This document contains the medical history of a 3-day old male neonate admitted with birth asphyxia and hyperbilirubinemia. It describes the mother's antenatal, natal and postnatal history. On examination, the neonate was found to have birth asphyxia with signs suggestive of hypoxic ischemic encephalopathy (HIE) stage 1 and physiological jaundice. The document discusses perinatal asphyxia, neonatal hypoxia, fetal monitoring techniques and recent advances in management of HIE including therapeutic hypothermia.

2.  B/O G, 3 days old male baby
 1st born of non consanguinous parents
 Informant –mother ,reliability –good
 DOB-9th feb,2017at 5.05 a.m
 Age at examination – 4th day
 Baby did not cry after birth and hence admitted in
NICU

3. ANTENATAL HISTORY
 Age at marriage-23
 No preconceptional Folic acid taken
 Conceived soon after marriage.
 Registered at nearby phc at 3months
Pregnancy detected by UPT at 3 months of
amenorrhea
 LMP -10/5/16 EDD-17/02/17
 Weight gain – 7kg
 Blood Group – O positive

4. 1ST TRIMESTER
 No h/o hyperemesis gravidarum
 No h/o fever / rash / post auricular swelling
 No h/o drug intake, radiation exposure
 No h/o bleeding pv
 Dating scan done at 3 months and said to be normal

5. 2nd TRIMESTER
 Quickenning felt at 5th month. Able to percieve the
fetal movements thereafter
 Took iron and calcium tablets from 4th month
 No h/o bleeding pv
 No h/o PIH/GDM/Anemia complicating pregnancy
 Inj TT 2 doses given at 5th and 7th month
 No Anomaly scan done at 5th month

6. 3rd TRIMESTER
 No h/o PIH/GDM/UTI
 Able to perceive fetal movements well
 USG done at 7th month.No congenital anomalies,no
oligo and polyhydramnios

7. NATAL HISTORY
 Mother developed labour pains on 9th feb at around 1
am,went to nearby PHC and was told to have CPD,and
referred here for safe confinement
 Mother doesn’t know about the rupture of mambranes
and colour of liquor
 Delivered after 4hours,a male baby with birth weight
2.8kg
 Did not cry after birth
 Was resuscitated and admitted in NICU

8. POSTNATAL HISTORY
 Baby was given Expressed breast milk on 2nd day of
birth
 Given to mother for Direct breast feeds on 3rd day
 Developed Jaundice on 3rd day
 No H/o seizures

9. FAMILY HISTORY
23 2 23
Non consanguinous marriage
No h/o hereditary disorders in family members

10. SOCIO ECONOMIC HISTORY
 Thatched house
 4 members in family
 Use fire woods for cooking
 Use bore water for driking
 Toilet facility not available
 Monthly income rs :10000
 Upper lower class

11. SUMMARY
 3days old term neonate,first born to non
consanguinous marriage,AGA with birth asphyxia and
Neonatal hyperbilirubinemia

12. GENERAL EXAMINATION
 Cry & activity –good
 Colour-Icterus + till thighs
 Posture-arms flexed,legs flexed &abducted
 Breathing- abdomino thoracic
 Iv cannula in lt foot

13. VITALS
 Normothermic
 All peripheral pulses felt
 HR-130/min,regular. RR-48/min
 CRT <2sec
 4 limb saturation > 94%

14. ANTHROPOMETRY
 Weight 2.6 Kg , Between 10th and 50th centile
 LENGTH 46cms- Between 10th and 50th centile
 HC-34cms- Between 50th and 90th centile
 CC-31cms

15. HEAD TO FOOT EXAMINATION
 SKIN –icterus till thighs +,no pallor/cyanosis
/haemangioma /mongolian spots/mottling
 HEAD&SKULL – Hair normal,AF –open 2.5:2.5 cm
flat, PF- closed,No cephalhematoma,cranio
tabes,sutures normal
 EYES: opened, no discharge, no hypertelorism,no
cataract
 NOSE: normal

16.  ORAL CAVITY :normal,No asymmetry ,No cleft lip or
palate
 EARS-Well curved pinna,good recoil
 NECK :Normal
 Chest-breast bud and areola normal,No retractions
 Abdomen no distension ,Umbilical cord healthy
 BACK –normal,No sacral dimple/tuft of hair
 Genitalia – B/L testes descended,Scrotum good
rugosity
 Anus- normal and patent

17.  Limbs normal
 Hip-ortolani,Barlow negative

18. SYSTEMIC EXAMINATION
 CARDIOVASCULAR SYSTEM:
Inspection: no chest wall deformity
Apical impulse @ left 5th ICS Lat to MCL
no subcostal retractions/intercostal retractions
palpation: inspectory findings confirmed
auscultation: S1 S2 heard
no murmurs.

