Hemorrhagic Stroke

Bleeding into brain tissue or meningeal spaces.

Intracranial hemorrhage accounts for about 20% of strokes. Intracranial hemorrhage is most often caused by aneurysms, vascular malformations, bleeding disorders, hypertension, amyloid angiopathy, and use of illicit drugs.

Subarachnoid Hemorrhage

Bleeding into the subarachnoid space.

Subarachnoid hemorrhage accounts for about 10% of all strokes but for a much higher percentage of deaths due to stroke. Subarachnoid hemorrhage increases the pressure within the cranium, impairs the drainage of cerebrospinal fluid (CSF), and irritates the arteries at the base of the brain. The blood is usually released quickly into the subarachnoid space at arterial pressure and becomes widely dispersed around the brain and spinal cord. Delayed vasoconstriction of the cerebral arteries, beginning >= 48 hours after hemorrhage and possibly continuing for >= 1 week, is common. Vasoconstriction with delayed brain ischemia is likely when the hemorrhage is large or produces thick focal collections of blood.

Etiology

The most common causes are vascular malformations, cerebral aneurysms, bleeding disorders (most often due to use of anticoagulants), head trauma, and amyloid angiopathy (degenerative hyalinization of the arteries in the brain and subarachnoid spaces). Vascular malformations rarely cause subarachnoid hemorrhage in elderly patients. Aneurysms occur in the elderly but slightly less commonly than in younger persons. Also, vascular malformations and saccular aneurysms are less likely to be life threatening in persons > 60; dangerous ones have usually ruptured before that age.

Head trauma, common among the elderly because of their tendency to fall, is often undiagnosed. After a fall, patients are often confused or amnesic and cannot clearly describe the event. The physician may incorrectly attribute blood in CSF to a spontaneous subarachnoid hemorrhage rather than to trauma, thus needlessly performing angiography to search for aneurysms.

Amyloid angiopathy can cause subarachnoid or intracerebral hemorrhage. Patients often have multiple, recurrent bleeding episodes. Dementia may coexist because of Alzheimer-like changes in the cortex.

Symptoms and Signs

Symptoms and signs of subarachnoid hemorrhage are no different in the elderly than in younger patients. Patients invariably have headache. Headache often begins suddenly, usually during physical activity, and becomes severe almost immediately. The pain is usually diffuse, but at times it is most severe at the back of the head and neck and may radiate down the back or down the lower limbs in a sciatic pattern. Nausea and vomiting, due to the sudden increase in intracranial pressure, are common. Usually, patients cannot perform any activity and often become restless, agitated, and confused.

At presentation, patients are usually not paralyzed and often do not have important focal neurologic signs (eg, hemiparesis, hemisensory loss, hemianopia). During physical examination, the most apparent abnormality is usually a change in the level of consciousness, resulting in restlessness, delirium, sleepiness, stupor, or coma. Stiff neck, difficulty concentrating, impaired short-term memory, and impaired extensor plantar reflexes are also common.

Vasoconstriction may occur after surgical manipulation of the arteries, especially if blood is released into the subarachnoid space during or after the procedure. If vasoconstriction and delayed brain ischemia develop, focal signs (eg, hemiparesis) can occur and are, with headache and decreased alertness, the most common findings.

Cardiac arrhythmias, hydrocephalus, and rebleeding are common complications.

Diagnosis

The approach to diagnosis is the same for elderly and for younger patients. The most important diagnostic tests are CT, lumbar puncture, and angiography. MRI may be used instead of CT. When performed within 24 to 48 hours of hemorrhage, unenhanced CT scans are likely to show blood as hyperdensity in the cisterns, between the cerebral gyri, or in the ventricles. Subarachnoid hemorrhages that are small or that occurred days before may not be visible. CT can also detect small contusions, subdural hematomas, and skull fractures; sometimes, enhanced CT can detect an aneurysm. Restlessness and agitation interfere with the patient's ability to cooperate during cranial CT and thus may compromise quality.

All symptomatic patients have grossly visible blood-stained CSF under increased pressure when lumbar puncture is performed within hours or a few days of the hemorrhage. If patients have severe unexplained headache, CT is usually performed before lumbar puncture. However, if patients have no focal neurologic signs or papilledema and can walk normally, a lumbar puncture can be safely performed without CT.

Computed tomography angiography and magnetic resonance angiography are also useful for finding large aneurysms, but standard catheter angiography is the definitive test for determining their location, size, and shape. If the diagnosis of subarachnoid hemorrhage has been confirmed, angiography is usually delayed until the patient is fit for surgery.

In patients with vasoconstriction, CT scans show no new bleeding but may show a hypodense area of cerebral infarction. Angiography shows general or focal vasoconstriction. Transcranial Doppler ultrasonography, which can measure blood flow velocities in intracranial arteries, is very useful for detecting vasoconstriction and monitoring its severity. CT or lumbar puncture can detect rebleeding.

Treatment

When the cause is an aneurysm or vascular malformation, the involved vessels are clipped or coated before the next bleeding episode. When the cause is use of warfarin, hypoprothrombinemia must be quickly reversed with vitamin K or fresh frozen plasma. When the cause is head trauma, immediate evaluation and treatment of accompanying brain contusions, hematomas, and lacerations are necessary.

