GENERAL PAST OBSTETRIC HISTORY ANTENATAL CARE OBSTETRIC/MEDICAL COMPLICATIONS LABOR DELIVERY IMMEDIATE CARE AT BIRTH FEEDING HISTORY POSTNATAL PROBLEMS FAMILY HISTORY PAST MEDICAL PROBLEMS PERSONAL/SOCIAL HISTORY

Least disturbing examination should be done first

Assess the state,posture, spontaneous activity, colour, any obvious respiratory distress or malformations

5 states of an infant are: Deep sleep Light sleep Awake & quiet Awake & active Awake & crying

Temperature Measured in the apex of the axilla—3min

Cold stress Assessed by touching the abdomen,

palms/soles In cold stress palms and soles are colder to

touch than the abdomen

Respiratory rate

40-60 breaths/min

Heart rate

Faster in preterms compared to term Normal range : 110-160 beats/min Bradycardia(<100/min) – heart disease Tachycardia(>160/min) – sepsis , anaemia,

fever or CCF

BP Flush method Doppler monitoring Direct intravascular measurement

Capillary refill time Estimated by applying firm pressure on the

sternum area for 5 sec Refill time is prolonged in case of

hypothermia and shock

LOW BIRTH WT : <2.5KG

VERY LOW BIRTH WT :<1.5KG

EXTREMELY LOW BIRTH WT : <1KG

Aberrant growth pattern is assessed by plotting the wt against the GA on a standard intrauterine growth curve

Appropriate for gestational age (AGA) Wt between 10th and 90th percentile

Small for gestational age (SGA) Wt falls below 10th percentile

Large for gestational age (LGA) Wt falls above 90th percentile for GA

Length : abt 50cmsHead circumference : 33-37cms at birthChest circumference : 3cm less than head circumference If the difference is more than 3cm -- IUGR

Ponderal Index Wt(gm)/length(cm3) x 100 <2 – asymmetrical growth retardation ≥2 – normal or symmetrical growth

retardation

PRE-TERM INFANTS Deep sole creases are absent or limited to

anterior 1/3rd

Breast nodule is <5mm Ear cartilage has poor elastic recoil Hair is fuzzy Testes are at the external ring and

scrotum has few rugosities Labia majora are widely separated

exposing labia minora and clitoris

SKIN AND HAIR Skin looked for scaliness , elasticity,

thickness , edema,rashes, lesions like hemangioma

Jaundice By compressing on the skin Colour imparted by the Hb in the blood

vessels is eliminated and the yellow colour due to bilirubin is high-lighted

Ecchymoses, petechiae—birth trauma

Lanugo hair - fine hair of fetal period that is shed at 28wks and later at term

Nails – hypoplastic finger nails indicate inutero exposure to valproate

HEAD AND FONTANELLESMolding – Gives the impression of a cliff with rise on

one side and a sharp fall on the other sideSynostosis - Feels like a mountain range with rise on both

sides of elevation

Craniotabes – Skull feel soft like a ping pong ball Due to delayed ossification and resorption of

bones Benign condition in neonates that resolves

spontaneously

Common Located in the

subcutaneous plane

Maximum size and firmness at birth

Softens progressively from birth & resolves within 2 or 3 days

Diffuse , crosses suture lines

Less common Located over parietal

bone,bw skull & periosteum

Increasing in size for 12-24hrs and then stable

Takes 3-6wks to resolve

Does not cross suture line ,has distinct margins

CAPUT SUCCEDANEUM CEPHALOHEMATOMA

Associated with linear fracture of skull bone in 5 – 25% ; hyperbilirubinaemia

Large fontanelles and split sutures : Raised ICP Certain chromosomal abnormalities Hypothyroidism Impaired bone growth like osteogenesis

imperfecta

NECK, FACE ,nose, EYES & EARS Neck masses-enlarged thyroid,scm

tumor,cystoid hygroma. Facial nerve paresis-birth injury. Absence of depressor anguli oris Nose – size,shape,patency,secretions , flaring Bilateral chaonal atresia

Natal teeth , retention cysts-disappear in few weeks.

