Hemorrhagic Stroke

Subarachnoid Hemorrhage

A subarachnoid hemorrhage (hemorrhage into the subarachnoid space) may occur as a result of an AVM, intracranial aneurysm, trauma, or hypertension. The most common causes are a leaking aneurysm in the area of the circle of Willis and a congenital AVM of the brain

Increased Intracranial Pressure

An increase in ICP can occur after either an ischemic or a hemorrhagic stroke but almost always follows a subarachnoid hemorrhage, usually because of disturbed circulation of CSF caused by blood in the basal cisterns. Neurologic assessments are performed frequently, and if there is evidence of deterioration from increased ICP (due to cerebral edema, herniation, hydrocephalus, or vasospasm), CSF drainage may be instituted by ventricular catheter drainage. Mannitol may be administered to reduce ICP. When mannitol is used as a long-term measure to control ICP, dehydration and disturbances in electrolyte balance (hyponatremia or hypernatremia; hypokalemia or hyperkalemia) may occur. Mannitol pulls water out of the brain tissue by osmosis and reduces total body water through diuresis. The patient's fluid balance is monitored continuously and is assessed for signs of dehydration and for rebound elevation of ICP. Other interventions may include elevating the head of the bed, sedation, hyperventilation, and use of hypertonic saline

Intracerebral Hemorrhage

An intracerebral hemorrhage, or bleeding into the brain tissue, is most common in patients with hypertension and cerebral atherosclerosis, because degenerative changes from these diseases cause rupture of the blood vessel. An intracerebral hemorrhage may also result from certain types of arterial pathology, brain tumors, and the use of medications (e.g., oral anticoagulants, amphetamines, and illicit drug use). Bleeding occurs most commonly in the cerebral lobes, basal ganglia, thalamus, brain stem (mostly the pons), and cerebellum (Hickey, 2009). Occasionally, the bleeding ruptures the wall of the lateral ventricle and causes intraventricular hemorrhage, which is frequently fatal.

Intracranial (Cerebral) Aneurysm

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, which results in a defect in the vessel wall with subsequent weakness of the wall; a congenital defect of the vessel wall; hypertensive vascular disease; head trauma; or advancing age. Any artery within the brain can be the site of a cerebral aneurysm, but these lesions usually occur at the bifurcations of the large arteries at the circle of Willis . The cerebral arteries most commonly affected by an aneurysm are the internal carotid artery, anterior cerebral artery, anterior communicating artery, posterior communicating artery, posterior cerebral artery, and middle cerebral artery. Multiple cerebral aneurysms are not uncommon

Assessment and Diagnostic Findings

Any patient with suspected stroke should undergo a CT scan or MRI to determine the type of stroke, the size and location of the hematoma, and the presence or absence of ventricular blood and hydrocephalus. Cerebral angiography confirms 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 negative, and subarachnoid hemorrhage must be confirmed. Lumbar puncture in the presence of increased ICP could result in brain stem herniation or rebleeding. When diagnosing a hemorrhagic stroke in a patient younger than 40 years, some clinicians obtain a toxicology screen for illicit drug use.

Implementing Aneurysm Precautions.

Cerebral aneurysm precautions are implemented for the patient with a diagnosis of aneurysm to provide a nonstimulating environment, prevent increases in ICP, and prevent further bleeding. The patient is placed on immediate and absolute bed rest in a quiet, nonstressful environment, because activity, pain, and anxiety elevate the blood pressure, which increases the risk for bleeding. Visitors, except for family, are restricted The head of the bed is elevated 15 to 30 degrees to promote venous drainage and decrease ICP. Some neurologists, however, prefer that the patient remain flat to increase cerebral perfusion. Any activity that suddenly increases the blood pressure or obstructs venous return is avoided. This includes the Valsalva maneuver, straining, forceful sneezing, pushing oneself up in bed, acute flexion or rotation of the head and neck (which compromises the jugular veins), and cigarette smoking. Any activity requiring exertion is contraindicated. The patient is instructed to exhale through the mouth during voiding or defecation to decrease strain. No enemas are permitted, but stool softeners and mild laxatives are prescribed. Both prevent constipation, which would cause an increase in ICP, as would enemas. Dim lighting is helpful, because photophobia (visual intolerance of light) is common. Coffee and tea, unless decaffeinated, are usually eliminated. Anti-embolism stockings or sequential compression devices may be prescribed to decrease the incidence of DVT resulting from immobility. The legs are observed for signs and symptoms of DVT (tenderness, redness, swelling, warmth, and edema), and abnormal findings are reported. The nurse administers all personal care. The patient is fed and bathed to prevent any exertion that might increase the blood pressure. External stimuli are kept to a minimum, including no television, no radio, and no reading. Visitors are restricted in an effort to keep the patient as quiet as possible. This precaution must be individualized based on the patient's condition and response to visitors. A sign indicating this restriction should be placed on the door of the room, and the restrictions should be discussed with both patient and family. The purpose of aneurysm precautions should be thoroughly explained to both the patient (if possible) and family

Hypertension

Hypertension is the most common cause of intracerebral hemorrhage, and its treatment is critical. Specific goals for blood pressure management, which are individualized for each patient, remain controversial. Blood pressure goals may depend on the presence of increased ICP. Clinical trials are currently ongoing to further investigate control of blood pressure in intracerebral hemorrhage. Systolic blood pressure may be lowered to prevent hematoma enlargement. If blood pressure is elevated, antihypertensive therapy (labetalol [Trandate], nicardipine [Cardene], nitroprusside [Nitropress], hydralazine [Apresoline]) may be prescribed. During the administration of antihypertensive agents, hemodynamic monitoring is important to detect and avoid a precipitous drop in blood pressure, which can produce brain ischemia. Stool softeners are used to prevent straining, which can elevate the blood pressure

