Free Nursing Essays - A stroke or cerebrovascular accident is the sudden interruption of blood flow to part of the brain
Definition and nature of a stroke
A stroke or cerebrovascular accident is the sudden interruption of blood flow to part of the brain, causing infarction (death) of brain cells and destroying or impairing body function controlled by that part of the brain. It is an episode of sudden neurological dysfunction with symptoms lasting more than 24 hours and is a major manifestation of cerebrovascular disease (any abnormality of vessel, blood flow or quality of blood resulting in ischemia or hemorrhage). When a stroke occurs the neurological outcomes are a result of the location of the insult.
Aetiology of illness or disease refers to the cause of diseases
Ischemic strokes account for an estimated 85% of the total of strokes.1 This can then be broken down into strokes resulting from atherosclerosis (20%), embolic (20%), idiopathic (30%) and other causes (15%).1
Atherosclerosis means hardening of the arteries and describes a pattern seen in three vascular diseases.2 Atherosclerosis is the formation of hard plaques in the muscular wall of arteries. It primarily affects elastic arteries and myocardial infarction, stroke and sudden cardiac death are all serious complications of the disease.2
Atheromas are sparse at first but as the disease progresses they increase in number.2 In small arteries they can occlude the blood flow altogether. The plaques can also weaken the muscular walls of large arteries resulting in aneurysm. The plaques may also break off and impede blood flow of the artery or become a thrombus and travel in the circulating blood. Thrombi may then lodge in the heart resulting in myocardial infarction or in the pulmonary arteries impeding blood flow to the lungs or in the cerebral arteries resulting in stroke. The impact of atherosclerosis is therefore great as the complications of the disease are numerous and often fatal.
There are both modifiable and non-modifiable risk factors associated with stroke. The factors that can’t be changed are age, gender, sex and race. High blood pressure, diabetes mellitus, cardiac disease and increased blood lipids can all increase the risk of stroke.1 The presence of athererosclerosis in other parts of the body is also an indication that the cerebral vessels are involved in the disease. Diabetes mellitus increases the acceleration of the atherosclerotic process and can therefore increase the risk of stroke as well. See Table 1.
Table 1: Aetiology: Risk factors associated with stroke1
Age From 60-75% of all strokes occur in persons over 65 years of age
Sex Men have an increased risk of stroke possibly because of poorer control of hypertension and heart disease.
Race African Americans are twice as likely to develop thrombotic strokes and three times more likely to develop hemorrhagic strokes.
Hypertension Hypertension is a major risk factor for stroke particularly in combination with atherosclerosis. The improved diagnosis and treatment of hypertension has reduced the incidence of stroke.
Heart disease This is a major risk factor to stroke from atherosclerosis and emboli.
Diabetes This is associated with an increased rate of atherosclerosis.
Other Cigarette smoking, oral contraceptive use, family history of TIA or CVA, obesity, sedentary lifestyle, elevated serum cholesterol and triglycerides
Hypertension is the most important risk factor of all emphasizing the need for the patient to be taking medication to appropriately normalize their blood pressure. High Blood Pressure promotes the formation of atherosclerosis in intracranial and extra cranial arteries and causes hardened lipid deposits to form in small penetrating blood vessels.2 Smoking raises the haemotocrit, increases platelet aggregation, lowers HDL (good cholesterol) and accelerates atheroma formation. Hyperlipidaemia is linked to increasing atherosclerotic disease therefore being tied in with the most common cause of stroke. Cardiogenic embolism is a common cause of stroke and this can result from atrial fibrillation and other arrhythmias, valvular heart disease, prosthetic heart valves, myocardial infarction, infective endocarditis, left ventricular hypertrophy, congestive heart failure, anemia and unstable angina. An increased haemotocrit as a result of smoking can cause a higher rate of atherosclerosis due to the high viscosity of the blood and increased rate of damage to the vessel wall. Conversely anemia causes turbulence which can increase thrombi production.2
It is thought that TIAs occur when microemboli break off from atherosclerotic plaque lesions. TIAs can also be triggered from events that temporarily decrease blood supply to the brain.1 TIAs are present in 60% of stroke patients and are the most important predictor of stroke.
