Therapeutic Management of Stroke as a Method of Preventing Secondary Events - Literature review Example

Therapeutic management of stroke to prevent secondary events in patients who have experienced an ischaemic stroke or transient ischaemic attack (TIA)Pathophysiology and Clinical manifestations Adams et al. (2008) found that transient ischaemic attack (ITA) has often been likened to stroke but the two are only similar and not exactly the same. The major difference with these two is that in ITA, the interruption of blood flow occurs only temporarily whiles in stroke there is more of a permanent blockage in the blood flow (Bornstein, Silvestrelli, Caso and Parnetti, 2012). Alexander (2011) linked the similarity in cases of stroke and ITA to similarity in pathophysiology and clinical manifestations as well. Rashid, Leonardi-Bee and Bath (2013) however posited that duration of manifestation of symptoms is a major issue in ITA as in ITA, the symptoms are only kindly to be the same as what is seen in stroke in the first 24 hours or less. Writing specifically on the pathophysiology of ITA and its clinical manifestation, Iadecola and Gorelick (2012) stressed that the primary pathophysiology of the disease is the underlying heart or blood vessel disease, which manifests in several forms, including atherosclerotic vascular disease. Atherosclerotic vascular diseases have been associated with ischaemic stroke and actually considered a major cause of ischaemic stroke or transient ischaemic attack (ITA) (Rothwell, 2011). This is because the onset of atherosclerotic vascular diseases has actually been linked with the occurrence of occlusive lesions which take place in major intracranial and extracranial arteries. Meanwhile, any form of inhabitation of supply of blood to the heart could be associated with possible breakdown in the active functioning of the brain (Adams et al., 2008). Rashid, Leonardi-Bee and Bath (2013) noted that with the onset of atherosclerotic vascular disease which is the primary pathophysiology of both stroke and ITA, the damage to lesions resulting from occlusive lesions bring about further secondary manifestations, necessary for diagnosis. As this occlusive lesions, which is a form of severely stenotic lesions occur at the major intracranial and extracranial arteries, they lead to the narrowing of small penetrating arteries of the brain and thus the cause or onset of secondary events in patients with TIA (Fayad, 2006). In relation to the current research problem, Bornstein, Silvestrelli, Caso and Parnetti (2012) found that where there pathophysiology and clinical manifestation shows clear possibility of ITA, it is very important that immediate management steps are taken to avert further secondary events, leading to stroke. This is because there is only a thin line from the transition point from ITA to stroke. For example Adams et al. (2008) noted secondary manifestations that take place largely in the brain, which is a case similar with both ITA and stroke. Fayad (2006) however held the position that for the secondary manifestations to take place in the brain, it is always necessary and expected that primary pathologies will be experienced as the secondary manifestations are actually the result of one or more of the primary pathologies, which include but not limited to hypertension, atherosclerosis leading to coronary artery disease, dyslipidemia, heart disease, and hyperlipidemia (Rothwell, 2011). Therapeutic Management Alexander (2011) made an important underlying statement to the management of stroke in patients with history of TIA with the goal of preventing the onset of secondary events. According to the statement, treatment of any form of stroke ought to look very directly into the cause, whether the stroke is ischaemic or hemorrhagic. But when it comes to TIA, the issue of how much time has elapsed since the start of symptoms is an issue that Iadecola and Gorelick (2012) regarded as being very important. For patients with the history of TIA, it can be expected that symptoms and clinical manifestations have fully passed. But even in such cases, the use of therapeutic management is said to be highly applicable when no secondary events have been noted yet. Once this is done, Choi-Kwon et al. (2013) admonished the need to look at the use of therapeutic management as an approach to acute management where therapies are used to prevent recurrent stroke. With this said, Indredavik et al. (2013) noted that the best way to use therapeutic management is to prevent events and diseases associated with the pathophysiology of the disease. Due to the effect of such primary pathologies such as hypertension on stroke in patients with TIA, the use of comprehensive antihypertensive therapies have been largely recommended (Choi-Kwon et al., 2013). These look directly at Class IIb and Level of Evidence C in patients. According to Ronning and Guldvog (2012), in the use of antihypertensive therapies in the management