admitted for

previous three days in a local hospital and later referred

to our hospital since the onset of weakness. On

examination he had tachypnoea and tachycardia with

nasal flaring and intercostal retraction. Saturation was

maintained with oxygen. CNS examination showed

hypotonia with loss of head control and flaccid paralysis

of all four limbs with just flickering movements and

DTR 1+. On respiratory system examination, bilateral

air entry present, normal vesicular breath sounds heard

with crepitations and conducted sounds. Per abdomen

was distended with no organomegaly and diminished

bowel sounds.

Initial diagnosis of acute flaccid paralysis/

quadriparesis was made, probably Guillain Barre

Syndrome or Acute Demyelinating Encephalomyelitis.

Routine blood investigation was sent and MRI brain was

done. MRI showed normal study. ECG leads in the

monitor showed normal QRS complex and flat T wave.

Serum electrolytes were traced which showed severe

hypokalemia, potassium of 1.3mEq/L. Hence the

diagnosis of Hypokalemia was made and potassium

infusion started. Initial rapid correction of 1mEq/Kg

given over one hour and later 24 hour correction

continued. By 12 hours of treatment the infant was

symptomatically better and started moving his limbs.

Investigation done are as shown in the table.


31/1/17 31/1/17 1/02/17 2/2/17 3/2/17

Hb 8.9

TC 17400

PCV 25.6

Pl C 4.64 lc

RGS 160

Urea 18 13.3 9.6 10.3

Creatinen 0.6 0.51 0.5 0.48

S. Na 136 135.3 133.8 135.9 137

S. K 1.3 2.7 3.6 4.2 3.9

S. Cl 106 104.1 103 106.7 107

Ionised Cal 5.83

BUN 8.3 mg/dl ABG 31/1/17 Serum

Osmolality

283.9

mOsm/Kg

Urine Na 87.1 mmol/L Ph 7.214 Urine

Osmolality

332.9

mOsm/Kg

Urine K 19.9 mmol/L PCo2 29.4 TTKG 12.6

Urine Cl 91.1 mmol/L PO2 129

Urine Creat 20.3mg/dl HCO3 12.9

Urine UN 333 mg/dl BE -14.9

Once hypokalemia was diagnosed urine

investigation was sent as mentioned in the above table.

Even though serum potassium was 1.3mEq/L, trans-

tubular potassium gradient (TTKG) was 12.6 which was

very high. This tells us that excess urinary loss was the

reason for hypokalemia. On further enquiry about the

medications received in the previous hospital, we got to

know that the infant was treated with Inj Ceftriaxone, Inj

Amikacin, Inj Hydrocortisone and salbutamol.

Amikacin and hydrocortisone both causes hypokalemia

with renal loss of potassium and salbutamol causes shift

of potassium from extracellular to intracellular

compartment. Thus we concluded that the infant was

suffering from drug induced hypokalemia.

Discussion

Drugs forms the major part of the management of a

sick child. There are many drug interactions which occur

especially when treated with multiple medications.

Electrolyte disturbances are major drug interaction

which can be life threatening. Hypokalemia is a known

side effect in many drugs as mentioned in the above

table. High index of suspicion is required for early

diagnosis and apt treatment.

Determining the etiology of the hypokalemia is

essential in order to appropriately manage patients. As

previously noted, hypokalemia can be caused by

medical conditions, acute illnesses, or medications. It is

important to explore each potential cause for every

patient who presents with hypokalemia.

Conclusion

In the absence of early detection and treatment,

hypokalemia can cause serious complications that could

be life-threatening. The vast majority of hypokalemia

cases are drug-induced, as was finally evident in this

case. Our patient exhibited profound hypokalemia with

significant symptoms. Fortunately, the etiology was

identified relatively early. As clinicians monitoring

patient therapy, we must be vigilant in identifying

potentially drug-induced disease as early as possible. In

doing so, we can assist in early treatment interventions to

improve patient outcomes and decrease lengths of stay

while preventing untoward reactions and associated

medical complications.

Reference :

1. Weiner DI, Wingo CS. Hypokalemia: consequences,

causes, and correction. J Am Soc Nephrol

1997;8(7):1179–1188.