19.  RESPIRATORY SYSTEM:
Chest wall moves symmetrically with
respiration.
RR – 48/min
Normal vesicular breath sounds heard.
Bilateral air entry +.
No added sounds.

20. ABDOMEN
All quadrants move equally with respiration
Liver palpable 1 cm below RCM,soft and rounded
Spleen not palpable
Hernial orifices free
Renal angle free
Umbilical cord clamped and Health
Bowel sounds +

21. NEUROLOGICAL EXAMINATION
 Alert
 Upper limb flexed at elbow,lower limbs flexed at both
hip and knee
 Does not Fix and follows light
 After stimulation, has a sustained cry
 Startle response +

22. CRANIAL NERVE EXAMINATION
 Does not fix on light
 Blinks on showing light
 red reflex (+),B/L Pupils equally reacting to light
 Dolls eye movement(+)
 No facial deviation while crying
 sucking and swallowing +
 Palatal movement equal,uvula centre
 Good cry volume+

23. Motor Examination
 Arm Recoil – Brisk
 Popliteal angle – 90degrees
 Scarf sign – Elbow does not reach midline
 Heel to ear –90 degrees
 180 degree flip test – Pulled to sit,head lag +,
 Ventral suspension – Head flexed,Arms and legs
extended
 Prone – Hips and knees flexed

24. NEONATAL REFLEXES
 Sucking ,rooting present
 Grasp reflex present
 Stepping,placing present
 ATNR(+)
 Moro reflex+
 Galant reflex+
 DTR – Biceps,Knee and Ankle +
 Sperficial Reflexes – Plantar – withdrawal response

25. Diagnosis
 3 days old Term/AGA/Male neonate with Birth
asphyxia with HIE sequelae ,Probably stage 1 with
physiological jaundice

26. DISCUSSION
Perinatal asphyxia
condition during the first and second stage of labour in
which impaired gas exchange leads to fetal hypoxaemia &
hypercarbia
identified by fetal acidosis as measured in umbilical
artery pH.
Neonatal hypoxia, ischaemia & asphyxialack of o2 ,blood
flow & gas exchange to fetus or newborn
Neonatal encephalopathy
describes an abnormal neurobehavioural state
consisting of decreased level of consciousness and usually
other signs of brain stem and/or motor dysfunction

27. Hypoxic- ischaemic encephalopathy
neonatal encephalopathy following severe birth
asphyxia or perinatal hypoxia
Hypoxic- ischaemic brain injury
refers to neuropathology attributable to hypoxia
and/or ischaemia as is evidenced by biochemical (CK-
BB), EEG,Neuroimaging,MRI, CT or pathologic
abnormalities.

28. ETIOLOGY
• Maternal factors:
hypertension( acute or chronic), hypotension,
infection(chorioamnionitis), diabetes, hypoxia from pulmonary or
cardiac disorders.
• Placental factors:
abnormal placentation,abruption, infarction, fibrosis
• Uterine factors: Rupture
• Umbilical cord accidents: entanglement, prolapse, true knot,
compression
• Fetal factors: anaemia, infection, etc
• Neonatal factors: cyanotic congenital heart disease,
PPHN,Cardiomyopathy.

30. CLINICAL FEATURES
 Encephalopathy- must have depressed consiousness
whether mild,moderate or severe
Mild-hyperalert or jittery state
Moderate & severe-more impaired responses to stimuli
such as light,touch or even noxious stimuli
 Brain stem dysfunction-abnormal or absent brain stem
reflexes(pupillary,corneal,oculo cephalic,cough & gag
reflex)

31.  Motor abnormalities-generalised hypotonial,weakness
& abnormal posture with lack of flexor
tone(symmetric)over days to weeks initial hypotonia
may evolve into spasticity & hyperreflexia
 Seizures-50% of newborns,start within 24hrs of HI
insult.seizures may be subtle tonic or clonic.EEG-gold
standard for diagnosing neonatal seizures particularly
in HIE
 Increased ICP-result from diffuse cerebral edema-
reflects extensive cerebral necrosis-poor prognosis

