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Cerebrovascular Accident CVA

Dec 20, 2019

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Cerebrovascular Accident CVA. Cerebrovascular Accident. Results from ischemia to a part of the brain or hemorrhage into the brain that results in death of brain cells . Approximately 750,000 in USA annually Third most common cause of death #1 leading cause of disability

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Cerebrovascular AccidentCVA

Cerebrovascular Accident • Results from ischemia to a part of the brain or hemorrhage into the brain that results in death of brain cells. • Approximately 750,000 in USA annually • Third most common cause of death • #1 leading cause of disability • 25% with initial stroke die within 1 year • 50-75% will be functionally independent • 25% will live with permanent disability • Physical, cognitive, emotional, & financial impact

Cerebrovascular AccidentRisk Factors • Nonmodifiable: • Age – Occurrence doubles each decade >55 years • Gender – Equal for men & women; women die more frequently than men • Race – African Americans, Hispanics, Native Americans, Asian Americans -- higher incidence • Heredity – family history, prior transient ischemic attack, or prior stroke increases risk

Cerebrovascular AccidentRisk Factors Controllable Risks with Medical Treatment & Lifestyle Changes: High blood pressure DiabetesCigarette smoking TIA (Aspirin)High blood cholesterol ObesityHeart Disease Atrial fibrillation Oral contraceptive use Physical inactivity Sickle cell disease Asymptomatic carotid stenosisHypercoagulability

CVA – Risk Factors

Cerebrovascular AccidentAnatomy of Cerebral Circulation • Blood Supply • Anterior: Carotid Arteries – middle & anterior cerebral arteries • frontal, parietal, temporal lobes; basal ganglion; part of the diencephalon (thalamus & hypothalamus) • Posterior: Vertebral Arteries – basilar artery • Mid and lower temporary & occipital lobes, cerebellum, brainstem, & part of the diencephalon • Circle of Willis – connects the anterior & posterior cerebral circulation

Cerebrovascular AccidentAnatomy of Cerebral Circulation • Blood Supply • 20% of cardiac output—750-1000ml/min • >30 second interruption– neurologic metabolism is altered; metabolism stops in 2 minutes; brain cell death < 5 mins.

Cerebrovascular AccidentPathophysiology • Atherosclerosis: major cause of CVA • Thrombus formation & emboli development • Abnormal filtration of lipids in the intimal layer of the arterial wall • Plaque develops & locations of increased turbulence of blood - bifurcations • Increased turbulence of blood or a tortuous area • Calcified plaques rupture or fissure • Platelets & fibrin adhere to the plaque • Narrowing or blockage of an artery by thrombus or emboli • Cerebral Infarction: blocked artery with blood supply cut off beyond the blockage

Cerebrovascular AccidentPathophysiology • Ischemic Cascade • Series of metabolic events • Inadequate ATP adenosine triphosphate production • Loss of ion homeostasis • Release of excitatory amino acids – glutamate • Free radical formation • Cell death • Border Zone: reversible area that surrounds the core ischemic area in which there is reduced blood flow but which can be restored (3 hours +/-)

CVA? - Call 911 • Sudden numbness or weakness of face, arm, or leg, especially on one side of the body. • Sudden confusion or trouble speaking or understanding speech. • Sudden trouble seeing in one or both eyes. • Sudden trouble walking, dizziness, or loss of balance or coordination • Sudden severe headache with no known cause.

Cerebrovascular AccidentTransient Ischemic Attack • Temporary focal loss of neurologic function • Caused by ischemia of one of the vascular territories of the brain • Microemboli with temporary blockage of blood flow • Lasts less than 24 hrs – often less than 15 mins • Most resolve within 3 hours • Warning sign of progressive cerebrovascular disease

Cerebrovascular AccidentTransient Ischemic Attack • Diagnosis: • CT without contrast • Confirm that TIA is not related to brain lesions • Cardiac Evaluation • Rule out cardiac mural thrombi • Treatment: • Medications that prevent platelet aggregation • ASA, Plavix • Oral anticoagulants

Cerebrovascular AccidentClassifications Based on underlying pathophysiologic findings

Cerebrovascular AccidentClassifications • Ischemic Stroke • Thrombotic • Embolic • Hemorrhagic Stroke • Intracerebral Hemorrhage • Subarachnoid Hemorrhage • Aneurysm • Berry or Saccular

Cerebrovascular AccidentClassifications • Ischemic Stroke—inadequate blood flow to the brain from partial or complete occlusions of an artery--85% of all strokes • Extent of a stroke depends on: • Rapidity of onset • Size of the lesion • Presence of collateral circulation • Symptoms may progress in the first 72 hours as infarction & cerebral edema increase • Types of Ischemic Stroke: Thrombotic StrokeEmbolic Stroke

CVA Recognition

Cerebrovascular AccidentIschemic – Thrombotic Stroke • Lumen of the blood vessels narrow – then becomes occluded – infarction • Associated with HTN and Diabetes Mellitus • >60% of strokes • 50% are preceded by TIA • Lacunar Stroke: development of cavity in place of infarcted brain tissue – results in considerable deficits – motor hemiplegia, contralateral loss of sensation or motor ability

Cerebrovascular AccidentThrombotic Stroke

Cerebrovascular AccidentCommon Sites of Atherosclerosis

Cerebrovascular AccidentIschemic – Embolic Stroke • Embolus lodges in and occludes a cerebral artery • Results in infarction & cerebral edema of the area supplied by the vessel • Second most common cause of stroke – 24% • Emboli originate in endocardial layer of the heart – atrial fibrillation, MI, infective endocarditis, rheumatic heart disease, valvular prostheses • Rapid occurrence with severe symptoms – body does not have time to develop collateral circulation • Any age group • Recurrence common if underlying cause not treated

Cerebrovascular AccidentEmbolic Stroke

Cerebrovascular AccidentGoals for Management • Immediate – assess & stabilize • ABCs, VS • Neurologic screening • Oxygen if hypoxic • IV access • Check glucose • Activate stroke team – CODE GREEN • 12-lead EKG • Immediate Neuro Assessment • Establish symptom onset • Review hx • Stroke Scale • Facial droop; arm drift; abnormal speech

Cerebrovascular AccidentGoals for Management • CT Scan – No hemorrhage: • Consider Fibrinolytic therapy • Check for exclusions • tPA • No anticoagulants or antiplatelet therapy for 24 hours • If not a candidate: Antiplatelet Therapy • CT Scan – Hemorrhage: • Neurosurgery? • If no surgery: Stroke Unit • Monitor BP and treat Hypertension • Monitor Neuro status • Monitor blood glucose and treat as needed • Supportive therapy

Cerebrovascular AccidentHemorrhagic Stroke • Hemorrhagic Stroke • 15% of all strokes • Result from bleeding into the brain tissue itself • Intracerebral • Subarachnoid

Cerebrovascular AccidentHemorrhage Stroke Intracerebral Hemorrhage • Rupture of a vessel • Hypertension – most important cause • Others: vascular malformations, coagulation disorders, anticoagulation, trauma, brain tumor, ruptured aneurysms • Sudden onset of symptoms with progression • Neurological deficits, headache, nausea, vomiting, decreased LOC, and hypertension • Prognosis: poor – 50% die within weeks • 20% functionally independent at 6 months

Cerebrovascular AccidentHemorrhage Stroke Intracerebral Hemorrhage

Cerebrovascular AccidentHemorrhagic-Subarachnoid • Hemorrhagic Stroke–Subarachnoid Hemorrhage • Intracranial bleeding into the cerebrospinal fluid-filled space between the arachnoid and pia mater membranes on the surface of the brain