2. Gennari FJ. Hypokalemia. N Engl J Med

1998;339(7):451–458.

3. Brophy DF. Disorders of potassium and magnesium

homeostasis. In: DiPiro JT, Talbert RL, Yee GC, et

al., eds. Pharmacotherapy: A Pathophysiologic


Approach, 9th ed. New York, New York: McGraw-

Hill; 2014.

4. Unwin RJ, Luft FC, Shirley DG. Pathophysiology

and management of hypokalemia: a clinical

perspective. Nat Rev Nephrol 2011;7(2):75–84.

5. Walmsley RN, White GH. Occult causes of

hypokalemia. Clin Chem 1984;30(8):1406– 1408.

6. Clausen T. Hormonal and pharmacological

modification of plasma potassium homeostasis.

Fundam Clin Pharmacol 2010;24(5):595–605.

7. Huang CL, Kuo E. Mechanism of hypokalemia in

magnesium deficiency. J Am Soc Nephrol

2007;18(10):2649–2652.

8. Daly K, Farrington E. Hypokalemia and

hyperkalemia in infants and children:

pathophysiology and treatment. J Pediatr Health

Care 2013;27(6):486–495.

9. Wilson B, Paul P, Mehta S. Hypokalemia secondary

to bupropion sustained release overdose. J Child

Adolesc Psychopharmacol 2013;23(1):57–60.

10. Izgi C, Erdem G, Mansuroglu D, et al. Severe

hypokalemia probably associated with sertraline

use. Ann Pharmacother 2014;48(2):297–300.

11. Trifanescu RA, Danciulescu MR, Carsote M, Poiana

C. Hypokalemia periodic paralysis as first sign of

thyrotoxicosis. J Med Life 2013;6(1):72–75.

12. Usami E, Kimura M, Kanematsu T, et al. Evaluation

of hypokalemia and potassium supplementation

during administration of liposomal-amphotericin B.

Exp Ther Med 2014;7(4):941–946.


Miliary Tuberculosis with Scoliosis : A Case Report

Madhu GN1

, Siva Saranappa SB2, Saipraneeth Reddy

3*

1,2,3 Associate Professor, Department of pediatrics, KIMS, Bangalore

Correspondence : Dr. Saipraneeth Reddy Guda Junior Resident, M.D.Pediatrics,

Department of Pediatrics, Kempegowda Institute of Medical Sciences , Bangalore

Email id: [email protected]. Ph: 8105701308

Introduction :

Tuberculosis is a disease of poverty that affects

mostly young adults in their most productive years.

Spinal tuberculosis is one of the oldest diseases known to

mankind and has been found in Egyptian mummies

into the diseased vertebral body. Although early

diagnosis and prompt treatment are essential for the

prevention of severe disability, the diagnostic challenges

inherent to spinal TB are enhanced.

The objective of this report is to describe a case of

dating back to 3400 BC[1]. The spine is the most miliary tuberculosis with rare association of scoliosis of

common and the most dangerous site for skeletal

tuberculosis because of high vascularity and relative

scarcity of phagocytic cells.

The abnormality of spinal deformity depends on

how many vertebrae are diseased. Commonly, as the

deformity worsens, a sharp angle (the gibbus) appears.

Uncommonly, the destruction is not symmetrical, so the

spine rotates. The disease is popularly known as Pott's

spine.[2]

Approximately 10 % of pat ients with

extrapulmonary tuberculosis have skeletal involvement.

Spinal tuberculosis accounts for almost 50% cases of

the thoracic spine in children .

Case Report :

A 16 years old adolescent boy with history of

chronic productive cough since 7 months and upper back

pain since 3 months presented with fever since 10 days

and hurried respiration since 7 days and significant loss

of weight. He was working in masonry since 2 years, is a

active smoker and alcoholic since 1 year.

