Oxbridge Free Nursing Essay | Stroke Neurological Blood Brain

Essay title - Define what a stroke is and the cause of the patient's stroke. The significance of the illness on the patient and the conflict between diabetes and strokes

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Introduction

Critically analyse, with reference to appropriate contemporary research / literature, the nursing role in caring for a patient during the acute phase (first 72hrs) of this condition.

“When they burst in, pushing the device ahead of them, I thought it meant I was being ejected to make room for another patient…….I could still not imagine any connection between a wheelchair and me.

No-one had yet given me an accurate picture of my situation, and I clung to the certainty, based on bits and pieces I had overheard, that I would very quickly recover movement and speech”

Jean-Dominique Bauby; 1997 The diving bell and the butterfly. Fourth Estate. London (pp15)

In the US, someone has an attack every 45 seconds, and there is a stroke related death every three minutes.^w2

Body of the essay

Stroke is an acute neurological injury in which blood supply to a part of the brain is interrupted. Give no of people who die of stroke in uk and the devastating effect Stroke is also a leading cause of adult disability. According to data from the Framingham Heart Study, 31% of stroke survivors in the study needed help caring for themselves; 20% needed help when walking; and 71% had a diminished ability to work.1 Deficits from stroke may involve weakness or paralysis, decreased sensation, decreased memory, decreased ability to think, speak, or eat.

Disability from stroke tends to be permanent, although rehabilitation therapies sometimes lead to recovered ability. Stroke survivors may return to work, may be left utterly helpless, but will most likely find themselves somewhere between these two extremes.

Therefore a thorough understanding of stroke's pathophysiology, presentation, investigation, and current and future treatments is crucial.

Strokes may either be hemorrhagic or ischemic. Eighty eight per cent of all strokes are ischemic, 9% are due to intracerebral hemorrhage, and 3% are due to subarachnoidA haemorrhage. ^w2

Strokes may either be haemorrhagic or ischaemic. Eighty eight per cent of all strokes are ischaemic, 9% are due to intracerebral haemorrhage, and 3% are due to subarachnoid haemorrhage. ^w2

Haemorrhagic stroke

Intracranial haemorrhage may occur within the brain parenchyma (intracerebral haemorrhage) or within the surrounding meningeal spaces (including epidural haematoma, subdural haematoma, and subarachnoid haemorrhage).

In intracerebral haemorrhage, bleeding occurs directly into the brain parenchyma. In addition to the area of the brain injured by the haemorrhage, the surrounding brain can be damaged by pressure produced by the mass effect of the haematoma. A general increase in intracranial pressure may occur.

Non-traumatic intracerebral haemorrhage is usually due to hypertensive damage to blood vessel walls. Chronic hypertension causes lipohyalinosis, fibrinoid necrosis, and the development of Charcot-Bouchard aneurysms in arteries throughout the brain, which may then rupture. Non-traumatic intracerebral haemorrhage may also be due to excessive cerebral blood flow (for example, haemorrhagic transformation of an ischaemic infarct); rupture of an aneurysm or an arteriovenous malformation; an arteriopathy (for example, cerebral amyloid angiopathy); a coagulopathy; a vasculitis; haemorrhagic necrosis (for example, due to tumour or infection); or venous outflow obstruction (for example, cerebral venous thrombosis).

Non-penetrating and penetrating cranial trauma are also common causes of intracerebral haemorrhage.

Strokes due to hypertension more commonly occur in sites such as the basal ganglia, thalamus, pons, cerebellum, and other brainstem sites, whereas those due to other causes more commonly occur in lobar regions (particularly the parietal and occipital lobes).

Subarachnoid haemorrhage usually occurs after rupture of a berry aneurysm in the circle of Willis. Other uncommon causes include trauma, hypertensive haemorrhage, vasculitides, tumours, and coagulopathies. This results in blood accumulating in the basal cisterns and around the brainstem.

Ischaemic stroke

An acute vascular occlusion results in ischaemia in the dependent area of the brain. About 80% of ischaemic strokes are due to thromboses and emboli. The most common sites of thrombotic occlusion are cerebral artery branch points, particularly in the distribution of the internal carotid artery. Arterial stenosis precipitated by turbulent blood flow, atherosclerosis, and platelet adherence cause blood clots to form. Less common causes of thromboses, particularly seen in younger stroke patients, include cervical artery dissection, essential thrombocythaemia, polycythemia, sickle cell anaemia, protein C deficiency, fibromuscular dysplasia of the cerebral arteries, and cocaine misuse.^w3

Emboli may arise from the heart, the extracranial arteries, or, rarely, the right sided circulation (paradoxical emboli), and can occlude the vasculature. Furthermore, rarely infective causes of emboli, such as subacute bacterial endocarditis, may cause occlusion, as may emboli due to iatrogenic causes, such as a cardiac prosthesis.