of stroke, the main objective of the therapist is to suppress the pathophysiology of the disease as well as its clinical manifestation. With this said, it would be noted that blood pressure controls play a very important role in the implementation of therapeutic management of stroke to prevent secondary events in patients who have previously experienced TIA. The first approach to therapeutic management of stroke therefore looks to the use of lifestyle changes which adopts modifications to lifestyle in the areas of weight loss, exercising, reducing alcohol intake, reduction in sodium intake, enhancing the intake of potassium, magnesium and calcium, reducing the intake of cholesterol and saturated fats, and limiting stress, smoking and caffeine intake (Corsini et al., 2013). Ronning and Guldvog (2012) however argued that most forms of lifestyle modifications have not been able to control the onset of pathophysiology and clinical manifestation of stroke. Owing to this, the use of lifestyle modifications have been noted to be relevant in cases where they are used for the purpose of limiting the possible exposure to the use of drug therapy. This means that drug therapy should be the ultimate goal in therapeutic management of stroke as drug therapy measures cardiac and vascular damage associated with the incidence of stroke (Indredavik et al. 2013). Whiles using drug therapy, the following medications may be recommended: diuretics, beta-blockers, ACE inhibitors, calcium channel blockers, ARNs, direct-acting vasodilators, and peripherally acting agents (Corsini et al., 2013). Pharmacist’s contribution to patient care The important roles of drug therapy in the whole therapeutic management of stroke for the prevention of secondary events in patients who have experienced TIA have already been established. Even the fact that very important and delicate forms of medications and drugs may be involved, it is always important that the pharmacist’s contribution to patient care will always be clearly defined (Cipolle, Strand and Morley, 2012). On the whole, Council on Credentialing in Pharmacy (2013) admonished the need to ensure that the pharmacist’s contribution is played in a manner that follows the use of the pharmacist’s patient care process showed in figure 1 below. Source: Joint Commission of Pharmacy Practitioners (2014) Based on figure 1, Cipolle, Strand and Morley (2012) noted that the overall aim that should characterize the pharmacist’s contribution is the need to play medical supervisory role. For example, it is important for the pharmacist to determine when it is best for the patient to start, not to start, or stop taking medications associated with the therapeutic management. The pharmacist has also been noted to have a crucial role to play in the monitoring and determination of the onset of side effects that come with the use of drugs in the medication therapy (Joint Commission of Pharmacy Practitioners, 2014). What is more, follow-up must be a constant part of the care process and this should be done within 1 to 2 months after starting therapy. Within the therapy process also, the pharmacist has a role to play in frequently adjusting medications based on patient response to therapy (Council on Credentialing in Pharmacy, 2013). Conclusion The literature review focused directly on the management of stroke by looking at therapeutic management interventions that seek to prevent the recurrent stroke in patients who have experienced an ischaemic stroke or ITA. The approach to the therapeutic management was focused on the minimisation of the effect or risk factors associated with the inception of atherosclerotic vascular disease. This is because the inception of atherosclerotic vascular disease has been noted to be the pathophysiology for the transition from ITA to secondary events of stroke. This was an important review given the fact that it tended to bridge most forms of gaps in literature where the management of stroke have mostly looked at curative approaches rather than preventive ones such as the therapeutic management. What is more, there has been documented evidence of the benefits of the use of therapeutic management approaches, especially when it comes to the issue of possible side effects associated with the management process. Going into the future, the use of therapeutic management is expected to be an adaptive approach for most patients who have showed cleared resistance to other forms of interventions that have often looked at the curative and medicinal approach to handling the disease. Appendix Summary Therapeutic Framework Information for 3 chosen drugs Therapeutic management of stroke to prevent secondary events in patients who have experienced an ischaemic stroke or transient ischaemic attack (TIA) Drug Name Chlorothiazide Atenolol Amlodipine Drug Group Thiazide diuretics Beta blockers Calcium channel blockers Legal Classification Prescription only Prescription only Prescription only How the