On examination, he was febrile, with tachypnea

(44/min) and tachycardia(120/min), pallor present,

lymph nodes were not palpable. BCG scar present,

drooping of left shoulder present. Respiratory systemic skeletal tuberculosis.[3] It occurs as a result of the examination revealed trachea deviated to left side, hematogenous spread or erosion of adjacent caseating

lymphnodes after a primary pulmonary infection that is

not generally evident in children as they are more

vulnerable to the occurrence of discitis because of the

persistence of the anastomosis between the motor end

plate and the spinal disc.[4]

The paradiscal regions of vertebrae are affected in

98% of TB spine lesion. The tuberculous lesion starts as a

paradiscal inflammation. Gradually as disease

progresses the vertebral end plates become structurally

weak and intervertebral disc starts ballooning/herniating

crowding of lower ribs on left side, decreased breathing

movements on left side of chest. Vocal fremitus and

vocal resonace decreased on left side. On percussion,

impaired note in left infra clavicular, axillary,

interscapular and infrascapular region and dull note in

left mammary, infra mammary and infra-axillary region.

Decreased breath sounds are present on the left side in

mammary, inframammary, axillary, infraaxillary,

interscapular and infrascapular areas. Examination of

spine showed deviation of upper thoracic spine to the

right in the interscapular region, no local tenderness

Abstract : Tuberculosis spine though common in developing countries, presentation as a scoliosis is usually rare

with non specific findings. This is the case report of a 16 years old adolescent boy presented with cough since 7

months and back pain since 3 months. On examination, tachycardia and tachypnea present, respiratory system is

abnormal with decreased air entry and breathing movements on the left side. Chest x ray revealed deviation of

upper thoracic vertebrae towards right and lower lung fields showing multiple bilateral opacities. Computed

tomography chest revealed wedge compression fracture of T5 vertebrae leading to scoliosis, and fibrosis with

underlying consolidation in the left lung fields, and upper paratracheal and aorticopulmonary lymph nodes. Child

was started on ATT and responded well, scoliosis correction was planned in future.

Keywords : Scoliosis, fibrosis, Miliary Tuberculosis, wedge compression fracture.

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figure 2

present (figure 1). No neurological sequelae found.

Figure 1: Dropping of left shoulder and right side

deviation of upper thoracic vertebrae(scoliosis)

Laboratory examination revealed hemoglobin- 12.1

gm/dl, total leukocyte count-4.1 x 109/L, Differential

leukocyte count- P79%, L20% 1%, ESR 09 mm 1 hr.

Mantoux test was negative, gastric lavage for AFB was

negative on two occasions. A chest radiograph revealed

multiple reticulonodular opacities in bilateral lower lung

fields, fibrosis of left lower lung fields with underlying

collapse and deviation of upper thoracic vertebrae to

right side with underlying wedge compression fracture.

(Figure 2)

CT chest revealed multiple nodular opacities in

both lungs, consolidation with air bronchogram noted in

the medial basal, posterior basal and lateral basal

segment of right lower lobe, anterior segment of left

upper lobe and superior basal and posterior basal

segment of left lower lobe. Left lung volume loss. Thick

left pleural collection with sub pleural fibrosis noted in

the left lower lobe. Wedge compression fracture with

osteolytic noted on T5 vertebral body with gibbus

formation(figure 3). Few subcentric upper paratracheal

and aorticopulmonary lymph nodes noted.

Discussion :

Miliary TB is common disease in areas where TB

is endemic. It is the widespread dissemination of

Mycobacterium tuberculosis from hematogenous

spread. The infection is characterized by the

appearance of numerous small nodular lesions that

resemble millet seeds on chest radiography [5]. CT

scanning of the chest may help to better define

abnormalities in patients with vague findings on chest

radiography

In vertebrae, the segment most often affected is

the thoracic spine[6]. In this case study, the patient had

residual scoliosis in the thoracic spine related to the

wedge compression of T5 vertebral bodies. Possibly,

the low specificity of the clinical condition and the

limited suspicion with regard to TB as the cause of

thoracic pain were responsible for the delay in

diagnosis. This delay also favours the occurrence of

residual deformity, since the destruction of bone is

slow and progressive.

Demonstration of tubercle bacilli in the skeletal

lesion is the gold standard for diagnosis of TB [7].