Small vessel disease within the brain causes a further 20% of ischaemic strokes. These are usually in patients with generalised small vessel disease - for example, hypertensive and diabetic patients. Multiple small emboli or an in situ process called lipohyalinosis (in which multiple microatheromata occlude the vessels) are thought to be responsible.

system of categories of subtypes of ischaemic stroke mainly based on cause has been developed for the "Trial of Org" 10 172 in acute stroke treatment (TOAST).^w4 This classification denotes five subtypes of ischaemic stroke - large artery atherosclerosis, cardioembolism, small vessel occlusion, stroke of other determined cause, and stroke of undetermined cause.

In all cases, loss of perfusion to a part of the brain results in an "ischaemic cascade" (fig 1). Conse- quently the initial ischaemic insult is locally amplified.

The high intracellular calcium acti- vates various enzymes that cause the destruction of the cell. Free radicals, arachidonic acid, and nitric oxide are generated by this process leading to further neuronal damage. Within hours to days of a stroke occurring, specific genes are activated that cause the formation of cytokines and other factors that in turn cause further inflammation and microcirculatory compromise. The area of damage thus spreads rapidly after the initial ischaemic event.

Risk factors

Stroke has numerous risk factors, some of which (such as increasing age and systolic blood pressure) are risk factors for both ischaemic and haemorrhagic stroke, however, other factors are more specific for type of stroke. The table gives important risk factors and their relative risk.

Risk factors for stroke

Risk factor	Description	Relative risk*
Ischaemic stroke
Age ^w5	For each successive 10 years after age 55	1.74
Family history ^w6	Paternal history of stroke or transient ischaemic attack	2.4
	Maternal history of stroke or transient ischaemic attack	1.4
	Parental history of coronary heart disease	3.33
Systolic blood pressure ^w5	For each 10 mm Hg increase	1.15
Atrial fibrillation ^{w7 w8}	For successive decade of life above age 55, incidence doubles; non-valvular atrial fibrillation accounts for 1.5% strokes in people aged 50-59 years, rising to 23.5% in people aged 80-89 years	3-5
Myocardial disease ^w8	Coronary heart disease	2
	Electrocardiographic left ventricular hypertrophy	3
	Cardiac failure	3-4
Diabetes mellitus ^w9	People with diabetes mellitus have increased susceptibility to atherosclerosis and increased atherogenic risk factors, particularly hypertension, obesity and abnormal blood lipids; known diabetes mellitus	2.45
	Asymptomatic people who have a high average blood glucose (=225 mg/dl)	1.43
Cigarette smoking ^w10	-	1.9
Alcohol ^w11	Complex associated dependent on amount (J shaped association) and race
Previous transient ischaemic attack ^w2	-	2.3
Carotid stenosis ^w12	-	2.03
Haemorrhagic stroke
Age ^{w13 w14}	Incidence increases exponentially with increasing age; relative risk for 85 year olds compared with 70-74 year olds	2.5
Systolic blood pressure ^w15	110-139 mm Hg	1
	140-179 mm Hg	4
	=180 mm Hg	8
Anticoagulation (international normalised ratio) ^w14	<3.0	1
	3.5-3.9	4.6

*Confidence intervals omitted for clarity

Clinical presentation

Stroke should be considered in any patient presenting with an acute neu- rological deficit (focal or global) or altered level of consciousness. Patients' symptoms vary depending on the area of the brain affected and the extent of the damage.

Because of the importance of get- ting people who have had a stroke into hospital as rapidly as possible, there has been extensive research into prehospital assessment by patients themselves, family members, and prehospital care personnel, such as emergency medical technicians. The Cincinnati prehospital stroke scale has been developed using the three most important items (facial paresis, arm drift, and abnormal speech) derived from the stroke scale of the National Institutes of Health.^w16

The Los Angeles prehospital stroke screen assesses for a unilateral arm drift, handgrip strength, and facial paresis.^w17 Regardless of the scale used, it is important to increase public awareness as to the presenta- tion of stroke to decrease the time from onset to presentation in hospi- tal. In the UK, a campaign is cur- rently being run by the Stroke Association called FAST (the face arm speech test), which guides the public to present at hospital immedi- ately in the case of facial weakness, arm weakness, or speech disturbance.

No features of the history can accurately distinguish between ischaemic and haemorrhagic stroke. But haemorrhagic stroke is perhaps more likely if the presentation includes features of raised intracranial pressure (such as nausea, vomiting, and headache). Seizures are also more common in hemor- rhagic stroke than in ischaemic stroke, occurring in up to 28% of hemorrhagic strokes. Meningism, the symptoms of meningeal irritation associated with acute febrile illness or dehydration without actual infection of the meninges, may also result from blood in the ventricles after a haem- orrhagic stroke.