drug works in the condition Drug works by increasing the supply of sodium to the collecting ducts. It functions through the process of slowing down the heart and reducing workload within the heart. Functions by inhibiting the movement of calcium ions into vascular smooth muscle cells and cardiac muscle cells. The usual adult dose (route, dose, frequency) Oral (capsules, tablets, oral solution) given in 25 mg orally once daily. Oral or IV given in 50 mg orally once a day. To be continued for 1 to 2 weeks for full effect. Oral (tablets) to be taken in dosage of 5 mg orally once a day Patient monitoring to check that the drug is working Periodic monitoring of electrolytes should be in place to check if drug is working. Hospitalization and intensive monitoring is recommended as treatment is symptomatic. Monitoring for the drug working should be focused on ensuring that there are binds to both dihydropyridine and nondihydropyridine binding sites. Important side-effects caused by the drug and monitoring for these side-effects blood in urine or stools, bloody urine, cracks in the skin, darkened urine and dizziness, faintness, or lightheadedness, all of which must be monitored by the focusing on electrolytes Blurred vision, shortness of breath, sweating, tightness in chest, unusual tiredness or weakness, and wheezing. All these must be monitored by taking periodic symptomatic data of patient. Shortness of breath, tightness in the chest, wheezing, and Swelling of the ankles or feet. Monitoring should take place by the use of close physical monitoring. Important drug interactions arsenic trioxide, cisapride, lithium, and Nexterone (amiodarone) Aquaphyllin (theophylline), Bronkodyl (theophylline), methacholine, and ritodrine Anzemet (dolasetron), itraconazole, Onmel (itraconazole), and Sporanox PulsePak (itraconazole) Important disease interactions (Contra-indications and Cautions) Renal failure or insufficiency. As a precaution, should not be taken if this disease is registered Type II diabetes and so should not be recommended for patients with the disease Severe coronary artery disease. Precaution should be taken by using alternative drugs. What the patient should be told about their medicine Patient should be told that medicine should be taken only under supervision and that any side effects should be reported immediately It is important for patient to remain under close monitoring and so patient should be told that they are due for the medicine only when they have sufficient time to remain under close surveillance. Side effects must be reported immediately. Patient should be told that medicine should be taken only under supervision. Side effects must be reported immediately. References Adams RJ, Albers G, Alberts MJ, et al. (2008). “Update to the AHA/ASA recommendations for the prevention of stroke in patients with stroke and transient ischemic attack.” Stroke. Vol. 39 No. 5: pp. 1647-1652 Alexander RW. (2011). “Hypertension and the pathogenesis of atherosclerosis: oxidative stress and the mediation of arterial inflammatory response: a new perspective.” Hypertension; Vol. 25 No. 2: pp. 155-161 Bornstein N, Silvestrelli G, Caso V and Parnetti L. (2012). “Arterial hypertension and stroke prevention: an update.” Clin Exp Hypertens. Vol. 28 No. 4: pp. 317-326 Choi-Kwon S, Yang YH, Kim EK, Jeon MY and Kim JS. (2013). “Nutritional status in acute stroke: undernutrition versus overnutrition in different stroke subtypes.” Acta Neurol Scand; Vol. 98 No. 3: pp. 187–192. Cipolle RJ, Strand LM and Morley PC. (2012). Pharmaceutical Care Practice: The Patient Centered Approach to Medication Management, 3rd ed. New York: McGraw-Hill. Corsini A, Pazzucconi F, Arnaboldi L, et al. (2013). “Direct effects of statins on the vascular wall.” J Cardiovasc Pharmacol. Vol. 31 No. 5: pp. 773-778 Council on Credentialing in Pharmacy (2013). “Scope of Contemporary Pharmacy Practice: Roles, Responsibilities, and Functions of Pharmacists and Pharmacy Technicians. J Am Pharm Assoc. Vol. 20 No. 10: pp. 35-69. Fayad P. (2006). “Secondary prevention measures after a stroke—should they target stroke or heart disease?” Nat Clin Pract Neurol; Vol. 2 No. 12: p.646-647 Iadecola C. and Gorelick PB. (2012). “Hypertension, angiotensin, and stroke: beyond blood pressure.” Stroke; Vol. 35 No. 2: pp. 348-350 Indredavik B, Bakke F, Slordahl SA, Rokseth R and Haheim LL. (2013). “Stroke unit treatment: 10-year follow-up.” Stroke Vol. 30 No. 3: pp. 1524–1527. Rashid P, Leonardi-Bee J. and Bath P. (2013). “Blood pressure reduction and secondary prevention of stroke and other vascular events: a systematic review.” Stroke. Vol. 34 No. 11: pp. 2741-2748 Ronning OM. and Guldvog B. (2012). “Stroke units versus general medical wards, I: twelve- and eighteen-month survival: a randomized, controlled trial.” Stroke; 29: pp. 58–62. Rothwell PM. (2011). “The interrelation between carotid, femoral and coronary artery disease.” . Eur Heart J. Vol. 22 No. 1: pp. 11-14 Read More