However, previous reports claim that no series was

able to do so in all cases, and empirical treatment is

recommended when spinal TB is suspected [8,9].

Hence in our case, we started on Anti tuberculous

treatment and scoliosis correction was planned for

future .

Sarah et al., in a retrospective study of 21

patients with tuberculous spondylitis, with an average

age of 9.7 years old, from an endemic area and with

diagnosis in up to four months, verified that back pain

is the most common symptom. Microbiological

diagnosis was confirmed in 67% of cases by a culture

of vertebral biopsy or paraspinal abscess, 20% by acid

fast bacilli (AFB) and conventional PCR tests. The

thoracic spine suffering from vertebral collapse was

found in most cases and 8 patients had compression of

the spinal cord and 5 were left with residual

deformities[10].

In the most severe form of Pott's disease, spinal

deformation and collapse can compress the spinal

cord, thus causing neurological disorders such as

paresis and paralyses[11]. In this case report, the

patient did not display neurological signs, despite the

compressive effects exerted by the sideward

displacement in the T5 and adjacent vertebral bodies.

Unlike adults, who have a higher incidence of

neurological symptoms with more localized

inflammatory signals, in children, the disease is

characterized by an extensive and diffused

figure 2: wedge compression fracture and b/l lower lobe opacities with fibrotic bands on left side.

figure 3: fibrotic bands and compression fracture of vertebral body of T5


involvement, and the low incidence of Pott's paraplegias

or tetraplegias[12]. Histological analysis of the lesions,

although nonspecific, demonstrated diagnostic value by

providing evidence of chronic granulomatous

inflammation, as found in most cases[12].

Concomitant pulmonary or genitourinary TB is

reported in 40-50% adults but in only 12% children from

Indian series.[13] In our case report, there is associated

miliary tuberculosis with fibrotic bands and spinal TB

(scoliosis).

A report of spinal TB including five cases from

Belgium assesses that doctors did not consider TB as an

initial diagnosis although the patients had severe back

pain and this caused delay in the diagnosis [14]. In our

case, we also think that delay of the diagnosis caused a

worse condition.

The primary diagnosis of spinal TB in our patient

was based on a combination of clinical and radiological

findings. The learning points in this case report are the

need for a high index of suspicion, value of a careful

history and how a radiological classical finding helped in

diagnosing spinal TB. In conclusion, severe forms of TB

can be caused by delay of diagnosis and inappropriate

treatment. Early diagnosis of this progressive disease can

save young patients from death or permanent disability.

Acknowledgments :

We thank concerned radiologists, KIMS

Bangalore, for assistance in interpreting the radiological

findings and all staff of the paediatrics departments who

helped in appropriate management and care for this

child.

References :

1 Taylor GM, Murphy E, Hopkins R, Rutland P, Chistov Y. First

report of Mycobacterium bovis DNA in human remains from the

Iron Age. Microbiology 2007;153(4):1243–9.

2 Dobson J. Percivall Pott. Ann R Coll Surg Eng 1972;50(1):54–65.

3 Gautam MP, Karki P, Rijal S, Singh R. Pott's spine and Pott's

paraplegia. J Nep Med Assoc 2005;44(159):106–15.

4. Schettino LC, Carelli LE, Barbosa MO. Tuberculose vertebral:

análise descritiva de uma série de casos submetidos a tratamento

cirúrgico. Coluna/Columna 2010; 9:119-125

5. K l a u s - D i e t e r L ( 2 0 0 7 ) M i l i a r y t u b e r c u l o s i s .

Available:http://emedicine.medscape.com/article /969401-

overview. Accessed 26 March 2009.

6. Cabral MML, Azevedo BCCA, Montenegro LML, Montenegro

RA, Lima AS, Schindler HC. Espondilite tuberculosa em

adolescente. J Bras Pneumol 2005; 31:261-264.

7. Handa U, Garg S, Mohan H, Garg SK: Role of fine-needle

aspiration cytology in tuberculosis of bone. Diagn Cytopathol

2010, 38(1):1–4.