Cerebrovascular AccidentHemorrhagic-Subarachnoid • Commonly caused by rupture of cerebral aneurysm (congenital or acquired) • Saccular or berry – few to 20-30 mm in size • Majority occur in the Circle of Willis • Other causes: Arteriovenous malformation (AVM), trauma, illicit drug abuse • Incidence: 6-16/100,000 • Increases with age and more common in women

Cerebrovascular AccidentHemorrhagic-SubarachnoidCerebral Aneurysm • Warning Symptoms: sudden onset of a severe headache – “worst headache of one’s life” • Change of LOC, Neurological deficits, nausea, vomiting, seizures, stiff neck • Despite improvements in surgical techniques, many patients die or left with significant cognitivedifficulties

Hemorrhagic-SubarachnoidCerebral Aneurysm • Surgical Treatment: • Clipping the aneurysm – prevents rebleed • Coiling – platinum coil inserted into the lumen of the aneurysm to occlude the sac • Postop: Vasospasm prevention – Calcium Channel Blockers

Hemorrhagic-SubarachnoidCerebral Aneurysm – Surgical Tx

Hemorrhagic-SubarachnoidCerebral Aneurysm – Coiling

Cerebrovascular AccidentClassification

Cerebrovascular AccidentClinical ManifestationsMiddle Cerebral Artery Involvement • Contralateral weakness • Hemiparesis; hemiplegia • Contralateral hemianesthesia • Loss of proprioception, fine touch and localization • Dominant hemisphere: aphasia • Nondominant hemisphere – neglect of opposite side; anosognosia – unaware or denial of neuro deficit • Homonymous hemianopsia – defective vision or blindness right or left halves of visual fields of both eyes

Cerebrovascular AccidentClinical ManifestationsAnterior Cerebral Artery Involvement • Brain stem occlusion • Contralateral • weakness of proximal upper extremity • sensory & motor deficits of lower extremities • Urinary incontinence • Sensory loss (discrimination, proprioception) • Contralateral grasp & sucking reflexes may be present • Apraxia – loss of ability to carry out familiar purposeful movements in the absence of sensory or motor impairment • Personality change: flat affect, loss of spontaneity, loss of interest in surroundings • Cognitive impairment

Cerebrovascular AccidentClinical ManifestationsPosterior Cerebral Artery & Vertebrobasilar Involvement • Alert to comatose • Unilateral or bilateral sensory loss • Contralateral or bilateral weakness • Dysarthria – impaired speech articulation • Dysphagia – difficulty in swallowing • Hoarseness • Ataxia, Vertigo • Unilateral hearing loss • Visual disturbances (blindness, homonymous hemianopsia, nystagmus, diplopia)

Cerebrovascular AccidentClinical Manifestations • Motor Function Impairment • Caused by destruction of motor neurons in the pyramidal pathway (brain to spinal cord) • Mobility • Respiratory function • Swallowing and speech • Gag reflex • Self-care activities

Cerebrovascular AccidentClinical ManifestationsRight Brain – Left Brain Damage

Cerebrovascular AccidentClinical Manifestations • Affect • Difficulty controlling emotions • Exaggerated or unpredictable emotional response • Depression / feelings regarding changed body image and loss of function

Cerebrovascular AccidentClinical Manifestations • Intellectual Function • Memory and judgment • Left-brain stroke: cautious in making judgments • Right-brain stroke: impulsive & moves quickly to decisions • Difficulties in learning new skills

Cerebrovascular AccidentClinical Manifestations • Communication • Left hemisphere dominant for language skills in the right-handed person & most left-handed persons -- Aphasia/Dysphasia • Involvement Expression & Comprehension • Receptive Aphasia (Wernicke’s area): sounds of speech nor its meaning can be understood – spoken & written • Expressive Aphasia (Broca’s area): difficulty in speaking and writing • Dysarthria: Affects the mechanics of speech due to muscle control disturbances – pronunciation, articulation, and phonation

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Learn about the nursing care management of patients with cerebrovascular accident in this nursing study guide .

Table of Contents

• What is Cerebrovascular Accident? 

Classification

Risk factors, pathophysiology, statistics and epidemiology, clinical manifestations, complications, assessment and diagnostic findings, medical management, surgical management, nursing assessment, nursing diagnosis, nursing care planning & goals, nursing interventions, discharge and home care guidelines, documentation guidelines.

• Practice Quiz: Cerebrovascular Accident (Stroke)

What is Cerebrovascular Accident?

A cerebrovascular accident (CVA), an ischemic stroke or “brain attack,” is a sudden loss of brain function resulting from a disruption of the blood supply to a part of the brain.

• Cerebrovascular accident or stroke is the primary cerebrovascular disorder in the United States.
• A cerebrovascular accident is a sudden loss of brain functioning resulting from a disruption of the blood supply to a part of the brain.
• It is a functional abnormality of the central nervous system .
• Cryptogenic strokes have no known cause, and other strokes result from causes such as illicit drug use, coagulopathies, migraine, and spontaneous dissection of the carotid or vertebral arteries.
• The result is an interruption in the blood supply to the brain, causing temporary or permanent loss of movement, thought, memory , speech, or sensation.

Strokes can be divided into two classifications.

• Ischemic stroke. This is the loss of function in the brain as a result of a disrupted blood supply.
• Hemorrhagic stroke. Hemorrhagic strokes are caused by bleeding into the brain tissue, the ventricles, or the subarachnoid space.

The following are the nonmodifiable and modifiable risk factors of Cerebrovascular accident:

Nonmodifiable

• Advanced age (older than 55 years)
• Gender (Male)
• Race (African American)
• Hypertension
• Atrial fibrillation
• Hyperlipidemia
• Asymptomatic carotid stenosis and valvular heart disease (eg, endocarditis, prosthetic heart valves)
• Periodontal disease

The disruption in the blood flow initiates a complex series of cellular metabolic events.

• Decreased cerebral blood flow. The ischemic cascade begins when cerebral blood flow decreases to less than 25 mL per 100g of blood per minute.
• Aerobic respiration. At this point, neurons are unable to maintain aerobic respiration.
• Anaerobic respiration. The mitochondria would need to switch to anaerobic respiration, which generates large amounts of lactic acid , causing a change in pH and rendering the neurons incapable of producing sufficient quantities of ATP.
• Loss of function. The membrane pumps that maintain electrolyte balances fail and the cells cease to function.

Stroke is a worldwide phenomenon suffered through all walks of life.

• Morbidity: In 2005, prevalence of stroke was estimated at 2.3 million males and 3.4 million females; many of the approximately 5.7 million U.S. stroke survivors have permanent stroke-related disabilities.
• Mortality: In 2004, stroke ranked fifth as the cause of death for those aged 45 to 64 years and third for those aged 65 years or older (National Heart, Lung and Blood Institute [NHLBI], 2007), with 150,000 deaths (American Heart Association and American Stroke Association, 2008); hemorrhagic strokes are more severe, and mortality rates are higher than ischemic strokes, with a 30-day mortality rate of 40% to 80%.
• Cost: Estimated direct and indirect cost for 2008 was $65.5 billion (American Heart Association and American Stroke Association, 2008).
• Stroke is the third leading cause of death after heart disease and cancer .
• Approximately 780, 000 people experience a stroke each year in the United States.
• Approximately 600, 000 of these are new strokes, and 180, 000 are recurrent strokes.
• About 5.6 million noninstitutionalized stroke survivors are alive today.
• Stroke is the leading cause of serious, long-term disability in the United States.
• Direct and indirect costs for stroke cost $65.5 billion in 2008.
• Strokes are usually hemorrhagic (15%) or ischemic/nonhemorrhagic (85%).
• Ischemic strokes are categorized according to their cause: large artery thrombotic strokes (20%), small penetrating artery thrombotic strokes (25%), cardiogenic embolic strokes (20%), cryptogenic strokes (30%), and other (5%).

