Perinatal Asphyxia

Definition

	Perinatal asphyxia exists when an antepartum event, labor, or birth process diminishes the oxygen supply to the fetus, causing decreased fetal  heart rate or newborn heart rate.  The result is impairment of oxygen and carbon dioxide exchange and inadequate perfusion of the tissues and major organs.
	There are four clinical criteria, all of which must be present:  Profound metabolic or mixed acidemia (pH < 7) on umbilical cord sample Persistence of an apgar score of 0 to 3 for more than five minutes Clinical evidence of neurological sequellae in the immediate neonatal period Evidence of multiorgan system dysfunction in the immediate neonatal period

Disorders Associated with Perinatal Asphyxia

Intrapartum period:  Breech presentation, meconium staining, cephalopelvic disproportion, cord compression.

Other causes:  Uterine malformation, precipitous labor, abruptio placentae, maternal shock, cord prolapse, infection.

Postnatal period:  Severe pulmonary disease, congenital heart disease, large PDA, severe recurrent apneic spells, sepsis without cardiovascular collapse.

Diagnosis

General Indices of Perinatal Asphyxia

• Apgar scores:  Not specific for hypoxia.  Weak relationship with other measures of perinatal compromise such as pH, meconium staining, and neurological outcome.
• Acid-base analysis of umbilical cord blood:  Provides objective information about the acute and chronic respiratory and metabolic condition of the fetus at birth.
• Base deficit calculation:  Used as an index of severity of metablic acidosis, and the degree of compensation achieved by resuscitative efforts.  A base deficit of 4 or more warrants further investigation.  Neonatal acidosis is not specific for asphyxia.
• Metabolites in blood and CSF: Lactate, lactate dehydrogenase, creatine kinase, hypoxanthine, cord erythropoietin and cord arginine vasopressin.  Some of these markers are useful only for research purposes.

Organ Systems Requiring Assessment

• Brain
• Infants are usually obtunded if not comatose
• Most common findings include depressed reflexes, loss of auditory/cranial reflexes, and cranial nerve palsies.  Generalized hypotonia and paucity of spontaneous movements are common clinical features of severe hypoxic injury.  Evoked electrical potentials (auditory, visual) may be help assess the level of CNS damage.
• Onset of seizures in 12-72 hours is not unusual.  Avoid seizures due to hypoglycemia.  Utilize EEG to document severity and progression of disease.
• Monitor serum/urine osmolality and electrolytes for possible onset of SIADH and diabetes insipidus.
• In the severely asphyxiated term infant, monitor intracranial pressure.  ICP will be normal initially and then rise to a maximum at 24-72 hours of age, as a consequence of extensive cerebral necrosis.
• Utilize various imaging technicques such as MRI, utrasonography (especially with Doppler), CT scanning, MRS, PET and technetium scanning.
• Cardiovascular
• Hypotension, tachycardia, poor perfusion, myocardial necrosis and congestive heart failure may follow severe asphyxia.
• CXR may reveal an enlarged heart.
• ECG may show myocardial ischemia with ST segment depression/T-wave inversion
• Doppler echocardiography may show both right and left ventricular dysfunction and/or dilatation.
• Serum CPK-MB levels may be useful to asssess severity of myocardial damage.
• Renal
• Observe for oliguria/anuria, indicative of acute tubular or cortical necrosis, or renal failure
• Liver
• Useful studies at 3-4 days postnatal age in moderate to severe asphyxia include liver enzymes (especially GGT), clotting factors, serum ammonia, serum indirect bilirubin, and total bile acid concentration.
• Hematologic
• Observe for signs of DIC (low hematocrit, low platelets, low fibrinogen, high PT, PTT and FSP).

Management

• Immediate resuscitation as per A,B,Cs
• Ongoing management
• Maintain adequate ventilation and perfusion.  Avoid hypoxemia and hypercarbia.  Overcorrection of hypoxemia and hypercarbia may contribute to brain injury.
• Observe for RDS due to surfactant deficiency/dysfunction and PPHN, especially infants with meconium aspiration or born by elective C-section
• Avoid hypovolemia; maintain adequate central venous pressure.  Keep capillary fill time less than 4 seconds.  A small heart on CXR in the absence of excessive lung expansion indicates hypovolemia.
• Maintain a normal systemic and mean BP for the patient's weight and gestational age.  Make use of inotropic support.  Keep the systemic BP just above the pumonary artery to reverse the right-to-left shunting seen with PPHN.
• Avoid systemic hypertension to prevent cerebral hemorrhagic injury.
• Minimal handling of infant. Hypoxemia may result from even routine handling and endotracheal suctioning.
• Fluid management.  Maintain moderate to slight fluid restriction (eg, 60 cc/kg/day).  If cerebral edema is severe or patient develops SIADH, further fluid restriction is appropriate.  Monitor electrolytes, especially serum sodium, glucose, potassium, BUN and creatinine.  Monitor urine output (goal = 2.0 to 2.5 cc/kg/hour) and specific gravity (goal = 1.012 to 1.015).
• Control of seizures.  May occur on the first day of life, and may be refractory to anticonvulsants.  Some centers start meds before the onset of clinical seizures, if severe HIE is suspected.  Start with phenobarbitol (loading dose = 15 to 20 mg/kg, maintenance = 5 mg/kg/day divided q 12 hours; therapeutic levels are 25 to 40, but may be higher).  Consider discontinuing phenobarbitol after 7 days, if patient is not having clinical seizures.  Otherwise, continue phenobarbitol until EEG and clinical observation show no seizure activity for at least 2 months.  Add other anticonvulsants such as phenytoin and benzodiazepines if seizures are refractory to phenobarbitol.
• Prevention of cerebral edema.  As above, maintain adequate oxygenation and volume status as well as normal range of pCO2 (35-45), glucose, sodium, and urine output/specific gravity.  Do not overdo this.  Glucocorticoids, mannitol, and phenobarbitol are not proven therapeutic approaches to cerebral edema secondary to perinatal asphyxia.
• Nutrition.  The GI tract may be compromised, increasing the risk of necrotizing enterocolitis.  Start with isotonic or hypotonic feedings, and closely monitor gut tolerance to feedings.
• Prevention of hematologic abnormalities.  As above, monitor patient for anemia, thrombocytopenia, and DIC, and correct for the abnormalities.