Cerebrovascular Accident Nursing Management

Introduction

A sudden loss of function resulting from the disruption of blood supply to a part of the brain, commonly referred to as a cerebral vascular accident (CVA) or stroke, occurs when there is a sudden interruption of blood flow to the brain. This interruption is typically caused by obstruction or rupture in one or more blood vessels that supply oxygen to the nerve cells in the brain. As a result, there is a sudden disruption of oxygen supply to the affected area of the brain, leading to temporary or permanent neurological dysfunction. A CVA is defined as the sudden interruption of cerebral circulation in one or more blood vessels supplying the brain, resulting in neurological symptoms that persist for longer than 24 hours.

Causes of CVA

Stroke, also known as a “brain attack,” can be caused by three different conditions affecting the cerebral arteries, all of which lead to similar clinical symptoms:

Cerebral Thrombosis: In elderly individuals, the cerebral arteries may be affected by arteriosclerosis, a condition where the artery walls become thickened and roughened. This can lead to obstruction of blood flow and the formation of blood clots. These clots, known as thrombi, can block the artery, cutting off the blood supply to part of the brain.
Cerebral Hemorrhage: The rupture of a blood vessel within the brain can result in bleeding into the brain tissue. This condition is more common among individuals with hypertension (high blood pressure).
Cerebral Embolism: An embolus, or detached clot, may become lodged in one of the cerebral arteries, leading to a stroke. This type of stroke is often associated with conditions where a clot forms on the left side of the heart and travels through the bloodstream to block a cerebral vessel. Diseases that frequently cause clot formation on the left side of the heart include:
- Mitral stenosis with atrial fibrillation
- Myocardial infarction (heart attack)
- Subacute bacterial endocarditis
A transient ischemic attack (TIA), also known as a ministroke, is a brief episode characterized by symptoms similar to those of a stroke. It occurs due to a temporary decrease in blood supply to a part of the brain. Most TIAs last only a few minutes. While TIAs have the same underlying cause as ischemic strokes, they differ in duration and impact. Unlike a stroke, which involves a prolonged lack of blood supply and can result in permanent brain damage, TIAs do not cause lasting effects on the brain. However, experiencing a TIA increases the risk of a full-blown stroke that could lead to permanent damage.

Each of these conditions can result in a stroke by disrupting the normal blood flow to the brain, leading to neurological dysfunction and potentially permanent damage

Risk factors of CVA

Cerebrovascular accidents (CVAs), commonly known as strokes, can have various risk factors, including:

Hypertension (high blood pressure): High blood pressure is a significant risk factor for stroke. It can damage blood vessels over time, increasing the likelihood of blockages or ruptures that lead to strokes.
Smoking: Smoking tobacco products can damage blood vessels and increase the risk of blood clots, both of which can lead to strokes.
Diabetes: Diabetes increases the risk of stroke, particularly if blood sugar levels are poorly controlled. High blood sugar levels can damage blood vessels and increase the likelihood of clot formation.
High Cholesterol: Elevated levels of cholesterol, especially low-density lipoprotein (LDL) cholesterol (“bad” cholesterol), can lead to the buildup of plaque in the arteries (atherosclerosis), increasing the risk of blockages that cause strokes.
Obesity and Physical Inactivity: Being overweight or obese and leading a sedentary lifestyle are associated with various cardiovascular risk factors, including high blood pressure, high cholesterol, and diabetes, all of which increase the risk of stroke.
Poor Diet: A diet high in saturated fats, trans fats, cholesterol, and sodium can contribute to the development of cardiovascular risk factors such as high blood pressure and high cholesterol, increasing the risk of stroke.
Excessive Alcohol Consumption: Heavy alcohol consumption can raise blood pressure and increase the risk of atrial fibrillation, a type of irregular heartbeat that is a risk factor for stroke.
Atrial Fibrillation (AFib): AFib is a type of irregular heartbeat that can cause blood clots to form in the heart. If a clot travels to the brain, it can cause a stroke.
Previous Stroke or Transient Ischemic Attack (TIA): Having a prior stroke or TIA increases the risk of future strokes.
Family History: A family history of stroke or certain genetic conditions that predispose individuals to stroke can increase the risk.
Age: The risk of stroke increases with age, with the majority of strokes occurring in people over the age of 65.
Gender: Men have a higher risk of stroke than women, although women are more likely to die from stroke.
Ethnicity: Certain ethnic groups, such as African Americans, Hispanic Americans, and Native Americans, have a higher risk of stroke compared to Caucasians.