Four important stroke syndromes are caused by disruption of particular cerebrovascular distributions.

Anterior cerebral artery - This prima- rily affects frontal lobe function, which results in altered mental status, con- tralateral lower limb weakness and hypoaesthesia, and gait disturbance.

Middle cerebral artery - This com- monly results in contralateral hemi- paresis, contralateral hypoaesthesia, ipsilateral hemianopia, and gaze preference toward the side of the lesion. Agnosia, a loss in ability to recognise objects, persons, sounds, shapes or smells, in the absence of a specific sensory deficit or memory loss, is common.

Receptive or expressive aphasia may result if the lesion occurs in the dominant (mainly left) hemisphere. Neglect (behaviour as if the contralateral sensory space does not exist) may result when the lesion occurs in the parietal cortex.

Fig 2 Computed tomograph after ischaemic stroke, showing oedema in insular cortex, as shown by solid arrows (open arrows show normal side). Reproduced from Chokski et al ^w27 with permission of Anderson Publishing

Posterior cerebral artery - This affects vision and thought, producing homonymous hemianopia, cortical blindness, visual agnosia, altered mental status, and impaired memory.

Vertebrobasilar artery - causes a wide variety of cranial nerve, cerebellar, and brainstem deficits. These include vertigo, nystagmus, diplopia, visual field deficits, dysphagia, dysarthria, facial hypoaesthesia, syncope, and ataxia. Loss of pain and temperature sensation occurs on the ipsilateral face and contralateral body.

Investigations

After the necessary basic blood tests (including full blood count, biochemistry, and coagulation studies) and cardiac monitoring with electrocardiogram, a non-contrast head computed tomography scan is essential for rapidly distinguishing ischaemic from haemorrhagic stroke and may be able to define the anatomic distribution of the stroke. This is crucial because treatments for each type of stroke differ.

Within six hours of the onset of ischaemic stroke, most patients will have a normal computed tomography scan. After 6-12 hours, sufficient oedema may collect into the area of the stroke so that a region of hypo- density may be seen on the scan.

Radiological clues before this include:

Insular ribbon sign (loss of definition of grey-white interface in the lateral margins of the insula due to oedema in the insular cortex; fig 2) ^w18

Hyperdense middle cerebral artery sign (fig 3)^w19

Hypoattenuation in the lentiform nucleus (fig 4)

Sulcal obliteration

Shifting due to oedema

Loss of grey-white matter differentiation.^{w20 w21}

These are all due to an increasing level of oedema in the brain, however, they rely on a high level of expertise of the radiologist and are often not present. Computed tomography scans also may fail to show some parenchymal haemorrhages smaller than 1 cm as a result of low resolution.

Conventional magnetic resonance imaging is not as sensitive as computed tomography for detecting haemorrhage in the acute setting. But newer techniques, such as perfusion and diffusion weighted magnetic resonance examinations, are more sensitive imaging methods for diagnosis in acute settings. Ischaemic areas can be determined within minutes or hours. But use of these methods has been restricted because they are not generally available and are difficult to employ under emergency conditions, particularly as they involve a patient lying flat for 40 minutes when they may be agitated or have a level of cardiorespiratory compromise.

Perfusion brain computed tomography, conversely, is a new imaging method capable of providing information about ischaemic brain tissue, which can be used in emergency conditions.^{w22 w23} Perfusion is measured by monitoring the passage of contrast material (non-ionic iodine) through the brain using computed tomography. Perfusion examination of the entire brain is not possible yet, and because only a few neighbouring sections can be imaged, the anatomical region must be clinically determined. Various studies have shown that computed tomography perfusion scans yield comparable information to diffusion weighted magnetic resonance imaging scans.^{w24 w25} But the entire brain cannot be analysed using perfusion computed tomography scanning, which is the major drawback, and further research is required to obtain an ideal investigation. Both types of investigation used have a high detection rate for haemorrhagic stroke.

Further investigations may include carotid duplex scanning for patients in whom carotid artery stenosis or occlusion is suspected, and transcranial Doppler ultrasound for evaluating the more proximal vasculature, including the middle cerebral artery, intracranial carotid artery, and vertebrobasilar artery. Echocardiography may be used for patients in whom cardiogenic embolism is suspected, and trans- oesophageal echocardiography may be used to detect a suspected thoracic aortic dissection, or transthoracic echocardiography for suspected acute myocardial infarction.

Computed tomography angiography is useful for patients with acute ischaemic stroke in whom accurate analysis of the cerebrovascular anatomy is required, particularly preoperatively. ^w26

Refer a friend and get 10% off your next order

Competing interests: None declared.