Strokes are caused by the following:

• Large artery thrombosis . Large artery thromboses are caused by atherosclerotic plaques in the large blood vessels of the brain.
• Small penetrating artery thrombosis. Small penetrating artery thrombosis affects one or more vessels and is the most common type of ischemic stroke.
• Cardiogenic emboli. Cardiogenic emboli are associated with cardiac dysrhythmias, usually atrial fibrillation .

Stroke can cause a wide variety of neurologic deficits, depending on the location of the lesion, the size of the area of inadequate perfusion, and the amount of the collateral blood flow. General signs and symptoms include numbness or weakness of face, arm, or leg (especially on one side of the body); confusion or change in mental status; trouble speaking or understanding speech; visual disturbances; loss of balance, dizziness, difficulty walking; or sudden severe headache.

General signs and symptoms include numbness or weakness of face, arm, or leg (especially on one side of the body); confusion or change in mental status; trouble speaking or understanding speech; visual disturbances; loss of balance, dizziness, difficulty walking; or sudden severe headache.

• Numbness or weakness of the face. Without adequate perfusion, oxygen is also low, and facial tissues could not function properly without them.
• Change in mental status. Due to decreased oxygen, the patient experiences confusion.
• Trouble speaking or understanding speech. Cells cease to function as a result of inadequate perfusion.
• Visual disturbances. The eyes also need enough oxygen for optimal functioning.
• Homonymous hemianopsia. There is loss of half of the visual field.
• Loss of peripheral vision. The patient experiences difficulty seeing at night and is unaware of objects or the borders of objects.
• Hemiparesis. There is a weakness of the face, arm, and leg on the same side due to a lesion in the opposite hemisphere.
• Hemiplegia. Paralysis of the face, arm, and leg on the same side due to a lesion in the opposite hemisphere.
• Ataxia. Staggering, unsteady gait and inability to keep feet together.
• Dysarthria. This is the difficulty in forming words.
• Dysphagia . There is difficulty in swallowing.
• Paresthesia. There is numbness and tingling of extremities and difficulty with proprioception.
• Expressive aphasia. The patient is unable to form words that is understandable yet can speak in single-word responses.
• Receptive aphasia. The patient is unable to comprehend the spoken word and can speak but may not make any sense.
• Global aphasia. This is a combination of both expressive and receptive aphasia.
• Hemiplegia, hemiparesis
• Flaccid paralysis and loss of or decrease in the deep tendon reflexes (initial clinical feature) followed by (after 48 hours) reappearance of deep reflexes and abnormally increased muscle tone (spasticity)

Communication Loss

• Dysarthria (difficulty speaking)
• Dysphasia (impaired speech) or aphasia (loss of speech)
• Apraxia (inability to perform a previously learned action)

Perceptual Disturbances and Sensory Loss

• Visual-perceptual dysfunctions (homonymous hemianopia [loss of half of the visual field])
• Disturbances in visual-spatial relations (perceiving the relation of two or more objects in spatial areas), frequently seen in patients with right hemispheric damage
• Sensory losses: slight impairment of touch or more severe with loss of proprioception; difficulty in interrupting visual, tactile, and auditory stimuli

Impaired Cognitive and Psychological Effects

• Frontal lobe damage: Learning capacity, memory, or other higher cortical intellectual functions may be impaired. Such dysfunction may be reflected in a limited attention span, difficulties in comprehension, forgetfulness, and lack of motivation.
• Depression , other psychological problems: emotional lability, hostility, frustration, resentment, and lack of cooperation.

Primary prevention of stroke remains the best approach.

• Healthy lifestyle. Leading a healthy lifestyle which includes not smoking, maintaining a healthy weight, following a healthy diet, and daily exercise can reduce the risk of having a stroke by about one half.
• DASH diet. The DASH ( Dietary Approaches to Stop Hypertension ) diet is high in fruits and vegetables, moderate in low-fat dairy products, and low in animal protein and can lower the risk of stroke.
• Stroke risk screenings. Stroke risk screenings are an ideal opportunity to lower stroke risk by identifying people or groups of people who are at high risk for stroke.
• Education. Patients and the community must be educated about recognition and prevention of stroke.
• Low-dose aspirin . Research findings suggest that low-dose aspirin may lower the risk of stroke in women who are at risk.

If cerebral oxygenation is still inadequate; complications may occur.

• Tissue ischemia . If cerebral blood flow is inadequate, the amount of oxygen supplied to the brain is decreased, and tissue ischemia will result.
• Cardiac dysrhythmias. The heart compensates for the decreased cerebral blood flow, and with too much pumping, dysrhythmias may occur.

Any patient with neurologic deficits needs a careful history and complete physical and neurologic examination.

• CT scan . Demonstrates structural abnormalities, edema , hematomas, ischemia, and infarctions. Demonstrates structural abnormalities, edema, hematomas, ischemia, and infarctions. Note: May not immediately reveal all changes, e.g., ischemic infarcts are not evident on CT for 8–12 hr; however, intracerebral hemorrhage is immediately apparent; therefore, emergency CT is always done before administering tissue plasminogen activator (t-PA). In addition, patients with TIA commonly have a normal CT scan
• PET scan. Provides data on cerebral metabolism and blood flow changes.
• MRI. Shows areas of infarction, hemorrhage , AV malformations, and areas of ischemia.
• Cerebral angiography. Helps determine specific cause of stroke, e.g., hemorrhage or obstructed artery, pinpoints site of occlusion or rupture. Digital subtraction angiography evaluates patency of cerebral vessels, identifies their position in head and neck, and detects/evaluates lesions and vascular abnormalities.
• Lumbar puncture . Pressure is usually normal and CSF is clear in cerebral thrombosis, embolism, and TIA. Pressure elevation and grossly bloody fluid suggest subarachnoid and intracerebral hemorrhage. CSF total protein level may be elevated in cases of thrombosis because of inflammatory process. LP should be performed if septic embolism from bacterial endocarditis is suspected.
• Transcranial Doppler ultrasonography. Evaluates the velocity of blood flow through major intracranial vessels; identifies AV disease, e.g., problems with carotid system (blood flow/presence of atherosclerotic plaques).
• EEG. Identifies problems based on reduced electrical activity in specific areas of infarction; and can differentiate seizure activity from CVA damage.
• Skull x-ray. May show a shift of pineal gland to the opposite side from an expanding mass; calcifications of the internal carotid may be visible in cerebral thrombosis; partial calcification of walls of an aneurysm may be noted in subarachnoid hemorrhage.
• ECG and echocardiography .  To rule out cardiac origin as source of embolus (20% of strokes are the result of blood or vegetative emboli associated with valvular disease, dysrhythmias, or endocarditis).
• Laboratory studies to rule out systemic causes: CBC, platelet and clotting studies, VDRL/RPR, erythrocyte sedimentation rate (ESR), chemistries ( glucose , sodium ).

Patients who have experienced TIA or stroke should have medical management for secondary prevention.

• Recombinant tissue plasminogen activator would be prescribed unless contraindicated, and there should be monitoring for bleeding.
• Increased ICP. Management of increased ICP includes osmotic diuretics , maintenance of PaCO2 at 30-35 mmHg, and positioning to avoid hypoxia through elevation of the head of the bed.
• Endotracheal Tube. There is a possibility of intubation to establish patent airway if necessary.
• Hemodynamic monitoring. Continuous hemodynamic monitoring should be implemented to avoid an increase in blood pressure .
• Neurologic assessment to determine if the stroke is evolving and if other acute complications are developing

Surgical management may include prevention and relief from increased ICP.

