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Hypoxic-Ischemic

Encephalopathy
DR. MAHMOUD MOHAMED OSMAN
MBBCH, MSc (Pedia), MRCPCH (UK), FRCP (Edinburgh)
Consultant Pediatrician & Neonatologist
Al Yammamah Hospital, MOH
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Hypoxic-Ischemic Encephalopathy…………..

LEARNING OBJECTIVES:

 Introduction
 Definition
 Risk factors
 Causes
OF HYPOXIC-ISCHEMIC
 Pathophysiology
ENCEPHALOPATHY
 Clinical features
 Diagnosis
 Managament
 Prognosis

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Hypoxic-Ischemic Encephalopathy…………..

INTRODUCTION:
 Anoxia is a term used to indicate the consequences of complete
lack of oxygen as a result of a number of primary causes.
 Hypoxemia refers to decreased arterial concentration of oxygen.
 Hypoxia refers to a decreased oxygenation to cells or organs.
 Ischemia is insufficient blood flow to cells or organs that to
maintain their normal function.
 Hypoxic-ischemic encephalopathy Is an abnormal neurobehavioral
state in which the predominant pathogenic mechanism is impaired
cerebral blood flow that may result in neonatal death or be
manifested later as cerebral palsy or developmental delay.

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Hypoxic-Ischemic Encephalopathy…………..

• Despite major advances in fetal monitoring technology


and knowledge of fetal and neonatal pathologies;
hypoxic-ischemic encephalopathy (HIE), remains a
serious condition that causes significant mortality and
long-term morbidity.
ETIOLOGY
• Asphyxia can occur in the antepartum or intrapartum
period as a result of impaired gas exchange across the
placenta.
• That leads to the inadequate provision of oxygen and
removal of carbon dioxide and hydrogen from the fetus.
• Asphyxia can also occur in the postpartum period, usually
secondary to pulmonary, cardiovascular, or neurologic
abnormalities.
• Hypoxic-ischemic encephalopathy is characterized by
clinical and laboratory evidence of acute or subacute brain
injury due to asphyxia (hypoxia, ischemia, and acidosis).
• Most often, the exact timing and underlying cause remain
unknown
Hypoxic-Ischemic Encephalopathy…………..

RISK FACTORS

Preconceptual Antepartum Intrapartum


• IDDM • Severe pre- • Breech
• Thyroid disease eclampsia • Cord prolapse
• Fertility • Placental • Emergency
treatments abruption C-section
• Nulliparity • IUGR • Induction
• Advanced • Antepartum • Maternal
maternal age. haemorrhage pyrexia
CAUSES OF FETAL HYPOXIC-ISCHEMIC INSULT:

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Pathophysiology
 After an episode of hypoxia and ischemia,
anaerobic metabolism occurs and generates
amounts of lactate, inorganic phosphates,
glutamate, free radicals and nitric oxide.
 The initial circulatory response of the fetus is
transient maintenance of perfusion of the
brain, heart, and adrenals in preference to
the lungs, liver, kidneys, and intestine.

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Pathophysiology……….

Cardiovascular Response to Asphyxia


Pathophysiology……….

 The pathology of hypoxia-ischemia depends on the


affected organ and the severity of the injury; these lead to
signs of coagulation necrosis and cell death.
 Term infants demonstrate neuronal necrosis of the cortex
and parasagittal ischemic injury, that manifest clinically as
cortical atrophy, focal seizures and hemiplegia.

 Preterm infants demonstrate Periventricular leukomalacia


(later, spastic diplegia), basal ganglia injury, and IVH.
 If fetal distress produces gasping, the amniotic fluid
contents (meconium, squames, lanugo) are aspirated into
the trachea or lungs.

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Pathophysiology……….

Patterns of brain injury in hypoperfusion:

 The premature neonatal brain


has a ventriculopetal vascular
pattern, and hypoperfusion
results in a periventricular border
zone of white matter injury.

 The term infant, develops a


ventriculofugal vascular pattern
as the brain matures, and the
border zone during hypoperfusion
is more peripheral with subcortical
white matter and parasagittal
cortical injury. Premature Term
Parasagittal Watershed Area (Mature baby)

The parasagittal parenchyma (the watershed zone) is at risk for


ischemic injury from hypoperfusion
Clinical Manifestations:
 Continuous fetal heart rate recording may reveal a slow
heart rate; or variable or late deceleration.
 These signs should lead to giving high oxygen to the
mother and consideration of immediate delivery to avoid
fetal death and CNS damage.
 The presence of meconium-stained amniotic fluid is
evidence that fetal distress has occurred.
 At birth, affected infants may be depressed and may fail
to breathe spontaneously; with pallor, cyanosis, a slow
heart rate, and unresponsiveness to stimulation.
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Clinical Manifestations…………
Clinical Manifestations………..

 During the next hours, they may remain


hypotonic, change to a hypertonic state, or to a
normal tone.
 Cerebral edema may develop and result in
profound brainstem depression.
 During this time, seizure activity may occur;
it may be severe and refractory to the usual
doses of anticonvulsants.
 Seizures in asphyxiated newborns may also be
due to hypocalcemia, hypoglycemia, or infection.
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Clinical Manifestations………..