References ^w1-w27 are on studentbmj.com.

K A L Carroll, fifth year medical student, Imperial College, London Email: katherine.carroll@imperial.ac.uk J Chataway, consultant neurologist, St Mary's Hospital, London

studentBMJ 2006;14:309-352 September ISSN 0966-6494

http://www.studentbmj.com/issues/06/09/education/319.php#top

Cerebral Embolism Formation

In addition to thrombotic occlusion at the site of cerebral artery atherosclerosis, ischemic infarction can be produced by emboli arising from proximally situated atheromatus lesions to vessels located more distal in the arterial tree [Mohr JP, Sacco RL. In: Barnett HJM, et al (eds). Stroke. Pathophysiology, Diagnosis, and Management. New York: Churchill Livingstone, 1992:271].

A small clot may break off from a larger thrombus and be carried to other places in the bloodstream. When the embolus reaches an artery too narrow to pass through and becomes lodged, blood flow distal to the fragment ceases, resulting in infarction of distal brain tissue due to lack of nutrients and oxygen.

As a cause of stroke, embolism accounts for approximately 32% of cases.

DEFINITION

A stroke is defined as a sudden loss of brain function caused by a blockage or rupture of a blood vessel to the brain. Stroke can be subdivided into two types: ischemic and hemorrhagic. Ischemic stroke accounts for 85% of all cases. Hemorrhagic stroke can be further subclassified as intracerebral and subarachnoid. This chapter provides an overview of the broad field of stroke, with particular emphasis on ischemic stroke.

PREVALENCE

Stroke is the leading cause of morbidity and the third-leading cause of mortality in the United States. Approximately 150,000 deaths per year are attributed to stroke. It is also the most common neurologic reason for hospitalization. Although we have made great strides in the treatment of stroke, the overall incidence will continue to rise as our population ages. Primary and secondary prevention of stroke is important to decrease its incidence and its associated morbidity.

PATHOPHYSIOLOGY

Ischemic Stroke

In ischemic stroke, interruption of the blood supply to the brain results in tissue hypoperfusion, hypoxia, and eventual cell death secondary to a failure of energy production. Three main mechanisms are involved in the development of ischemic stroke, and they are associated with atherothrombotic, embolic, and small-vessel diseases. Less common causes include coagulopathies, vasculitis, dissection, and venous thrombosis.

Atherothrombotic Disease

In atherothrombotic disease, lipid deposition leads to the formation of plaque, which narrows the vessel lumen and results in turbulent blood flow through the area of stenosis. The turbulence of the flow and the resultant alterations in flow velocities lead to intimal disruption or plaque rupture, both of which activate the clotting cascade. This causes platelets to become activated and adhere to the plaque surface, where they eventually form a fibrin clot. As the lumen of the vessel becomes more occluded, ischemia develops distal to the obstruction and can eventually lead to an infarction of the tissue that is dependent on the parent vessel for oxygen delivery.

Unenhanced computed tomography (CT) detects evidence of remote embolic ischemic stroke in the left frontal cortex (middle cerebral artery distribution) and in the left mesial occipital lobe (posterior cerebral artery distribution).

Figure 2

Embolic Disease

Embolic stroke occurs when dislodged thrombi travel distally and occlude vessels downstream (Figure 2).One-half of all embolic strokes are caused by atrial fibrillation; the rest are attributable to a variety of causes, including (1) left ventricular dysfunction secondary to acute myocardial infarction or severe congestive heart failure, (2) paradoxical emboli secondary to a patent foramen ovale, and (3) atheroemboli. These latter vessel-to-vessel emboli often arise from atherosclerotic lesions in the aortic arch, carotid arteries, and vertebral arteries.

CT demonstrates the lacunar infarcts that are typical of small-vessel ischemic stroke.

Figure 3

Small-Vessel Disease

Small-vessel ischemia can occur when microatheromata occlude the orifice of penetrating arteries (Figure 3). Another mechanism is associated with lipohyalinosis, in which pathologic changes in the tunica media and the adventitia of penetrating arteries occur in the presence of chronic hypertension. Elevated blood pressure causes endothelial injury that disrupts the blood-brain barrier. This in turn leads to a deposition of plasma proteins and eventually degeneration of the tunica media smooth muscle. The smooth muscle is replaced with collagenous fibers, which inhibit the elasticity of the blood vessel. This causes the vessel lumen to narrow and eventually activates the clotting cascade, leading to thrombosis. Small-vessel ischemic disease typically results in lacunar infarcts, which were named for the small "lakes" (lacunae) that are found at autopsy in affected patients.