• Carotid endarterectomy. This is the removal of atherosclerotic plaque or thrombus from the carotid artery to prevent stroke in patients with occlusive disease of the extracranial cerebral arteries.
• Hemicraniectomy. Hemicraniectomy may be performed for increased ICP from brain edema in severe cases of stroke.

Nursing Management

After the stroke is complete, management focuses on the prompt initiation of rehabilitation for any deficits.

During the acute phase , a neurologic flow sheet is maintained to provide data about the following important measures of the patient’s clinical status:

• Change in level of consciousness or responsiveness.
• Presence or absence of voluntary or involuntary movements of extremities.
• Stiffness or flaccidity of the neck.
• Eye opening, comparative size of pupils, and pupillary reaction to light.
• Color of the face and extremities; temperature and moisture of the skin.
• Ability to speak.
• Presence of bleeding.
• Maintenance of blood pressure.

During the postacute phase , assess the following functions:

• Mental status (memory, attention span, perception, orientation, affect, speech/language).
• Sensation and perception (usually the patient has decreased awareness of pain and temperature).
• Motor control (upper and lower extremity movement); swallowing ability, nutritional and hydration status, skin integrity, activity tolerance, and bowel and bladder function.
• Continue focusing nursing assessment on impairment of function in patient’s daily activities.

Based on the assessment data, the major nursing diagnoses for a patient with stroke may include the following:

• Impaired physical mobility related to hemiparesis, loss of balance and coordination, spasticity, and brain injury .
• Acute pain related to hemiplegia and disuse.
• Deficient self-care related to stroke sequelae.
• Disturbed sensory perception related to altered sensory reception, transmission, and/or integration.
• Impaired urinary elimination related to flaccid bladder , detrusor instability, confusion, or difficulty in communicating.
• Disturbed thought processes related to brain damage.
• Impaired verbal communication related to brain damage.
• Risk for impaired skin integrity related to hemiparesis or hemiplegia and decreased mobility.
• Interrupted family processes related to catastrophic illness and caregiving burdens.
• Sexual dysfunction related to neurologic deficits or fear of failure.

Main article: Cerebrovascular Accident (Stroke) Nursing Care Plans

The major nursing care planning goals for the patient and family may include:

• Improve mobility.
• Avoidance of shoulder pain.
• Achievement of self-care.
• Relief of sensory and perceptual deprivation.
• Prevention of aspiration .
• Continence of bowel and bladder.
• Improved thought processes.
• Achieving a form of communication.
• Maintaining skin integrity .
• Restore family functioning.
• Improve sexual function.
• Absence of complications.

Nursing care has a significant impact on the patient’s recovery. In summary, here are some nursing interventions for patients with stroke:

• Positioning. Position to prevent contractures, relieve pressure, attain good body alignment, and prevent compressive neuropathies.
• Prevent flexion. Apply splint at night to prevent flexion of the affected extremity.
• Prevent adduction. Prevent adduction of the affected shoulder with a pillow placed in the axilla.
• Prevent edema. Elevate affected arm to prevent edema and fibrosis.
• Full range of motion. Provide full range of motion four or five times a day to maintain joint mobility.
• Prevent venous stasis. Exercise is helpful in preventing venous stasis, which may predispose the patient to thrombosis and pulmonary embolus.
• Regain balance. Teach patient to maintain balance in a sitting position, then to balance while standing and begin walking as soon as standing balance is achieved.
• Personal hygiene. Encourage personal hygiene activities as soon as the patient can sit up.
• Manage sensory difficulties. Approach patient with a decreased field of vision on the side where visual perception is intact.
• Visit a speech therapist. Consult with a speech therapist to evaluate gag reflexes and assist in teaching alternate swallowing techniques.
• Voiding pattern. Analyze voiding pattern and offer urinal or bedpan on patient’s voiding schedule.
• Be consistent in patient’s activities. Be consistent in the schedule, routines, and repetitions; a written schedule, checklists, and audiotapes may help with memory and concentration, and a communication board may be used.
• Assess skin. Frequently assess skin for signs of breakdown, with emphasis on bony areas and dependent body parts.

Improving Mobility and Preventing Deformities

• Position to prevent contractures; use measures to relieve pressure, assist in maintaining good body alignment, and prevent compressive neuropathies.
• Apply a splint at night to prevent flexion of affected extremity.
• Prevent adduction of the affected shoulder with a pillow placed in the axilla.
• Elevate affected arm to prevent edema and fibrosis.
• Position fingers so that they are barely flexed; place hand in slight supination. If upper extremity spasticity is noted, do not use a hand roll; dorsal wrist splint may be used.
• Change position every 2 hours; place patient in a prone  position for 15 to 30 minutes several times a day.

Establishing an Exercise Program

• Provide full range of motion four or five times a day to maintain joint mobility, regain motor control, prevent contractures in the paralyzed extremity, prevent further deterioration of the neuromuscular system, and enhance circulation. If tightness occurs in any area, perform a range of motion exercises more frequently.
• Exercise is helpful in preventing venous stasis, which may predispose the patient to thrombosis and pulmonary embolus.
• Observe for signs of pulmonary embolus or excessive cardiac workload during exercise period (e.g., shortness of breath, chest pain , cyanosis , and increasing pulse rate ).
• Supervise and support the patient during exercises; plan frequent short periods of exercise, not longer periods; encourage the patient to exercise unaffected side at intervals throughout the day.

Preparing for Ambulation

• Start an active rehabilitation program when consciousness returns (and all evidence of bleeding is gone, when indicated).
• Teach patient to maintain balance in a sitting position, then to balance while standing (use a tilt table if needed).
• Begin walking as soon as standing balance is achieved (use parallel bars and have a wheelchair available in anticipation of possible dizziness).
• Keep training periods for ambulation short and frequent.

Preventing Shoulder Pain

• Never lift patient by the flaccid shoulder or pull on the affected arm or shoulder.
• Use proper patient movement and positioning (e.g., flaccid arm on a table or pillows when patient is seated, use of sling when ambulating).
• Range of motion exercises are beneficial, but avoid over strenuous arm movements.
• Elevate arm and hand to prevent dependent edema of the hand; administer analgesic agents as indicated.

Enhancing Self Care

• Encourage personal hygiene activities as soon as the patient can sit up; select suitable self-care activities that can be carried out with one hand.
• Help patient to set realistic goals; add a new task daily.
• As a first step, encourage patient to carry out all self-care activities on the unaffected side.
• Make sure patient does not neglect affected side; provide assistive devices as indicated.
• Improve morale by making sure patient is fully dressed during ambulatory activities.
• Assist with dressing activities (e.g., clothing with Velcro closures; put garment on the affected side first); keep environment uncluttered and organized.
• Provide emotional support and encouragement to prevent fatigue and discouragement.

Managing Sensory-Perceptual Difficulties

• Approach patient with a decreased field of vision on the side where visual perception is intact; place all visual stimuli on this side.
• Teach patient to turn and look in the direction of the defective visual field to compensate for the loss; make eye contact with patient, and draw attention to affected side.
• Increase natural or artificial lighting in the room; provide eyeglasses to improve vision.
• Remind patient with hemianopsia of the other side of the body; place extremities so that patient can see them.

Assisting with Nutrition

• Observe patient for paroxysms of coughing, food dribbling out or pooling in one side of the mouth , food retained for long periods in the mouth, or nasal regurgitation when swallowing liquids.
• Consult with speech therapist to evaluate gag reflexes; assist in teaching alternate swallowing techniques, advise patient to take smaller boluses of food, and inform patient of foods that are easier to swallow; provide thicker liquids or pureed diet as indicated.
• Have patient sit upright, preferably on chair, when eating and drinking; advance diet as tolerated.
• Prepare for GI feedings through a tube if indicated; elevate the head of bed during feedings, check tube position before feeding , administer feeding slowly, and ensure that cuff of tracheostomy tube is inflated (if applicable); monitor and report excessive retained or residual feeding.