Pathophysiology of CVA

The brain requires a continuous supply of nutrients from the blood because it cannot store either oxygen (O2) or glucose. Blood is delivered to the brain through two major pairs of vessels: the internal carotids and vertebrals. Cerebral autoregulation is responsible for maintaining a relatively constant blood flow rate of 750 milliliters per minute to the brain. Cerebral blood vessels dilate or constrict in response to changes in blood pressure and carbon dioxide levels.

Ischemia, or reduced blood flow, can lead to the primary death of cerebral cells, resulting in cerebral infarction and the formation of a core of necrotic tissue. Additionally, there is a secondary area of tissue damage where cells are temporarily unable to function but may still be viable. Ischemia causes various harmful effects, including:

Impaired movement of calcium and potassium, with high levels of calcium triggering the activation of enzymes that attack neuron cell membranes.
Accumulation of oxygen (O2) free radicals, which disrupt calcium metabolism further.
Reduced glucose levels in the perfusion area lead to increased lactate production, worsening cellular damage, and acidosis.
Influx of fluid-activated white cells and coagulation factors, leading to further microcirculation blockage.

Stroke associated with hemorrhage is primarily due to an abrupt increase in intracranial pressure and ischemia, followed by cerebral edema. In intracerebral bleeding, blood is forced into adjacent brain tissue, forming a hematoma. This hematoma can compress tissue and even result in brain tissue displacement or herniation. Now, let’s discuss how a patient with CVA presents clinically.

Clinical Manifestations

The specific symptoms experienced by a patient will depend on the site and severity of ischemic damage. Symptoms may include:

Sudden weakness or paralysis of the face, arm, or leg, typically on one side of the body.
Sudden difficulty speaking or understanding speech.
Sudden vision problems in one or both eyes.
Sudden severe headache with no known cause.
Loss of balance or coordination.
Confusion, dizziness, or difficulty with walking.
Numbness or tingling, often on one side of the body.

These symptoms usually occur suddenly and require immediate medical attention. It’s essential to recognize the signs of stroke and seek prompt medical care to minimize damage and improve outcomes.

Motor Effects:

Hemiparesis, or hemiplegia, occurs on the side of the body opposite the site of ischemia.
Initially, muscles may be flaccid, but they can progress to become spastic.
Dysphagia: The swallowing reflex may also be impaired.
Dysarthria: difficulty articulating speech.

Bowel and Bladder:

Increased frequency, urgency, and urinary incontinence.
Constipation.
Bowel incontinence.

Language:

Aphasia: difficulty or inability to express oneself verbally or comprehend speech.
Alexia: inability to understand written words.
Agraphia: the inability to express oneself in writing.

Sensory-Perceptual:

Diminished response to superficial sensations such as touch, pain, pressure, heat, and cold.
Diminished proprioception: Loss of awareness of the positions of various body parts relative to each other and the environment.

Cognitive-Emotional:

Emotional lability and unpredictability.
Depression.
Memory loss.
Short attention span.
Impaired reasoning, judgment, and abstract thinking abilities.

As cerebral edema increases, there may be changes in mentation, including apathy, irritability, disorientation, memory loss, withdrawal, drowsiness, stupor, or coma.

Other clinical features may include:

Numbness or loss of sensation.
Weakness or paralysis on one side of the body.
Headache, neck stiffness, and rigidity.
Vomiting.
Seizures.

Medical Management:

Investigations:

a. CT scan: used to identify the site of infarction, hematoma, and any brain structure displacement.

b. MRI: Magnetic resonance imaging is utilized to determine the site of an infarction.

c. EEG: Electroencephalography detects abnormal nerve impulse transmission.

d. Lumbar puncture for CSF analysis: typically not performed routinely, especially in cases of increased intracranial pressure (IICP).

e. Cerebral Angiography: Helps pinpoint the site of rupture or occlusion and identify collateral blood circulation.

f. History: Patient history may reveal risk factors such as hypertension.

g. Coagulation studies: used to detect any coagulation abnormalities.

