Ischaemic stroke Essay Example

  • Category:
    Nursing
  • Document type:
    Case Study
  • Level:
    Undergraduate
  • Page:
    3
  • Words:
    2053

ISCHAEMIC STROKE 10

Assessment 1: Case Study

Pathophysiological Process Template

The template relates to the pathophysiology process of an Ischaemic stroke that affects the dominant left cerebral hemisphere.

Definition

Ischaemic stroke discussed in this context refers to sudden development of the focal neurological deficits that are precipitated by the abnormal decrease of cerebral blood flow and oxygen to the bran. The underlying causes of permanent reduction in the flow of oxygen and blood that lead to the Ischaemic stroke are clinically attributed to the complete or partial occlusion of cerebral artery (Norvin, 2010).

Aetiology

There varied disease conditions that can cause Ischaemic stroke. The most reported problem in this context is that narrowing of arteries in the neck or in the head (Stanford, Harris &Baker 2008). The problematic vasoconstriction is commonly caused atherosclerosis, or a gradual deposition of cholesterol on the arterial walls. When the arteries are extremely narrowed, there may be a tendency of cells collecting hence forming blood clots, which can easily block the arteries (thrombosis) or dislodge to become trapped in the arteries supplying the brain (embolism) (Blann, 2008).

Ischaemic stroke can also be caused by clotting of blood in the heart, which often results from irregular heartbeats, heat attack, or some form of abnormality of the heart valves. Other known causes of the stroke include drug abuse, traumatic injuries to the blood vessels of the head or diseases associated with blood clotting.

In the case at hand, Mr. Black was reported to have suffered hypertension for ten years, and it is one of the primary risk factors for stroke because of lipohyalinosis and increase in myocardial activity that cause injuries of blockages to the cerebral artery (Gupter & Field, 2009). The patient was also documented as a routine smoker doing a packet a day and the nicotine substance in cigarettes increases the risks o arterial narrowing, which increases the cardiac output hence raising the systolic blood pressure and pulse rate (Blann, 2008).

The patient in the case study was also obese with a MBI reported as 37.1. Obesity has increasingly been demonstrated as a major risk factor for increases in blood cholesterol deposition (Blum & Geyer, 2009). Additionally, Mr. Black drinks alcohol, which can increase the potential for developing heart complications that can lead to cardio-embolic stroke (Blann, 2008).

Pathogenesis

Ischaemic stroke occurs when a blockage to the arteries in the brain disrupts the blood and oxygen flow. This is because if the oxygen and nutrient supplies to the brain cells are interrupted for a few minutes, they start dying. According to Brandstater, Geyer and Gomez (2009), critical reductions in blood supply that cause shortage of flow into the cerebral vessel replenishing the left hemisphere are consistent with occurrence of ischaemic stroke. The abnormalities leading to the stroke result in structural alterations such as destruction in the motor neurons on the right side of the body accompanied by aphasia.

Clinical Features of Ischaemic Stroke

An historical focus for Ischaemic stroke patients revolves around the common lead factors with an aim of establishing the predisposing issues for atherosclerotic and cardiac diseases: hypertension, diabetes mellitus, cholesterol deposition, and other heart abnormalities (Blum & Geyer, 2009). The stroke is almost conclusive if a patient presents with acute neurologic deficit or variations in the level of consciousness.

The apparent clinical features of the stroke include acute hemiplegia, serious hemisensory loss, and permanent or partial hemianopia, monocular or loss of binocular visibility (Aurie, 2009). The patient may also present signs of acute aphasia, ataxia, and vertigo, and may be experiencing sudden reductions in levels of consciousness. In younger patients, historical elements that can form lead to suspicion of stroke include recent trauma that may have affected blood vessels, coagulophathies, complains about migraines, or excessive abuse of illicit drugs.

For Mr. Black, the sudden paralysis to the right arm, the weakness to his leg, the visible facial drooping, and the decreased sensation on the right side of the body clinically signalled Ishaemic stroke. Additionally, Mr. Black relayed signs of aphasia, difficulties in speaking, and reduction in the level of consciousness.

Course of the Ischaemic Stroke

The disease predisposes patients into risks of permanent disability. Baim (2006) cites intravenous thrombolysis and dedicated stroke centres as the main interventions that have shown potential for improving stroke outcomes.