Attaining Bowel and Bladder Control

• Perform intermittent sterile catheterization during the period of loss of sphincter control.
• Analyze voiding pattern and offer urinal or bedpan on patient’s voiding schedule.
• Assist the male patient to an upright posture for voiding.
• Provide highfiber diet and adequate fluid intake (2 to 3 L/day), unless contraindicated.
• Establish a regular time (after breakfast) for toileting.

Improving Thought Processes

• Reinforce structured training program using cognitive, perceptual retraining, visual imagery, reality orientation, and cueing procedures to compensate for losses.
• Support patient: Observe performance and progress, give positive feedback, convey an attitude of confidence and hopefulness; provide other interventions as used for improving cognitive function after a head injury.

Improving Communication

• Reinforce the individually tailored program.
• Jointly establish goals, with the patient taking an active part.
• Make the atmosphere conducive to communication, remaining sensitive to patient’s reactions and needs and responding to them in an appropriate manner; treat the patient as an adult.
• Provide strong emotional support and understanding to allay anxiety ; avoid completing patient’s sentences.
• Be consistent in schedule, routines, and repetitions. A written schedule, checklists, and audiotapes may help with memory and concentration; a communication board may be used.
• Maintain patient’s attention when talking with the patient, speak slowly, and give one instruction at a time; allow the patient time to process.
• Talk to aphasic patients when providing care activities to provide social contact.

Maintaining Skin Integrity

• Frequently assess skin for signs of breakdown, with emphasis on bony areas and dependent body parts.
• Employ pressure relieving devices; continue regular turning and positioning (every 2 hours minimally); minimize shear and friction when positioning.
• Keep skin clean and dry, gently massage the healthy dry skin and maintain adequate nutrition .

Improving Family Coping

• Provide counseling and support to the family.
• Involve others in patient’s care; teach stress management techniques and maintenance of personal health for family coping.
• Give family information about the expected outcome of the stroke, and counsel them to avoid doing things for the patient that he or she can do.
• Develop attainable goals for the patient at home by involving the total health care team, patient, and family.
• Encourage everyone to approach the patient with a supportive and optimistic attitude, focusing on abilities that remain; explain to the family that emotional lability usually improves with time.

Helping the Patient Cope with Sexual Dysfunction

• Perform indepth assessment to determine sexual history before and after the stroke.
• Interventions for patient and partner focus on providing relevant information, education, reassurance, adjustment
• of medications, counseling regarding coping skills, suggestions for alternative sexual positions, and a means of sexual expression and satisfaction.

Teaching points

• Teach patient to resume as much self care as possible; provide assistive devices as indicated.
• Have occupational therapist make a home assessment and recommendations to help the patient become more independent.
• Coordinate care provided by numerous health care professionals; help family plan aspects of care.
• Advise family that patient may tire easily, become irritable and upset by small events, and show less interest in daily events.
• Make a referral for home speech therapy. Encourage family involvement. Provide family with practical instructions to help patient between speech therapy sessions.
• Discuss patient’s depression with the physician for possible antidepressant therapy.
• Encourage patient to attend community-based stroke clubs to give a feeling of belonging and fellowship to others.
• Encourage patient to continue with hobbies, recreational and leisure interests, and contact with friends to prevent social isolation .
• Encourage family to support patient and give positive reinforcement.
• Remind spouse and family to attend to personal health and wellbeing.

Expected patient outcomes may include the following:

• Improved mobility.
• Absence of shoulder pain.
• Self-care achieved.
• Achieved a form of communication.
• Maintained skin integrity.
• Restored family functioning.
• Improved sexual function.

Patient and family education is a fundamental component of rehabilitation.

• Consult an occupational therapist. An occupational therapist may be helpful in assessing the home environment and recommending modifications to help the patient become more independent.
• Physical therapy. A program of physical therapy may be beneficial, whether it takes place in the home or in an outpatient program.
• Antidepressant therapy. Depression is a common and serious problem in the patient who has had a stroke.
• Support groups . Community-based stroke support groups may allow the patient and the family to learn from others with si milar problems and to share their experiences.
• Assess caregivers . Nurses should assess caregivers for signs of depression, as depression is also common among caregivers of stroke survivors.

The focus of documentation should involve:

• Individual findings including level of function and ability to participate in specific or desired activities.
• Needed resources and adaptive devices.
• Results of laboratory tests, diagnostic studies, and mental status or cognitive evaluation .
• SO/family support and participation.
• Plan of care and those involved in planning.
• Teaching plan.
• Response to interventions, teaching, and actions performed.
• Attainment or progress toward desired outcomes.
• Modifications to plan of care.

Practice Quiz: Cerebrovascular Accident (Stroke)

Here’s a 5-item practice quiz for this Cerebrovascular Accident (Stroke) Study Guide. Please visit our nursing test bank for more NCLEX practice questions .

1. As a cause of death in the United States, stroke currently ranks:

A. Second B. Third C. Fourth D. Fifth

2. The most common cause of cerebrovascular accident is:

A. Arteriosclerosis B. Embolism C. Hypertensive changes D. Vasospasm

3. The degree of neurologic damage that occurs with an ischemic stroke depends on the:

A. Location of the lesion. B. Size of the area of inadequate perfusion. C. Amount of collateral blood flow. D. Combination of the above factors.

4. The most common side effect of tPA is:

A. An allergic reaction . B. Bleeding. C. Severe vomiting . D. A second stroke in 6 to 12 hours.

5. The majority of strokes have what type of origin?

A. Cardiogenic emboli. B. Cryptogenic. C. Large artery thrombotic. D. Small artery thrombotic.

Answers and Rationale

1. Answer: B. Third

• B: Stroke is the third leading cause of death after heart disease and cancer .
• A: Cancer is the second leading cause of death in the United States.
• C: Stroke is not the fourth leading cause of death in the United States.
• D: Stroke is not the fifth leading cause of death in the United States.

2. Answer: A. Arteriosclerosis

• A: Small penetrating artery thrombosis affects one or more vessels and is the most common cause of cerebrovascular accident.
• B: Embolism is not the most common cause of cerebrovascular accident.
• C: Hypertensive changes are not the most common cause of cerebrovascular accident.
• D: Vasospasm is not the most common cause of cerebrovascular accident.

3. Answer: D. Combination of the above factors.

• D: Stroke can cause a wide variety of neurologic deficits, depending on the location of the lesion, the size of the area of inadequate perfusion, and the amount of the collateral blood flow.
• A: The degree of neurologic damage that occurs with an ischemic stroke depends on the location of the lesion.
• B: The degree of neurologic damage that occurs with an ischemic stroke depends on the size of the area of inadequate perfusion.
• C: The degree of neurologic damage that occurs with an ischemic stroke depends on the amount of collateral blood flow.

4. Answer: B. Bleeding.

• B: A patient taking tPA should be monitored for bleeding.
• A: Allergic reaction is not a side effect of tPA.
• C: Severe vomiting is not a side effect of tPA.
• D: A second stroke is not a side effect of tPA.

5. Answer: D. Small artery thrombotic.

• D: Small artery thrombotic is the most common type of origin for strokes.
• A: Cardiogenic emboli is not the most common type of origin for strokes.
• B: Cryptogenic is not the most common type of origin for strokes.
• C: Large artery thrombotic is not the most common type of origin for strokes.

Posts related to Cerebrovascular Accident (Stroke):

• 8+ Cerebrovascular Accident (Stroke) Nursing Care Plans
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8 thoughts on “Cerebrovascular Accident (Stroke)”

I’m impressed, I have been challenged to read more.

