Pediatric emergency medicine trisk 1006

Common postoperative complications include mass lesions,
infections, hydrocephalus, and infarctions.
Most occur in the immediate postoperative period, however, the
clinician must have a heightened clinical suspicion for weeks after
surgery.

Mass Lesions
Hematoma. A postoperative hematoma may be extra-axial, occurring in the
epidural or subdural space or intra-axial, occurring within the parenchyma
of the brain. The clinical presentation of these lesions is not specific, and
both should be included in the differential diagnosis for postoperative
patients who become increasingly lethargic and exhibit focal signs such as
hemiparesis, aphasia, cranial nerve palsy, or seizure. Changes in vital signs,
such as Cushing triad (hypertension, bradycardia, and abnormal respiratory
pattern), may reflect increasing ICP (see Chapter 59 Pain: Headache ).
A CT scan should be obtained if a developing hematoma is suspected and
the patient’s condition is stable enough to permit a rapid work-up. Patients
whose neurologic condition is deteriorating with decreasing levels of
consciousness require an endotracheal tube, not only for airway protection,
but to allow hyperventilation. The goal is a partial pressure of carbon
dioxide (PCO2 ) level between 30 and 35 torr. Hyperosmolar therapy may
be necessary for the acutely decompensating patient. Evidence exists for
use of hypertonic saline or mannitol to rapidly decrease ICP. Hypertonic
saline may be given acutely in bolus doses of 4 to 10 mL/kg of body
weight. Continuous infusions of 3% saline range between 0.1 mL and 1.0
mL/kg of body weight per hour. Alternatively, Mannitol is given as an
initial intravenous bolus of 1 to 1.5 g/kg body weight. Hematomas are
usually treated by reexploration and evacuation of the mass lesion.
The patient whose condition deteriorates many days or weeks after
craniotomy may have a chronic subdural hematoma. Treatment is to drain
by placement of burr holes with gentle aspiration, provided that the

collection is not associated with enclosing membranes. A chronic subdural
hematoma with membranes can be evacuated only by full craniotomy.


Brain Edema. Edema often accompanies neoplastic lesions and is more
commonly associated with metastatic tumors. On CT scan, brain edema
appears as an area of decreased density associated with brain shift. Brain
edema is commonly associated with ICH and contusion. Edema associated
with cerebral infarction generally indicates a severe stroke and may lead to
herniation. The treatment of brain edema depends on the cause of the
lesion. Edema (vasogenic edema) caused by neoplasia or inflammation
respond to treatment with steroids. The role of steroids in treating edema
caused by trauma, infarction, or anoxia is unproven. Brain edema (cytotoxic
edema) that occurs after surgery for trauma, infarction, or hemorrhage
represents increased tissue water and may require hyperosmolar therapy as
described above.
Pneumocephalus. Pneumocephalus is simply the accumulation of air in
the intracranial spaces. It commonly occurs after craniotomy if the air is not
completely evacuated before the bone flap is replaced. It may also occur
after a traumatic basilar skull fracture when air is introduced into the
subarachnoid space by communication with the exterior environment,
usually through the ethmoid, sphenoid, or frontal sinuses. A CT scan may
show the accumulation of air beneath a bone flap or in communication with
one of the sinuses. Most cases of pneumocephalus are treated with 100%
oxygen by a nonrebreather mask. Tension pneumocephalus marked by an
enlarging pocket of air causing mass effect (midline shift, sulcal
effacement, or both) demands more aggressive and invasive intervention.
Emergency surgery is necessary to resolve the mass effect.
Pneumocephalus can be an indication of CSF leakage. Although
pneumocephalus indicates a tear in the dura, a CSF leak indicates a

relatively large dural tear allowing a stream of CSF to flow. CSF may drain
through the ethmoid or sphenoid sinus complex, causing rhinorrhea;
through the mastoid air cells, causing otorrhea; or from the scalp suture
line. When rhinorrhea or otorrhea occur postoperatively, they should be
treated conservatively with a lumbar drain. If a seal is not accomplished
after 10 to 14 days of conservative treatment, surgical intervention is
necessary. The use of antibiotics to treat either pneumocephalus or
pneumocephalus with subsequent CSF leak is controversial. Treatment with
antibiotics should not be initiated unless signs and symptoms of CSF
infection develop.


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


meningitis, including fever; therefore, the diagnosis may depend entirely
upon examination of CSF and careful observation. If a shunt reservoir is
present, then CSF may be obtained with a shunt tap. As mentioned in a
prior section of the chapter, a CT scan or MRI of the brain should be
performed prior to lumbar puncture. Lumbar puncture in the backdrop of
unrecognized hydrocephalus or mass lesion may risk a potentially fatal
herniation syndrome. The manifestations of postoperative meningitis are
often much more subtle than those of the typical pneumococcal or
meningococcal variety. If signs of meningeal irritation should occur in
isolation or in association with any other changes, neurologic or metabolic,
examination of the CSF is mandatory before any antibiotics are
administered. Because cell count, glucose concentration, and protein

concentration are abnormal after craniotomy, an absolute diagnosis must
await the result of CSF culture or the demonstration of bacteria on Gram
stain. Empiric treatment with broad-spectrum intravenous antibiotics should
be started immediately following LP and directed at gram-positive cocci
and gram-negative organisms, as described in the previous section. The
antibiotic regimen should then be tailored once the final culture results and
sensitivities have been obtained.
Ventriculitis. The clinical picture of ventriculitis differs little from that of
meningitis, although the presentation is usually much more subtle.
Meningeal symptoms may be minimal and fever variable, whereas
alteration in mental status and neurologic function predominate. Both
meningitis and ventriculitis tend to occur in the postoperative period more
than 3 days after violation and contamination of the subarachnoid or
ventricular space. The only diagnostic test is microscopic and bacteriologic
examination of the ventricular fluid. As with meningitis, broad-spectrum
antibiotics should be initiated pending Gram stain and culture results.
Abscess. Brain abscess, or its immediate precursor, cerebritis, is relatively
rare in the postoperative period. If an abscess does not communicate with
the ventricular or subarachnoid space, meningeal signs will usually be
absent. The development of meningeal signs or infected CSF in the face of
focal deficits must heighten the clinician’s suspicion for abscess. However,
in 95% of cases of cerebral abscess, the CSF may be completely normal and