Hypoperfusion can occur as a result of (1) atherosclerotic disease that limits distal flow or (2) systemic hypotension, such as seen in patients who experience acute cardiacarrhythmia or cardiac arrest. A reduction in cerebral perfusion pressure activates the autoregulatory system. As the small arterioles constrict in an attempt to maintain pressure, ischemia can develop in the distal branches of the vascular tree. Areas of the brain that lies between two major vascular supplies (eg, the middle and anterior cerebral arteries) is known as a watershed area. These areas are especially prone to ischemia during episodes of systemic hypotension.

Hemorrhagic Stroke Intracerebral hemorrhage is the result of the rupture of a vessel within the brain parenchyma. The primary causes of these ruptures are hypertension and amyloid angiopathy; secondary precipitating factors are listed in Table 1. As with ischemic stroke, the location of an intracerebral hemorrhage determines the type of symptoms and the patient's overall outcome. For example, a small lobar hemorrhage might cause only a mild headache and subtle motor deficits, while a hemorrhage of the same size in the pons might result in a coma. Outcomes are also correlated with the volume of blood; hemorrhages greater than 60 ml are almost always fatal, regardless of their location.

Table 1:

Primary and Secondary Causes of Intracerebral Hemorrhage

Primary

Secondary

Hypertension

Amyloid angiopathy

Aneurysms

Arteriovenous malformations

Neoplasms

Trauma

Anticoagulation

Use of thrombolytics

Hemorrhagic conversion of ischemic stroke

Unenhanced CT shows a hypertensive hemorrhage in the right thalamus in addition to remote lacunar ischemic infarcts in the basal ganglia bilaterally.

Figure 4

Hypertension is a major cause of hemorrhages of the basal ganglia and brainstem (Figure 4). Chronic hypertension can lead to the formation of Charcot-Bouchard aneurysms in lipohyalinotic vessels, which can rupture. Common locations of hypertensive hemorrhages include the putamen, caudate, thalamus, pons, and cerebellum.

Amyloid angiopathy is a common cause of lobar hemorrhage (Figure 5). This disease process occurs in the elderly and is caused by a deposition of beta amyloid sheets in the tunica media of the vessel wall. The deposition of amyloid protein causes the vessels to become more rigid, fragile, and prone to rupture. Evidence of hemosiderin deposition in other areas of the brain on magnetic resonance imaging (MRI) might also be seen. This deposition indicates that the patient has experienced previous hemorrhage and provides indirect support for the presence of amyloid angiopathy; however, pathologic examination is necessary before a definitive diagnosis can be made.

Unenhanced CT demonstrates a left parietal intracranial hemorrhage, which is believed to have been caused by amyloid angiopathy.

Figure 5

SIGNS AND SYMPTOMS

There is tremendous variability in the signs and symptoms of stroke, but they have all been well documented. Depending on the severity of the stroke, patients can experience a loss of consciousness, cognitive deficits, speech dysfunction, limb weakness, hemiplegia, vertigo, diplopia, lower cranial nerve dysfunction, gaze deviation, ataxia, hemianopia, and aphasia, among others. Four classic syndromes that are characteristically caused by lacunar-type stroke are: pure motor hemiparesis, pure sensory syndrome, ataxic hemiparesis syndrome, and clumsy-hand dysarthria syndrome. Pure Motor Hemiparesis Patients with pure motor hemiparesis present with face, arm, and leg weakness. This condition usually affects the extremities equally, but in some cases it affects one extremity more than the other. The most common stroke location in affected patients is the posterior limb of the internal capsule, which carries the descending corticospinal and corticobulbar fibers. Other stroke locations include the pons, midbrain, and medulla. Pure Sensory Syndrome Pure sensory syndrome is characterized by hemibody sensory symptoms that involve the face, arm, leg, and trunk. It is usually the result of an infarct in the thalamus. Ataxic Hemiparesis Syndrome Ataxic hemiparesis syndrome features a combination of cerebellar and motor symptoms on the same side of the body. The leg is typically more affected than the arm. This syndrome can occur as a result of a stroke in the pons, the internal capsule, or the midbrain, or in the anterior cerebral artery distribution. Clumsy-Hand Dysarthria Syndrome Patients with clumsy-hand dysarthria syndrome experience unilateral hand weakness and dysarthria. The dysarthria is often severe, whereas the hand involvement is more subtle, and patients may describe their hand movements as "awkward." This syndrome is usually caused by an infarct in the pons. It should be remembered that not all focal neurologic symptoms are a result of stroke. Common stroke "mimickers" include hyper- and hypoglycemia, seizure, multiple sclerosis, hyperventilation, tumor, and complicated migraine. Finally, emphasis should be placed on educating patients on the warning signs of stroke and the importance of reaching a health care provider within 2 hours of symptom onset. With the significant advances that have improved the management of acute stroke, early treatment might reduce the degree of morbidity that is associated with first-ever strokes.