The article was helpful

Am so impressed with the write up am student will wish to develop a research topic in CVA

As a nursing student, I want to thank this article for the valuable information on cerebrovascular accident nursing management. Understanding the importance of proper care and management for stroke patients is a crucial aspect of my education and future practice as a nurse. This article has provided me with a deeper insight into the role of the nurse in promoting positive outcomes for stroke patients, and I am grateful for the opportunity to learn more about this important topic. Thank you!

very presented alihamudulillah i got something

Hi Mugoya, Wonderful to hear you gained something valuable from the study guide! If you’re curious about more or have any questions, feel free to reach out. Always here to help!

well explained great article for students ……… Kindly increase the number of mcqs

Hi Abdur, Thanks for the positive feedback on the article! I’m glad to hear it’s helpful for students. All of our practice questions are available at our Nursing Test Bank page . If there are specific topics you’d like to see more questions on, just drop a suggestion. Your input helps us create better resources!

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Case report

Clinical course of a 66-year-old man with an acute ischaemic stroke in the setting of a covid-19 infection, saajan basi.

1 Department of Stroke and Acute Medicine, King's Mill Hospital, Sutton-in-Ashfield, UK

2 Department of Acute Medicine, University Hospitals of Derby and Burton, Derby, UK

Mohammad Hamdan

Shuja punekar.

A 66-year-old man was admitted to hospital with a right frontal cerebral infarct producing left-sided weakness and a deterioration in his speech pattern. The cerebral infarct was confirmed with CT imaging. The only evidence of respiratory symptoms on admission was a 2 L oxygen requirement, maintaining oxygen saturations between 88% and 92%. In a matter of hours this patient developed a greater oxygen requirement, alongside reduced levels of consciousness. A positive COVID-19 throat swab, in addition to bilateral pneumonia on chest X-ray and lymphopaenia in his blood tests, confirmed a diagnosis of COVID-19 pneumonia. A proactive decision was made involving the patients’ family, ward and intensive care healthcare staff, to not escalate care above a ward-based ceiling of care. The patient died 5 days following admission under the palliative care provided by the medical team.

SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) is a new strain of coronavirus that is thought to have originated in December 2019 in Wuhan, China. In a matter of months, it has erupted from non-existence to perhaps the greatest challenge to healthcare in modern times, grinding most societies globally to a sudden halt. Consequently, the study and research into SARS-CoV-2 is invaluable. Although coronaviruses are common, SARS-CoV-2 appears to be considerably more contagious. The WHO figures into the 2003 SARS-CoV-1 outbreak, from November 2002 to July 2003, indicate a total of 8439 confirmed cases globally. 1 In comparison, during a period of 4 months from December 2019 to July 2020, the number of global cases of COVID-19 reached 10 357 662, increasing exponentially, illustrating how much more contagious SARS-CoV-2 has been. 2

Previous literature has indicated infections, and influenza-like illness have been associated with an overall increase in the odds of stroke development. 3 There appears to be a growing correlation between COVID-19 positive patients presenting to hospital with ischaemic stroke; however, studies investigating this are in progress, with new data emerging daily. This patient report comments on and further characterises the link between COVID-19 pneumonia and the development of ischaemic stroke. At the time of this patients’ admission, there were 95 positive cases from 604 COVID-19 tests conducted in the local community, with a predicted population of 108 000. 4 Only 4 days later, when this patient died, the figure increased to 172 positive cases (81% increase), illustrating the rapid escalation towards the peak of the pandemic, and widespread transmission within the local community ( figure 1 ). As more cases of ischaemic stroke in COVID-19 pneumonia patients arise, the recognition and understanding of its presentation and aetiology can be deciphered. Considering the virulence of SARS-CoV-2 it is crucial as a global healthcare community, we develop this understanding, in order to intervene and reduce significant morbidity and mortality in stroke patients.

A graph showing the number of patients with COVID-19 in the hospital and in the community over time.

Case presentation

A 66-year-old man presented to the hospital with signs of left-sided weakness. The patient had a background of chronic obstructive pulmonary disease (COPD), atrial fibrillation and had one previous ischaemic stroke, producing left-sided haemiparesis, which had completely resolved. He was a non-smoker and lived in a house. The patient was found slumped over on the sofa at home on 1 April 2020, by a relative at approximately 01:00, having been seen to have no acute medical illness at 22:00. The patients’ relative initially described disorientation and agitation with weakness noted in the left upper limb and dysarthria. At the time of presentation, neither the patient nor his relative identified any history of fever, cough, shortness of breath, loss of taste, smell or any other symptoms; however, the patient did have a prior admission 9 days earlier with shortness of breath.

The vague nature of symptoms, entwined with considerable concern over approaching the hospital, due to the risk of contracting COVID-19, created a delay in the patients’ attendance to the accident and emergency department. His primary survey conducted at 09:20 on 1 April 2020 demonstrated a patent airway, with spontaneous breathing and good perfusion. His Glasgow Coma Scale (GCS) score was 15 (a score of 15 is the highest level of consciousness), his blood glucose was 7.2, and he did not exhibit any signs of trauma. His abbreviated mental test score was 7 out of 10, indicating a degree of altered cognition. An ECG demonstrated atrial fibrillation with a normal heart rate. His admission weight measured 107 kg. At 09:57 the patient required 2 L of nasal cannula oxygen to maintain his oxygen saturations between 88% and 92%. He started to develop agitation associated with an increased respiratory rate at 36 breaths per minute. On auscultation of his chest, he demonstrated widespread coarse crepitation and bilateral wheeze. Throughout he was haemodynamically stable, with a systolic blood pressure between 143 mm Hg and 144 mm Hg and heart rate between 86 beats/min and 95 beats/min. From a neurological standpoint, he had a mild left facial droop, 2/5 power in both lower limbs, 2/5 power in his left upper limb and 5/5 power in his right upper limb. Tone in his left upper limb had increased. This patient was suspected of having COVID-19 pneumonia alongside an ischaemic stroke.

Investigations

A CT of his brain conducted at 11:38 on 1 April 2020 ( figure 2 ) illustrated an ill-defined hypodensity in the right frontal lobe medially, with sulcal effacement and loss of grey-white matter. This was highly likely to represent acute anterior cerebral artery territory infarction. Furthermore an oval low-density area in the right cerebellar hemisphere, that was also suspicious of an acute infarction. These vascular territories did not entirely correlate with his clinical picture, as limb weakness is not as prominent in anterior cerebral artery territory ischaemia. Therefore this left-sided weakness may have been an amalgamation of residual weakness from his previous stroke, in addition to his acute cerebral infarction. An erect AP chest X-ray with portable equipment ( figure 3 ) conducted on the same day demonstrated patchy peripheral consolidation bilaterally, with no evidence of significant pleural effusion. The pattern of lung involvement raised suspicion of COVID-19 infection, which at this stage was thought to have provoked the acute cerebral infarct. Clinically significant blood results from 1 April 2020 demonstrated a raised C-reactive protein (CRP) at 215 mg/L (normal 0–5 mg/L) and lymphopaenia at 0.5×10 9 (normal 1×10 9 to 3×10 9 ). Other routine blood results are provided in table 1 .

CT imaging of this patients’ brain demonstrating a wedge-shaped infarction of the anterior cerebral artery territory.

Chest X-ray demonstrating the bilateral COVID-19 pneumonia of this patient on admission.

Clinical biochemistry and haematology blood results of the patient

APTT, activated partial thromboplastin time; CRP, C-reactive protein; eGFR, estimated glomerular filtration rate; Hb, haemoglobin; INR, international normalised ratio; MCV, mean corpuscular volume; PT, prothrombin time; WCC, white cell count.

