Pediatric emergency medicine trisk 4023 4023

Hydrocephalus
Types of hydrocephalus in the postoperative period include a loculated
ventricle, communicating or noncommunicating. A loculated (“trapped”)
ventricle may cause symptoms resembling those caused by focal, expanding
mass lesions. A loculated ventricle occurs when the drainage pathway from
one lateral ventricle into the third ventricle is blocked. This blockage
typically results from unilateral IVH or from a midline shift. Diagnosis is
confirmed with CT and must be followed by permanent drainage of the
loculus. The treatment of choice is emergent ventriculostomy and
placement of a shunt.
The most common cause of communicating hydrocephalus is the
blockage of absorption pathways by subarachnoid blood. A CT scan shows
universal dilation of all ventricles. Lumbar puncture may demonstrate an
elevated opening pressure. Serial lumbar punctures may be performed as a
temporizing measure to diagnose and treat communicating hydrocephalus.
If the patient’s neurologic condition improves after lumbar puncture,
definitive treatment by shunting may be required.
Any lesion that causes an obstruction at the narrow fourth ventricular
inflow or outflow track can create noncommunicating or obstructive
hydrocephalus. Obstructive hydrocephalus is commonly associated with
lesions of the posterior fossa and is a dreaded complication of surgical
procedures to this area of the brain. Such lesions include cerebellar edema,
infarct, or an intraventricular blood clot in the fourth ventricle. Patients with
a noncommunicating hydrocephalus can never be safely treated with lumbar
puncture, because the pressure gradient created by this procedure places the
patient at risk of tonsillar herniation and sudden death. The patient may be
temporarily stabilized with a ventriculostomy to provide decompression by
draining CSF out of the intracranial cavity. Permanent shunt placement is
the definitive treatment for obstructive or noncommunicating
hydrocephalus.
Infection

Meningitis. Meningitis may occur as late as 4 weeks after surgery because
of violation of mastoid air cells in the face of a CSF leak. Unfortunately,
after craniotomy the patient may normally exhibit all of the clinical signs of