2. DEFINITION
It is the term used to designate the clinical and
neuropathological findings of an encephalopathy that
occurs in a full term infant who has experienced a
significant episode of intrapartum asphyxia.
3. Etiology of HIE
• Maternal:
– Cardiac arrest
– Asphyxiation
– Severe anaphylaxis
– Status epilepticus
– Hypovolemic shock
• Uteroplacental:
– Placental abruption
– Cord prolapse
– Uterine rupture
– Hyperstimulation with
oxytocic agents
• Fetal:
– Fetomaternal hemorrhage
– Twin to twin transfusion
– Severe isoimmune hemolytic
disease
– Cardiac arrhythmia
4. • Fifteen to 20% of infants with hypoxic-ischemic
encephalopathy (HIE) die in the neonatal period, and
25–30% of survivors are left with permanent
neurodevelopmental abnormalities (cerebral palsy,
mental retardation)
6. (1) inadequate oxygenation of maternal blood from
hypoventilation during anesthesia, cyanotic heart
disease, respiratory failure, or carbon monoxide
poisoning;
(2) low maternal blood pressure from acute blood loss,
spinal anesthesia, or compression of the vena cava and
aorta by the gravid uterus;
(3) inadequate relaxation of the uterus to permit placental
filling as a result of uterine tetany caused by the
administration of excessive oxytocin;
(4) premature separation of the placenta;
(5) impedance to the circulation of blood through the
umbilical cord as a result of compression or knotting of
the cord; and
(6) placental insufficiency from toxemia or postmaturity.
7. Hypoxic-Ischemic Encephalopathy in Term Infants
SARNAT AND SARNAT STAGING
SIGNS STAGE 1 STAGE 2 STAGE 3
Level of consciousness Hyperalert Lethargic Stuporous, coma
Muscle tone Normal Hypotonic Flaccid
Posture Normal Flexion Decerebrate
Tendon reflexes/clonus Hyperactive Hyperactive Absent
Myoclonus Present Present Absent
Moro reflex Strong Weak Absent
Pupils Mydriasis Miosis Unequal, poor light
reflex
Seizures None Common Decerebration
EEG Normal Low voltage changing
to seizure activity
Burst suppression to
isoelectric
Duration <24 hr if progresses;
otherwise, may remain
normal
24 hr to 14 days Days to weeks
Outcome Good Variable Death, severe deficits
8. Due to ischemia, anaerobic
Excitatory and toxic amino
ATP, failure of NaK ATPase
pump, depolarization of
metabolism, lactate &
acids, particularly
inorg.phosphates accumulate
Ca by activating xanthine
oxidase, N2O,PGs release
glutamate, accumulate in
neuronal cells, influx of Ca, Na&
Ca the osmotic activates damaged influx proteases tissue
of water
&
lipases which generates
Damage to cell
membranes &
free radicals
Diving sea reflex-
02 free radicals
Redistribution of blood to
infarction
more vital organs
12. Diagnosis
• There is no clear diagnostic test for HIE
• Abnormal findings on the neurologic exam in the
first few days after birth is the single most useful
predictor that brain insult has occurred in the
perinatal period
• Essential Criteria for Diagnosis of HIE:
– Metabolic acidosis (cord pH <7 or base deficit of >12)
– Early onset of encephalopathy
– Multisystem organ dysfunction
13. INVESTIGATIONS
• Exclude other causes of acute resp. distress
• Chest X ray- to exclude pneumothorax, CDH,
Congenital pneumonia
• Sepsis screening and bl. Culture
• Serum electrolytes
Hyponatremia – SIADH
Hyperkalemia – acute renal shutdown/ tissue
catbolism
Hyperphosphatemia, hypocalcemia – tissue injury
BUN & CREATININE, LACTATE, PYRUVATE, BRAIN
SPECIFIC CREATINE KINASE, HYPOXANTHINE, NON-ESTERIFIED
FFA
14. • Amplitude-integrated EEG (aEEG)
– When performed early, it may reflect dysfunction
rather than permanent injury
– Most useful in infants who have moderate to severe
encephalopathy
• Marginally abnormal or normal aEEG is very reassuring of
good outcome
• Severely abnormal aEEG in infants with moderate HIE raises
the probability of death or severe disability from 25% to
75%
15. • CRANIAL ULTRASOUND
On 2, 7,21 days & before discharge to ruleout
IVH. It shows echogenic focus head of caudate
or caudothalamic notch.
CT SCAN after 2 wks to prevent radiation
damage.
MRI: Most appropriate technique and is able to show
different patterns of injury. Presence of signal abnormality in
the internal capsule later in the first week has a very high
predictive value for neurodevelopmental outcome
16. MANAGEMENT
• TABC
• IV fluids – first 48hrs 10% dextrose to prevent
hypoglycemia
• Maintain 2/3 rd of fluid to prevent SIADH
• Ca gluconate 2ml/kg for 2 days
• 7.5% NaHCo3, 2-3ml/kg diluted with equal vol. of
distilled water or 5%D
• Hypotension by inotropes like dopamine, dobutamine
• Avoid mannitol- worsen due to endothelial damage in
HIE.
• Prophylactic Phenobarbitone to combat seizures.
17. Criteria for Hypothermia
• Hypothermia is not effective for every baby
– Currently only used in infants > 35 weeks
• Time interval between birth and initiation of
treatment important
– Treatment must be started within 6 hours of birth to be
effective
19. Hypothermia - Mechanism of Action
• Reduces cerebral metabolism, prevents edema
• Decreases energy utilization
• Reduces/suppresses cytotoxic amino acid accumulation
and nitric oxide
• Inhibits platelet-activating factor, inflammatory cascade
• Suppresses free radical activity
• Attenuates secondary neuronal damage
• Inhibits cell death
• Reduces extent of brain damage
– DEATH OR SEVERE DISABILITY AT 18 MONTHS OF AGE SIGNIFICANTLY
REDUCED!!
– Brain cooling DONE UPTO 72hrs.
20. CONTRAINDICATIONS TO COOLING
· Infants likely to require surgery during
first three days after birth
· Other abnormalities indicative of poor
long term outcome are present
e.g. structural anomalies
· Appears moribund
22. • Brain death after neonatal HIE is diagnosed
by the clinical findings of coma unresponsive
to pain, auditory, or visual stimulation; apnea
with Pco2 rising from 40 to over 60 mm Hg
without ventilatory support; and absent
brainstem reflexes (pupil, oculocephalic,
oculovestibular, corneal, gag, sucking). These
findings must occur in the absence of
hypothermia, hypotension, and elevated
levels of depressant drugs (phenobarbital).