Interestingly the patient, in this case, was clinically assessed in the accident and emergency department on 23 March 2020, 9 days prior to admission, with symptoms of shortness of breath. His blood results from this day showed a CRP of 22 mg/L and a greater lymphopaenia at 0.3×10 9 . He had a chest X-ray ( figure 4 ), which indicated mild radiopacification in the left mid zone. He was initially treated with intravenous co-amoxiclav and ciprofloxacin. The following day he had minimal symptoms (CURB 65 score 1 for being over 65 years). Given improving blood results (declining CRP), he was discharged home with a course of oral amoxicillin and clarithromycin. As national governmental restrictions due to COVID-19 had not been formally announced until 23 March 2020, and inconsistencies regarding personal protective equipment training and usage existed during the earlier stages of this rapidly evolving pandemic, it is possible that this patient contracted COVID-19 within the local community, or during his prior hospital admission. It could be argued that the patient had early COVID-19 signs and symptoms, having presented with shortness of breath, lymphopaenia, and having had subtle infective chest X-ray changes. The patient explained he developed a stagnant productive cough, which began 5 days prior to his attendance to hospital on 23 March 2020. He responded to antibiotics, making a full recovery following 7 days of treatment. This information does not assimilate with the typical features of a COVID-19 infection. A diagnosis of community-acquired pneumonia or infective exacerbation of COPD seem more likely. However, given the high incidence of COVID-19 infections during this patients’ illness, an exposure and early COVID-19 illness, prior to the 23 March 2020, cannot be completely ruled out.

Chest X-ray conducted on prior admission illustrating mild radiopacification in the left mid zone.

On the current admission, this patient was managed with nasal cannula oxygen at 2 L. By the end of the day, this had progressed to a venturi mask, requiring 8 L of oxygen to maintain oxygen saturation. He had also become increasingly drowsy and confused, his GCS declined from 15 to 12. However, the patient was still haemodynamically stable, as he had been in the morning. An arterial blood gas demonstrated a respiratory alkalosis (pH 7.55, pCO 2 3.1, pO 2 6.7 and HCO 3 24.9, lactate 1.8, base excess 0.5). He was commenced on intravenous co-amoxiclav and ciprofloxacin, to treat a potential exacerbation of COPD. This patient had a COVID-19 throat swab on 1 April 2020. Before the result of this swab, an early discussion was held with the intensive care unit staff, who decided at 17:00 on 1 April 2020 that given the patients presentation, rapid deterioration, comorbidities and likely COVID-19 diagnosis he would not be for escalation to the intensive care unit, and if he were to deteriorate further the end of life pathway would be most appropriate. The discussion was reiterated to the patients’ family, who were in agreement with this. Although he had evidence of an ischaemic stroke on CT of his brain, it was agreed by all clinicians that intervention for this was not as much of a priority as providing optimal palliative care, therefore, a minimally invasive method of treatment was advocated by the stroke team. The patient was given 300 mg of aspirin and was not a candidate for fibrinolysis.

Outcome and follow-up

The following day, before the throat swab result, had appeared the patient deteriorated further, requiring 15 L of oxygen through a non-rebreather face mask at 60% FiO 2 to maintain his oxygen saturation, at a maximum of 88% overnight. At this point, he was unresponsive to voice, with a GCS of 5. Although, he was still haemodynamically stable, with a blood pressure of 126/74 mm Hg and a heart rate of 98 beats/min. His respiratory rate was 30 breaths/min. His worsening respiratory condition, combined with his declining level of consciousness made it impossible to clinically assess progression of the neurological deficit generated by his cerebral infarction. Moreover, the patient was declining sharply while receiving the maximal ward-based treatment available. The senior respiratory physician overseeing the patients’ care decided that a palliative approach was in this his best interest, which was agreed on by all parties. The respiratory team completed the ‘recognising dying’ documentation, which signified that priorities of care had shifted from curative treatment to palliative care. Although the palliative team was not formally involved in the care of the patient, the patient received comfort measures without further attempts at supporting oxygenation, or conduction of regular clinical observations. The COVID-19 throat swab confirmed a positive result on 2 April 2020. The patient was treated by the medical team under jurisdiction of the hospital palliative care team. This included the prescribing of anticipatory medications and a syringe driver, which was established on 3 April 2020. His antibiotic treatment, non-essential medication and intravenous fluid treatment were discontinued. His comatose condition persisted throughout the admission. Once the patients’ GCS was 5, it did not improve. The patient was pronounced dead by doctors at 08:40 on 5 April 2020.

SARS-CoV-2 is a type of coronavirus that was first reported to have caused pneumonia-like infection in humans on 3 December 2019. 5 As a group, coronaviruses are a common cause of upper and lower respiratory tract infections (especially in children) and have been researched extensively since they were first characterised in the 1960s. 6 To date, there are seven coronaviruses that are known to cause infection in humans, including SARS-CoV-1, the first known zoonotic coronavirus outbreak in November 2002. 7 Coronavirus infections pass through communities during the winter months, causing small outbreaks in local communities, that do not cause significant mortality or morbidity.

SARS-CoV-2 strain of coronavirus is classed as a zoonotic coronavirus, meaning the virus pathogen is transmitted from non-humans to cause disease in humans. However the rapid spread of SARS-CoV-2 indicates human to human transmission is present. From previous research on the transmission of coronaviruses and that of SARS-CoV-2 it can be inferred that SARS-CoV-2 spreads via respiratory droplets, either from direct inhalation, or indirectly touching surfaces with the virus and exposing the eyes, nose or mouth. 8 Common signs and symptoms of the COVID-19 infection identified in patients include high fevers, severe fatigue, dry cough, acute breathing difficulties, bilateral pneumonia on radiological imaging and lymphopaenia. 9 Most of these features were identified in this case study. The significance of COVID-19 is illustrated by the speed of its global spread and the potential to cause severe clinical presentations, which as of April 2020 can only be treated symptomatically. In Italy, as of mid-March 2020, it was reported that 12% of the entire COVID-19 positive population and 16% of all hospitalised patients had an admission to the intensive care unit. 10

The patient, in this case, illustrates the clinical relevance of understanding COVID-19, as he presented with an ischaemic stroke underlined by minimal respiratory symptoms, which progressed expeditiously, resulting in acute respiratory distress syndrome and subsequent death.

Our case is an example of a new and ever-evolving clinical correlation, between patients who present with a radiological confirmed ischaemic stroke and severe COVID-19 pneumonia. As of April 2020, no comprehensive data of the relationship between ischaemic stroke and COVID-19 has been published, however early retrospective case series from three hospitals in Wuhan, China have indicated that up to 36% of COVID-19 patients had neurological manifestations, including stroke. 11 These studies have not yet undergone peer review, but they tell us a great deal about the relationship between COVID-19 and ischaemic stroke, and have been used to influence the American Heart Associations ‘Temporary Emergency Guidance to US Stroke Centres During the COVID-19 Pandemic’. 12

The relationship between similar coronaviruses and other viruses, such as influenza in the development of ischaemic stroke has previously been researched and provide a basis for further investigation, into the prominence of COVID-19 and its relation to ischaemic stroke. 3 Studies of SARS-CoV-2 indicate its receptor-binding region for entry into the host cell is the same as ACE2, which is present on endothelial cells throughout the body. It may be the case that SARS-CoV-2 alters the conventional ability of ACE2 to protect endothelial function in blood vessels, promoting atherosclerotic plaque displacement by producing an inflammatory response, thus increasing the risk of ischaemic stroke development. 13

Other hypothesised reasons for stroke development in COVID-19 patients are the development of hypercoagulability, as a result of critical illness or new onset of arrhythmias, caused by severe infection. Some case studies in Wuhan described immense inflammatory responses to COVID-19, including elevated acute phase reactants, such as CRP and D-dimer. Raised D-dimers are a non-specific marker of a prothrombotic state and have been associated with greater morbidity and mortality relating to stroke and other neurological features. 14

Arrhythmias such as atrial fibrillation had been identified in 17% of 138 COVID-19 patients, in a study conducted in Wuhan, China. 15 In this report, the patient was known to have atrial fibrillation and was treated with rivaroxaban. The acute inflammatory state COVID-19 is known to produce had the potential to create a prothrombotic environment, culminating in an ischaemic stroke.