Pathological changes that occur at the cellular level can result in disease. Atherosclerosis is one of these micro-pathological changes that can result in widespread damage and disease throughout the whole body and can be fatal. That is, the particular patient in this case had a stroke as a result of atherosclerotic changes that had taken place in his arteries. A plaque or thrombus formed at the micro level and then broke off into the circulation and blocked one of the arteries in his brain causing neurological deficit to the relative region and associated part of the body.
The formation of atherosclerosis at the cellular level and progression to disease
There are two theories to why atherosclerosis forms in the first place. The first theory hypothesizes that there is an increased cellular proliferation as a result of a raised intake of lipid from the blood. The second theory suggests that organization and continual growth of thrombi result in plaque formation. The latest theory is a mixture of the two and is called ‘Response to injury hypothesis’ and considers atherosclerosis to be a chronic inflammatory response of the arterial wall initiated by some form of injury to the endothelium.2
Atherosclerotic plaques develop as a result of the following steps1:-
1. The development of focal regions of endothelial injury that results in increased endothelial permeability and increased WBC (White Blood Cell) adhesion
2. The taking up of lipoproteins (mainly LDL) into the vessel wall
3. Adhesion of blood monocytes and other WBCs to the endothelium followed by migration of monocytes into the intima and their transformation into foam cells
4. Adhesion of platelets to the lesion
5. Release of factors from the platelets or WBCs that cause migration of smooth muscle cells from the media into the intima
6. Proliferation of smooth muscle cells in the intima and increased production of the extracellular matrix (ECM) leading to accumulation of collagen and proteoglycans
7. Increased accumulation of lipids
This patient has a history of cardiovascular disease and atherosclerosis of the coronary arteries. This is a sign that there are atherosclerotic changes occurring throughout the body. These cellular changes in the walls of arteries have resulted in not only a disease of the patient’s vessels but a secondary disease of the brain tissue called a stroke due to cerebral blood flow reduction.
The cellular changes of ischemia in the brain
Cerebral arterial occlusion may lead to focal ischemia and to infarction of a specific region of CNS tissue.2 The area of the brain affected determines whether a patient remains asymptomatic or develops a hemiplegia, a sensory deficit, blindness or some other deficit. The brain requires a continual supply of glucose and oxygen. When blood supply to a region is reduced the survival of the tissue depends on the collateral circulation, duration of the ischemia and the size and reduction of the flow. Neurons are the most sensitive cells in the body and it is useful to understand what is happening at the cellular level:-
The changes that occur after a cerebrovascular incident can be grouped into three different categories; early changes, subacute changes and repair.
Early changes occur 12-24 hours after the insult and include acute neuronal cell change (red neurons). These begin with the development of small vacuoles and then eosinophilia of the neuronal cytoplasm. Later pyknosis (cell nucleus is thickened into a dense mass) and karyorrhexis occur. Similar changes also take place in the Purkinje cells of the cerebellum and the oligodendrocytes.
Subacute changes occur at 24 hours to 2 weeks and include death of the tissue, an increase in macrophages, vascular proliferation and reactive giosis.2
Repair is seen after 2 weeks and is characterized by removal of the necrotic tissue and change in normal CNS structure. The neuron loss and gliosis produce an irregular destruction of the neocortex.
The outcome of this patient’s stroke depends on a number of risk factors including the available collateral circulation, the duration of the ischemia and the size and reduction of blood flow. The ability of the brain to repair will depend on the patient’s nutritional status, number of white blood cells available and extent of the damage.
Conclusion
This patient illustrates an example of how changes at the microscopic level due to risk factors such as smoking, diabetes, high blood lipids and ingestion of saturated fats/high calorie intake can result at cellular changes of the blood vessels resulting in disease. The brain may not be able to recover completely from this stroke and prevention is mandatory to prevent further damage.
Recommendations include follow up with hypertensive medication to gain better control of blood pressure. Regular monitoring of blood glucose, cholesterol and triglycerides with medication control if necessary. Referral to a dietician to help foster improved dietary changes to support the heart and reduce weight including implementation of good fats into the diet, increased fruit and vegetables and reduction of saturated fats from the diet.
References
1. Medical Surgical Nursing. Phipps, Sands and Marek. 1999. Mosby Inc, St Louis. Pp 1737-1757
2. Pathologic Basis of Disease. Robbins. Contran, Kumar and Collins. 1999. WB Saunders Company, Philadelphia. pp498-510
