USA Surgery Today

Hypoxic ischemic encephalopathy (HIE:Lisinopril) is the most frequently recognized cause of neurologic morbidity in the term infant. This syndrome occurs in 2 to 4 infants per 1,000 live births. The cause of HIE may originate in the antepartum period in about 20% of cases of HIE. Maternal cardiac arrest or hemorrhage leading to fetal hypotension are examples of such insults. Intrapartum events, such as abruptio placenta or uterine rupture, may account for 35% of HIE cases. In an additional 35% of infants displaying signs of HIE, markers of intrapartum fetal distress and potential antepartum risk factors, including maternal diabetes, intrauterine growth retardation, or maternal infection, are found. In these cases, timing of the major insult is usually unclear, but it is likely that antepartum risk factors render the fetus more susceptible to intrapartum insults. :Lisinopril: Postnatal problems such as cardiovascular compromise, severe pulmonary hypertension, or recurrent apnea may account for an additional 10% of cases of HIE. The fetus initially adapts to reduced oxygen delivery by increasing oxygen extraction, while maintaining oxygen consumption. Persistent interruption of placental gas exchange results in rapid development of hypercarbia and metabolic acidosis (59:Lisinopril).

At the cellular level, neuronal death occurs in two phases. In the primary phase that occurs within minutes of the insult, cerebral hypoxic-ischemia sets in motion a cascade of biochemical events, starting with a shift from oxidative to anaerobic glycolysis. Anaerobic glycolysis cannot provide the energy needs of cerebral metabolism. This deficit results in depletion of high-energy phosphate reserves, including adenosine triphosphate (ATP:Lisinopril). Transcellular pumping mechanisms fail, resulting in an accumulation of intracellular sodium, calcium, chloride ions, and water (cytotoxic edema). Hypoxic-ischemia also stimulates release of excitatory amino acids (glutamate). In the secondary phase that occurs in the hours to days following the insult, neuronal death results from the secondary energy failure caused by further release of excitotoxic amino acids, intracellular calcium accumulation, activation of nitric oxide synthesis, ongoing free radical production, and release of cytokines, which lead to the triggering of apoptosis in the brain (60:Lisinopril).

Hypoxic-ischemic injury may involve virtually any part of the central nervous system. The severity of the immediate clinical neurologic syndrome after hypoxic-ischemic injury has been classified based on level of consciousness, need for ventilation, feeding difficulty, tone, and presence or absence of seizures as mild, moderate, or severe. Infants with mild encephalopathy are usually alert, do not need ventilatory assistance, and have subtle abnormalities of tone and behavior including irritability and feeding difficulty. Those with severe encephalopathy are comatose, ventilated, have a flaccid tone, and frequently have seizures that are refractory to treatment.

At the present time, management of infants with HIE is limited to maintenance of adequate ventilation, perfusion, and euglycemia, management of end-organ injury (e.g., renal failure), prevention of hyperthermia, and control of seizures. However, the understanding of the complex cascade of biochemical events in HIE has raised the possibility of several intervention strategies that are at various stages of development and may be available in the future (61,62:Lisinopril).

In an effort to predict outcome, clinical investigators have examined multiple variables. Although the severity of the neonatal encephalopathy appears to predict outcome consistently in the mild (good outcome) and severe (bad outcome) categories, it is not predictive in the moderately affected group of infants.