Hypoxic Ischemic Encephalopathy

  Hypoxic Ischemic Encephalopathy :

state of hypoxia (arterial O2 lack), Ischemia (lack of perfusion) affecting CNS (Hypoxic Ischemic Encephalopathy) wich occurs in infants exposed to perinatal asphyxia presented by decreased Apgar score, cyanosis, pallor, convolutions, hypotonia, apnea within 12 hours after birth (variable severity).

Perinatal asphyxia: 

hypoxemia-hypercapnia and metabolic acidosis due to disturbed gas exchange in the placenta or lungs.

lung expansion doesn't occur within minutes after birth and is unable to establish ventilation and pulmonary perfusion.

manifested by increase respiratory effort(1ry hyperpnea) followed by 1ry apnea 1minute then rythmic gasping 8-10 gasps/min. for several minutes then 2ry apnea occurs.

Criteria of diagnosis ( profound metabolic or mixed acidosis and low Apgar score < 3 in 1st 5 minutes).

Pathology of HIE:

Hypoxia increases glycolysis in brain cells and decreases cerebral ATP leading to an increased amount of lactate, inorganic phosphate(inactivation of synapses and Na, K ATPase pumps) leads to the release of O2 free radicals glutamate-aspartate leads to membrane depolarization, increase Ca++influx and nitric oxide synthase leads to decreased of oxidative phosphorylation leads to DNA(neural) damage, cerebral vasodilatation and more ischemia leads to *cortex necrosis and/or selective neurological injury, especially in the full-term neonate.

                           *IVH and/or white matter injury especially in preterm neonates.

Risk factors:

*maternal factors:

diabetic mother

toxemia

hypertension

infections

addict

*Obstetrical factors:

placenta previa

cord prolapse

premature rupture 

IUGR

*postpartum factors:

respiratory distress syndrome

preterm 

sepsis

cardiac anomalies

CLINICAL MSANIFESTATION:(SARANT):

GRADE I:

alternating periods of lethargy, irritability, and jitteriness.

poor feeding.

increase muscle tone, exaggerated deep tendon reflexes, and Moro reflexes.

sympathetic excitation (increased heart rate and/or dilated pupil)

no symptoms resolve in 24 hours.

GRADE II:

lethargy.

poor feeding and depressed gag reflex.

hypotonia

decrease heart rate and/or pupil constriction.

50%-70% seizures in 24 hours.

GRADE III:

coma.

flaccidity.

fixed slightly reactive pupil.

apnea, bradycardia, and hypotension.

seizures uncommon

 **Multiorgan dysfunction:

• acute tubular necrosis (oliguria, polyuria, or hematuria).
• cardiomyopathy (hypotonia).
• pulmonary hypertension (tachypnea, hypoxemia).
• hepatic necrosis (increased ammonia, increased AST and ALT, jaundice).
• necrotizing enterocolitis (distension, bloody stool).
• adrenal insufficiency( decrease glucose, decrease Na+and decrease blood pressure).
• antidiuretic hormone insufficiency (oliguria, decrease Na+).

Differential diagnosis:

• other causes of neonatal seizure.
• viral encephalopathy.
• meningitis.
• congenital infection.
• narcotic and analgesic.

Investigation:

• cranial ultrasound (detect hemorrhage, edema especially in preterm babies).
• C.T. (early to detect hemorrhage, edema) 2-4 hours and late to detect brain injury 2-4 weeks).
• MRI.
• EEG and ABG.
• lumber puncture to exclude meningitis.
• Ca++, glucose, urea, creatinine, and urine electrolytes.
• creatine-kinase brain fraction increase in serum in HIE and IVH.
• neuron-specific enolase. 

Management:

• Perinatal (early resuscitation & treatment of meconium aspiration).
• Postnatal 
• NPO (48 hours) may be prolonged in severe cases.
• IV fluids with restriction
• Ventilation & Oxygenation.
• stabilization of circulation.
• Preserve body temperature.
• Renal stabilization.
• Anticonvulsant therapy.
• Brain dehydration methods.
• Correction of metabolic disorders:

            Hypoglycemia:
                                    *due to glycogen depletion (decreased glucose                                                                                                                   production) 2ry to catecholamine release & unexplained                                                                                   hyperinsulinism.   
                                     *slowly discontinue of glucose IVI to avoid rebound                                                                                          hypoglycemia.

           Hypercalcemia:

           Metabolic acidosis:

                                         *adequate perfusion.

                                          *academia with perinatal asphyxia inhibits surfactant production.

.     N.B. ➤ Mean blood pressure in full term(45-50mmHg) & in preterm (35-40mmHg).

                    hypovolemia is suspected in case of hypotension, oliguria, metabolic acidosis, and peripheral                          core temperature difference > 2.5 degrees.

                    treatment by fluid or plasma or albumin 10 ml /kg / 30 minutes, if there is no improvement                               suspect myocardial dysfunction.

              ➤Ashaxiated infants susceptible to fluid volume overload due to * SIADH 3-4 days after insult.

                                                                                                                      * Acute tubular necrosis.

PROGNOSIS:

poor prognosis in case of :

• stage III.
• poor APGAR score.
• multiorgan system dysfunction.
• C.T. abnormality.
• intractable seizures.
• periventricular leukomalacia.