Hemorrhagic strokes account for 15% of cerebrovascular disor-ders and are primarily caused by an intracranial or subarachnoid hemorrhage. Each year in the United States there are approxi-mately 50,000 intracerebral hemorrhages and 25,000 cases of subarachnoid hemorrhage from ruptured intracranial aneurysm (Pfohman & Criddle, 2001; Qureshi et al., 2001).
Patients generally have more severe deficits and a longer re-covery time compared to those with ischemic stroke (AHCPR, 1995). The mean cost per discharge for subarachnoid hemor-rhage was estimated at $39,994, compared to $21,535 for in-tracranial hemorrhage. The mean length of stay was 22 days for subarachnoid hemorrhage and 19 for intracranial hemorrhage (Matchar & Samsa, 2000).
Hemorrhagic strokes are caused by bleeding into the brain tis-sue, the ventricles, or the subarachnoid space. Primary intracere-bral hemorrhage from a spontaneous rupture of small vessels accounts for approximately 80% of hemorrhagic strokes and is primarily caused by uncontrolled hypertension (Qureshi et al., 2001). Secondary intracerebral hemorrhage is associated with arteriovenous malformations (AVMs), intracranial aneurysms, or certain medications (eg, anticoagulants and amphetamines) (Qureshi et al., 2001).
The pathophysiology of hemorrhagic stroke depends on the cause and type of cerebrovascular disorder. Symptoms are produced when an aneurysm or AVM enlarges and presses on nearby cranial nerves or brain tissue or, more dramatically, when ananeurysm or AVM ruptures, causing subarachnoid hemorrhage (hemorrhage into the cranial subarachnoid space). Normal brain metabolism is disrupted by the brain being exposed to blood; by an increase in ICP resulting from the sudden entry of blood into the subarachnoid space, which compresses and injures brain tissue; or by secondary ischemia of the brain resulting from the reduced perfusion pressure and vasospasm that frequently accompany subarachnoid hemorrhage.
An intracerebral hemorrhage, or bleeding into the brain sub-stance, is most common in patients with hypertension and cere-bral atherosclerosis because degenerative changes from these diseases cause rupture of the vessel. They also may be due to cer-tain types of arterial pathology, brain tumor, and the use of med-ications (oral anticoagulants, amphetamines, and illicit drugs such as crack and cocaine).
The bleeding is usually arterial and occurs most commonly in the cerebral lobes, basal ganglia, thalamus, brain stem (mostly the pons), and cerebellum (Qureshi et al., 2001). Occasionally, the bleeding ruptures the wall of the lateral ventricle and causes in-traventricular hemorrhage, which is frequently fatal.
An intracranial (cerebral) aneurysm is a dilation of the walls of a cerebral artery that develops as a result of weakness in the arterial wall. The cause of aneurysms is unknown, although research is ongoing. An aneurysm may be due to atherosclerosis, resulting in a defect in the vessel wall with subsequent weakness of the wall; a congenital defect of the vessel wall; hypertensive vascular dis-ease; head trauma; or advancing age.
Any artery within the brain can be the site of cerebral aneurysms, but they usually occur at the bifurcations of the large arteries at the circle of Willis (Fig. 62-5). The cerebral arteries most com-monly affected by an aneurysm are the internal carotid artery (ICA), anterior cerebral artery (ACA), anterior communicating artery (ACoA), posterior communicating artery (PCoA), poste-rior cerebral artery (PCA), and middle cerebral artery (MCA). Multiple cerebral aneurysms are not uncommon.
AVM is due to an abnormality in embryonal development that leads to a tangle of
arteries and veins in the brain without a
A subarachnoid hemorrhage (hemorrhage into the subarachnoid space) may occur as a result of an AVM, intracranial aneurysm, trauma, or hypertension. The most common cause is a leaking aneurysm in the area of the circle of Willis or a congenital AVM of the brain.
The patient with a hemorrhagic stroke can present with a wide variety of neurologic deficits, similar to the patient with ischemic stroke. A comprehensive assessment will reveal the extent of the neurologic deficits. Many of the same motor, sensory, cranial nerve, cognitive, and other functions that are disrupted following ischemic stroke are altered following a hemorrhagic stroke. Table 62-2 reviews the neurologic deficits frequently seen in stroke pa-tients. Table 62-3 compares the symptoms seen in right hemi-spheric stroke with those seen in left hemispheric stroke.
In addition to the neurologic deficits that are similar to is-chemic stroke, the patient with an intracranial aneurysm or AVM can have some unique clinical manifestations. Rupture of an aneurysm or AVM usually produces a sudden, unusually severe headache and often loss of consciousness for a variable period. There may be pain and rigidity of the back of the neck (nuchal rigidity) and spine due to meningeal irritation. Visual distur-bances (visual loss, diplopia, ptosis) occur when the aneurysm is adjacent to the oculomotor nerve. Tinnitus, dizziness, and hemi-paresis may also occur.
At times, an aneurysm or AVM leaks blood, leading to the for-mation of a clot that seals the site of rupture. In this instance, the patient may show little neurologic deficit. In other cases, severe bleeding occurs, resulting in cerebral damage followed rapidly by coma and death.