All patients should be monitored in a quiet room. Dehydration should be avoided, because it can lead to decreased cerebral blood flow. The sudden increase in intracranial pressure may increase systemic blood pressure; severe hypertension (> 170/110 mm Hg) should be controlled. However, because increased intracranial pressure increases venous pressure in the brain and in the dural venous sinuses, systemic blood pressure must exceed this elevated venous pressure if the brain is to be perfused.

Corticosteroids help control increased intracranial pressure and brain swelling. For example, dexamethasone 10 mg IV may be given, followed by 4 to 20 mg IV or IM q 6 h until response is maximal, then switching to oral corticosteroids. When vasoconstriction is present, both nimodipine and hypervolemic therapy should be considered.

Intracerebral Hemorrhage

Bleeding directly into the brain.

Bleeding destroys brain tissue because of effects of local pressure. Intracerebral hemorrhage accounts for about 10% of all strokes but for a much higher percentage of deaths due to stroke. After age 60, intracerebral hemorrhage is more common than subarachnoid hemorrhage. Usually, intracerebral hemorrhage arises from small arteries or arterioles.

Hypertension and coexisting degenerative changes due to aging increase susceptibility to intracerebral hemorrhage in the elderly. Bleeding disorders and use of anticoagulants pose additional risk and more often result in death than does intracerebral hemorrhage due to other conditions. Amyloid angiopathy contributes to up to 20% of intracerebral hemorrhages in patients > 70. Aneurysms and vascular malformations are uncommon causes. Occasionally, bleeding occurs into a previously unsuspected brain tumor, especially if it is metastatic.

Location of hemorrhage varies (see Figure 44-3). Warfarin-induced hemorrhages tend to occur in the lobes of the cerebrum and the cerebellum; they begin more insidiously and progress more gradually than hemorrhages due to other conditions. Hemorrhages due to amyloid angiopathy are almost always lobar. Traumatic hematomas are usually multiple. They are located on the surface of the brain, commonly on the orbital frontal lobes and tips of the temporal lobes, which are close to the rough bony ridges at the base of the skull.

Symptoms, Signs, and Diagnosis

The earliest symptoms result from loss of function subserved by the brain region in which the hemorrhage occurs. For example, hemorrhage into the left putamen and internal capsule causes right limb paralysis; hemorrhage in the right occipital lobe causes a left visual field defect; and cerebellar hemorrhage causes an inability to walk. The hemorrhage may expand within minutes, or at most a few hours, and act as a mass, increasing intracranial contents and pressure and causing headache, vomiting, and decreased alertness. However, these symptoms may not occur if the hemorrhage remains small. Nearly 50% of elderly patients with small to moderate intracerebral hemorrhages do not have headache and remain alert because previous atrophy in the brain provides additional space to accommodate the extra contents. On examination, signs of focal abnormality of brain function are apparent (see Table 44-9).

If intracerebral hemorrhage progresses, consciousness usually decreases and focal neurologic signs increase. For example, on admission, a patient with a right putamenal hemorrhage may have left hemiparesis, conjugate deviation of the eyes to the right, an extensor left plantar reflex, and normal pupils. If the hematoma expands or the region surrounding the hematoma becomes edematous, the right plantar reflex may become extensor, the eyes may not move horizontally in either direction, the right pupil may become dilated and fixed, and stupor may develop. Without aggressive treatment, patients whose condition worsens in this manner have a high mortality rate.

On CT scans, hematomas appear as white, hyperdense, well-circumscribed lesions. CT can also show location and size, drainage into the ventricles or onto the brain's surface, shifts of intracranial contents, and unsuspected tumors or vascular malformation adjacent to the hematoma. If the patient is anemic, the hematoma may appear hypodense or may have a fluid level.

MRI shows the extent and dissection of the hemorrhage in the coronal and sagittal planes better than CT. MRI and magnetic resonance angiography can show vascular malformations. Differentiation between hemorrhage and ischemia is less obvious on routine MRI scans than on CT scans. Fluid-attenuating inversion recovery and gradient-echo susceptibility MRI (sensitive to the presence of iron-containing compounds and calcium) are often required to detect very recent hemorrhages. MRI clearly shows hemosiderin from old hemorrhages.

Treatment

Patients with large hemorrhages usually die before treatment can be initiated. Those with small hemorrhages, which are self-contained and self-limited, require little treatment except preventive measures (eg, controlling hypertension). Although severe hypertension (> 170/100 mm Hg) should be controlled, blood pressure should not be reduced to normal levels, because doing so could compromise cerebral perfusion. Corticosteroids and osmotic drugs (eg, mannitol, glycerol) may help control increased intracranial pressure (see Table 44-10). Moderate-sized (2- to 4-cm) hematomas are the most important to treat, especially if the patient's condition is worsening.

Surgical drainage of an expanding hematoma can be lifesaving. However, because surgical drainage substitutes a cavity for the hematoma, it does not diminish the extent of paralysis or other focal abnormalities. For these reasons, neurologic examination should be repeated frequently in patients with new intracerebral hemorrhages. Repeated CT scans often show enlargement of the hematoma and increased pressure effects.

Thalamic and pontine hematomas are not accessible surgically. Surgical decompression is most feasible for cerebellar hemorrhages and lobar hematomas near the brain surface. Some hematomas can be drained stereotactically, using a burr hole, rather than by craniotomy. Local instillation of a fibrinolytic drug can make the hematoma more liquid and facilitate stereotactic drainage.