 Heart failure and cardiogenic shock, respiratory


distress syndrome, gastrointestinal perforation,
and acute tubular necrosis may occur
(multiorgan failures).
 The severity of neonatal encephalopathy
depends on the duration and timing of injury.
Symptoms develop over a series of days.

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Clinical Manifestations………..

Clinical Staging of Hypoxic-Ischemic Encephalopathy:

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Multi-organ injuries
as consequences of

hypoxic-ischemic
encephalopathy
Diagnosis
Criteria for diagnosis of HIE:
 Profound metabolic or mixed acidemia (pH < 7)
in an umbilical artery blood sample, if obtained.
 Persistence of an Apgar score of 0-3 for longer
than 5 minutes.
 Neonatal neurologic sequelae.
(seizures, coma, hypotonia)
 Multiple organ involvement.
(kidney, lungs, liver, heart, intestines)
Diagnosis………

THE APGAR SCORE:


Diagnosis………

• There are no specific tests to confirm or exclude


a diagnosis of hypoxic-ischemic encephalopathy.

• The diagnosis is made based on the history,


physical and neurological examinations, and
laboratory evidence.
Diagnosis………

LABORATORY EVALUATION OF ASPHYXIA:

Serum electrolyte Markedly low serum sodium, potassium, and chloride


levels in the presence of reduced urine flow and
excessive weight gain may indicate acute tubular
damage or (SIADH) secretion, particularly during the
initial 2-3 days of life.

Renal function Serum creatinine levels, creatinine clearance, and


BUN levels
Cardiac & liver Assess the degree of hypoxic-ischemic injury to other
enzymes organs
Coagulation system Prothrombin time, partial thromboplastin time, and
fibrinogen levels.

ABG Assess acid-base status and to avoid hyperoxia and


hypoxia as well as hypercapnia and hypocapnia
Diagnosis………

NEUROIMAGING INCLUDES:
 MRI is the preferred imaging modality in neonates with HIE
because of its increased sensitivity and specificity early in the
process and its ability to outline the topography of the lesion.
 CT scans are helpful in identifying focal hemorrhagic lesions,
diffuse cortical injury, and damage to the basal ganglia.
 Ultrasonography has limited utility in evaluation of hypoxic
injury in the term infant; it is the preferred modality in
evaluation of the preterm infant.
 Amplitude-integrated electroencephalography (aEEG); or
EEG.

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MANAGAMENT
1. Hypothermia Therapy
 Selective head or whole body hypothermia of a core temperature of
33.5 C applied within 6 hours of birth for 48-72 hours is
neuroprotective.
 Possible mechanisms include:
1. Reduced metabolic rate and energy depletion.
2. Decreased excitatory transmitter release.
3. Reduced alterations in ion flux.
4. Reduced apoptosis due to hypoxic-ischemic encephalopathy.
5. Reduced vascular permeability, edema, and disruptions of
blood-brain barrier functions.
 Several clinical trials demonstrate that therapeutic hypothermia is a
promising therapy for mild-to-moderate cases of HIE. It reduces
mortality and major neurodevelopmental impairment.
MANAGAMENT……….

2. Aggressive treatment of seizures:


 It is critical and may necessitate continuous EEG monitoring.

 Phenobarbital, the drug of choice for seizures, is given as IV


loading dose (20 mg/kg); additional doses of 5-
10 mg/kg (up to 40-50 mg/kg total). And maintenance therapy
(5 mg/kg/24hr)
 Phenytoin (20 mg/kg loading dose) or lorazepam (0.1 mg/kg)
may be needed for refractory seizures.
 There is some clinical evidence that high-dose prophylactic
phenobarbital may decrease neurodevelopmental
impairment.
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MANAGAMENT……..

3. General supportive measures:


 Hyperthermia has been found to be associated with
impaired neurodevelopment, so it is important to
prevent hyperthermia before initiation of hypothermia.
 Careful attention to ventilatory status and,
hemodynamic status (adequate oxygenation, blood
pressure, acid-base balance); to prevent secondary
hypoxia or hypotension due to complications of HIE.
 Careful attention to possible infection is important.

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Olympic Cool Cap System
Prognosis:
1. In severe hypoxic-ischemic encephalopathy, the mortality
rate is reported as 25-50%.
2. As many as 80% of infants who survive severe HIE
develop serious complications, 10% develop moderately
serious disabilities, and as many as 10% are healthy.
3. The infants who survive moderately severe HIE 30-50%
may have serious long-term complications, and 10-20%
have minor neurological morbidities.
4. Infants with mild hypoxic-ischemic encephalopathy tend
to be free from serious CNS complications.
Hypoxic-Ischemic Encephalopathy…………..

Predictors of Mortality and Neurologic Morbidity after


Perinatal Hypoxic-Ischemic Insult

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Hypoxic-Ischemic Encephalopathy…………..

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