Prognosis depends on the neurologic condition of the patient, age, associated diseases, and the extent and location of an intra-cranial aneurysm. Subarachnoid hemorrhage from an aneurysm is a catastrophic event with significant morbidity and mortality (Pfohman & Criddle, 2001). Chart 62-6 discusses ethical issues related to the patient with a severe hemorrhagic stroke.
Any patient suspected of having a hemorrhagic stroke should un-dergo CT scanning to determine the size and location of the hematoma as well as the presence or absence of ventricular blood and hydrocephalus (Qureshi et al., 2001). CT scan and cerebral angiography confirm the diagnosis of an intracranial aneurysm or AVM. These tests show the location and size of the lesion and provide information about the affected arteries, veins, adjoining vessels, and vascular branches. Lumbar puncture is performed if there is no evidence of increased ICP, the CT scan results are neg-ative, and subarachnoid hemorrhage must be confirmed. Lumbar puncture in the presence of increased ICP could result in brain stem herniation or rebleeding. In diagnosing a hemorrhagic stroke in a patient younger than 40, some clinicians obtain a tox-icology screen for illicit drug use.
The Hunt-Hess classification system guides the physician in diagnosing the severity of subarachnoid hemorrhage after an aneurysmal bleed (Table 62-6). Classifying the patient by severity of neurologic deficit provides a baseline for future comparison.
Primary prevention of hemorrhagic stroke is the best approach and includes managing hypertension and ameliorating other sig-nificant risk factors (Pfohman & Criddle, 2001). Control of hy-pertension, especially in individuals over 55 years of age, clearly reduces the risk for hemorrhagic stroke (Qureshi et al., 2001). Additional factors are similar to the risks for ischemic stroke and include smoking, excessive alcohol intake, and high cholesterol (see Chart 62-2). Stroke risk screenings provide an ideal oppor-tunity to lower hemorrhagic stroke risk by identifying high-risk individuals or groups and educating the patients and the com-munity about recognition and prevention (Pfohman & Criddle, 2001).
A prevention effort unique to hemorrhagic stroke is to increase the public’s awareness about the association between phenyl-propanolamine (an ingredient found in appetite suppressants as well as cold and cough agents) and hemorrhagic stroke. Recent research has found that phenylpropanolamine is an independent risk factor for hemorrhagic stroke, especially in women (Kernan et al., 2000). Many products have been removed voluntarily from the market, but consumers should continue to look for this in-gredient on labels.
The goals of medical treatment of hemorrhagic stroke are to allow the brain to recover from the initial insult (bleeding), to prevent or minimize the risk for rebleeding, and to prevent or treat com-plications. Management consists of bed rest with sedation to pre-vent agitation and stress, management of vasospasm, and surgical or medical treatment to prevent rebleeding. Analgesics (codeine, acetaminophen) may be prescribed for head and neck pain. The patient is fitted with elastic compression stockings to prevent deep vein thrombosis, a threat to any patient on bed rest.
Potential complications include rebleeding; cerebral vasospasm resulting in cerebral ischemia; acute hydrocephalus, which results when free blood obstructs the reabsorption of cerebrospinal fluid (CSF) by the arachnoid villi; and seizures.
Immediate com-plications of a hemorrhagic stroke include cerebral hypoxia, de-creased cerebral blood flow, and extension of the area of injury. Providing adequate oxygenation of blood to the brain minimizes cerebral hypoxia. Brain function is dependent on available oxy-gen being delivered to the tissues. Administering supplemental oxygen and maintaining the hemoglobin and hematocrit at ac-ceptable levels will assist in maintaining tissue oxygenation.
Cerebral blood flow is dependent on the blood pressure, car-diac output, and integrity of cerebral blood vessels. Adequate hy-dration (IV fluids) must be ensured to reduce blood viscosity and improve cerebral blood flow. Extremes of hypertension or hy-potension need to be avoided to prevent changes in cerebral blood flow and the potential for extending the area of injury.
A seizure can also compromise cerebral blood flow. Seizures occur in approximately 5% of stroke patients (Berges et al., 2000). Observation for and appropriate treatment of seizure ac-tivity is an important component of care following a hemorrhagic stroke (Qureshi et al., 2001).
The development of cerebral vasospasm (narrowingof the lumen of the involved cranial blood vessel) is a serious com-plication of subarachnoid hemorrhage and accounts for 40% to 50% of the morbidity and mortality of those who survive the ini-tial intracranial bleed. The mechanism responsible for the spasm is not clear, but vasospasm is associated with increasing amounts of blood in the subarachnoid cisterns and cerebral fissures, as visualized by CT scan.
Vasospasm leads to increased vascular resistance, which im-pedes cerebral blood flow and causes brain ischemia and infarc-tion. The signs and symptoms reflect the areas of the brain involved. Vasospasm is often heralded by a worsening headache, a decrease in level of consciousness (confusion, lethargy, and disorientation), or a new focal neurologic deficit (aphasia, hemi-paresis [partial paralysis affecting one side of the body]).
Vasospasm frequently occurs 4 to 14 days after initial hemor-rhage when the clot undergoes lysis (dissolution), increasing the chances of rebleeding.
