Stroke Case Study | Pathophysiology and Care Delivery Plan

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11th Feb 2020 Nursing Case Study Reference this

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This paper will discuss the case study relating to the patient, Mrs Amelia Middleton, and answer a series of questions relating to the pathophysiology of stroke, nursing care of the patient, and response to pharmacological issues with her treatment

Question 1

Farrell & Dempsey (2014b) define the pathophysiological characteristics of an ischaemic stroke as being the disruption to cerebral blood supply due to an obstruction in a blood vessel (p. 1649). This disruption can be described as an ischaemic cascade, which commences with a fall in cerebral blood flow to less than 25mL/100g/min (p. 1649). When this occurs, neurons are unable to maintain aerobic respiration, causing a decrease in adenosine triphosphate (ATP) production. To combat this, mitochondria switch to anaerobic respiration, which produces large amounts of lactic acid, causes changes in cellular pH levels, anaerobic respiration is less efficient, and neurons are not capable of producing sufficient ATP to fuel the depolarisation processes (Farrell & Dempsey, 2014b, p. 1649; Craft, Gordon, & Tiziani, 2011). With the loss of ATP production, the active transport across the cell membrane ceases, leading to the destruction of the cell membrane, releasing more calcium and glutamate, vasoconstriction and generation of free radicals. As the cascade continues, intracellular pressures increase, causing oedema (Craft, et al., 2011, p. 192). This oedema reaches it maximum after about 72 hour, and slowly subsides over the following two weeks.

There are four types of haemorrhagic stroke, namely – intracerebral, intracranial cerebral aneurysm, arteriovenous malformations, and subarachnoid haemorrhage, all with varying pathophysiology (Farrell & Dempsey, 2014b, p. 1661). The most common type is the intracerebral haemorrhage, which is mostly found in patients with hypertension and cerebral atheroschlerosis. Certain types of arterial pathology, brain tumour, and the use of medications may also cause intracerebral haemorrhage (Farrell & Dempsey, 2014b). Bleeding related to the condition is most commonly arterial and normally occurs in the putamen and adjacent internal capsule, cerebral lobes, basal ganglia, thalamus, cerebellum and brain stem (Farrell & Dempsey, 2014b).

Intracranial aneurism is dilation of the walls of a cerebral artery developing because of weakness in the arterial wall (Farrell & Dempsey, 2014b). Presumed causes of aneurysms are weakness in arterial walls, congenital abnormalities, hypertensive vascular disease, head trauma, infection, or advancing age. Aneurysms can occur in any area of the brain but commonly occur at the circle of Willis arteries. Arteries affected by aneurysms are the internal carotid artery, anterior cerebral artery, anterior communicating artery, posterior communicating artery, posterior cerebral artery and middle cerebral artery (Farrell & Dempsey, 2014b).

Arteriovenous malformations are caused by abnormalities in embryonic development or are the result of trauma. It is the formation of a mass of arteries and veins without a capillary bed, whose absence, leads to dilation of arteries and veins with eventual rupture. This type of haemorrhage is common in younger people (Farrell & Dempsey, 2014b).

Subarachnoid haemorrhage may occur because of arteriovenous malformation, intracranial aneurysm, trauma or hypertension. Most common causes are leaking aneurysms in the area of the circle of Willis or a congenital arteriovenous malformation of the brain (Farrell & Dempsey, 2014b).

Both ischaemic and haemorrhagic stroke have modifiable and non-modifiable precipitating factors. Modifiable factors are those that can be changed and include:

History of cardiovascular disease

Hypertension

Smoking

Diabetes

Atrial Fibrillation

Obesity

Diet

Physical inactivity

(Al-Asadi & Habib, 2014; Jarvis, 2012)

Non-modifiable factors are those that cannot be changed or altered, and in concert with modifiable risk factors, can indicate populations at higher risk. The factors are:

Age

Gender

Low birth weight

Ethnicity

Genetic disorders

 

(Al-Asadi & Habib, 2014; Jarvis, 2012)

Question 2

The nursing care required for the patient within the first 24 hours would initially include a neurological assessment, especially if thrombolytic therapy has been administered (Hinkle & McKenna Guanci, 2007). Nurses need to use the Glasgow coma scale (GCS), check vital signs pupil reaction and limb assessment. If the GCS falls during or after treatment, patients need to have an urgent CT scan to exclude haemorrhagic stroke. These observations need to be recorded every 15 minutes for the first 2 hours after thrombolytic therapy, then every hour for the next 24 to 48 hours (Hinkle & McKenna Guanci, 2007). Oxygen therapy will only need to be administered if the patient becomes hypoxic, which occurs if the oxygen saturation (SaO2) levels fall below 95% saturation. Blood sugar levels need to be monitored, as it is common for post stroke patients to become hyperglycaemic. Patients also need to be in an electric bed with the cot sides up and the head at a 30-degree angle, which reduces the risks of choking and falls (Catangui & Slark, 2012). Suction should be available at the bedside in case of angioedma. Electrocardiograms need to be performed regularly to detect any abnormal changes in heart rhythm. The patient is already in atrial fibrillation but this may alter if thrombolytic therapy is administered, as such, this requires assessment on an hourly basis. The nurse should also take the time to provide information to family members regarding the patient’s treatment (Felicilda-Reynaldo, 2013). The patient and family need to be informed why thrombolytic therapy is needed, what the desired outcomes are and if there are any adverse effects. When this treatment is needed, it is often in an emergency and can be frightening for family members to see their loved one in pain or distress (Felicilda-Reynaldo, 2013).

