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 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 50cms
Head circumference :
 33-37cms at birth
Chest 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 FONTANELLES
Molding –
 Gives the impression of a cliff with rise on
one side and a sharp fall on the other side
Synostosis -
 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% ;
hyperbilirubinaemi
a
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 abnormal
Plantar 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
 Aetiology
1)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
OR
Due 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,bu
lging 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
 INVESTIGATION
1. Serum total bilirubin
2. Blood group of mother and baby: detects any
incompatability
3. 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
DIAGNOSIS
1. 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 ways
1. 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 LIGHT
Special 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
phototherapy
Room temp should be 25-28c
Undress the baby compltly except the
diaper
Cover 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
Thank
you

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.Newborn

  • 1.
  • 2.  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
  • 3.  Least disturbing examination should be done first  Assess the state,posture, spontaneous activity, colour, any obvious respiratory distress or malformations
  • 4. 5 states of an infant are:  Deep sleep  Light sleep  Awake & quiet  Awake & active  Awake & crying
  • 5. 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
  • 7. 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
  • 8. BP  Flush method  Doppler monitoring  Direct intravascular measurement
  • 9. 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
  • 10.  LOW BIRTH WT : <2.5KG  VERY LOW BIRTH WT :<1.5KG  EXTREMELY LOW BIRTH WT : <1KG
  • 11.  Aberrant growth pattern is assessed by plotting the wt against the GA on a standard intrauterine growth curve
  • 12. 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
  • 13. Length :  abt 50cms Head circumference :  33-37cms at birth Chest circumference :  3cm less than head circumference  If the difference is more than 3cm -- IUGR
  • 14. Ponderal Index  Wt(gm)/length(cm3) x 100  <2 – asymmetrical growth retardation  ≥2 – normal or symmetrical growth retardation
  • 15. 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
  • 16. 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
  • 17.  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
  • 18. HEAD AND FONTANELLES Molding –  Gives the impression of a cliff with rise on one side and a sharp fall on the other side Synostosis -  Feels like a mountain range with rise on both sides of elevation
  • 19. Craniotabes –  Skull feel soft like a ping pong ball  Due to delayed ossification and resorption of bones  Benign condition in neonates that resolves spontaneously
  • 20.  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
  • 21.  Associated with linear fracture of skull bone in 5 – 25% ; hyperbilirubinaemi a
  • 22. Large fontanelles and split sutures :  Raised ICP  Certain chromosomal abnormalities  Hypothyroidism  Impaired bone growth like osteogenesis imperfecta
  • 23. 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
  • 24.  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
  • 25.  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
  • 26. 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
  • 27.  Spine – spina bifida . Masses and scoliosis  Anal opening – for patency and position
  • 28. GENITALIA (MALE & FEMALE)  Examined by hips abducted in the supine position  Urethra- patency  Clitoris - clitoromegaly
  • 29. EXTREMITIES  Make sure that arms and limbs are fully movable  Nail hypoplasia , syndactyly , polydactyly , oligodactyly , unequal limbs  CTEV – calcaneovalgus / equinovarus deformity
  • 31.  CHEST  CVS  ABDOMEN  MUSCULOSKELETAL SYSTEM  NUEROLOGICAL EXAMINATION  CRANIAL NERVES  MOTOR EXAMINATION  PRIMARY NEONATAL REFLEXES  SENSORY EXAMINATION
  • 32.  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
  • 33. Auscultation  Absent respiratory sounds and presence of bowel sounds– r/o diaphragmatic hernia
  • 34.  Heart disease:  Tacypnea , cyanosis or both  Position of apex beat  Congenital diaphragmatic hernia  Pneumothorax
  • 35.  Unusual flatness/scaphoid shape of abdomen – congenital diaphragmatic hernia  Visible gastric / bowel patterns indicating ileus or other obstructions  Tenderness of abdomen – necrotising enterocolitis
  • 36.  Developmental dysplasia of hips (DDH)  1 in 800 live births  Family history  Breech delivery  2 tests  Ortolani’s test  Barlow maneuver
  • 37.  CRANIAL NERVES  MOTOR EXAMINATION  PRIMARY NEONATAL REFLEXES  SENSORY EXAMINATION
  • 38.  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.