32. MULTIORGAN DYSFUNCTION
Kidney-Most commonly
affected
Proximal tubule affected by
decreased perfusion-ATN with
oliguria
cardiac Transient MI.ECG-ST depression in mid
precardium & T inversion in left
precardium
GIT Increased risk of bowel ischemia & NEC
Haematology DIC(damage to blood vessels),poor
production of clotting factors &
platelets
Liver dysfunction Isolated elevation of hepatocellular
enzymesDIC,hypoglycemia etc..
Pulmonary effects Increased PVR-PPHN ,pulmonary
hemorrhage,pulmonary edema etc..

33. SARNAT AND SARNAT STAGING

34. LEVENE GRADING OF HIE
FEATURE
S
MILD MODERAT
E
SEVERE
Consiousness irritable Lethargic comatose
Tone Some
hypotonia
Moderate
hypotonia
Severe
hypotonia
Seizures NIL present persistent
Sucking/breat
hing
Poor suck Unable to suck Unable to
sustain
spontaneous
breathing

35. Is it the birth asphyxia causing the
hypoxia or the Intrauterine chronic
hypoxia due to fetal causes causing
birth asphyxia ?????

36. PRIMARY Vs SECONDARY APNEA

37. FETAL MONITORING
 Fetal activity record
 Human placental lactogen
 Estriol
 Nonstress Monitoring
 Oxytocin challenge test
 Fetal biophysical profile
 Doppler velocimetry studies
 Fetal scalp Blood monitoring

38. NON STRESS TEST
 Fetal heart rate
 Uterine contractions
 Fetal movements

42. CARDIOTOCOGRAPHY
 Electronic fetal monitoring
 FH recorded by external transducer using usg doppler

43. Baseline variability
 Normal baseline variability 5 – 25 bpm
 Non-reassuring baseline var. - < 5 bpm
for > 40 min but < 90 min
 Abnormal baseline var. < 5 bpm for 90 min

44. Baseline variability is reduced in
the following
 Reduced baseline variability is seen in fetal hypoxiaemia
and when combined with deceleration it is evidence of fetal
acidosis
 Analgesic drug in labour
 Narcotics in labour
 MgSO4 when given for eclampsia & PTL

45. Accelerations occur during labour and it is very
reassuring
 Often asso. with fetal movements
 Can occur without any stimulation in labour
 Fetal stimulation during pelvic examination
 Fetal scalp blood sampling.
(ab.of such .acc. during labour however is not necessarily an
unfavourable sign unless coincidental with other non
reassuring changes)

46. (type-1) Early deceleration
 Pressure exerted on the head during contr. sti. para
sym. causing slowing of FHR(due to vagal sti.)
 Occurs early with respect to Ut. contr. The nadir of
deceleration corresponds to peak of contr. & return
to baseline with the end of contr.

47. Late deceleration (type-2)
 Commences after onset of contr., reaches nadir after peak of
contr. & FRH returns to baseline after contr. has passed away.
 Occurs in placental insuffi. like HT, PE

48. Variable deceleration (Type III)
 Commonest type seen during labour due to cord compression
 Variable in shape, size and timing in reference to Ut. contr.
 Depends on if umb vein compression or vein + artery – variable
dece
It is ≥ 15bpm in amplitude & lasting ≥ 15 acc – 2mts

49. BIOPHYSICAL PROFILE

53. Ominous sign
 Absence of Umbilical artery end diastolic flow
 Reversal of flow
 Indicator of fetal hypoxia or acidemia

54. RECENT ADVANCES IN HIE

55. SIGNIFICANT PREDICTORS OF HIE
 Chest compressions for more than 1 minute
 Onset of respiration after 20 mins
 Base deficit in cord blood more than 16mmol/l
 Risk of adverse outcome 93% when all 3 present

56. BIOMARKERS
 CLINICAL PARAMETERS –
Sarnat stage I – Normal neurological
outcome,Mortality 1 %
Stage II – Mortality 20% - 37%
Stage III- Mortality or morbidity almost 100%
Apgar score and cord ABG not precise