Question 3

Thrombolysis is the division of a blood clot or thrombus by the infusion of a fibrinolytic agent (drugs that are capable of breaking down fibrin, the main constituent of blood clots) into the blood (Tiziani, 2013). Thrombolytic agents act by activating plasminogen to form a proteolytic enzyme, plasmin, which attaches to fibrin, and consequently, breaks down the clot (Tiziani, 2013; Catangui & Slark, 2012); this process is called clot resolution. Thrombolytic agents vary in there action, for example, Alteplase and Reteplase, are recombinant tissue plasminogen activator (r-tPA) drugs that have fibrin specific actions, adhering to fibrin bound plasminogen, Tenecteplase, a genetically engineered tissue plasminogen activator (tPA) shares similar traits (Tiziani, 2013; Catangui & Slark, 2012). In contrast, Streptokinase is a non-specific plasminogen activator, which attaches itself to both fibrin bound plasminogen and unbound plasminogen (Tiziani, 2013).

The use of thrombolytic agents on stroke patients is time-critical. Catangui & Slark (2012), supported by Hinkle & McKenna Guanci (2007) and Farrell & Dempsey (2014b), describe a set of contraindications for the use of thrombolysis in stroke patients, these include age, blood pressure greater that 185mmHg/110mmHg, GCS score less than 8, time from onset of symptoms less than 4½ hours, or previous stroke or myocardial infarction. This is not an exhaustive list, but is relevant to the case study patient. From these indicators it can be shown that the patient falls into a category that contraindicates the use of thrombolysis in the treatment of her condition, i.e. her blood pressure is 200mm/Hg/110mm/Hg, and that it has been at least 6 hours since onset of conditions.

Question 4

Aspirin is both a non-steroidal anti-inflammatory (NSAID) and anti-platelet drug (Tiziani, 2013, p. 4 & 511). In its NSAID function, the drug acts to inhibit prostaglandin production, which is a mediator of inflammatory response and thermoregulation (McKenna & Lim, 2012). The anti-platelet properties of the drug inhibit the production of thromboxane A2, which is a vasoconstrictor that normally increases platelet aggregation (McKenna & Lim, 2012). Contraindications for this drug are for people with allergies to Salicylates, haemorrhage, and gastrointestinal bleeding (Tiziani, 2013; McKenna & Lim, 2012). Administration is by oral pathway. In the context of this case study, because the patient is not eligible for thrombolysis, aspirin would be beneficial in lowering the risk of further stroke by reducing the chance of further thrombosis forming through its anti-platelet properties. The risks in this context are exacerbation of her hypertension and possible bleeding; however, in this circumstance the prescription of aspirin is appropriate.

Carvedilol is a lipophilic vasodilating non-cardioselective β-blocker (Leonetti & Egan, 2012). This drug is used to treat hypertension by blocking norepinephrine binding to α1-adrenergic receptors in addition to both β1-adrenergic and β2-adrenergic receptors (Leonetti & Egan, 2012). Contraindications for this drug include bradycardia, heart block, diabetes, and bronchospasms (McKenna & Lim, 2012). Administration is by oral pathway. In the context of the case study, the administration of carvedilol is desirable because of her hypertension. It is further suggested that carvedilol contributes to a reduction in cardiac arrhythmias such as atrial fibrillation (Watson & Lip, 2006). The risk associated with this drug include hepatic failure, oedema, and deterioration if the patient is in heart failure (McKenna & Lim, 2012; Tiziani, 2013)

Atorvostatin is a hydroxymethylglutaryl co-enzyme A (HMG-CoA) reductase inhibitor used to treat hypercholesterolaemia or hyperlipidaemia (McKenna & Lim, 2012). The drug acts to inhibit production of cholesterol by blocking HMG-CoA reductase from completing the synthesis of cholesterol (Tiziani, 2013). Administration is by oral pathway. In the context of this case study, Atorvostatin is not indicated for administration without further investigation into potential underlying causes, such as, heart disease or hypercholesterolaemia.

Question 5

In the context of this case study, atrial fibrillation could indicate heart disease, but further investigation would be necessary to determine this. Factors such as age, hypertension, ischaemic stroke, family history of myocardial infarction, and erratic pulse are evident and are all indicators towards heart disease (Bordignon, Corti & Bilato, 2012). McKenna & Lim (2012, p. 676) also associate coronary artery disease, myocardial inflammation, valvular disease, cardiomegaly, and rheumatic heart disease with atrial fibrillation.

Pharmacologically, the drugs considered for intervention include heparin, warfarin, and carvedilol (Watson & Lip, 2006). Both Heparin and Warfarin are anticoagulant drugs. Heparin is a fast acting, intra-venous or subcutaneously administered anticoagulant used in the acute setting, with changeover to orally administered warfarin, whose anticoagulant effect is evident after 36-72 hour, for longer-term use (Tiziani, 2013; McKenna & Lim, 2012). In context of the case study, aspirin use would be discontinued if heparin and warfarin were administered, as these drugs are recorded as having an adverse reaction (Tiziani, 2013; McKenna & Lim, 2012). These drug types have contraindications for active and potential bleeding, so issues such as haemorrhoid bleeding may exclude these drugs from administration (Tiziani, 2013).

As previously stated, Carvedilol is a nonselective β-blocker (Leonetti & Egan, 2012). This drug is administered orally and are safe in combination with heparin or warfarin (Tiziani, 2013). Contraindications for this drug include bradycardia, heart block, diabetes, and bronchospasms (McKenna & Lim, 2012). This drug had both antihypertensive properties and has been shown to reduce cardiac arrhythmias such as atrial fibrillation (Watson & Lip, 2006). The risk associated with this drug include hepatic failure, oedema, and deterioration if the patient is in heart failure (McKenna & Lim, 2012; Tiziani, 2013).

Conclusion

This paper has discuss and identified the pathophysiology of stroke, discussed the nursing care of the stroke patient, and identified and discussed pharmacological interventions available to treat the patient.

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