Page 1132 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 84: Cerebrovascular Disease 771

with hemispheric lobar hemorrhages and patients without hypertension,
or in any subgroup, including those with atrial fibrillation or other causes should be sought, such as arteriovenous malformations
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other cardioembolic sources. or saccular aneurysms. Amyloid angiopathy becomes increasingly
• Hemicraniectomy reduces mortality in patients with large important in patients in the seventh, eighth, and ninth decades. These
hemispheric infarcts and depressed level of consciousness who hemorrhages usually occur in the subcortical hemispheric white matter
are operated within 48 hours of stroke onset. and may be multiple. Previous microhemorrhages in parietal and occipi-
• Treatment of Intracerebral Hemorrhage tal lobes are often visible on magnetic resonance images. Hemorrhage
due to anticoagulant and thrombolytic drugs may affect any part of the
The following statements can be made based on good clinical trial data brain. Rarer causes of intracerebral hemorrhage occurring in patients
• Prophylaxis for deep venous thrombosis with low-dose subcu- with other systemic diseases include thrombocytopenia, hemophilia,
taneous heparin or heparinoids may be instituted safely on the and disseminated intravascular coagulation. Primary or metastatic brain
second day after the hemorrhage and reduces subsequent deep tumors will rarely present as ICH.
venous thrombosis if begun before day 4. Nontraumatic spontaneous subarachnoid hemorrhage (SAH) is
• In patients with systolic blood pressure of 150 to 220 mm Hg, almost always due to a ruptured saccular aneurysm. Aneurysms may
also rupture into the brain parenchyma, producing intracerebral hem-
rapid pharmacological reduction of systolic pressure by 27 mm Hg
within the first hour is safe but does not improve outcome. orrhage as well. Saccular aneurysms are most commonly located on
the large arteries at the base of the brain. Both congenital and acquired
• Craniotomy and clot evacuation in patients with supratentorial factors appear to play a role in the postnatal development of aneu-
ICH, either superficial or deep, is of no benefit. rysms. Acquired factors include atherosclerosis, hypertension, and
• Treatment of Subarachnoid Hemorrhage hemodynamic stress. In patients with infective endocarditis, mycotic
The following statements can be made based on good clinical trial data aneurysms of more distal arteries may form and sometimes rupture.
• Oral nimodipine at a dose 60 mg every 4 hours for 21 days after Other causes of SAH include ruptured arteriovenous malformations
(cerebral and spinal) and fistulae, cocaine abuse, pituitary apoplexy,
hemorrhage reduces poor outcome. and intracranial arterial dissection. In some cases, particularly SAH
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• Early definitive treatment reduces the risk of rebleeding. ventral to the midbrain or restricted to cortical sulci, the cause cannot
• For aneurysms amenable to both endovascular coiling and be determined.
surgical clipping, endovascular treatment is beneficial.
• Intravascular volume contraction should be avoided. CLINICAL AND LABORATORY DIAGNOSIS
The initial diagnostic evaluation of the patient with suspected stroke
serves (1) to determine whether neurologic symptoms are due to cere-
brovascular disease or to some other condition, such as peripheral nerve
injury, intracranial infection, tumor, subdural hematoma, multiple scle-
ETIOLOGY rosis, epilepsy, or hypoglycemia; and (2) to distinguish among different
types of cerebrovascular disease that require different treatments. The
Cerebrovascular diseases can be divided into three categories: cerebral clinical history and examination remains the cornerstone of this process.
ischemia and infarction, intracerebral hemorrhage, and subarachnoid Cerebrovascular disease typically produces focal brain dysfunction of sud-
hemorrhage. Cerebral ischemia and infarction are caused by processes den onset in a single location. The primary exception to this is aneurysmal
that reduce cerebral blood flow. Reductions in whole brain blood flow SAH, which usually presents as a sudden onset of severe headache, with or
due to systemic hypotension or increased intracranial pressure (ICP) may without nausea, vomiting, or loss of consciousness. In some cases, a less
produce infarction in the distal territories or border zones of the major severe aneurysmal hemorrhage may present as a headache of moderate
cerebral arteries. More prolonged global reductions cause diffuse hemi- intensity, neck pain, and nonspecific symptoms. A high index of suspicion
spheric damage without localizing findings or, at its most severe, produce is needed in order to avoid missing the diagnosis of SAH. Focal brain
brain death. Prolonged regional reductions can lead to focal brain infarc- dysfunction may not always cause an obvious hemiparesis. Neurologic
tions. Local arterial vascular disease accounts for approximately 65% to deficits such as neglect, agnosia, aphasia, visual field defects, or amne-
70% of all focal brain infarctions. In most cases, arterial disease serves sia may be the only manifestations of brain infarction or hemorrhage.
as a nidus for local thrombus formation with or without subsequent Multiple small brain infarcts may produce impaired consciousness with
distal embolization. Focal arterial stenosis in combination with systemic minimal or no focal neurologic deficits, mimicking metabolic, or toxic
hypotension is a very rare cause of focal brain infarction. Atherosclerosis encephalopathy. The clinical distinction between cerebral infarction and
is the most common cause of local disease in the large arteries supplying intracerebral hemorrhage is unreliable as both produce sudden focal defi-
the brain. Disease of smaller penetrating arteries may cause small deep cits. Large hemorrhages may produce vomiting or unconsciousness, but
(lacunar) infarcts. While emboli arising from the heart cause approxi- so may infarcts in the vertebrobasilar circulation. The initial neurologic
mately 30% of all cerebral infarcts in a general population, they assume examination provides a baseline for monitoring the subsequent clinical
more importance in ICU patients. Atrial fibrillation is the most common course. A thorough medical evaluation is necessary to detect systemic
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of these causes. Atherosclerotic emboli following heart surgery, infec- diseases that may be the cause of the cerebrovascular problem. Careful
tive endocarditis, nonbacterial thrombotic endocarditis, and ventricular evaluation of the heart is imperative to detect conditions that might pre-
mural thrombus secondary to acute myocardial infarction or cardio- dispose to embolization, particularly atrial fibrillation, recent myocardial
myopathy should all be considered in the appropriate circumstances. infarction, and more rarely, infective endocarditis.
More rare causes of cerebral infarction must also be considered in the X-ray computed tomography (CT) is the diagnostic neuroimaging test
ICU. These include dissections of the carotid or vertebral artery (after of choice for patients with acute stoke. It is rapid and can be performed
direct neck trauma, “whiplash” injuries or forced hyperextension during easily on acutely ill patients. Acute intracerebral hemorrhage is easily
endotracheal intubation), intracranial arterial or venous thrombosis identified by noncontrast CT. Cerebral infarction may not be demon-
secondary to meningeal or parameningeal infections, and paradoxical strated by CT for several days. If the infarct is small enough, it may never
embolization from venous thrombosis via a patent foramen ovale. 1 be apparent. Magnetic resonance diffusion weighted imaging is more
Hemorrhage into the basal ganglia, thalamus, and cerebellum in sensitive than CT for lesion detection in the early period following isch-
middle-aged patients with long-standing hypertension is the most emic infarction. Due to its higher resolution, magnetic resonance imag-
common type of intracerebral hemorrhage. In hypertensive patients ing (MRI) is also superior for detecting small infarcts (especially those in

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