Cleft palate Eyes;-subconj.hge.pupils,reactive to light Visual tracking assessment of the examiners

face Globe – 70% of adult size Cornea – 80% of adult size

Gross hearing – look for blink on response to noise

Accessory auricles & pre-auricular skin tags are a common finding that may be associated with renal anomalies

UMBILICUS , ANUS & SPINE Inspect no.of vessels in the cord, Single umbilical artery – renal and GI

anomalies. IUGR babies – long and thin cord with very

little Wharton jelly Palpate base of cord for presence of hernia

Spine – spina bifida . Masses and scoliosis Anal opening – for patency and position

GENITALIA (MALE & FEMALE) Examined by hips abducted in the supine

position Urethra- patency Clitoris - clitoromegaly

EXTREMITIES Make sure that arms and limbs are fully

movable Nail hypoplasia , syndactyly , polydactyly ,

oligodactyly , unequal limbs CTEV – calcaneovalgus / equinovarus

deformity

SYSTEMIC EXAMINATION

CHEST CVS ABDOMEN MUSCULOSKELETAL SYSTEM NUEROLOGICAL EXAMINATION

CRANIAL NERVES MOTOR EXAMINATION PRIMARY NEONATAL REFLEXES SENSORY EXAMINATION

APdia ≈ transverse dia Respiratory distress

Nasal flaring Grunting Tachypnea Intercostal & subcostal retraction

May indicate: Pneumonia RDS Delayed reabsorption of lung fluid Any other cardiorespiratory cause

Auscultation Absent respiratory sounds and presence of

bowel sounds– r/o diaphragmatic hernia

Heart disease: Tacypnea , cyanosis or both

Position of apex beat Congenital diaphragmatic hernia Pneumothorax

Unusual flatness/scaphoid shape of abdomen – congenital diaphragmatic hernia

Visible gastric / bowel patterns indicating ileus or other obstructions

Tenderness of abdomen – necrotising enterocolitis

Developmental dysplasia of hips (DDH) 1 in 800 live births Family history Breech delivery 2 tests Ortolani’s test Barlow maneuver

CRANIAL NERVES MOTOR EXAMINATION PRIMARY NEONATAL REFLEXES SENSORY EXAMINATION

CRANIAL NERVES Responds to soaked peppermint -32wks of gestatn. By 26wks blinks in response to light,at term fixation

and following is well established. Colour vision – 2 months Startles / blinks to loud sound – 28wks. Suck swallow co-ordination -32wks. Suck swallow breathing -34wks.

MOTOR EXAMINATION Minimal resistance to passive manipulation in

all limbs – by 28wks Distinct flexor tone in lower limbs – by 32wks

Differential hypotonia Selective hypotonia in the upper and the

proximal muscle group compared to the lower and distal group

Seen in early phase of hypoxic ischaemic encephalopathy

Ankle clonus Upto 5-10 beats accepted as normal in a

newborn Clonus of more than a few beats beyond 3

months of age is abnormalPlantar response If elicited by thumb nail- flexion response If elicited by pin drag- extension response

MORO REFLEX Best elicited by sudden dropping of baby’s

head in relation to trunk Response consists of opening of the hands

and the extension and abduction af the upper extremities ; followed by anterior flexion (embracing) of upper extremities with an audible cry

Hand opening present by 28wks Extension & abduction by 32wks Anterior flexion by 37wks Audicle cry appears by 32wks Moro reflex disappears by 3-6months in

normal infants

Most common cause of depressed / absent Moro reflex – generalised disturbance of CNS

Most useful abnormality of the Moro reflex to elicit is distinct asymmetry– feature of root plexus or nerve disease

Palmar grasp present by 28wks and strong by 32 wks This allows lifting of baby by 37wks . This

becomes less consistent on development of voluntary grasping at 2months

Elicited by stroking the palmar aspect of the hand taking care that the childs dorsum of hand should not touch examination cot.child grasps the finger.

