Tumors

Patients with brain tumors can present with headache, neurologic deficits, and seizures. New-onset seizures should be investigated by brain computed tomography (CT) or magnetic resonance imaging (MRI). Supratentorial tumors typically cause motor or sensory changes or cranial nerve dysfunction. Patients with tumors located in or near the optic chiasm, temporal lobe, parietal lobe, and occipital lobe should have a comprehensive neuro-ophthalmologic examination to formally evaluate visual fields.

Hydrocephalus is a major complication of supratentorial tumors, which can lead to herniation and, if not treated in a timely fashion, may cause rapid, progressive physiologic decompensation and ultimately death. If a tumor is proximate to the sella or is located in the suprasellar region, it is imperative to perform a comprehensive evaluation of the patient’s pituitary hormonal status, including serum levels of prolactin, follicle-stimulating hormone, luteinizing hormone, thyroid-stimulating hormone, adrenocorticotropic hormone, growth hormone, insulin-like growth factor-1, cortisol, and alpha subunit.

Tumors in the posterior fossa should be evaluated for evidence of cranial nerve dysfunction or brain stem compression. Hypertension, bradycardia, or an altered respiratory pattern (Cushing’s triad) can indicate brain stem compression. More subtle signs of this complication include agitation or an altered level of consciousness.

Acoustic neuromas arising from the eighth cranial nerve can cause loss of hearing, and these patients should be evaluated with an audiogram.

Hematomas

Hematomas are often associated with significant head trauma necessitating direct admission to the ICU. However, bleeding may result from minor head trauma in the elderly because of brain atrophy and subsequent traction on bridging veins in the subdural space. Intraparenchymal hematomas can arise from trauma or may occur spontaneously secondary to hypertension, amyloid angiopathy, or an underlying lesion. In general, subdural hematomas arise from venous injury, whereas epidural hematomas are arterial in nature. Because blood extravasates at a higher pressure from arteries compared to veins, epidural hematomas often progress more rapidly than subdural hematomas.

The classic presentation of epidural hematomas is a brief episode of unconsciousness from concussion, a subsequent lucid interval, followed by progressive mental status deterioration. In clinical practice, however, patients rarely present in this fashion. The overwhelming majority of subdural and epidural hematomas arise in the supratentorial space, although they can occur in the posterior fossa as well. Subdural hematomas often cause headaches, confusion, aphasia, hemiparesis, or seizures. Epidural hematomas commonly present with a decrease in level of consciousness. Chronic subdural hematomas occur most often in the elderly and can present in a variety of manners including a decrease in the level of consciousness, focal hemiparesis, severe headaches, or new-onset seizures.

Acute subdural hematomas usually require a craniotomy for clot evacuation. Patients with chronic subdural hematomas can be treated in an expectant fashion. Although most chronic subdural hematomas can be evacuated using burr hole drainage, those that are not fully liquefied or that are loculated may require a full craniotomy for evacuation. In the elderly, brain atrophy may prevent reexpansion of the brain following subdural evacuation, which can lead to recurrent hematomas.

Epidural hematomas usually expand more rapidly because of the arterial bleeding underlying the pathology and often need to be evacuated more expeditiously than subdural hematomas. A clot that causes mass effect, midline shift, or a significant neurologic deficit should be evacuated immediately. The indications for evacuation of intraparenchymal hematomas are unclear, as these surgeries have not been shown to improve neurologic deficits but only represent lifesaving procedures. The Surgical Trial in Intracerebral Haemorrhage (STICH), completed in 2005, compared a strategy of early surgical decompression (within 72 hours of presentation) with conservative medical management. In this large (n = 1033 representing 83 hospitals in 27 countries) randomized trial, there was no difference on early or 6-month mortality between the two groups. Although there were no overall benefits to early surgical intervention (primary outcome), there was a small benefit to surgical decompression noted in younger patients with hematomas that came within 1 cm of the cortical surface.

Aneurysms and Arteriovenous Malformations

Aneurysms typically present after rupture, causing subarachnoid hemorrhage and a headache that is often described as the “worst headache of my life.” Arteriovenous malformations present most commonly with hemorrhage and seizures though they can also manifest as a focal neurologic deficit or coma. The causes of hemorrhage are myriad but they frequently occur during physical activity, bowel movements, or sexual intercourse.

Patients with subarachnoid hemorrhage present with varying levels of consciousness, ranging from fully alert to comatose. The Hunt and Hess classification is used to estimate the patient’s clinical status and prognosis (Table 89.1).

Hunt and Hess grades 1 to 3 are considered low grade and these patients are considered to be good surgical candidates for aneurysm occlusion. Grades 4 and 5 are considered high grade and represent a poor prognosis, with a meaningful survival that is usually quoted to be less than 10%. These patients should be treated with endovascular occlusion.

Management is dictated by the initial neurologic deficit.

Neurocritical Care Monitoring

Key principles in neurocritical care, regardless of the pathology or procedure, include the prevention of secondary insults to the brain, ischemic or otherwise, and the maintenance of cerebral blood flow (CBF). Traditionally, these goals have been achieved through monitoring of intracranial pressure (ICP) and maintenance of an appropriate cerebral perfusion pressure (CPP) (Chapter 41). Intraparenchymal bolts for measuring ICP are inserted in patients with a neurologic exam that is difficult to follow, typically equivalent to a Glasgow Coma Scale of 8 or less. Cerebral perfusion pressure is calculated as the difference between mean arterial pressure (MAP) and ICP. Standard thresholds for intervention are an ICP greater than 20 mm Hg or a CPP less than 60 mm Hg, although care should be tailored on an individual basis.

Treatment of intracranial hypertension should be based on a stepwise algorithm starting with sedation (Chapter 5) and osmotic therapy (i.e., mannitol or hypertonic saline). Hyperventilation can be used acutely to lower ICP but is not useful for the long-term management of elevated ICP. If these strategies do not control intracranial hypertension, cerebrospinal fluid drainage via ventriculostomy placement and institution of pharmacologic paralysis (Chapter 6) may be necessary. Decompressive hemicraniectomy and pentobarbital coma are often reserved for intractable intracranial hypertension.

Other methods of monitoring cerebral physiology have been explored because of evidence that ICP- and CPP-based care sometimes fail to detect episodes of cerebral compromise. Brain oxygen electrodes are a useful adjunct for detecting brain hypoxia, and there are data to support improved clinical outcomes using this technology. In addition to their traditional role in seizure management, electroencephalography (EEG) can be utilized to detect ischemia using various algorithms. Cerebral microdialysis is a method for analyzing cellular metabolites in the brain. The lactate-pyruvate ratio is the most well-studied marker of cerebral metabolic dysfunction, but it, along with other microdialysis markers, is primarily a research tool currently and therefore is not routinely used in the clinical setting.