Documentos de Académico
Documentos de Profesional
Documentos de Cultura
Hemorrhagic strokes account for 15% to 20% of cerebrovascular disorders and are primarily caused by intracranial or subarachnoid hemorrhage.
Hemorrhagic strokes are caused by bleeding into the brain tissue, the ventricles, or the subarachnoid space. Primary intracerebral hemorrhage from a spontaneous rupture of small vessels accounts for approximately 80% of hemorrhagic strokes and is caused chiefly by uncontrolled hypertension. Subarachnoid hemorrhage results from a ruptured intracranial aneurysm (a weakening in the arterial wall) in about half the cases
Another common cause of intracerebral hemorrhage in the elderly is cerebral amyloid angiopathy, which involves damage caused by the deposit of beta-amyloid protein in the small and medium-sized blood vessels of the brain. Secondary intracerebral hemorrhage is associated with arteriovenous malformations (AVMs), intracranial aneurysms, intracranial neoplasms, or certain medications (eg, anticoagulants, amphetamines).
The mortality rate has been reported to be as high as 43% at 30 days after an intracranial hemorrhage . Patients who survive the acute phase of care usually have more severe deficits and a longer recovery time compared to those with ischemic stroke.
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 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.
Intracerebral Hemorrhage
An intracerebral hemorrhage, or bleeding into the brain substance, 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 (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. Occasionally, the bleeding ruptures the wall of the lateral ventricle and causes intraventricular hemorrhage, which is frequently fatal.
Arteriovenous Malformations
An AVM is 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.
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.
Clinical Manifestations
The patient with a hemorrhagic stroke can present with a wide variety of neurologic deficits, similar to the patient with ischemic stroke. The conscious patient most commonly reports a severe headache Many of the same motor, sensory, cranial nerve, cognitive, and other functions that are disrupted after ischemic stroke are also altered after a hemorrhagic stroke. Other symptoms that may be observed more frequently in patients with acute intracerebral hemorrhage (compared with ischemic stroke) are vomiting, an early sudden change in level of consciousness, and possibly focal seizures due to frequent brain stem involvement .
Clinical Manifestations
Rupture of an aneurysm or AVM usually produces a sudden, unusually severe headache and often loss of consciousness for a variable period of time. There may be pain and rigidity of the back of the neck (nuchal rigidity) and spine due to meningeal irritation. Visual disturbances (visual loss, diplopia, ptosis) occur if the aneurysm is adjacent to the oculomotor nerve. Tinnitus, dizziness, and hemiparesis may also occur. In other cases, severe bleeding occurs, resulting in cerebral damage, followed rapidly by coma and death.
Prevention
Primary prevention of hemorrhagic stroke is the best approach and includes managing hypertension and ameliorating other significant risk factors. Control of hypertension, especially in people older than 55 years of age, clearly reduces the risk for hemorrhagic stroke. Additional risk factors are increased age, male gender, and excessive alcohol intake). A prevention effort unique to hemorrhagic stroke is to increase the public's awareness about the association between phenylpropanolamine (PPA, an ingredient found in appetite suppressants as well as cold and cough agents) and hemorrhagic stroke.
Complications
Potential complications of hemorrhagic stroke 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.
Vasospasm
The development of cerebral vasospasm (narrowing of the lumen of the involved cranial blood vessel. 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. Monitoring for vasospasm may be performed through the use of bedside transcranial Doppler ultrasonography (TCD) or follow-up cerebral angiography). Vasospasm leads to increased vascular resistance, which impedes cerebral blood flow and causes brain 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).
Increased ICP
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. If the patient shows evidence of deterioration from increased ICP (due to cerebral edema, herniation, hydrocephalus, or vasospasm).
Systemic Hypertension
Preventing sudden systemic hypertension is critical in the management of intracerebral hemorrhage. Although specific goals for blood pressure management are individualized for each patient, systolic blood pressure may be lowered to less than 150 mm Hg to prevent hematoma enlargement . If blood pressure is elevated, antihypertensive therapy .
