Cerebrovascular Accident

‘Cerebrovascular diseases are the third most common cause of death in western countries’ (Stevens and Lowe 2000 pg 436). The most frequent neurological manifestation of cerebrovascular disease is a sudden onset of dysfunction due to insufficient cerebral blood supply. This has been termed as a Cerebrovascular Accident (CVA) or stroke. For the purpose of this portfolio the author has observed, partaken in, researched and evaluated the nursing interventions and care received by a patient admitted to hospital following a cerebral infarction.

The patient, whom I will refer to under the pseudonym of John, is an eighty four year old man who lived alone with some family support. ‘Older people are at higher risk of a stroke and from the age of fifty-five onwards, the chances of having a stroke more than double every ten years’ (MacWalter and Fraser 2003 pg 8). This is a biological trait that cannot be altered but is an important risk factor taken into consideration when a stroke is suspected.

John’s health status prior to admission showed a medical history of hypertension and high cholesterol levels. These medical conditions are the main possible causes of a Cerebrovascular accident alongside his contributing lifestyle factors and social history, such as smoking. ‘Constricting the blood supply and promoting clotting are two ways in which smoking can make it more likely that a stroke will occur’ (MacWalter and Fraser 2003 pg 9).

A Cerebrovascular Accident is diagnosed from a patient’s medical history and current clinical findings as a result of extensive tests and investigations. Pathophysiological Processes The clinical definition of a Cerebrovascular Accident is defined by Stevens and Lowe (2000 pg 437) as ‘a sudden onset of a non-traumatic focal neurological deficit that causes death or lasts for over twenty-four hours’. This results in insufficient blood supply to the brain therefore affecting cells by the disruption in the supply of oxygen.

The causes of strokes are divided into two main groups; Ischaemic, caused by cerebral infarction and haemorrhagic, caused by intracerebral and subarachnoid haemorrhage. ‘It is characterised by a variable degree of neurological deficit produced either as a consequence of cerebral ischaemia caused by a thrombosis, embolism and/or atherosclerosis, or as a result of cerebral haemorrhage’ (Montague, Watson and Herbert 2005 pg 117). An Ischaemic stroke is the most common type and occurs when there is a blockage in an artery in the brain.

The word ischaemia relates to an interruption to blood flow, this interruption can be in the form of either a thrombosis (blood clot) an embolus, carried into the artery by the circulatory flow from a clot elsewhere, or as a result of a disease process in which the arteries are thickened or narrowed. John was diagnosed with suffering an Ischaemic stroke with the causal factors being atheroma affecting the right anterior cerebral vessels.

Clinical features of an Ischaemic stroke usually develop abruptly and depending on the site, cause and extent of brain damage, may include symptoms such as loss of consciousness, hemiparasis or hemiplegia of one side of the body, asymmetry of facial features, problems with balance and co-ordination, language and visual difficulties, dysphagia and incontinence (British Medical Association 2002). Sensation, movement or function controlled by the damaged area of the brain is impaired, however each patient’s symptoms differ depending upon the type of stroke suffered.

Symptoms depend on the lobes of the brain that have been affected. The anatomy of the brain includes the cerebral cortex which is divided into two hemispheres, left and right, and as the cranial nerves descend they cross over. The left lobes of the cortex control the movements and senses on the right side of the body e. g. voluntary movement, personality and mood, speech, bladder control, attention to stimuli and concentration etc.

Similarly the right lobes of the cortex control movements and senses on the left side of the body e. g. eeling texture and shapes, dressing, special imaging, interpreting vision, facial recognition, orientation etc (Martini 2002). When admitted John presented with a sudden onset of left-sided weakness affecting his arm and leg and reducing co-ordination. This was then followed by visual disturbances in the form of blurred and double vision, a severe headache, confusion, slightly slurred speech, dysphagia, urinary incontinence and a period of unconsciousness. Stroke symptoms are initially exaggerated by the swelling and distortion of the injured neural tissue (Martini 2002).

Underlying the development of the Ischaemic stroke was the development of atherosclerosis and the contributing factors of hypertension and hyperlipidaemia. Atherosclerosis is the process that refers to the hardening and obstruction of arteries. ‘It is due to deposits of lipids and other substances, in the form of atheromatous plaque in the intima of the medium and large arteries’ (Montague, Watson and Herbert 2005 pg 431). Atheroma is the term given to the cholesterol-based plaque, as this collects it blocks off part of the lumen restricting blood flow.

In addition to this atheroma predisposes thrombosis, where platelets adhere to the surface of the atheroma initiating the formation of a blood clot. This is what occurred in the case of John as thrombosis occluded the blood supply to the right anterior cerebral lobe resulting in Ischaemic tissue. Largely the level of cholesterol in the blood stream determines the risk of developing atherosclerosis, which can be dependent upon dietary and genetic factors (Campbell 2003).

