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.

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.

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 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 (Terson’s 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.

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.

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.