Complications

A stroke may be mild and leaving temporary disabilities but a severe case may leave the patient permanently disabled. The interruptions to the blood flow in the brain can cause a patient a loss in the ability to control some muscles especially those in the face and can also lead to irreversible paralysis.

The stroke may complicate ability to talk or swallow. If the patient loses the ability to move muscles in the mouth and throat, the ability to speak, eat, and swallow is compromised or lost. For instance, stroke can make patients experience slurred speech (dysarthria) because of the loss of the ability to coordinate muscles in the mouth.

Stroke can impose permanent pain, cause memory loss, or even make the patient emotionally problematic. Many people that have suffered stroke end up losing their memory or having difficulties in thinking (Baker, 2008). Additionally, people who have experienced stroke can lose the ability to control their emotions and can become prone to depression. Mr. Black experienced many of the complications observed by Sanford (2008): paralysis and body weakness and limited control over muscle movement.

Prognosis

The Ishaemic and embolic types of stroke have been documented to be more prevalent among middle and old aged men compared with women. According to Sanford (2008), 20-25% of stroke survivors can experience recurrence, and some patients can respond to treatment and improve from ishchaemic stroke.

Diagnosis

The immediate diagnostic approach includes examination of the muscle movement ability, ability to see with both eyes, ability to talk, swallow or eat, and difficulties in movement. The Magnetic Resonance Imaging (MRI), Computerized Tomography (CT) for brain, and PET scans can generate conclusive images of target brain areas showing the extent of damage if any, brain activity, and ultimately the location of the stroke (Porth & Maffin, 2009). Laboratory tests for different targets: cardiac enzymes, urea, full blood count, and blood glucose among others can help in establishing any inconsistencies in the blood.

Treatment

Intravenous throbolysis is recommendable for Mr. Black, which would improve re-perfusion and this should be done not more than three hours of symptoms identification (Spencer & Barnett, 2012). Antiplatelet medicine should be administered to aid reducing the development of thrombus. Spencer and Barnett (2012) observe that treatment of stroke should consider stable nutritional support and therapeutic prescriptions for rehabilitating the affected areas.

Prevention

Lifestyle management is the primary preventive feature in the contemporary society. People should continually exercise to remain health and avoid drug abuse, heavy alcohol drinking, and eating junk food that lacks in nutritional value.

According to Baker (2008), the secondary preventive approach entails the anitplatelet therapies for patients affected by the disease.

Mr. Black’s Clinical Manifestations and Relation to Structural and Functional Changes

Structural

The event of stroke attack s characterized by sudden changes in the energy metabolism and causes depolarization of cells, which distorts calcium ion balance in the intra-cellular space, increased lactate levels, acidosis and release of free radicals (Hossmann & Heiss, 2010). In the event of a severe interruption, there is sudden death of cells.

The structural changes characteristic of Mr. Black’s stroke is presented by Jenkins, and Tortora (2013). In the context of the ischaemic stroke affecting the left dominant cerebral artery, abnormalities in the middle cerebral artery play a big role. This is because the arteries perfuse the main blood and oxygen routes in the brain, which implies that a blockage causes impaired oxygen and glucose flow thus affecting the biochemical and electrophysiologic activity of the neural cells.

The stroke disrupts the potential of the neural membrane, affects the neurons, and results in reduced adenosine triphosphate (ATP) and phosphocreatine. The impacts of the interruptions cause lactic acidosis because the accumulation of lactate and hydrogen ions reduce the systemic PH.

Functional Changes

The left dominant and middle cerebral arteries are the main parts of the brain that are adversely affected. Changes in brain activity include significant deficits to the right body function. Blann (2008) argues that impairment of frontal lobes, parietal cortices, and basal ganglia cause a deficit in the motor functioning, which can affect functions such as mobility, binocular vision, memory and behaviour. Stroke affects primary somatosensory region of the body hence causing sensory deficits.