Elevated lipid levels, or hyperlipidaemia, may be a result of metabolic disease e. g. diabetes or possibly high fat diets, especially saturated fats and high dietary cholesterol and plays a role in the progression of atherosclerosis. ‘There is no definitive causal relationship between saturated fat intake in the diet and the serum cholesterol levels but there is evidence that unsaturated fatty acids lower blood cholesterol whereas saturated fats tend to raise it (Montague, Watson and Herbert 2005 pg 432).

Cholesterol is one of the lipids circulated in the blood flow and is an important constituent of cells and is involved in the formation of hormones and bile salts. Cholesterol transported by circulatory flow in the form of low-density lipoproteins (LDL’s) is a risk factor for conditions such as atherosclerosis whilst cholesterol in the form of high-density lipoproteins (HDL’S) protects against arterial diseases.

The optimum values agreed upon by medical professionals is a total cholesterol level less than 5. 2 mmol/L, HDL cholesterol 0. 8-1. 8 mmol/L (male) 0. 8-2. mmol/L (female) and LDL cholesterol between 1. 3 and 4. 9 mmol/L (MacWalter and Fraser 2003). When admitted John’s total cholesterol level was 7. 9 mmol/L, which linked to a raised blood pressure of 180 mmHg systolic over 92 mmHg diastolic. Most authorities now agree that a resting systolic value above 140 mmHg and a diastolic persistently exceeding 90 mmHg indicates hypertension. Persistent hypertension is a common disease and approximately 50% of people in England aged 65-74 are hypertensive and this percentage increases for people even older (Marieb 2001).

An average of three or more blood pressure readings are taken at rest, several days apart and if that average exceeds the upper limits of what is considered normal for that patient then hypertension is diagnosed. ‘In the past there was more attention paid to the diastolic pressure value but there is increasing evidence that the height of the systolic blood pressure is a better predictor of both heart attacks and strokes’ (Beevers et al. 2001; Montague, Watson and Herbert 2005 pg 486). Increased arterial pressure has an adverse effect as it places physical stress on the walls of blood vessels throughout the body.

This can then promote the development of atherosclerosis, which in turn puts the individual at a greater risk of suffering a stroke. The other risk factor in John’s case is a lifestyle issue, as he had a regular nicotine intake through smoking approximately fifteen cigarettes a day. The mechanisms linking smoking and atherosclerosis are complex and nicotine is thought to increase platelet adhesion and carbon monoxide increases the permeability of the arterial endothelium, enhancing plaque formation (Montague, Watson and Herbert 2005).

Clinical Tests and Investigations A number of diagnostic procedures were performed when John was admitted; these were to pinpoint the type of stroke and to help decide on the most appropriate treatment. On admission he was hypertensive and a full set of observations where taken monitoring vital signs such as blood pressure, temperature, pulse oximetry and respiration rate. These characteristic signs and symptoms can often detect abnormalities of the vascular system.

Respiratory patterns give the clearest indication of how the brain is functioning, this is because the process of respiration is controlled by more than one area of the brain and any disease that affects those areas can cause abnormal respiratory patterns. The rate and pattern of Johns respirations was noted at 22 breaths per minute, faster than the average and termed trachypnoea, this was then constantly re-evaluated after oxygen therapy was commenced, to identify any improvement or deterioration. ‘Rate and depth determine the type of respiration.

The normal rate at rest is approximately 14-18 breaths per minute in an adult’ (Dougherty and Lister 2004 pg 459). Pulse oximetry was then monitored to evaluate the effectiveness of the commenced oxygen therapy. Blood pressure was monitored to evaluate the condition of the patient and assess vascular stability and the effectiveness of medication to treat hypertension, this was then re-evaluated four hourly. ‘It is essential to have an early knowledge of any change in blood pressure, as this may indicate a deterioration in condition and requires prompt treatment’ (Dougherty and Lister 2004 pg 450).

Observations such as respiration patterns, pulse oximetry and blood pressure provide a baseline for further comparisons and can also be a possible indication of intercranial pressure in stroke patients. ‘When intercranial pressure is greater than 33mmHg for even a short time, cerebral blood flow is significantly reduced. The resulting ischaemia stimulates the vasomotor centre, causing systemic blood pressure to rise’ (Dougherty and Lister 2004 pg0491). Analysis of a sample of blood was undertaken to give information on the health of major organs and any chemical imbalances in the blood indicating a disease process.