DIAGNOSIS

The evaluation of stroke should focus on determining its cause in order to tailor appropriate therapy. Different patterns of signs can provide clues as to both the location and the mechanism of a particular stroke. Symptoms suggestive of a brainstem stroke include vertigo, diplopia, bilateral abnormalities, lower cranial nerve dysfunction, gaze deviation (toward the side of weakness), and ataxia. Indications of higher cortical dysfunction-such as neglect, hemianopsia, aphasia, and gaze preference (opposite the side of weakness)-suggest hemispheric dysfunction with involvement of a superficial territory from an atherothrombotic or embolic occlusion of a mainstem vessel or peripheral branch. The pattern of motor weakness is also a helpful clue. Ischemia of the cortex supplied by the middle cerebral artery typically causes weakness that (1) is more prominent in the arm than in the leg and (2) involves the distal muscles more than the proximal muscles. Conversely, involvement of an area supplied by the superficial anterior cerebral artery results in weakness that (1) is more prominent in the leg than the arm and (2) involves proximal upper extremity (shoulder) muscles more than distal upper extremity muscles. Flaccid paralysis of both the arm and leg (unilateral) suggests ischemia of the descending motor tracts in the basal ganglia or brainstem. This is often caused by an occlusion of a penetrating artery as a result of small-vessel disease. All patients should undergo an imaging study of the brain. The development of MRI has been a significant advancement in all phases of stroke management. It can often identify small strokes that cannot be seen on CT. Diffusion-weighted imaging can generally detect acute ischemic infarcts that are less than 7 days old; this can be especially useful in patients who have experienced multiple previous strokes. Magnetic resonance angiography (MRA) is a noninvasive means of evaluating the status of both intra- and extracranial vessels; however, it can overestimate the presence and degree of stenosis, and studies are under way to determine its accuracy. Other noninvasive methods of assessing the cerebral circulation include Transcranial Doppler Ultrasonography and CT angiography. For now, cerebral angiography remains the gold standard for visualizing the intra- and extracranial circulation. The risk of angiographic complications is approximately 1%. Patients with an ischemic stroke that is potentially referable to the carotid circulation should undergo either carotid duplex sonography or MRA of the extracranial carotids in an effort to identify the presence of significant carotid artery stenosis. A transthoracic echocardiogram (TTE) should be performed to evaluate the possibility of a cardioembolic source. The use of contrast or agitated saline should be considered in order to increase the yield in the detection of a patent foramen ovale (PFO). A transesophageal echocardiogram is superior to a TTE for evaluating the atrial appendage and aortic arch and for identifying the presence of a PFO or an atrial septal aneurysm.

