Postresuscitative management of the asphyxiated term/preterm infant

Following severe perinatal asphyxia the newborn can be affected by multi-organ dysfunction in spite of successful delivery room resuscitalion. Central nervous system was the most frequently involved, followed by the kidney, lung, heart, and intestine. Hypotension and heart failure are two of the most serious complications of severe asphyxia as they are associated with secondary ischaemic injury to the CNS, myocardium (endocardial ischemia), kidneys (renal failure) and intestine (NEC). Pulmonary complications with an asphyxiated infant ranges from minimal oxygen requirement to persistent hypertension of the newborn and massive pulmonary hemorrhage. Renal involvement varies from oliguria to azotemia depending on the initial insult. Asphyxia causes activation and consumption of coagulation factors and reduces platelet procluction and compromise platelet function. While other organs may recover, the consequence of brain damage is long-term abnormal neurologic sequelae.
Postresuscitative management ot the asphyxiated infant can be classified in two steps. The first step is the general supportive care in which clinical management is directed at maintenance of adequate ventilalion, cerebrovascular perfusion and adequate blood glucose levels. For this purpose the infant's cardiopulmonary status should be monitored and signs of multiorgan system dysfunction sought and treated where appropriate. The second step is neuroprotective therapy, which should be planned according to the phase of postasphyxial injury. After the hypoxic insult, phases of recovery are characterized by the alteralions in cerebral blood flow, EEG intensity, and cortical impedance that occur in the first 5 days after perinatal asphyxia. They have been referred as: reperfusion phase (+0-4 hours), latent phase (0-8 hours), secondary energy failure phase (8-72 hours), late phase>72 hours. Current therapy that can be applied in clinical practice includes osmotic agents, barbiturates, allopurinol, ascorbic acid, deferoxamine. ıbuprofen and magnesium. Future therapies will be combination of modalities including rescue hypothermia and various pharmacological approaches such as monosialogangliosides, growth factors, gene therapy with anti-apopitotic agents or calcium binding proteins that are appropriate for the phase and mechanism of the postasphyxial injury.