A full blood count was performed which measure the amount of haemoglobin and the amount of red and white blood cells, as well as platelet levels that may have revealed a haemorrhage, as changes may indicate blood loss, or an infection. The normal range of red blood cells, for an adult male, are 4. 7-6. 1 m/mm3 and the range for haemoglobin is 14-18g/dl (Martini 2002). Johns blood results revealed red and white cell counts and haemoglobin were within normal limits, which meant an infection, and haemorrhagic stroke could be ruled out.

A platelet count and electrolyte levels where then analysed and results showed a raised platelet count which indicated vascular thrombosis and increased sodium levels, 151mmol/L, which was thought to be the result of essential hypertension. Normative values of sodium levels within the blood are 135-145mEq/L (Martini 2002). Urea and electrolytes give an indication of liver function and sodium, potassium and chloride levels are electrolytes that function in cerebral nerve transmission (Watson and Fawcett 2003).

A lipid profile was carried out to determine the low-density and high-density lipoprotein levels as well as total cholesterol; the high result of 7. 9 mmol/L reflected the potential for cerebral atheroma. A preliminary diagnosis of an intracerebral event was made after blood results from a Troponin T blood test revealed no myocardial damage, indicating no myocardial infarction was suffered. These blood tests were repeated as necessary throughout his inpatient stay to evaluate the effects of the treatment prescribed and medications administered.

The structural basis of the preliminary diagnosis of an Ischaemic stroke was determined by the use of different scans. An echocardiogram, which is ultrasonography of the heart, was performed to assess the functioning and structure of the heart chambers, valves, walls and coronary arteries and diagnose blood clots in the heart. This is done because strokes can be caused by a blood clot that has travelled in the circulatory flow to the brain. ‘Arterial fibrillation, a damaged heart valve or recent myocardial infarction can cause clots in the heart which can migrate to the brain (British Medical Association 2002).

Johns echocardiogram showed a probable CVA although thrombosis was not found in the heart, it also identified occasional ectopic beats, which were of no major concern, but an electrocardiogram (ECG) trace was taken to determine heart rate and rhythm as well as damage caused by persistent hypertension. Heart rate can be determined through the study of ECG and abnormal wave patterns occur when cardiac abnormalities such as myocardial infarction or chamber hypertrophy, occur in the conduction system. A CT (Computerised Tomography) scan of the brain was then performed to confirm diagnosis.

Johns CT scan showed cerebral ischaemia in the periventricular white matter. ‘CT scans are able to determine whether the stroke is due to a bleed or blockage, the hemisphere in which the damage has occurred and the size of the damaged area. This is therefore an extremely valuable diagnostic tool (MacWalter and Fraser 2003 pg 41). Nursing Interventions and Care Evidence-based practice can be defined as ‘care that is based on procedures underpinned by the conscientious, explicit and judicious use of current best evidence’ (Mann 1996; Dougherty and Lister 2004 pg 2).

The National Institute for Clinical Excellence develops guidelines for health professionals about the effectiveness of particular interventions for specific client groups. Evidence-based and good practice in stroke rehabilitation is based on current research, which has been appraised, national standards such as those set out in the National Service Framework for Older People and local policies relating to procedures. For patients who have had an Ischaemic stroke the National Institute of Clinical Excellence has issued guidelines on the secondary prevention of further Ischaemic strokes.

Treatment is recommended to commence with an antiplatelet drug e. g. Aspirin (NICE 2004). On diagnosis John was commenced on 200mg of Aspirin daily, this is an antiplatelet drug, which inhibits platelet aggregation reducing clotting tendencies. ‘According to the Antithrombic Trialists (ATT) collaboration, Aspirin has been shown to reduce occlusive vascular events by 23% on high risk patients’ (Albers et al. 2004). He was closely monitored by nursing staff for any adverse reactions as aspirin is related to bleeding problems including haemorrhagic stroke and gastrointestinal bleeding (BNF 2005).

However, the benefits of antiplatelet treatment are considered to outweigh the risks of major bleeding. Drug therapy was also commenced to treat the underlying cause of John’s stroke. He was commenced on Bendrofluazide 2. 5mg daily; to reduce blood pressure in a gentle graduated fashion. The recommended dosage is 2. 5-10mg daily and this was started once his sodium level was within normal range. ‘Generally therapy to lower blood pressure in the acute phase of a stroke is not recommended as it may compromise blood flow to the brain (MacWalter and Fraser 2003 pg 61).

Bendrofluazide is a diuretic used as an antihypertensive (BNF 2005). John was also commenced on a low dose lipid-regulating drug called Simvastatin, 20mg daily, to reduce the levels and change the proportions of cholesterol in the bloodstream. The recommended dosage is between 10-80mg daily (BNF 2005). Current research is being undertaken on the benefits of using clot-dissolving enzymes in the acute stroke phase and results of this research may further influence drug therapy for Ischaemic stroke patients.