THERAPY

Early Drug Treatment Intravenous (IV) tissue plasminogen activator (t-PA) was approved for use in ischemic stroke in 1996, and it radically changed our approach to acute stroke. Because it must be given within 3 hours of symptom onset, rapid and efficient evaluation is essential for all patients with stroke-like symptoms who are potential t-PA candidates. In the National Institute of Neurological Diseases and Stroke (NINDS) trial, on which the approval was based, patients who were treated with recombinant t-PA were 30% more likely to experience an excellent recovery at 3 months than were patients who received placebo.¹ This benefit was seen in patients with all stroke subtypes. However, t-PA was also associated with a 6.4% incidence of symptomatic intracranial hemorrhage, which represents a 10-fold increase in risk. To minimize this risk, strict adherence to national guidelines is essential.² Some of the contraindications to t-PA therapy include uncontrolled blood pressure (>185/110 mm Hg on repeated measurements), a history of brain hemorrhage, abnormal coagulation factors (international normalized ratio [INR] >1.7; partial thromboplastin time >1.5 times normal; platelet count <100 K/uL), and a history of major surgery during the previous 14 days. The nationally recommended inclusion and exclusion criteria should be reviewed for each stroke patient for whom t-PA is being considered. An accurate assessment of the timing of the stroke is also crucial. If the onset of the stroke was not witnessed, then the time the patient was last known to be neurologically at baseline should be used. For example, if a patient went to bed neurologically normal and awoke with stroke symptoms, the moment of stroke onset is considered to be the time the patient went to bed (assuming that the patient did not get up during the night). Patients older than 77 years of age and those whose strokes are severe (National Institutes of Health stroke scale score >22) are at increased risk for symptomatic intracerebral hemorrhage. Even so, these patients benefited from t-PA in the NINDS trial. Inpatient Management The inpatient management during the weeks following a stroke also has a significant impact on outcomes. For example, caring for patients in a stroke unit rather than in a general ward prevents 1 additional death for every 32 patients treated. The impressive benefit of stroke unit care is believed to be attributable to the adherence to standard stroke-specific management practices. One of these practices is an evaluation of swallowing function, which should be performed routinely. If dysphagia is present, steps to avoid aspiration should be taken. Another important precaution is to deliver prophylaxis against deep venous thrombosis (DVT) to nonambulatory patients with either subcutaneous heparin or intermittent compression stockings. Stroke patients have an increased risk of DVT and the subsequent life-threatening complication of pulmonary embolism, which is the most common cause of death during the 2 to 4 weeks following a stroke. Careful control of the patient's blood glucose levels and temperature should also be a priority because hyperglycemia and fever have been shown to result in poorer outcomes. Aspirin has been found to be of modest but significant benefit during the acute phase of stroke. According to the combined results of two large trials that enrolled a total of 35,580 patients, aspirin therapy resulted in 9 fewer deaths or nonfatal strokes per 1000 patients during the first few weeks poststroke among patients who were treated within 48 hours of the onset of their initial stroke.³^,4 In contrast, there is no evidence from trials that supports the use of intravenous heparin or heparin-like products during the acute phase of stroke. The efficacy of these medications in acute stroke has been evaluated in two randomized controlled trials. In the International Stroke Trial (IST), researchers used a factorial design to randomize 19,435 patients with ischemic stroke to treatment with one of six regimens: (1) subcutaneous heparin at 5,000 IU twice daily, (2) subcutaneous heparin at 12,500 IU twice daily, or (3) no heparin; in addition, patients on each of these three regimens either did or did not also receive 300 mg/day of aspirin.³ The investigators found no significant differences in the rates of recurrent stroke, death at 14 days, or death or dependency at 6 months between patients who did and did not receive heparin. The other study, the Trial of ORG 10172 in Acute Stroke Treatment (TOAST), was a smaller but more detailed study.⁵ The TOAST investigators randomized 1281 patients to receive either the IV low-molecular-weight heparinoid ORG 10172 or placebo. They found no statistically significant difference between the two groups with respect to the primary criterion of a favorable outcome, which was a Glasgow Outcome Scale score of 1 or 2 at 3 months. Although a post hoc analysis of the TOAST data revealed that ORG 10172 provided a significant benefit for patients with atherothrombotic disease, this finding must be viewed with caution and must be confirmed by randomized studies that are specifically targeted to this population. It is also possible that anticoagulation might benefit other specific patient populations-such as those with multiple embolic risk factors, prosthetic valves, or vertebrobasilar insufficiency-but more data are needed.

PREVENTION

Table 2:

Non-Modifiable Risk Factors for Stroke

Race/ethnicity

Family history

Risk Factor Control Risk factors for stroke are either modifiable or non-modifiable. Among the latter are age, sex, race/ethnicity, and family history (Table 2). Beginning at age 55 years, the rate of stroke doubles every decade. Men are more likely than women to experience early stroke (prior to age 65 yr) and carotid artery stenosis. With respect to race, blacks have a higher incidence of both ischemic and hemorrhagic stroke than do non-Hispanic whites. This difference has been ascribed to the higher prevalence of hypertension and diabetes among blacks.

Table 3:

Modifiable Risk Factors for Stroke⁶

Risk Factor	Relative Risk
Hypertension	2-4
Diabetes	1.8-6
Smoking	1.8
Hyperlipidemia	1.8-2.6
Carotid stenosis*	2.0
Atrial fibrillation	2.6-4.5

*Asymptomatic

The modifiable risk factors for stroke include hypertension, diabetes, cigarette smoking, hyperlipidemia, carotid artery stenosis, atrial fibrillation, excessive alcohol consumption, and physical inactivity (Table 3).

Hypertension

The most important modifiable risk factor is hypertension, which increases the risk of stroke 2- to 4-fold. This higher risk is seen in both systolic and diastolic hypertension as well as in isolated systolic hypertension in the elderly. Blood pressure control significantly reduces the risk of stroke; it has been shown to prevent 30 strokes for every 1000 patients treated. According to the current recommendation of the Stroke Council of the American Heart Association (AHA), blood pressure should be maintained at less than 140/90 mm Hg.⁶

Diabetes

Diabetes increases stroke risk 1.8- to 6-fold. Although there is no clear evidence that normalizing blood glucose values itself specifically reduces stroke risk, the Stroke Council's guidelines clearly state that hyperglycemia should be controlled to reduce the risk of microvascular complications.⁶

Smoking

Approximately 27% of men and 22% of women in the United States smoke cigarettes. Smokers have a relative risk of stroke in the range of 1.8, and the estimated population attributable risk of stroke due to smoking is 18%. Fortunately, this increased risk disappears within 5 years of smoking cessation.

