Late Post Traumatic Ventriculomegally Does It Requires CSF Diversion ?

Hydrocephalus, Ventriculomegally

Post Traumatic Hcp

Aim of the study is : 1. prevelance of ventriculomegally in post traumatic patients after head trauma 2. To determine the incidence of surgically treated ventriculomegally within 6 months from head injury in a series of consecutive adult patients undergoing acute head CT following injury. 3. importance of csf diversion in post traumatic ventriculomegally

Ventricular enlargement is a common finding after severe head injury.This is generally attributed to dysfunctional of perfusion and absorption of cerebrospinal fluid (CSF) or secondary to an atrophic process from neuronal loss.\[ late post-traumatic ventriculomegally may be developed weeks to months after brain injury. Late post traumatic ventriculomegally incidence peaked within three months after injury . Its incidence deeply varies among series (0.7-50%), and this is mainly due to very different diagnostic criteria Therefore, given the very high number of patients with traumatic brain injury (TBIs), patients presenting with late post-traumatic ventriculomegally are not infrequent. The choice of the term ventriculomegally in the title reflects the difficulty in differentiating a ventricular enlargement (secondary to post-traumatic brain damage with atrophy) from an active hydrocephalic process. Those patients with subarachnoid hemorrhage (SAH) had a threefold risk of developing ventriculomegally compared to patients with no SAH during the 2-year follow-up period. Also, decompressive craniectomy and the presence of subdural hygroma after craniectomy seem to increase the risk for ventriculomegally.In craniectomy, the proximity of the craniotomy to the skull midline might increase the risk as well. Other possible risk factors for post traumatic ventriculomegaly include: increased age, cerebrospinal fuid infection, and intraventricular hemorrhage . Inflammation-mediated adhesions related to intracranial hemorrhages can explain the predisposition to post traumatic ventriculomegally. In fact, practically all patients with post-traumatic ventricular enlargement present with symptoms of post-taumatic Lesions and almost never present with the Hakim-adams trriad. Some of them present nonspecific symptoms, especially arrested clinical improvement during rehabilitation programs, impaired consciousness or a worsening neurologic status . A classic clinical feature to suspect post traumatic ventriculomegally after TBI is poor improvement or stagnation of recovery . Early recognition of post traumatic ventriculomegally is essential in the follow-up of patients with TBIs, as cerebrospinal fluid diversion (ventricular shunting) has been shown to improve outcome during rehabilitation

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