Mr. Black’s Clinical Manifestations

As aforementioned the stroke in the left hemisphere can result from varied imbalances in the brain including the interruption of blood and oxygen and blood flow to the cerebral artery, distortion in pH balance, neural and cellular death, and imbalances in nutritional chemicals (Blann, 2008). The stroke often causes motor deficits on the right side of the body accompanied by destruction in the frontal lobes. Stroke causes impairment of parietal cortices, and basal ganglia causing the deficit in the motor functioning, which can affect functions such as mobility, binocular vision, memory and behaviour. Stroke affects primary somatosensory region of the body hence causing sensory deficits (Blann, 2008).

The implication of the stroke to Mr. Black is extensive because he may suffer paralysis in the right arm and movement difficulties in the right leg. The potential of adverse effects on the left dominant cerebral cortex and the Broca’s, which control comprehension and language, can cause complications in communication.

Modes of Action: Alteplase and Assasantin

Alteplase

Alteplase is a generic name for a medicine used for thrombolytic therapy in ischaemic stroke, which is administered to revive blood and oxygen flow, reduce the extent of cell death and limit tissue necrosis (ref). The medicine is a serine protease comprising of two primary chains: A and B. The A chain is active for fibrin binding and improvement of the plasminogen activation (Gonzales & Gotta, 2008). The B-chain helps in production of local fibrinolysis that improves the re-perfusion of obstructed vessels.

Assasantin

The Assasantin is medicine used in treating stroke. The drug is administered to reduce recurrence of strokes or transient ischaemic attacks. The medicine has an anticoangulant and antithrombotic, and inhibits teh uptake of adenosine by red blood cells thus limiting development of platelets. The primary function of the drug is to prevent platelets in the blood from causing vasoconstriction associated with stroke.

References

Auriel, E. (2009). Anatomy and pathophysiology of stroke. In N. M. Bornstein (Ed.), Stroke: Practical guide for clinicians. Tel Aviv, Israel: Karger.

Baim, D.S. (Eds.) (2006).Grossman’s cardiac catheterization, angiography, and intervention. Philadelphia, PA: Lippincott Williams & Wilkins.

Baker, M. D. (2008). Stroke prevention in clinical practice. London, UK: Springer-Verlag London.

. London, UK: M& K Update Ltd.Deep vein thrombosis and pulmonary embolism: A guide for practitionersBlann, A. (2009).

Blum, A., & Geyer, D. J. (2009). Tobacco and stroke. In J.D. Geyer & C.R. Gomez (Eds.), Stroke: A practical approach. Philadelphia, PA: Lippincott Williams & Wilkins.

Brandstater, E. M., Geyer, D. J., & Gomez, R. C. (2009). Stroke localization. In J.D. Geyer & C.R. Gomez (Eds.), Stroke: A practical approach. Philadelphia, PA: Lippincott Williams & Wilkins.

Philadelphia, PA: Lippincott Williams & Wilkins.Stroke: A practical approach. Geyer, J.D., & Gomez, C.R. (Eds.) (2009).

Gopnzales, N. R., & Grotta, J.C. (2008). Alteplase for acute ischaemic stroke. Expert Review of Cardiovascular Therapy, 4(3), 301-18.

Gupta, S., & Field, M. J. (2009). Chronic hypertension. In J.D. Geyer & C.R. Gomez (Eds.). Stroke: A practical approach. Philadelphia, PA: Lippincott Williams & Wilkins.

Hossman, A. K., & Heiss, W. (2010). Neuropathology and pathophysiology of stroke. In M. Brainin & W. Hesiss (Eds.), Text book of stroke medicine. New York, NY: Cambridge University Press.

Jenkins, W. G., & Tortora, J. G. (2013). Anatomy and physiology: From science to life. (3rd ed.). Hoboken, NJ: Wiley & Sons.

Norving, B. (2010). Etiology, pathophysiology and imaging: Common causes of ischaemic stroke. New York, NY: Cambridge University Press.

Porth, C. M., & Matfin, G. (Eds.). (2009). Pathophysiology: Concepts of altered health states. (8th ed.). Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins.

ed.). Marrickville, NSW Australia: Elsevier Australia.nd (2Medical-surgical nursing: Assessment and management of clinical problemsSanford, T.J. (2008). Nursing management: Patient with stroke. In D. Brown & Edward, H. (Eds.).

Spencer, D., & Barnett, M. J. H. (2012). Stroke prevention, treatment, and rehabilitation. New York, NY: McGraw-Hill Company.