Medical Treatment:

Medical management typically involves physical rehabilitation, dietary adjustments, drug therapy, and supportive care to assist patients in adapting to specific deficits, such as speech impairment and paralysis.

Respiratory Support: Ensures maintenance of the airway and delivery of oxygen as necessary. Intermittent positive-pressure breathing (IPPB) and chest physiotherapy are important interventions.
IV Fluids: Administered to maintain fluid and electrolyte balance. Fluid intake may be restricted while there is a risk of increased intracranial pressure (IICP).
Positioning: During the acute stage, bed rest is recommended. Activity levels are gradually increased as the patient’s condition improves. The head of the bed (HOB) is often elevated to 30°, as prescribed. In cases of hemorrhagic stroke or patients with IICP, elevating the HOB helps decrease cerebral perfusion and improve venous outflow.
Diet: If swallow and gag reflexes are diminished or if the patient has decreased level of consciousness (LOC), the patient may be kept NPO (nothing by mouth) and may require a gastric tube for feeding. A low-sodium and low-fat diet may be prescribed to mitigate other risk factors.

Pharmacotherapy:

Tissue Plasminogen Activator (TPA): Administered to eligible patients within a three-hour window of the stroke occurring to help dissolve clots and improve recovery. TPA can only be given if doctors are certain it will not worsen bleeding in the brain.
Anticoagulants: Heparin sodium and warfarin sodium may be prescribed for patients with cerebrovascular accidents (CVAs) or transient ischemic attacks to prevent further thrombosis.
Antihypertensive Agents: Medications like Nifedipine may be used to control very high blood pressure, which can lead to cerebral edema and IICP.
Antiplatelet Medications: Aspirin, in conjunction with dipyridamole or sulfinpyrazone, may be prescribed to prevent platelet aggregation and thrombus formation.
Glucocorticosteroids and Osmotic Diuretics: Drugs like Dexamethasone and Mannitol may be used to prevent or reduce cerebral edema.
Gastrointestinal Protection: Antacids and histamine H-receptor blockers (e.g., ranitidine) may be administered to reduce the risk of gastrointestinal hemorrhage from stress-induced gastric ulcers.
Antiepileptic Drugs: Medications such as phenytoin or phenobarbital may be prescribed to control and prevent seizures.
Sedatives/Tranquilizers: Drugs like diphenhydramine may be used cautiously to promote rest without further impairing neurological function.
Analgesics: Acetaminophen may be administered to control headaches.
Stool softeners: Docusate or bisacodyl may be given to prevent straining, which can lead to increased IICP.
Hemodilution: administration of albumin and crystalloid fluids to decrease blood viscosity and improve cerebral blood flow.

Hydration is encouraged through fluids and volume expanders to optimize cerebral perfusion.

Nursing Care:

Objectives:

Prevent complications associated with stroke.
Maintain a clear airway.
Provide a nutritious diet.
Facilitate the patient’s return to their normal or near-normal functional state.

Nursing care for a stroke patient necessitates comprehensive support, including assistance with all activities of daily living.

Environment/Position:

The patient is ideally cared for in the intensive care unit for close monitoring during the acute or critical phase.
Bed rest is recommended with the head of the bed elevated at 30° to prevent the tongue from obstructing the airway.
Supplemental oxygen, preferably 100% from a cylinder, may be administered as needed.
Maintain a quiet and restful environment, avoiding activities known to increase intracranial pressure.
Assist the patient in changing positions every 2 hours and encourage independent movement in bed as soon as possible.
Position the affected arm with the hand elevated above the wrist and the wrist above the elbow to aid venous return and reduce swelling.
Shoulders should be positioned neutrally with support as necessary to prevent joint issues.
Take care to avoid excess pressure on the shoulder joint, which is prone to subluxation and contractures.
Elevate heels off the mattress to prevent pressure injuries and position feet to prevent foot drop.
Splint your hands firmly to prevent contractures.
Avoid a supine position to prevent aspiration; maintain a side-lying position with the head of the bed elevated 10 to 20°.
Perform pressure area care and use elbow and heel protection to prevent sores.

Observation:

Immediately after admission, focus on monitoring the patient’s neurological status and preventing complications.
Regularly assess vital signs and perform neurological checks to detect signs of increased intracranial pressure.
Use the Glasgow Coma Scale to evaluate consciousness and neurological responses.
Check for signs of pressure, shearing, or friction damage during position changes.
Change the patient’s position every 2 hours and document it in the chart.
Maintain strict recording of input and output, especially with the presence of an indwelling urethral catheter; assess for signs of infection; and collect urine samples for examination.

