Perinatal asphyxia can result in systemic effects, including neurologic insult, respiratory distress and pulmonary hypertension, and liver, myocardial, and renal dysfunction. Depending on the severity and timing of the hypoxic insult, a neonate with hypoxic-ischemic encephalopathy due to perinatal asphyxia can demonstrate a variety of neurologic findings. Using the Sarnat staging for encephalopathy can be useful. In Sarnat Stage I, the least severe stage, there is generalized sympathetic tone and the neonate may be hyper-alert with prolonged periods of wakefulness, mydriasis and increased deep tendon reflexes. In Sarnat Stage II, the neonate may be lethargic or obtunded, with decreased tone, strong distal flexion, and generalized parasympathetic tone with miosis, bradycardia and increased secretions. Seizures are common in Sarnat Stage II. Sarnat Stage III, the most severe, is characterized by a profoundly decreased level of consciousness, flaccid tone, decreased deep tendon reflexes and very abnormal EEG. Clinical seizures are less common in Sarnat Stage III due to the profound injury in the brain preventing the propagation of clinical seizures.

A chest radiograph may determine the need for intubation and/or need for exogenous surfactant therapy. An arterial blood gas is useful in diagnosing respiratory versus metabolic acidosis and degree of hypoxemia. Liver damage can be determined by serum transaminase levels and coagulation factors. Troponin and CK-MB can be useful in determining myocardial insult and creatinine and blood urea nitrogen can ascertain the extent of renal dysfunction. Physiologically stressed infants rapidly deplete glucose stores and can develop profound hypoglycemia. Frequent blood glucose checks during the critical period of resuscitation are recommended.[7][8][9][8]

Therapeutic hypothermia is the treatment for neonatal hypoxic-ischemic encephalopathy. Following the immediate primary neuronal injury, during which there is an interruption of oxygen and glucose to the brain, there is a latent period of up to 6 hours before a secondary phase of injury occurs as the injured areas are reperfused, and damaged cells lyse, releasing toxic neurotransmitters. The goal of therapeutic hypothermia is to intervene during the latent period and minimize damage from the secondary neuronal injury. Therapeutic hypothermia, when started within six hours of injury decreases mortality and severe disability from 62% to 48% and increases survival with the normal outcome from 24% to 40% with a number needed to treat of six to seven. Whole body cooling appears to be more effective at decreasing death than selective head cooling, but both modalities are effective at decreasing severe disability and a combined outcome of death and severe disability. Infants with moderate encephalopathy (Sarnat Stage II) benefit most from therapeutic hypothermia. Importantly, cooling does not appear to decrease death at the cost of more severely neurologic impairment in survivors. Side effects associated with therapeutic hypothermia include peripheral vasoconstriction, diuresis, cardiac dysfunction, arrhythmias, coagulopathy, thrombocytopenia, stridor, leukocyte dysfunction, pulmonary hypertension and subcutaneous fat necrosis (calcium deposits in the skin). Therapeutic hypothermia can be delivered safely with specialized equipment and monitoring in sophisticated medical centers. [10][11][12][13][14]

The treatment of respiratory distress, pulmonary hypertension, coagulopathy and myocardial dysfunction is supportive. Infants with respiratory distress and pulmonary hypertension may require intubation, surfactant, oxygen and inhaled nitric oxide. Coagulopathy is treated with the prudent use of blood products to maintain oxygen-carrying capacity and coagulation. Myocardial dysfunction may result in a need for vasopressors. Renal dysfunction may result in oliguria or anuria; therefore, use of crystalloid fluid and blood products should be cautious.

• Brain tumors

• Developmental defects

• Genetics of Methylmalonic acidemia

• Genetics of Propionic acidemia

• Infections

• Neuromuscular disorders including neonatal myopathy

Birth asphyxia is not an uncommon event, and because of its high morbidity and mortality, the condition is best managed by an interprofessional team. However, the long-term prognosis of these infants has been difficult to assess. In the short term, the condition is reported to have a mortality in excess of 30%, with the majority of deaths occurring within the first few days after birth. Those infants who survive are often left with mild to severe neurological deficits, and they also end up dying from aspiration or systemic infections. Long-term survivors have been found to have disabling cerebral palsy, inadequate mental development or low psychomotor scores, seizures, blindness, and severe hearing impairment. The management of these infants, in the long run, is complex and prohibitively expensive. [3][15](Level V)