A review of the current treatment methods for posthaemorrhagic hydrocephalus of infants

Posthaemorrhagic hydrocephalus (PHH) is a major problem for premature infants, generally requiring lifelong care. It results from small blood clots inducing scarring within CSF channels impeding CSF circulation. Transforming growth factor – beta is released into CSF and cytokines stimulate deposition of extracellular matrix proteins which potentially obstruct CSF pathways. Prolonged raised pressures and free radical damage incur poor neurodevelopmental outcomes. The most common treatment involves permanent ventricular shunting with all its risks and consequences

Brain development and perinatal vulnerability to cerebral damage

The recent exponential rise in detailed magnetic resonance (MR) imaging studies has emphasized the concept of gestationally determined regional vulnerability in the brain: the site and nature of the injury sustained being determined by a combination of the characteristics of the insult, the specific tissue and cell vulnerability and the gestation of the infant. The type of insult may also be partly dependent on gestation. However, it is now known that acute perinatal hypoxic ischemic events, previously considered characteristic for the term born neonate presenting with hypoxic-ischemic encephalopathy (HIE), may occur at earlier points in gestation [1, 2]. Nevertheless, such events occur less often in the infant born preterm where lesions develop in similar brain regions and in other areas characteristically more vulnerable in more premature babies (Fig. 127.1). Similarly, white matter (WM) lesions, which are considered the hallmark of injury to the preterm brain because they are characteristic of perinatal injury relating to inflammation, infection or hypoglycemia in the term brain, may also occur in a small percentage of neonates with an encephalopathy (Fig. 127.2) [3]