Nutrition and Fluids:

Assess the patient’s swallowing reflexes before initiating feeding, which may be through a nasogastric tube (NGT).
Ensure proper placement of the NGT to prevent choking.
Provide a highly nutritious diet through the NGT, including items like milk, soup, custard, and light porridge.
Ensure that feeds are at a safe temperature to prevent gastrointestinal burns.
Administer fluids cautiously to prevent cerebral edema.

Elimination:

Monitor for constipation and provide stool softeners if necessary to prevent straining.
Apply barrier cream to the perineal area to prevent skin excoriation from uncontrolled bowel movements.

Hygiene:

Assist with all hygiene needs, including bedpan use, pressure area care, mouth care, and catheter care.
Maintain a dry, clean environment for the patient.

Exercises and Rehabilitation:

Incorporate active physical therapy into the rehabilitation plan, focusing on positioning to prevent contractures and skin breakdown.
Encourage coughing and deep breathing exercises, along with frequent position changes, to prevent mucus pooling and promote lung ventilation.
Encourage early mobilization and exercise, even while in bed, to prepare for future activities and maintain optimism about recovery.
Perform passive range of motion (ROM) exercises regularly to prevent joint immobility, contractures, and muscle weakness and stimulate circulation.
Assist the patient out of bed as soon as medically permitted and involve physiotherapists to guide exercises.
Provide assistance with using mobility aids such as walkers or wheelchairs.
Consult with a speech therapist if speech has been affected and teach compensatory techniques.

Health Education:

Educate the patient’s family about residual deficits and set realistic expectations for the patient’s abilities.
Stress the importance of physiotherapy for ongoing rehabilitation.
Encourage a low-cholesterol and low-sodium diet, weight reduction if necessary, and avoidance of smoking and excessive alcohol consumption.
Emphasize the importance of regular follow-up appointments to promote full recovery.

Complications of Cerebrovascular Accident (CVA)

Complications of Cerebrovascular Accident (CVA), commonly known as stroke, may include:

Motor Deficits: Weakness or paralysis of muscles, typically on one side of the body (hemiparesis or hemiplegia), which can lead to difficulties with mobility and activities of daily living.
Sensory Deficits: Loss of sensation or altered sensation in affected limbs or areas of the body, which can impact coordination and perception.
Speech and Language Impairments: Aphasia, dysarthria, or other communication difficulties may arise due to damage to areas of the brain responsible for language processing and production.
Cognitive Impairments: Memory loss, confusion, impaired reasoning, and decreased attention span may occur, affecting the individual’s ability to think clearly and perform cognitive tasks.
Emotional and Behavioral Changes: Emotional lability, depression, anxiety, irritability, and changes in mood or personality can result from the emotional impact of stroke and neurological damage.
Swallowing Difficulties: Dysphagia, or difficulty swallowing, can lead to aspiration pneumonia, malnutrition, and dehydration if not managed effectively.
Pain: Some individuals may experience pain, especially in the affected limbs, due to nerve damage or changes in sensation.
Muscle Spasticity: Increased muscle tone and involuntary muscle contractions may occur, leading to stiffness, spasms, and difficulty with movement.
Deep Vein Thrombosis (DVT) and Pulmonary Embolism: Immobility and reduced mobility increase the risk of blood clots forming in the deep veins of the legs, which can travel to the lungs and cause a pulmonary embolism.
Pressure Ulcers: Prolonged immobility and decreased sensation increase the risk of pressure ulcers (bedsores) developing, particularly in areas subjected to pressure or friction.
Urinary and Bowel Dysfunction: Incontinence, urinary retention, and constipation may occur due to neurological damage affecting bladder and bowel control.
Secondary Stroke: Individuals who have experienced a stroke are at increased risk of having another stroke, particularly if underlying risk factors are not effectively managed.
Dependence and Disability: Stroke survivors may require ongoing assistance with activities of daily living and may experience varying degrees of disability, impacting independence and quality of life.

These complications highlight the importance of comprehensive rehabilitation and management strategies to minimize disability, improve recovery, and enhance the individual’s overall well-being following a stroke.