Hypoxic Ischemic Encephalopathy

Definition of Terms
Anoxia
indicate the consequences of complete lack of oxygen as a result of a number of primary causes

Hypoxia
arterial concentration of oxygen that is less than normal

Ischemia
refers to blood flow to cells or organs that is insufficient to maintain their normal function

 Hypoxic-ischemic encephalopathy
is an important cause of permanent damage to CNS cells that may result in neonatal death or be manifested later as cerebral palsy or mental deficiency 15 to 20% of infants with hypoxic-ischemic encephalopathy die in the neonatal period 25-30% of survivors are left with permanent neurodevelopmental abnormalities (cerebral palsy, mental retardation).

 Prevention is critical because no specific therapy can reverse the CNS injury

Etiology
Fetal Hypoxia
inadequate oxygenation of maternal blood as a result of:
hypoventilation during anesthesia cyanotic heart disease respiratory failure carbon monoxide poisoning

 low maternal blood pressure as a result of

the hypotension that may complicate spinal anesthesia from compression of the vena cava and aorta by the gravid uterus

inadequate relaxation of the uterus to permit placental filling as a result of

uterine tetany caused by the administration of excessive oxytocin

premature separation of the placenta

 impedance to the circulation of blood through the umbilical cord as a result of compression or knotting of the cord uterine vessel vasoconstriction by cocaine placental insufficiency from numerous causes, including toxemia and postmaturity

 After birth hypoxia may be caused by

anemia severe enough to lower the oxygen content of the blood to a critical level, as after severe hemorrhage or hemolytic disease shock severe enough to interfere with the transport of oxygen to vital organs as a result of:
overwhelming infection massive blood loss intracranial or adrenal hemorrhage

 failure of oxygenation of an adequate amount of blood as a result of:

severe forms of cyanotic congenital heart disease pulmonary disease

Pathophysiology
total fetal hypoxia, bradycardia, hypotension, decreased cardiac output

severe metabolic as well as respiratory acidosis occur

initial circulatory response of the fetus is increased shunting through the ductus venosus, ductus arteriosus, and foramen ovale, with transient maintenance of perfusion of the brain, heart, and adrenals in preference to the lungs (because of pulmonary vasoconstriction), liver, kidneys, and intestine.

 Early congestion, fluid leak from increased capillary permeability, and endothelial cell swelling
lead to signs of coagulation necrosis and cell death Congestion and petechiae are seen in the pericardium, pleura, thymus, heart, adrenals, and meninges

 Prolonged intrauterine hypoxia may result in PVL and pulmonary arteriole smooth muscle hyperplasia
which predisposes the infant to pulmonary hypertension

fetal distress produces gasping

amniotic fluid contents (meconium, squames, lanugo) are aspirated into the trachea or lungs

 combination of chronic fetal hypoxia and acute hypoxic-ischemic injury after birth
results in gestational age-specific neuropathology

Term infants demonstrate neuronal necrosis of the cortex (later, cortical atrophy) and parasagittal ischemic injury Preterm infants demonstrate PVL (later, spastic diplegia), status marmoratus of the basal ganglia, and IVH

 Term more often than preterm infants have focal or multifocal cortical infarcts that produce focal seizures and hemiplegia

Clinical Manifestations
Intrauterine growth restriction with increased vascular resistance may be the first indication of fetal hypoxia During labor, the fetal heart rate slows, and beat-to-beat variability declines fetal scalp blood analysis may show a pH less than 7.20 acidosis usually has both metabolic and respiratory components

SignsStage 1Stage 2Stage 3 Level of consciousnessHyperalertLethargicStuporous, coma Muscle toneNormalHypotonicFlaccid PostureNormalFlexionDecerebrate Tendon reflexes/clonusHyperactiveHyperactiveAbsent MyoclonusPresentPresentAbsent Moro reflexStrongWeakAbsent PupilsMydriasisMiosisUnequal, poor light reflex SeizuresNoneCommonDecerebration ElectroencephalographicNormalLow voltage changing to seizure activityBurst uppression to isoelectric Duration<24 hr if progresses; otherwise, may remain normal24 hr to 14 daysDays to weeks OutcomeGoodVariableDeath, severe deficits

 the presence of yellow, meconium-stained amniotic fluid is evidence that fetal distress has occurred birth, these infants are frequently depressed and fail to breathe spontaneously Pallor, cyanosis, apnea, a slow heart rate, and unresponsiveness to stimulation are also signs of hypoxic-ischemic encephalopathy

 CNS dysfunction, congestive heart failure and cardiogenic shock, persistent pulmonary hypertension (persistent fetal circulation), respiratory distress syndrome, gastrointestinal perforation, hematuria, and acute tubular necrosis are associated with perinatal asphyxia After delivery, hypoxia is due to respiratory failure and circulatory insufficiency

Treatment
supportive and directed at the organ system manifestations Careful attention to ventilatory status and adequate oxygenation, blood volume, hemodynamic status, acid-base balance, and possible infection is important

Prognosis