It is believed that early surgery to clip the aneurysm prevents rebleeding and that removal of blood from the basal cisterns around the major cerebral arteries may prevent vasospasm. The IV administration of the calcium-channel blocker nimodipine during the critical time in which vasospasm may occur may pre-vent delayed ischemic deterioration. Advances in technology have led to the introduction of interventional neuroradiology for the treatment of aneurysms. Endovascular techniques may be used in selected patients to occlude the artery supplying the aneurysm with a balloon or to occlude the aneurysm itself. As more studies on these techniques are completed, their use will increase.
Management of vasospasm remains difficult and controver-sial. Based on one theory that vasospasm is caused by an increased influx of calcium into the cell, medication therapy may be used to block or antagonize this action and prevent or reverse the ac-tion of vasospasm already present. Calcium-channel blockers may include nimodipine (Nimotop), verapamil (Isoptin), and nifedi-pine (Procardia). Other therapy for vasospasm is aimed at mini-mizing the deleterious effects of the associated cerebral ischemia and includes fluid volume expanders and induced arterial hyper-tension, normotension, or hemodilution.
An increase in ICP can follow either an ischemicor hemorrhagic stroke but almost always follows a subarachnoid hemorrhage, usually because of disturbed circulation of CSF caused by blood in the basal cisterns. If the patient shows evi-dence of deterioration from increased ICP (due to cerebral edema, herniation, hydrocephalus, or vasospasm), CSF drainage may be instituted by cautious lumbar puncture or ventricular catheter drainage, and mannitol is given to reduce ICP. When mannitol is used as a long-term measure to control ICP, dehy-dration and disturbances in electrolyte balance (hyponatremia or hypernatremia; hypokalemia or hyperkalemia) may occur. Man-nitol acts by pulling water out of the brain tissue by osmosis as well as by reducing total-body water through diuresis. The pa-tient is monitored for signs of dehydration and for rebound ele-vation of ICP.
Preventing sudden systemic hyperten-sion is critical in hemorrhagic stroke management. The goal of therapy is to maintain the systolic blood pressure at about 150 mm Hg. If blood pressure is elevated, antihypertensive therapy (labetalol [Normodyne], nicardipine [Cardene], nitroprusside [Nitropress]) may be prescribed. Hemodynamic monitoring by arterial line during the administration of antihypertensives is im-portant to detect and avoid a precipitous drop in blood pressure, which can produce brain ischemia. Because seizures cause blood pressure elevation, antiseizure agents are administered prophy-lactically. Stool softeners are used to prevent straining, which can also elevate the blood pressure.
Many patients with a primary intracerebral hemorrhage are not treated surgically. However, surgical evacuation is strongly rec-ommended for the patient with a cerebellar hemorrhage if the di-ameter exceeds 3 cm and the Glasgow Coma Scale score is below 14 (Qureshi et al., 2001). Surgical evacuation is most frequently accomplished via a craniotomy.
The patient with an intracranial aneurysm is prepared for sur-gical intervention as soon as the condition is considered stable. The Hunt-Hess classification system guides the physician in diagnosing the severity of subarachnoid hemorrhage after an aneurysm bleeds and in timing the surgery (see Table 62-6). Mor-bidity and mortality from surgery are high if the patient is stu-porous or comatose (grade IV or V). Surgical treatment of the patient with an unruptured aneurysm is an option (Pfohman & Criddle, 2001).
The goal of surgery is to prevent bleeding in an unruptured aneurysm and further bleeding in an already ruptured aneurysm. This objective is accomplished by isolating the aneurysm from its circulation or by strengthening the arterial wall. An aneurysm may be excluded from the cerebral circulation by means of a lig-ature or a clip across its neck. If this is not anatomically possible, the aneurysm can be reinforced by wrapping it with muslin or some other substance to provide support and induce scarring.
An extracranial-intracranial arterial bypass may be performed to establish collateral blood supply to allow surgery on the aneurysm. Alternatively, an extracranial method may be used, whereby the carotid artery is gradually occluded in the neck to re-duce pressure within the blood vessel. After ligation of the carotid artery, there is some risk for cerebral ischemia and sudden hemi-plegia because during the surgical procedure, there is a temporary occlusion of the blood supply to the brain (unless a temporary by-pass shunt is used). In anticipation of these complications, cere-bral blood flow and internal carotid pressure may be measured to identify patients at risk for postoperative ischemic episodes.
Several less invasive endovascular treatments are now being used for aneurysms. These procedures are performed by neuro-surgeons in neurointerventional radiology suites. Two procedures are endovascular treatment (occlusion of the parent artery) and aneurysm coiling (obstruction of the aneurysm site with a coil). While associated with lower risks than intracranial surgery in gen-eral, secondary stroke and rupture of the aneurysm are still po-tential complications (Pfohman & Criddle, 2001).
Postoperative complications include psychological symptoms (disorientation, amnesia, Korsakoff ’s syndrome, personality changes), intraoperative embolization, postoperative internal artery occlusion, fluid and electrolyte disturbances (from dys-function of the neurohypophyseal system), and gastrointestinal bleeding.