  • 39.  MOTOR EXAMINATION  Minimal resistance to passive manipulation in all limbs – by 28wks  Distinct flexor tone in lower limbs – by 32wks
  • 40. 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
  • 41. 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 abnormal Plantar response  If elicited by thumb nail- flexion response  If elicited by pin drag- extension response
  • 42. 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
  • 43.  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
  • 44.  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
  • 45.
  • 46. 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.
  • 47. 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
  • 48.
  • 49.  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
  • 50.
  • 51.  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
  • 52.
  • 53.  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)
  • 54.  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  Aetiology 1)The increased bilirubin production due to break down of fetal RBC’s
  • 55. 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
  • 56.  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
  • 57.  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%
  • 58.
  • 59.  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
  • 60.  Due to decreased or delayed feeding OR Due 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
  • 61.  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
  • 62.  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
  • 63.  Needs no treatment  Very rarely phototherapy may be required  If the breast milk is with held for 48 hrs,the jaundice comes down dramatically
  • 64.  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
  • 65.  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
  • 66.  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
  • 67.  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
  • 68.  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
  • 69.  Deposition of free unconjugated bilirubin in basal ganglia and subthalamic nuclei of brain
  • 70.  PHASE1  Poor suck, lethargy, hypotonia, depressed sensorium, loss of morro,decreased tendon reflexes  PHASE 2  Hypertonia of extensors,fever,retrocoloitis,opisthotonus,bu lging AF,spasm,twitching  PHASE3  High pitched cry, convulsion , death
  • 71.  Choreoathetoid CP  Upward gaze palsy  SNHL  MR  Delayed motor skills
  • 72.  Hypoproteinemia  Sulfonamides  Acidosis  FFA  Asphyxia  Prematurity  Inf.
  • 73. 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
  • 74.  INVESTIGATION 1. Serum total bilirubin 2. Blood group of mother and baby: detects any incompatability 3. 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
  • 75.  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
  • 76.
  • 77.  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
  • 78. 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
  • 79.  INTRAHEPATIC  METABOLIC  Tyrosinemia  Galactosemia  Gauchers  Neiman pick  CF  Hypothyroidism
  • 80.  HBV,HCV,  TORCH  IDIOPATHIC—NENONATAL HEPATITIS
  • 82.  EHBA  Choledochal cyst  Bile duct stenosis
  • 83.  Rule out cholestasis by noting the urine and stool colour and checking the level of direct bilirubin DIAGNOSIS 1. Investigations to rule out cholestasis( stool colour, urine colour, direct and indirect bilirubin levels 2. 2. Investigations to rule out ongoing haemolysis, G6PD screen
  • 84.  3. Investigations to rule out hypothyroidism  4. Investigations to rule out UTI
  • 85.  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
  • 86. 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
  • 87.  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.
  • 88.
  • 89.  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
  • 90.  Phototherapy acts by several ways 1. 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.
  • 91.  As it is excreted slowly it is not a major mechanism for decrease in TSB.
  • 92.  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
  • 93.  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 
  • 94. TYPES OF LIGHT Special 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.
  • 95.  Efficacy of phototherapy depends upon irradiance, surface area exposed, distance from phototherapy unit, initial TSB level and adequacy of breast feeding.
  • 96.  Sunlight is relatively ineffective because of low blue content of light.  Hyperpyrexia and skinburns occur in prolonged sunlight exposure
  • 97. Procedure for providing phototherapy Room temp should be 25-28c Undress the baby compltly except the diaper Cover the eyes with a patch that should not block the eyes. Keep baby at a distance 30-45cm from the light source
  • 98.
  • 99.  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).
  • 100.  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
  • 101. SIDE EFFECTS:  Rash, over heating, dehydration and diarrhoea,hyperthermia,bronze baby,retinal damage,DNA breaks.
  • 102.
  • 103.
  • 104.
  • 105.  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
  • 106. 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.
  • 107. 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
  • 108.
  • 109. PHENOBARBITONE: INDUCES GLUCORONYL TRANSFERASE ENZYME THUS IMPROVES CONJUGATION AS WELL AS UPTAKE AND EXCRETION OF BILIRUBIN BY LIVER CELLS
  • 110.  TIN  ZINC  Decrease formation of bilirubin by inhibiting heme oxygenase
  • 111.
  • 112.  Babies with serum bilirubin ≥20 mg/dl  Those who req.exchange transfusion  BERA-3 mnths
  • 113.  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
  • 114.  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