Introduction
Neurosurgical emergencies frequently are initiated by increased intracranial
pressure (ICP). Some causes of increased intracranial pressure (ICP) may be directly
related to a cerebral mass. Acute obstructive hydrocephalus, occurring from a variety of
etiologies, may cause elevations in ICP. Treatment of patients with increased intracranial
pressure follows the same guidelines as the care for any critically ill patient, namely:
establishing an airway, breathing for the patient if necessary, and supporting
circulation. Additional benefit for the patient can be gained by the use of osmotic agents
to help alter the intracranial pressure. The following information outlines the more
typical cases of neurosurgical emergencies which might be expected while caring for an
active duty population.
Subarachnoid Hemorrhage
One source of rapid elevation of intracranial pressure is subarachnoid hemorrhage
(SAH). The leading cause for SAH is trauma. Those patients without a history of trauma
usually bleed into their subarachnoid space from aneurysms, arteriovenous malformations
(AVM), tumors, strokes, etc. The more common causes of nontraumatic SAH are aneurysms and
AVMs.
Diagnosis
The diagnosis is made by documenting historical findings to include an excruciating
headache, coupled with photophobia, nausea, and vomiting. Any of these symptoms may be
present in other medical conditions and are not prerequisites. Patients may have mild
headache initially, without photophobia. Patients exams may vary considerably from
those that present with mild headache to those that present in coma. The cardinal sign of
basilar meningeal irritation is a stiff neck. Frequently patients with a SAH will present
with some evidence of neck stiffness. Upon examination many times the patient will prefer
to keep their eyes closed for comfort, will have rigid board-like neck stiffness, and may
be nauseated. Elevation of blood pressure may also be remarkable even with young patients.
Neurologic exam
Neurologic examination should pursue abnormalities in any of the following areas:
mental status, cranial nerves, motor and sensory exams, or cerebellar function. Patients
may be obtunded due to the irritating effect of subarachnoid blood, however other patients
may only have a mild headache. The third nerve cranial nerve is most commonly affected.
The patient may present with ptosis and a dilated pupil (due to 3rd nerve compression from
an expanding posterior communicating aneurysm). Unilateral hemiparesis may represent the
presence of a hematoma from hemorrhage into the cerebral cortex from an aneurysm.
Similarly, the patient may have signs of mass effect, seizures, or other focal
abnormalities from a large clot. More often than not, however, the patient has evidence of
generalized cortical dysfunction manifested by depression in the level of consciousness.
Ocular hemorrhages are common in SAH, occurring in up to 25 percent of cases. The
hemorrhage can be subhyaloid (preretinal) seen as a bright red spot near the optic disc,
intraretinal surrounding the fovea, or within the vitreous humor (Tersons syndrome).
Diagnostic studies
Diagnosis is simplified by rapid sequence CT scanning, when available. However,
aboard ships other than the USNS Comfort or Mercy, scanning is not available, and
therefore secondary procedures must be relied upon. Certainly even when CT scanning is
negative and the suspicion is high, lumbar puncture is used for diagnosis. The major
complication of lumbar puncture is causing an alteration in the transmural pressure of the
aneurysm, causing it to re-hemorrhage, with usually catastrophic results.
Therefore, if CT is available ashore, and logistics allow for transportation, then
scanning should always be performed first. If this is impossible, the use lumbar puncture
in the diagnosis is justified.
Lumbar puncture
Confusion frequently arises from a bloody lumbar puncture. If the bloody CSF clears
as the second and third tubes of CSF are collected, and if the fluid is found to be
xanthochromic after centrifugation of the tubes, then the likelihood that the patient had
a SAH is high. However if the fluid never clears, and the fluid is clear after
centrifugation then the patient most likely did not have a SAH. However, it is
theoretically possible to perform a lumbar puncture on a patient and find clear CSF (i.e.,
no xanthochromia) if the lumbar puncture is performed very early on. Therefore, if the
suspicion remains that the patient had a SAH, after CSF is drawn that shows no
xanthochromia, then the patient should be treated as though he or she had a SAH.
Definitive treatment
The definitive treatment of a patient with a SAH from an aneurysm or AVM is
surgery. Obviously, logistics may not allow for immediate transfer of the patient to the
care of a neurosurgeon. It is difficult at times to differentiate between a SAH of an
aneurysm and AVM, and therefore guidelines must be adhered to which deal with a worst case
scenario. The guidelines that follow therefore will deal with a hypothetical patient who
had a SAH from an aneurysmal bleed. The possibility of re-rupture in these patients is
more dangerous than with a patient with an AVM.
Initial management
The ABCs must be evaluated and stabilized. In general, the use of hyperventilation
in aneurysm patients is to be avoided in light of the possibility of compounding the
ischemic effects of vasospasm. PCO2 levels should be maintained between 31-35mm if
hyperventilation is to be used. If mass effect still threatens the patient, then
dehydrating agents such as Mannitol or
Lasix may be used. We generally use
Mannitolin
lower doses of 0.25mg/kg, since the dehydration effect is obtained without causing
prerenal shutdown from hypovolemia.
Electrolyte abnormalities
Patients with SAH frequently may have abnormalities of their electrolytes, most
commonly with hyponatremia. Low sodium may lead to exacerbation of seizures, which if the
sodium is low enough may make the seizures extremely difficult to treat. As stated before,
the general idea is not to fluid restrict these patients, and although the patient may be
considered to have the syndrome of inappropriate antidiuretic hormone (SIADH), it is
probably best to treat these patients with 3% saline solution as opposed to fluid
restriction. IV fluids should at least be kept at maintenance levels unless the patient is
demonstrating signs of incipient herniation. Vigilance must be maintained to verify that
calcium and magnesium levels are not too low, since low levels may also precipitate
seizures.
Other considerations
Cardiac arrhythmias may occur with SAH. Close monitoring in the initial stages of
SAH (at least 48 hours), will help signal the need for therapy in these particular
patients. Hypertension (systolic blood pressure greater than 180 mm Hg) may also be
extremely difficult to treat, at times requiring either the use of nipride or
nitroglycerin, labetalol, or hydralazine. Systolic blood pressure should be kept to
a maximum of 155 mm Hg in the scenario of SAH from aneurysmal rupture. Many times pain
treatment will assist with the control of hypertension. We prefer IV morphine because of
its analgesic control and because it can be easily reversed to allow for an accurate
neurologic exam.
Management of seizures
Seizures must be treated with patients who had a SAH. In general, unless
contraindicated, we treat patients with Dilantin. The loading dose for this drug is
15mg/kg and should not be given too rapidly due to the potential for complete heart block.
Some neurosurgeons prefer phenobarbital, in light of its sedating effect, its effect on
blood pressure, as well as seizure control. Phenobarbital
can be given in 30mg aliquots
with the upper limit of adequate levels around 300mg loading dose. Care must be maintained
at high levels for respiratory arrest.
Environmental management
Because one of the biggest fears is rebleeding, patients should be kept
comfortable, in darkened and quiet surroundings, with stool softeners, and in an
environment that is as nonstressful as possible. Pain control can assist in making
patients as comfortable as possible.
Disposition
The objective should be eventual transfer to a medical facility where
neurosurgical capabilities are present. Air evacuation is possible depending on logistics
and the presence tertiary medical facilities. Using a Hunt classification of SAH severity
for description may provide further valuable information for a neurosurgical colleague.
Hunt Classification of SAH
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