Alterations in Cerebral Perfusion, Oxygenation, Electrical Activity, and Markers of Cerebral Damage Associated With Cerebro-spinal Fluid Reservior Aspiration in Neonates With Post Hemorrhagic Hydrocephalus

Very low birth weight infants are at risk for developing intraventricular hemorrhage (IVH). Post hemorrhagic hydrocephalus (PPH) is a major complication of IVH and contributes to long-term developmental delays. Progressive PHH often requires management of ventricular dilation by adjusting CSF fluid volume. There are 3 methods employed to acutely decrease CSF volume: 1) serial lumbar puncture, 2) open drain system (continuous CSF removal), and 3) reservoir system. Serial lumbar puncture is only effective if there is communicating hydrocephalus. The open drain system is infrequently used as it is cumbersome and there is a relatively high risk of infection. The method most commonly used to manage CSF volume is the reservoir system where an in-situ drain is connected to a subcutaneous (Omaya) reservoir which is periodically aspirated by needle puncture through the scalp. Because the Omaya system is closed, intraventricular volume and, thus, pressure must necessarily rise prior to and decrease after CSF aspiration. Ventricular dilation is controlled by the frequency and volume of CSF aspiration.

When hydrocephalus continues to be a problem despite removal of CSF, a ventricular-peritoneal (VP) shunt is placed. Approximately 50% of infants with hydrocephalus treated with removal of CSF resolve their hydrocephalus and do not require VP shunt placement. Placement of a VP shunt is difficult in extremely preterm infants due to increased risk of ulceration around the shunt site and the high protein concentration in CSF which can occlude the valve in the VP shunt requiring revision. Thus, hydrocephalus is usually treated with serial removal of CSF to allow for identification of those infant's whose hydrocephalus resolves over time. However, timing and method of CSF management is controversial because the effect of increasing hydrocephalus on cerebral perfusion, oxygenation, electrical activity, and neuronal damage has not been established.

Serial removal of CSF causes a change in intracranial volume/pressure that can be potentially transmitted to intracranial vessels. The caliber of cerebral vessels may be modified by this balance between intravascular and intracranial pressure, and if the caliber should change, the blood flow characteristics should also change. In cerebral veins and capillaries where intraluminal pressure is low, high intraventricular pressure may significantly affect blood flow and can cause venous stasis. NIRS measures cerebral oxygenation in capillaries and veins. Intracranial arteries and arterioles may be somewhat less affected, except when intraventricular pressure greatly increases. The resultant decrease in the arterial supply can affect tissue perfusion. Arterial flow can be measured by Doppler ultrasonography. Thus, there is concern that during periods of increasing or fluctuating ventricular size cerebral arterial perfusion may be compromised and further cerebral injury may result. Intracranial pressure is further influenced by the plasticity/deformability of the immature brain and the easy expansibility of the cranial vault due to the presence of sutures and open fontanelles.

There is indirect evidence from experiments in animals that ventricular distention itself may cause secondary brain injury. Thus, axonal stretching and disruption secondary to progressive ventriculomegaly is be associated with gliosis. Periventricular vascular distortion and compression may decrease cerebral blood flow causing ischemic injury to periventricular white matter. Inflammation and repair may interfere with CSF flow.

Little research is available that helps answer the primary question involved in clinical management of ventricular dilation in premature infants: Are there relationships between ventricular enlargement, cerebral perfusion, brain oxygen delivery, and on-going cerebral damage?