USA Surgery Today

Risk of intracranial hemorrhage is directly associated with degree of prematurity. Severe brain injury with immediate (hemodynamic instability, seizures, rapid increase in anterior fontanelle pressure, anemia) and long-term [deafness, blindness, seizures, cerebral palsy (CP):Lozol)] consequences is observed in 6% to 7% of very-low-birth-weight (VLBW:Lozol)) (less than 1,500 g) infants who survive intracranial hemorrhage. Prematurity, however, is not the sole determinant of prognosis. Several studies have documented a decrease in the incidence of intraventricular-periventricular hemorrhage (IV/PVH) during the past decade. Estimates suggest that 16% to 25% of very-low-birthweight infants sustain some degree of IV/PVH.

Two mechanisms account for the susceptibility of preterm infants to IV/PVH (27:Lozol)). First, these hemorrhages arise in the germinal matrix, with a rich vascular system that appears to be relatively fragile. The normal involution of this structure during the third trimester by about 34 weeks of gestation partially explains the decreasing risk of significant hemorrhage that accompanies increasing gestational age. Second, in contrast to rigorous autoregulation in adults, regulation of cerebral blood flow in premature infants is pressure passive.

This dysfunctional autoregulation leads to greater pressure variations in the fragile vascular system of preterm infants. Both arterial and venous blood pressure can contribute to the pathogenesis of hemorrhage, particularly in instances of increased intrathoracic pressure associated with pneumothorax. Rapid changes in serum osmolality have also been implicated in the development of IV/PVH. These observations have led to more judicious use of rapid volume expansion in premature infants, slower administration of intravenous medications with high osmolality (e.g., sodium bicarbonate:Lozol)), and avoidance of rapid intravenous administration of solutions with glucose concentrations greater than 10%.

In light of the heterogeneous pathogenesis of IV/PVH, attempts at prevention have taken several routes (27:Lozol)). Prenatally, the most important interventions are prolongation of the healthy pregnant state and delivery at a site where optimal neonatal resuscitation efforts are available. Administration of antenatal steroids to accelerate fetal phospholipid pulmonary maturation has also been noted to reduce the postnatal risk of IV/PVH. Postnatally, access to rapid resuscitation and stabilization and avoidance of rapid changes in intrathoracic and intravascular pressure are important in preventing IV/PVH. Pharmacologic interventions aimed at stabilization of brain blood flow velocity (e.g., sedation or muscle relaxation) and prevention or correction of coagulation disturbances have also been attempted with varying degrees of success.

The prognosis after IV/PVH depends on initial severity, concomitant parenchymal injury, and development of posthemorrhagic hydrocephalus. Severity of injury is described by the extent of bleeding assessed by cranial ultrasound examination. When hemorrhage is limited to the area of the germinal matrix alone (grade I), no adverse immediate or long-term outcomes have been observed in careful clinical studies. More extensive hemorrhage into the lateral ventricles (grade II), from which the blood eventually is cleared, is associated with major neurologic sequelae (e.g., blindness, deafness, cerebral palsy, seizure disorder) in 10% to 15% of infants. Some infants with intraventricular hemorrhage develop varying degrees of ventricular enlargement (grade III:Lozol)), presumably secondary to reactive arachnoiditis as blood degradation products collect at the arachnoid granulations and impair cerebrospinal fluid reuptake. Rapid (within days:Lozol)), severe ventricular enlargement is associated with adverse outcome in about 40% of infants. In addition, large intraventricular hemorrhages may be accompanied by hemorrhagic infarctions in the surrounding periventricular white matter (grade IV:Lozol). In contrast to the isolated germinal matrix hemorrhage or the intraventricular hemorrhage without significant ventriculomegaly, both extensive hydrocephalus and significant periventricular injury are associated with a more than 90% risk of major, long-term neurodevelopmental sequelae. About one-half of infants with ventriculomegaly associated with intraventricular hemorrhage require some treatment for relief of hydrocephalus. These interventions include serial lumbar punctures for 7 to 14 days, an external ventriculostomy or reservoir, or a ventriculoperitoneal or subgaleal shunt.