57. SEROMARKERS
 Under trial
 S100B
 Neuron specific enolase
 IL 1B,IL 6

58. MRI and MRS
 Abnormal signal intensity in the posterior limb of
Internal capsule
 Basal ganglia and thalamic signal abnormalities
 Severe white matter abnormalities
 Deep grey matter Lactate/NAA –MR biomarker with
sensitivity 82% and specificity 95%

59. aEEG
 Abnormal aEEG at 48 to 72 hrs predicts adverse
neurodevelopmental outcomes and sooner the
abnormalities disappear better the prognosis
 Sensitivity 93%and Specificity 90%
 Good neurodevelopmental outcomes if onset of SWC
before 36hrs
 Normalisation of aEEG takes lesser time in non cooled
infants than those treated with Hypothermia

60. Other Electrophysiological studies
 VEP
 BERA
 SEP
 Have prognostic value

61. Near Infrared Spectroscopy [NIRS]
 Bedside and noninvasive technique
 To moniter cerebral oxygenation stsus in HIE
 Under evaluation

66. EXCLUSION CRITERIA
Inability to initiate cooling by 6 hrs of age
Major congenital abnormality
Major chromosomal abnormality
Severe growth restriction(<1800 g BW)
Infant is moribund and will not receive
any further aggressive treatment
Refusal of consent by parent
Refusal of consent by consulting neonatologist

68. NEURO PROTECTIVE STRATEGIES

69. XENON
 NMDA antagonist,inhibits AMPA and kainate
receptors
 Reduction in NT release and inhibition of apoptosis
 Neuroprotective and synergistic with Hypothermia in
HIE
 Very expensive and requires special ventilators

70. ERYTHROPOIETIN[Epo]
 Hematopoetic growth factor
 Neuroprotective,Anti inflammatory and anti apoptotic
 Safe dose -300 or 500 U/Kg every other day
 Improves neurological outcome at 18 m in moderate
HIE

71. N – ACETYL CYSTEINE
 Free radical scavenger
 Restores Glutathione,attenuates reperfusion
injury,decreases inflammation and NO production
 Decreases incidence of PVL in preterm infants by 39%

72. MELATONIN
 Free radical scavenger
 Indirect antioxidant
 Neuroprotective and synergistic with hypothermia in
HIE

73. ANTICONVULSANTS
 Prophylactic Phenobarbitone – before cooling is
ineffective
 Topiramate – modulates AMPA,GABA A ion
channels,Na and Ca channels,Neuroprotective
 Levitiracetam – Regulates AMPA and NMDA mediated
excitatory synaptic transmission

74. ALLOPURINOL
 Inhibits Xanthine oxidase
 Free radical scavenger
 Decrease reperfusion injury and brain damage
 More trials needed

75. MAGNESIUM SULPHATE
 Naturally occuring NMDA receptor antagonist
 Decreases inflammatory cytokines,platelet
aggregationand essential for glutathione synthesis
 Postnatal MgSO4 improves short term neurological
outcome in term infants with perinatal asphyxia

76. Strategies under Consideration
 Drugs – Indomethacin,Bumetanide,Sodium
cromoglycate,Minoclcline,Pomegranate polyphenols,2
–immunobiotin,necrostatin
 Growth factors – Nerve GF,Insulin like GF 1,Brain
derived neurotrophic factor
 Cord blood SCT –Immunomodulation,release of
growth factors,anti apoptotic mechanisms
 Brain tonics [Piracetam] – widely used without any
scientific basis

77. POINTS TO PONDER
 HIE is a common cause of neonatal morbidity and
mortality
 Adequate intensive care and supportive measures will
improve neurodevelopmental outcome
 Therapeutic hypothermia has become the standard of care
in developed countries,but yet to become a routine clinical
practice in India
 Other nover neuroprotective therapies are under
investigations
 Apart from clinical parameters,EEG and MRI are a great
value in assessing the severity of HIE and predicting the
long term neurodevelopmental outcome

78. Reference
 INDIAN JOURNAL OF PRACTICAL PEDIATRICS •
IJPP is a quarterly subscription journal of the Indian
Academy of Pediatrics committed to presenting
practical pediatric issues and management updates in
a simple and clear manner
 Indexed in Excerpta Medica, CABI Publishing.
 Vol.16 No.3 JUL.- SEP. 2014

79. THANKYOU