8. Garg RK, Somvanshi DS: Spinal tuberculosis: a review. J Spinal

Cord Med 2011, 34(5):440–454.

9. Wang D: Diagnosis of tuberculous vertebral osteomyelitis in a

developed country and literature review. Spinal Cord 2005,

43(9):531–542.

10. Eisen S, Honywood L, Shingadia D, Novelli V. Spinal

tuberculosis in children. Arch Dis Child 2012; 97:724-729.

11. Jacobs RF, Starke JR. Tuberculosis in children. Med Clin North

Am 1993; 77:1335-1351

12. Arcelis RRM, Marques HHS, Matielo RLB, Sakane PT, Baldacci

ER.Tuberculose Ostearticular em crianças. Pediatria (São Paulo)

2006; 28:169-174.

13. Tuli SM. Tuberculosis of the spine. In: Tuli SM. ed.

Tuberculosis of the skeletal system. J.P. Brothers, New Delhi

1991; 132- 253.

14. Alame T, Dierckx P, Ninane V, Sergysels R (1996) Spinal

tuberculosis: a report of five cases and a review. Monaldi Arch

Chest Dis 51: 362-368.

http://emedicine.medscape.com/article


A Term Neonate with Congenital Pulmonary Airway Malformation

Nitin M, Sudha Rudrappa, Girish G Dept of Pediatrics, Mysore Medical College and Research Institute, Mysore 570001

Correspondence : Dr. Nitin M. Dept of Pediatrics, Mysore Medical College and Research Institute, Mysore 570001

e-mail : [email protected]

Introduction : Congenital pulmonary airway

malformation (CPAM), formerly known as cystic

adenomatoid malformation consists of hamartomatous

or dysplastic lung tissue mixed with more normal lung,

generally confined to 1 lobe1.

Case report : A full term male newborn, delivered

on 25/6/2015 by normal vaginal delivery at Cheluvamba

hospital, Mysore with 2.5 kg birth weight, with

uneventful antenatal and natal history, breast fed within

1hour of life with no prelacteal feeds given, was

apparently normal till 26hours of life, later shifted to

NICU from mothers side in view of hurried breathing

and refusal of feeds since morning. There was no

suggestive of cyanosis, suck rest suck cycle, forehead

sweating or temperature disturbance like hypo or

hyperthermia. There was no history of PROM, maternal

pyrexia and UTI in the mother. Baby passed urine and

meconium by 24hours.

On examination, baby was pink and alert, with

good cry, suck and activity. Heart rate was 140

beats/min, peripheral pulses were well felt, respiratory

rate 76 cycles/min, CFT was < 2sec, SPO2 - 92% at room

air. Except for nasal flaring upper respiratory tract was

normal. Lower respiratory tract examination reveled

subcostal and intercostal retractions with fine crackles

heard over right mammary, axillary and scapular

regions. Other systems were within normal limits.

In view of the history and examination findings

provisional diagnosis of congenital pneumonia was

made and newborn was started on started on IV fluids,

oxygen by hood 6l/min and antibiotics – Inj

Cefotaxime and Inj Amikacin. Congenital heart

disease and metabolic disease were other differential

diagnosis. Chest X ray was done which showed right

paracardiac patch. Sepsis workup was within normal

limits (TC – 10,500/mm3 , DC – N40 L58 M2, BNR –

0.2, micro ESR – 5mm/hr, Blood culture – No growth).

ABG and RFT were within normal limits. Baby was

started with NGF on day 3 of life 15ml/kg and

gradually increased by 15ml/kg/day.

Since the condition of the baby didn't improve,

repeat sepsis workup was done on day 4 of life which

showed raised CRP and elevated counts of

20,500cells/mm3 , subsequently antibiotics were

revised to Inj Piperacillin-tazobactum and Inj

Amikacin. As the baby's condition was not improving

and that we noticed a systolic murmur on day 8 of life,

made us plan an ECHO which showed tiny PDA2mm,

PFO 4mm.

As the ECHO finding didn't correlate with the

clinical condition USG thorax was done which was

normal. Subsequently contrast CT thorax was

planned. It showed focal consolidation changes in the

apical and posterior segments of the right upper lobe.

