HYPOXIC ISCHEMIC

ENCEPHALOPATHY
DR. MANSOOR
ELAHI

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.

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

 Fifteen to 20% of infants with hypoxicischemic encephalopathy (HIE) die in

the neonatal period, and 2530% of
survivors are left with permanent
neurodevelopmental abnormalities
(cerebral palsy, mental retardation)

FETAL HYPOXIA CAUSED BY

VARIOUS DISORDERS IN
MOTHER

(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.

Hypoxic-Ischemic Encephalopathy in Term Infants

SARNAT AND SARNAT STAGING
SIGNS
Level of
consciousness
Muscle tone
Posture
Tendon
reflexes/clonus
Myoclonus
Moro reflex
Pupils

STAGE 1
Hyperalert

STAGE 2
Lethargic

STAGE 3
Stuporous, coma

Normal
Normal
Hyperactive

Hypotonic
Flexion
Hyperactive

Flaccid
Decerebrate
Absent

Present
Strong
Mydriasis

Present
Weak
Miosis

Seizures
EEG

None
Normal

Duration

<24 hr if
progresses;
otherwise, may
remain normal
Good

Common
Low voltage
changing to
seizure activity
24 hr to 14 days

Absent
Absent
Unequal, poor
light reflex
Decerebration
Burst suppression
to isoelectric

Outcome

Variable

Days to weeks

Death, severe
deficits

Patho physiology of HIE`s

Due to ischemia,
Excitatory
and toxic
anaerobic
metabolism,
amino
ATP, failure acids,
of NaK ATPase
lactate
&
pump,
depolarization
of
particularly
Ca
by
activating
inorg.phosphates
Ca activates
neuronal
cells, influx of
glutamate,
xanthine
oxidase,
accumulate
Ca,
Na&
osmotic
proteasesinflux
& of

accumulate in the
water
N2O,PGs
release
free
Damage
to
cell
lipases
which
Diving
sea reflexdamaged
tissue
radicals
membranes
generates 02
&
free
Redistribution
of
radicals
blood
to more
infarction
vital organs

Potential pathways for brain injury after

hypoxia-ischemia.

MULTIORGAN SYSTEMIC EFFECTS OF

ASPHYXIA
SYSTEM
EFFECT
Central nervous system Hypoxic-ischemic encephalopathy,
infarction, intracranial hemorrhage,
seizures, cerebral edema, hypotonia,
hypertonia
Cardiovascular
Myocardial ischemia, poor contractility,
cardiac stun, tricuspid insufficiency,
hypotension
Pulmonary
Pulmonary hypertension, pulmonary
hemorrhage, respiratory distress
syndrome
Renal
Acute tubular or cortical necrosis
Adrenal
Adrenal hemorrhage
Gastrointestinal
Perforation, ulceration with hemorrhage,
necrosis
Metabolic
Inappropriate secretion of antidiuretic
hormone, hyponatremia, hypoglycemia,
hypocalcemia, myoglobinuria

What is
the
diagnosis
?

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

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

 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%

 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

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.

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

COOL CAP

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.

CONTRAINDICATIONSTOCOOLING

Infantslikelyto requiresurgeryduring first

three daysafter birth
Otherabnormalitiesindicativeofpoor
longtermoutcomearepresent
e.g.structuralanomalies
Appearsmoribund

Newer Treatment modalities:

 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).