Some early case studies produced in Wuhan describe patients in the sixth decade of life that had not been previously noted to have antiphospholipid antibodies, contain the antibodies in blood results. They are antibodies signify antiphospholipid syndrome; a prothrombotic condition. 16 This raises the hypothesis concerning the ability of COVID-19 to evoke the creation of these antibodies and potentiate thrombotic events, such as ischaemic stroke.

No peer-reviewed studies on the effects of COVID-19 and mechanism of stroke are published as of April 2020; therefore, it is difficult to evidence a specific reason as to why COVID-19 patients are developing neurological signs. It is suspected that a mixture of the factors mentioned above influence the development of ischaemic stroke.

If we delve further into this patients’ comorbid state exclusive to COVID-19 infection, it can be argued that this patient was already at a relatively higher risk of stroke development compared with the general population. The fact this patient had previously had an ischaemic stroke illustrates a prior susceptibility. This patient had a known background of hypertension and atrial fibrillation, which as mentioned previously, can influence blood clot or plaque propagation in the development of an acute ischaemic event. 15 Although the patient was prescribed rivaroxaban as an anticoagulant, true consistent compliance to rivaroxaban or other medications such as amlodipine, clopidogrel, candesartan and atorvastatin cannot be confirmed; all of which can contribute to the reduction of influential factors in the development of ischaemic stroke. Furthermore, the fear of contracting COVID-19, in addition to his vague symptoms, unlike his prior ischaemic stroke, which demonstrated dense left-sided haemiparesis, led to a delay in presentation to hospital. This made treatment options like fibrinolysis unachievable, although it can be argued that if he was already infected with COVID-19, he would have still developed life-threatening COVID-19 pneumonia, regardless of whether he underwent fibrinolysis. It is therefore important to consider that if this patient did not contract COVID-19 pneumonia, he still had many risk factors that made him prone to ischaemic stroke formation. Thus, we must consider whether similar patients would suffer from ischaemic stroke, regardless of COVID-19 infection and whether COVID-19 impacts on the severity of the stroke as an entity.

Having said this, the management of these patients is dependent on the likelihood of a positive outcome from the COVID-19 infection. Establishing the ceiling of care is crucial, as it prevents incredibly unwell or unfit patients’ from going through futile treatments, ensuring respect and dignity in death, if this is the likely outcome. It also allows for the provision of limited or intensive resources, such as intensive care beds or endotracheal intubation during the COVID-19 pandemic, to those who are assessed by the multidisciplinary team to benefit the most from their use. The way to establish this ceiling of care is through an early multidisciplinary discussion. In this case, the patient did not convey his wishes regarding his care to the medical team or his family; therefore it was decided among intensive care specialists, respiratory physicians, stroke physicians and the patients’ relatives. The patient was discussed with the intensive care team, who decided that as the patient sustained two acute life-threatening illnesses simultaneously and had rapidly deteriorated, ward-based care with a view to palliate if the further deterioration was in the patients’ best interests. These decisions were not easy to make, especially as it was on the first day of presentation. This decision was made in the context of the patients’ comorbidities, including COPD, the patients’ age, and the availability of intensive care beds during the steep rise in intensive care admissions, in the midst of the COVID-19 pandemic ( figure 1 ). Furthermore, the patients’ rapid and permanent decline in GCS, entwined with the severe stroke on CT imaging of the brain made it more unlikely that significant and permanent recovery could be achieved from mechanical intubation, especially as the damage caused by the stroke could not be significantly reversed. As hospitals manage patients with COVID-19 in many parts of the world, there may be tension between the need to provide higher levels of care for an individual patient and the need to preserve finite resources to maximise the benefits for most patients. This patient presented during a steep rise in intensive care admissions, which may have influenced the early decision not to treat the patient in an intensive care setting. Retrospective studies from Wuhan investigating mortality in patients with multiple organ failure, in the setting of COVID-19, requiring intubation have demonstrated mortality can be up to 61.5%. 17 The mortality risk is even higher in those over 65 years of age with respiratory comorbidities, indicating why this patient was unlikely to survive an admission to the intensive care unit. 18

Regularly updating the patients’ family ensured cooperation, empathy and sympathy. The patients’ stroke was not seen as a priority given the severity of his COVID-19 pneumonia, therefore the least invasive, but most appropriate treatment was provided for his stroke. The British Association of Stroke Physicians advocate this approach and also request the notification to their organisation of COVID-19-related stroke cases, in the UK. 19

Learning points

• SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) is one of seven known coronaviruses that commonly cause upper and lower respiratory tract infections. It is the cause of the 2019–2020 global coronavirus pandemic.
• The significance of COVID-19 is illustrated by the rapid speed of its spread globally and the potential to cause severe clinical presentations, such as ischaemic stroke.
• Early retrospective data has indicated that up to 36% of COVID-19 patients had neurological manifestations, including stroke.
• Potential mechanisms behind stroke in COVID-19 patients include a plethora of hypercoagulability secondary to critical illness and systemic inflammation, the development of arrhythmia, alteration to the vascular endothelium resulting in atherosclerotic plaque displacement and dehydration.
• It is vital that effective, open communication between the multidisciplinary team, patient and patients relatives is conducted early in order to firmly establish the most appropriate ceiling of care for the patient.

Contributors: SB was involved in the collecting of information for the case, the initial written draft of the case and researching existing data on acute stroke and COVID-19. He also edited drafts of the report. MH was involved in reviewing and editing drafts of the report and contributing new data. SP oversaw the conduction of the project and contributed addition research papers.

Funding: The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

Competing interests: None declared.

Patient consent for publication: Next of kin consent obtained.

Provenance and peer review: Not commissioned; externally peer reviewed.

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Ischemic stroke: A case study

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• Martinez, Rudolf Cymorr Kirby P.
• Rudolf Cymorr Kirby P. Martinez, PhD, MA, RN, CAA, LMT, CSTP, FRIN
• Sigma Affiliation

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This presents an analysis of a case of Ischemic stroke in terms of possible etiology, pathophysiology, drug analysis and nursing care

Clinical Focus: Adult Medical/Surgical

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Cerebro Vascular Accident (CVA)-A Medical Case Study

• Sophia G. 1
• 1. Lecturer, Department of Medical Surgical Nursing, DR. B.R. Ambedkar Institute of Nursing, Dr. B. Ramch Campus, Bangalore, India

Description

Objectives: To perform a health assessment, identify the nursing needs and prevent complication, formulate nursing diagnosis, provide comprehensive nursing care, learn about cerebro vascular accident and its management teach family members and patients in detail about follow-up care. Methods of collection: case sheet, wife. Sample : MICU. Setting : Government Rajaji hospital, Madurai. Conclusion: By this care study, I got an opportunity to provide comprehensive nursing care to my client who had cerebrovascular accident. It is of paramount importance for the nurses to become competent in providing nursing care for the patients with these problems.

(6-18)MEDICAL CASE STUDY-format (1).pdf

Files (761.8 kb), additional details.

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• Lewis. Text book of Medical Surgical Nursing.9th edition. Mosby. st. Louin Missouri. 2011.
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