With the CT findings diagnosis of CPAM type 3 was

made and the parents were counseled regarding the

surgical option, but they were not willing. Meanwhile

the condition of the neonate improved and was

discharged with oral antibiotics. Subsequently the

child developed 2 episodes of pneumonia localized to

the same right lung fields. At present the child is 7

month old with weight of 5.9 kg and the parents have

consented for surgery.

Abstract : Aterm newborn presented at 26 hr of life with hurried breathing and refusal of feeds, the antenatal and

natal history being uneventful. On examination the newborn had hypoxia and mild respiratory distress. A

provisional diagnosis of congenital pneumonia was made and was started on antibiotics and oxygen.

Subsequently the sepsis work up and other investigations including ECHO turned out to be normal except for the

chest X-ray finding of paracardial patch. The persistence of signs with absence of sepsis and major congenital

heart disease made us plan CT thorax which showed findings of congenital pulmonary airway malformation.

Subsequently the child was discharged. In view of recurrent pneumonia the child is being planned for surgery and

is und follow up.

Keywords : newborn, respiratory distress, Congenital pulmonary airway malformation

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Discussion :

CPAM may present before or after birth. Lesions

are characterized by an increase in structures

resembling bronchioles that are lined by columnar

epithelium; cartilage usually is absent2. It occurs in

approximately 1-4 in 100,000 births. Prenatal

ultrasonographic findings are classified as

macrocystic (single or multiple cysts >5 mm) or

microcystic (echogenic cysts <5 mm). Five

histological patterns have been described. Type 0

(acinar dysplasia) is least common, prognosis is

poorest for this type, and infants die at birth. Type 3

(<10%) is seen mostly in males; the lesion is a mixture

of microcysts and solid tissue with bronchiole-like

structures lined with cuboidal ciliated epithelium and

maldevelopment of terminal bronchiolar structures.

Patients can present in the newborn period or early

infancy with respiratory distress, recurrent respiratory

infection, and pneumothorax. CT allows accurate

diagnosis and sizing of the lesion and is indicated even

in asymptomatic neonates1.

Serial ultrasound monitoring of congenital cystic

lung lesions has demonstrated that a significant

proportion of these lesions decrease in size and may

regress spontaneously; therefore, antenatal treatment

is not usually required3.In view of spontaneous

resolution, surgery may be delayed for asymptomatic

infants. In the postnatal period, surgery is indicated for

symptomatic patients1.

This neonate presented in the postnatal period

with history and examination findings of Congenital

pneumonia, but the CT scan revealed the diagnosis.

Here the antenatal USG missed the diagnosis. In view

of recurrent pneumonia the infant is being followed up

and planned for surgical resection of the lesion.

Conclusion :

CPAM is one of the very rare congenital

anomalies of the lung. Antenatal USG can pick up the

diagnosis. Only symptomatic cases should be taken up

for surgery as there are chances of spontaneous

recovery.

Acknowledgement : No funding or sponsorship.

References : 1. Blatter JA, Finder JD. Congenital disorders of the lung. In:

Kliegman RM, Stanton BF, St Geme JW, Schor NF, eds. Nelson

Textbook of Pediatrics. 20th

ed. Philadelphia, PA: Elsevier

2016:2057-2059.

separated by areas of nonciliated cuboidal epithelium.

The prognosis for this type, like type 0, is poor1.

The lesion probably results from an embryologic

2. Hanzinski TA. Congenital disorders of the lower respiratory tract.

In: In: Rudolph CD, Rudolph AM, Hostetter MK, Lister G, Siegel

NJ. Rudolph”s text book of Pediatrics. 21st ed. McGraw Hill 2003.

3. Sfakianaki AK, Copel JA. Congenital Cystic Lesions of the Lung:

injury before the 35th

day of gestation, with Congenital Cystic Adenomatoid Malformation and

Bronchopulmonary Sequestration. Rev Obstet Gynecol.

2012;5(2):85-93.








S.S. Institute of Medical Sciences and Research Centre,

Davangere - 577005, Karnataka, India

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