Medical Management
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 for rebleeding, and to prevent or treat complications. Management is primarily supportive and consists of bed rest with sedation to prevent 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 sequential compression devices to prevent deep vein thrombosis (DVT) .
Surgical Management
In many cases, a primary intracerebral hemorrhage is not treated surgically. However, if the diameter of the hematoma exceeds 3 cm and the Glasgow Coma Scale score decreases, .surgical evacuation is strongly recommended for the patient with a cerebellar hemorrhage. Surgical evacuation is most frequently accomplished via a craniotomy . The patient with an intracranial aneurysm is prepared for surgical intervention as soon as his or her condition is considered stable. Morbidity and mortality from surgery are high if the patient is stuporous or comatose (Hunt-Hess grade 4 or 5). Surgical treatment of the patient with an unruptured aneurysm is an option.
Surgical Management
The goal of surgery is to prevent bleeding in an unruptured aneurysm or 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 ligature or a clip across its neck. If this is not anatomically possible, the aneurysm can be reinforced by wrapping it with some substance to provide support and induce scarring. Several less invasive endovascular treatments are now being used for aneurysms. These procedures are performed by neurosurgeons in neurointerventional radiology facilities. Two procedures are endovascular treatment (occlusion of the parent artery) and aneurysm coiling (obstruction of the aneurysm site with a coil). Although these techniques are associated with lower risks than intracranial surgery in general, secondary stroke and rupture of the aneurysm are still potential complications
Altered level of consciousness Sluggish pupillary reaction Motor and sensory dysfunction Cranial nerve deficits (extraocular eye movements, facial droop, presence of ptosis) Speech difficulties and visual disturbance Headache and nuchal rigidity or other neurologic deficits
Nursing Interventions Optimizing Cerebral Tissue Perfusion 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. Relieving Sensory Deprivation and Anxiety Sensory stimulation is kept to a minimum for patients on aneurysm precautions. For patients who are awake, alert, and oriented, an explanation of the restrictions helps reduce the patient's sense of isolation. Reality orientation is provided to help maintain orientation.
Monitoring and Managing Potential Complications Vasospasm Seizures Hydrocephalus Blood in the subarachnoid space or ventricles impedes the circulation of CSF, resulting in hydrocephalus. A CT scan that indicates dilated ventricles confirms the diagnosis. Hydrocephalus can occur within the first 24 hours (acute) after subarachnoid hemorrhage or several days (subacute) to several weeks (delayed) later. Symptoms vary according to the time of onset and may be nonspecific. Acute hydrocephalus is characterized by sudden onset of stupor or coma and is managed with a ventriculostomy drain to decrease ICP
Rebleeding The rate of recurrent hemorrhage is approximately 2% after a primary intracerebral hemorrhage. Hypertension is the most serious risk factor, suggesting the importance of appropriate antihypertensive treatment . Hyponatremia After subarachnoid hemorrhage, hyponatremia is found in 10% to 40% of patients.Laboratory data must be checked frequently, and hyponatremia (defined as a serum sodium concentration of less than 135 mEq/L) must be identified as early as possible. The physician needs to be notified of a low serum sodium level that has persisted for 24 hours or longer
Promoting Home and CommunityBased Care Teaching Patients Self-Care Continuing Care Evaluation Expected Patient Outcomes
Expected patient outcomes may include the following: Demonstrates intact neurologic status and normal vital signs and respiratory patterns
Is alert and oriented to time, place, and person Demonstrates normal speech patterns and intact cognitive processes Demonstrates normal and equal strength, movement, and sensation of all four extremities Exhibits normal deep tendon reflexes and pupillary responses
Is free of complications
Exhibits absence of vasospasm Exhibits normal vital signs and neuromuscular activity without seizures Verbalizes understanding of seizure precautions Exhibits normal mental status and normal motor and sensory status Reports no visual changes