Tonic neck response Elicited by rotation of the head Causes extension of the upper extremity on

the side to which face is rotatedand flexion of upper extremity on the side of the occiput

This disappears by 6-7 months

Even a neonate of 28wks has the ability to discriminate touch & pain

Pain results in alerting & slight motor activity and then later withdrawal and cry

Jaundice is an important problem in the first week of life

High bilirubin levels may be toxic to the developing CNS and may cause neurological impairment

60 % of term newborn will become visibly jaundiced in the first week of life

Most cases –benign ,no intervention needed

5-10%-clinically significant jaundice

Normal phenomenon in new borns Due to accumulation of unconjugated

bilirubin Appears beyond 1st day of life Peaks in 3-4 days Disappears by 7-10 days in a normal new

born Max. level of bilirubin is less than 12 mg/dl Preterm –it may go upto 14 mg/dl and

duration also will be prolonged(10-14 days)

Appearance of icterus on 1st day of life indicates a highly accelerated production of bilirubin starting from intrauerine life

Commonest cause-Rh or ABO Incompatibility

Aetiology1)The increased bilirubin production due to

break down of fetal RBC’s

2)The immaturity of hepatic conjugating mechanisms to handle bilirubin load

3)Delayed establishment of effective feeding which contribute to increased enterohepatic circulation

4)Defective uptake and excretion of bilirubin by the immature hepatocyte

Most common causes of jaundice depending o its day of appearance:

day 1:blood group incompatibility,usually Rh incompatibility, HS, G6PD

day 2-3:physiological jaundice, crigler najjar

later:sepsis,breast milk jaundice,neonatal cholestasis due to neonatal hepatitis or extra hepatic biliary atresia

Cong. Inf- CMV,rubella,toxo

Icterus in face only:approximately serum bilirubin is 4-6mg%

Icterus up to upper trunk:apprxm serum bilirubin is6- 8 mg%

Icterus upto lower trunk and thighs:8-12 mg%

Icterus upto lower legs and arms:12-14 mg%

Icterus of palms and soles:>15 mg%

Referred to as an elevation of TSB levels to the extent where treatment of jaundice is very likely to result into benefit than harm.

STB levels have been arbitarily defined as pathological if it exceeds 5 mg/dl on first day,10 mg/dl on 2nd day or 15 mg/dl thereafter in term babies

Appearance of jaundice within 24 hrs,TSB levels above expected normal range,presence of clinical jaundice beyond 3 wks and conjugated bilirubin

Due to decreased or delayed feeding ORDue to low volume of milk produced in first

2-3 days appears between 24-72 hrs of age,peaks by

5-15 days of life and disappears by the third week of life

Commonest cause of physiological jaundice

Milk of certain mothers contain some inhibitors of conjugation ( pregnanediol, non esterified long chain fatty acids etc)

So their babies may develop a mild unconjugated hyperbilirubinemia by 2nd or 3rd week of life

Unlikely in the first few days of life as breast milk secretion takes time to establish

These babies must be investigated for prolonged jaundice

A diagnosis should be considered if it is unconjugated(not staining the nappies)

And other causes for prolongation like continuing hemolysis,extravasated blood,G6PD Deficiency and hypothyroidism

Needs no treatment

Very rarely phototherapy may be required

If the breast milk is with held for 48 hrs,the jaundice comes down dramatically

Newborns detected to have yellow discoloration of skin beyond the legs

OR

when their clinically assessed TsB levels approach phototherapy range, should have lab confirmation of TSB

Important causes of jaundice in neoates include:

1)hemolytic:Rh compatibility,ABO incompatibility,G6PD Deficiency,thalassemias,heriditary spherocytosis

2)non hemolytic:prematurity,extravasated blood,inadequate feeding,polycythemia,idiopathic,breast milk jaundice

Is the newborn term or preterm? basic pathophysiology of jaundice is same in term and preterm neonates but babies at lower gestation are at a high risk of dvp brain damage at lower levels Is there any hemolysis? setting of Rh or ABO

Incompatibility,onset of jaundice within 24hrs, presence of pallor, hepatosplenomegaly, presence of haemolysis on the peripheral blood smear, raised reticulocyte count ( more than 8%), rapid rise of bilirubin ( more than 5mg/dl in 24hrs or more than .5mg/dl/hr should raise a suspicion of haemolytic jaundice

Is the baby otherwise sick( sepsis, asphyxia) or healthy?