Cerebral Hypoxia and Decreased Blood Flow

Immediate complications of a hemorrhagic stroke include cerebral hypoxia, decreased cerebral blood flow, and extension of the area of injury. Providing adequate oxygenation of blood to the brain minimizes cerebral hypoxia. Brain function depends on delivery of oxygen to the tissues. Administering supplemental oxygen and maintaining the hemoglobin and hematocrit at acceptable levels will assist in maintaining tissue oxygenation. Cerebral blood flow depends on the blood pressure, cardiac output, and integrity of cerebral blood vessels. Adequate hydration (IV fluids) must be ensured to reduce blood viscosity and improve cerebral blood flow. Extremes of hypertension or hypotension 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, resulting in further injury to the brain. Observing for seizure activity and initiating appropriate treatment are important components of care after a hemorrhagic stroke

Arteriovenous Malformations (AVM)

Most AVMs are caused by an abnormality in embryonal development that leads to a tangle of arteries and veins in the brain that lacks a capillary bed. The absence of a capillary bed leads to dilation of the arteries and veins and eventual rupture. AVM is a common cause of hemorrhagic stroke in young people

complications

Potential complications of hemorrhagic stroke include rebleeding or hematoma expansion; 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

Prevention

Primary prevention of hemorrhagic stroke is the best approach and includes managing hypertension and ameliorating other significant risk factors. Control of hypertension can reduce the risk of hemorrhagic stroke. Additional risk factors are increased age, male gender, and excessive alcohol intake. Stroke risk screenings provide an ideal opportunity to lower hemorrhagic stroke risk by identifying high-risk individuals or groups and educating patients and the community about recognition and prevention

Vasospasm

The development of cerebral vasospasm (narrowing of the lumen of the involved cranial blood vessel) is a serious complication of subarachnoid hemorrhage and is a leading cause of morbidity and mortality in those who survive the initial subarachnoid hemorrhage. Of those with cerebral vasospasm, 15% to 20% die. The mechanism responsible for vasospasm is not clear, but it is associated with increasing amounts of blood in the subarachnoid cisterns and cerebral fissures, as visualized by CT scan. Monitoring for vasospasm may be performed through the use of bedside transcranial Doppler ultrasonography or follow-up cerebral angiography. Vasospasm most frequently occurs 7 to 10 days after initial hemorrhage, when the clot undergoes lysis (dissolution), and the chance of rebleeding is increased. It leads to increased vascular resistance, which impedes cerebral blood flow and causes brain ischemia (delayed cerebral ischemia) and infarction. 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, hemiparesis). Management of vasospasm remains difficult and controversial. 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. Medication may be effective in the treatment of vasospasm. 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 action of vasospasm if already present. The most frequently used calcium channel blocker is nimodipine (Nimotop). Current guidelines recommend that nimodipine be prescribed for all patients with subarachnoid hemorrhage. This is currently the only drug approved by the FDA for the prevention and treatment of vasospasm in subarachnoid hemorrhage Another therapy for vasospasm and the resulting delayed cerebral ischemia, referred to as triple-H therapy, is aimed at minimizing the deleterious effects of the associated cerebral ischemia and includes (1) fluid volume expanders (hypervolemia), (2) induced arterial hypertension, and (3) hemodilution. However, current research and guidelines now endorse euvolemia to prevent delayed cerebral ischemia and induced arterial hypertension for treatment of delayed cerebral ischemia

MEDICAL MGMT

The goals of medical treatment for hemorrhagic stroke are to allow the brain to recover from the initial insult (bleeding), to prevent or minimize the risk of rebleeding, and to prevent or treat complications. Management may consist of bed rest with sedation to prevent agitation and stress, management of vasospasm, and surgical or medical treatment to prevent rebleeding. If the bleeding is caused by anticoagulation with warfarin, the INR may be corrected with fresh-frozen plasma and vitamin K. Reversing the anticoagulation effect of the newer anticoagulants is more complicated. Protocols may include hemodialysis, the use of oral activated charcoal, administration of prothrombin complex concentrates, or administration of recombinant activated factor VII. If seizures occur, they are treated with antiseizure drugs such as phenytoin (Dilantin). Hyperglycemia should also be treated, and normoglycemia is recommended. The patient is fitted with sequential compression devices or anti-embolism stockings to prevent deep vein thrombosis (DVT). If the patient is not mobile after 1 to 4 days from the onset of the hemorrhage and there is documentation of the bleeding ceasing, then DVT prevention medications (low-molecular-weight heparin or unfractionated heparin) may be prescribed. Analgesic agents may be prescribed for head and neck pain. Fever should be treated with acetaminophen (Tylenol), iced saline boluses, and devices such as cooling blankets. After discharge, most patients will require antihypertensive medications to decrease their risk of another intracerebral hemorrhage

Pathophysiology

The pathophysiology of hemorrhagic stroke depends on the cause and type of cerebrovascular disorder. Symptoms are produced when a primary hemorrhage, aneurysm, or AVM presses on nearby cranial nerves or brain tissue or, more dramatically, when an aneurysm or AVM ruptures, causing subarachnoid hemorrhage (hemorrhage into the cranial subarachnoid space). Normal brain metabolism is disrupted by the brain's exposure 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.

Hemorrhagic stroke

hemorrhagic strokes are caused by bleeding into the brain tissue, the ventricles, or the subarachnoid space.