Treating the stroke symptoms is the first step to initiating rehabilitation. On admission to the ward John underwent a comprehensive assessment to identify his most important needs and concerns and decide on a plan of care in collaboration with other members of the multi-disciplinary team i. e. physiotherapists and occupational therapists. Nursing staff undertook an immediate bedside assessment of his swallowing reflex, this was achieved through the use of a water swallowing test which involved an examination of his ability to swallow 30mls of sterile water in 10mls intervals.

This highlighted some swallowing difficulties and a referral was made to a speech and language therapist (SALT) for a more comprehensive assessment. Whilst waiting for the SALT assessment John was managed with nil by mouth over night plus intravenous fluids. An explanation of this was given to John as research by Parker et al (2004 pg. 28) suggested that ‘patients with good awareness of the clinical indicators of dysphagia modify the way they drink by taking smaller volumes per swallow and drink more slowly than those with poor awareness’.

Once the Speech and Language Therapist had assessed John with different food consistencies a recommendation of a soft diet and syrup-thickened fluids was made. ‘It is essential for the nurse to be involved in all aspects of the patients therapy so that it can continue in the therapists absence’ (Montague, Watson and Herbert 2005 pg. 117). An assessment was then made of John’s Activities of Daily living, problems identified from this were addressed and short and long term outcomes were discussed.

His need for assistance with personal hygiene, due to his continued hemiparasis, meant the assistance of one person was needed for washing and dressing whilst encouraging and promoting independence and full range of movement. ‘The active promotion and restoration of independence is the goal for all patients following a stroke’ (Carr and Shepherd 2002; Montague, Watson and Herbert 2005 pg. 117). This was achieved through input from Occupational Therapists in the form of washing and dressing assessment and strategies to overcome the loss of the use of one side.

Further occupational work included bathroom and kitchen assessments as well as a home visit to ensure John would be able to cope once discharged. In the acute phase of John’s stroke he was bed bound and adequate pressure area care was essential to avoid skin breakdown. ‘Prevention of pressure sores is one of the most important responsibilities of any nurse caring for dependent older adults who have activity or mobility limitations’ (Miller 1999 pg. 393). Skin tissue breakdown can be attributed to impaired circulation and external pressure to an area or bony prominence.

Interventions used to combat the breakdown of tissue on Johns sacral and heel areas included repositioning at two hourly intervals, in accordance with hospital policies on the prevention of pressure sores, as well as assessment tools such as a the ‘Medley Score’ to evaluate the need for a pressure relieving mattress. It was also essential to position and support Johns affected limbs to reduce further complications and promote good alignment and assist with better mobility. ‘The shoulder can be prone to damage if the arm is not carefully positioned and protected’ (MacWalter and Fraser 2003 pg. 1).

A physiotherapist with the intention of improving muscle tone carried out an assessment of posture, movement and tone and mobility and John participated in planned physiotherapy sessions in the gym throughout his inpatient stay. Problems with elimination were identified in particular urinary incontinence and constipation. ‘Constipation is recognised as a serious problem in clinical practice, affecting 60% of those in stroke rehabilitation wards’ (Norton, Lockwood and Swift 2004 pg 2551).

Johns urinary incontinence was thought to result from impaired neurological function secondary to his Cerebrovascular accident, this diagnosis was made by an incontinence nurse to whom he was referred. Interventions to manage his incontinence included primarily the use of incontinence pads and monitored fluid intake. ‘If bladder fullness is not adequately achieved as in states of dehydration or limited fluid intake, the neurological mechanisms that control bladder emptying will not function effectively’ (Miller 1999 pg. 425). Secondary interventions included health promotion on adequate fluid intake and environmental modifications e. g.

Commode at bedside etc. Similar interventions were undertaken to prevent constipation, these include increased use of lactulose, which is an osmotic laxative that retains fluid in the intestine. It also included health promotion on lifestyle factors such as diet, fluid intake, increased mobility and toileting habits (Norton, Lockwood and Swift 2004). John was discharged from the rehabilitation ward after eight weeks and continued care included drug therapy of low dose Aspirin, 75mg daily, antihypertensive and cholesterol lowering drugs. As well as advice in the form of patient information leaflets on secondary prevention of strokes e. . smoking cessation.

Conclusion An Ischaemic stroke is a serious and complex disease process with many underlying developmental factors such as hypertension, atherosclerosis and lifestyle factors. Treatment and rehabilitation in a dedicated stroke unit is known to achieve better outcomes for stroke patients, this is partly due to the access to a multi-disciplinary team that includes physiotherapists and occupational therapists. The time taken to recover from a stroke is extremely viable and depends on the early interventions in the acute phase.

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