Presence of lethargy, poor feeding, failure to thrive, hepatosplenomegaly, temp instability or apnoea may be a marker of underlying serious disease

Does the infant have cholestatic jaundice? Presence of dark yellow

urine( staining clothes) or pale coloured stools will suggest cholestatic jaundice

Does the baby have any bilirubin induced brain disfunction( kernicterus) ?

These include presence of lethargy, poor feeding and hypotonia. Advanced signs include seizures, retrocollis, paralysis of upward gaze, and shrill cry

Deposition of free unconjugated bilirubin in basal ganglia and subthalamic nuclei of brain

PHASE1 Poor suck, lethargy, hypotonia, depressed

sensorium, loss of morro,decreased tendon reflexes

PHASE 2 Hypertonia of

extensors,fever,retrocoloitis,opisthotonus,bulging AF,spasm,twitching

PHASE3 High pitched cry, convulsion , death

Choreoathetoid CP Upward gaze palsy SNHL MR Delayed motor skills

Hypoproteinemia

Sulfonamides Acidosis FFA

Asphyxia Prematurity Inf.

Risk factors for development of severe hyperbilirubinemia

2. Jaundice observed in the first 24hr 3. Blood group incompatability with positive

direct antiglobulin test( DCT), other known haemolytic disease( G6PD deficiency)

4. Gestational age- 35-36wks 5. Previous sibling received phototherapy 6. Cephalhaematoma or significant bruising 7. If breast feeding is inadequate with

excessive weight loss

INVESTIGATION1. Serum total bilirubin2. Blood group of mother and baby: detects any

incompatability3. Direct Coombs test: detects presence of

antibody coating on fetal RBCs 4. Indirect Coombs test: detects the presence

of antibodies against fetal RBC in maternal serum

5. Haematocrit decreasd in haemolysis 6. Reticulocyte count: increased in

haemolysis 7. Peripheral smear: evidence of

haemolysis 8. G6PD levels in RBC 9. Others: sepsis screen, thyroid fn tests,

urine for reducing substances to rule out galactosemia, specific enzyme or genetic studies for Crigglar Najjar, Gilbert and other genetic enzyme deficiencies

The parents should be explained about the benign nature of jaundice

The mother should be encouraged to breast feed frequently

The new born should be exclusively breastfed with no top feeds, water or dextrose water

Mother should be told to bring the baby to the hospital if the baby looks deep yellow or palms and soles also have yellow staining

Any new born discharged prior to 72hrs of life should be evaluated again in the next 48hrs for assessment of adequacy of breast feeding and progression of jaundice

PROLONGED JAUNDICE BEYOND 3 WEEKS This is defined as persistence of

significant jaundice( 10mg/dl) beyond 3 weeks in a term baby

The common causes include breastmilk jaundice, extravasated blood, ongoing haemolytic disease, G6PD deficiency and hypothyroidism

INTRAHEPATIC

METABOLIC

Tyrosinemia Galactosemia Gauchers Neiman pick CF Hypothyroidism

HBV,HCV, TORCH

IDIOPATHIC—NENONATAL HEPATITIS

Injury hypoplasia

EHBA Choledochal cyst Bile duct stenosis

Rule out cholestasis by noting the urine and stool colour and checking the level of direct bilirubin

DIAGNOSIS1. Investigations to rule out cholestasis( stool

colour, urine colour, direct and indirect bilirubin levels

2. 2. Investigations to rule out ongoing haemolysis, G6PD screen

3. Investigations to rule out hypothyroidism

4. Investigations to rule out UTI

HEALTHY BABY

BIRTH WEIGHT PHOTOTHERAPY EXCHANGE TRANSFUSION

<1000 gm 5-7 11-13

1001-1500 gm 7-10 13-15

1501-2000gm 10-12 15-18

2001-2500 gm 12-15 18-20

SICK BABY

Gestation PHOTOTHERAPY EXCHANGE TRANSFUSION

<28 5-6 11-14

28-29 6-8 12-14

30-31 8-10 13-16

32-33 10-12 15-18

PHOTOTHERAPY

Phototherapy is the primary treatment in neonates with unconjugated hyperbilirubinemia.

This therapeutic principle was discovered rather serendipitously in England in the 1950s and is now arguably the most widespread therapy of any kind (excluding prophylactic treatments) used in newborns.

PHOTOTHERAPY Unconjugated bilirubin in skin gets

converted into water soluble isomers on exposure to light of a particular wavelength(460-490mm)

These isomers are water soluble, nontoxic and excreted in intestine and urine

For phototherapy to be effective, bilirubin needs to be present in the skin

Phototherapy acts by several ways1. Configurational isomerisation: The z

isomer of bilirubin are converted into E isomers

The reaction is instantaneous upon exposure to light

Reversible as bilirubin reaches the bile duct

After exposure of 8-12hrs of phototherapy this constitutes about 25% of STB which is nontoxic.

As it is excreted slowly it is not a major mechanism for decrease in TSB.

2. Stuctural isomerisation: Its irreversible  intramolecular

cyclization where bilirubin is converted into lumirubin

This is directly proportional to the dose of phototherapy

This product forms 2-6% of TSB which is rapidly excreted from the body

This mainly responsible for phototherapy induced decline in TSB

3. Photo oxidation: This is a minor reaction

Bilirubin converted into small polar products that are excreted in urine

although bilirubin is bleached through the action of light, the process is slow 

TYPES OF LIGHTSpecial blue lamps with a peak output at 460-490nm are the most efficient.

In India CFL phototherapy is most commonly used.

Nowadays blue LED are using instead of CFL as it has long life and is capable of delivering high irradiance.

Efficacy of phototherapy depends upon irradiance, surface area exposed, distance from phototherapy unit, initial TSB level and adequacy of breast feeding.

Sunlight is relatively ineffective because of low blue content of light.

Hyperpyrexia and skinburns occur in prolonged sunlight exposure

Procedure for providing phototherapyRoom temp should be 25-28c

Undress the baby compltly except the diaperCover the eyes with a patch that should not block the eyes.Keep baby at a distance 30-45cm from the light source

Ensure adequate breast feeding. Turn the baby after each feed to expose

maximum surface area of the baby to light Monitor temp every 2-4hrs. Measure TSB level every 12-24hrs. Record body weight daily Ensure that the baby passes adequate amnt

of urine(6-8 times/day).

Phototherapy should be provided continuously except during breast feeding sessions

Discontinue phototherapy when STB falls below age specific phototherapy cut off

Monitor for rebound STB rise after 24hrs of stopping phototherapy for babies with haemolytic disorders

SIDE EFFECTS: Rash, over heating, dehydration and

diarrhoea,hyperthermia,bronze baby,retinal damage,DNA breaks.

HIGH DOSE INTRAVENOUS IMMUNOGLOBULIN:

reduces need for exchange transfusion in hemolytic jaundice such as in Rh or ABO Incompatibility

blocks Fc receptor and inhibit hemolysis The 2004 AAP guidelines suggest a dose-500-

1000 mg/kg as slow infusion over 2 hrs

Double volume exchange transfusion (DVET)should be performed if the TSB levels reach to age specific cutoff for exchange transfusion or if infant has signs of bilirubin encephalopathy.

It is performed by pull and push technique using umbilical venous route.

Indication for DVET at birth in infants with Rh isoimmunisation

-cord bilirubin is 5mg/dl or more -cord Hb is 10g/dl or less.

-Reticulocyte >15% -previous sibling history

PHENOBARBITONE: INDUCES GLUCORONYL TRANSFERASE

ENZYME

THUS IMPROVES CONJUGATION AS WELL AS UPTAKE AND EXCRETION OF BILIRUBIN BY LIVER CELLS

TIN ZINC

Decrease formation of bilirubin by inhibiting heme oxygenase

Babies with serum bilirubin ≥20 mg/dl Those who req.exchange transfusion BERA-3 mnths

Antenatal investigation should include maternal blood grouping. Rh positive baby born to a Rh negative mother is at ahigh risk for hyperbilirubinemia and requires greater monitoring. Anti D injection after first obstetrical event ensures decreased risk of sensitisation in future pregnancies

Ensuring adequate breast feeding Parent education

Parent education regarding danger signs should include yellowish discolouration below knees and elbows or persistent jaundice beyond 15days as reason for immediate check up by health personnel.

High risk babies such as with large cephalhematoma or family history of jaundice should be asked to come for follow up after 3 days of discharge and reassessed

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