Hyperlipidemia

Lipid disorders have been shown to increase the risk of stroke by 1.8- to 2.6-fold.⁶ Most of the information regarding the effect of lowering cholesterol on stroke risk comes from secondary analyses of trials on the prevention of coronary disease, but it is prudent to use these guidelines when evaluating patients for stroke risk. The recently issued third report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) provides age- and gender-specific weighting algorithms to guide treatment decisions on the use of lipid-lowering agents. Tools for the immediate assessment of a particular individual's risk can be downloaded for use with personal digital assistants. In general, for primary prevention in the absence of cardiovascular disease, total cholesterol levels should be maintained below 240 mg/dL, LDL levels at less than 160 mg/dL (in patients who have <2 cardiovascular risk factors), and HDL concentrations at greater than 40 mg/dL. Tighter control of hyperlipidemia is indicated for patients who have a history of stroke or cardiovascular disease; their goal LDL level is less than 100 mg/dL, their target HDL level is greater than 40 mg/dL, and their recommended total cholesterol level is less than 200 mg/dL. Keep in mind, however, that total cholesterol levels lower than 160 mg/dL have been associated with an increased risk of intracerebral hemorrhage.

Asymptomatic Carotid Artery Stenosis

The Asymptomatic Carotid Atherosclerosis Study (ACAS) showed that carotid endarterectomy is beneficial in primary stroke prevention in patients who have high-grade asymptomatic carotid stenosis.⁷ In this trial, investigators compared medical management with endarterectomy plus medical management in 1662 patients who had stenoses greater than 60%. Endarterectomy was associated with a 53% reduction in 5-year relative risk, which amounts to an absolute risk reduction of 1% per year. Moreover, the combined rate of surgical and angiographic complications in this trial was very low (2.3%); a complication rate greater than 4.5%, which is closer to the rates seen in other studies, would have negated the benefit of endarterectomy seen in this trial. Therefore, the current AHA guidelines recommend carotid endarterectomy for patients with an asymptomatic stenosis greater than 60% only if (1) the surgeon performing the procedure has a morbidity/mortality rate of less than 3% and (2) the patient has a life expectancy of at least 5 years.⁶^,8

Symptomatic Carotid Artery Stenosis

The benefit of carotid endarterectomy in patients with symptomatic high-grade carotid artery stenosis was well demonstrated in two large trials. The North American Symptomatic Carotid Endarterectomy Trial (NASCET) was a rigorously performed, randomized, controlled trial that compared carotid endarterectomy with medical management in 659 symptomatic patients who had angiographically proven stenosis of 70% to 99%.⁹ The researchers found that the risk of ipsilateral stroke at 2 years was 9% in the surgical group and 26% in the medical group, a difference that translated into a 51% reduction in relative risk of stroke or death over 2 years in the endarterectomy group. The European Carotid Surgery Trial was another randomized controlled study of patients with symptomatic carotid artery stenosis, and it yielded similar results.¹⁰ A third trial-a Veterans Affairs Cooperative Studies Program trial¹¹-was prematurely stopped after the results of the previous two trials became known.

The benefit of carotid endarterectomy is much greater in symptomatic patients than in asymptomatic patients. According to data from NASCET and ACAS, in which the same method was used to measure stenosis, carotid endarterectomy prevented one stroke or death in 1 year for every 12 symptomatic patients who were so treated; the corresponding figure for asymptomatic patients was 1 for every 85 patients treated.

The NASCET investigators also compared endarterectomy with medical treatment in patients with symptomatic disease whose stenoses were only moderate (50% to 69%).¹² They found that the 5-year stroke rates were 15.7% in the endarterectomy group and 22.2% in the medical group (p=.045). In this group, carotid endarterectomy would prevent one stroke or death in 1 year in for every 77 patients treated.

According to current guidelines, surgical treatment should be offered to all patients with symptomatic stenosis greater than 70% who are good candidates for surgery.⁸^,13 Patients with a 50% to 69% stenosis should be selected carefully, and the decision to operate should be based on symptoms and stroke risk factors.¹³

Carotid angioplasty and stenting are exciting new and less invasive therapies for carotid artery stenosis. These procedures might be especially useful in patients who are at high surgical risk. However, they are still investigational.

Atrial Fibrillation

The incidence of stroke among patients with atrial fibrillation is approximately 5% per year. Adjusted-dose warfarin has been shown in numerous trials to be the treatment of choice for prevention of stroke in these patients. Warfarin reduces stroke risk by approximately 68%, while antiplatelet agents reduce this risk by only 21%. A target INR of 2.5 (range: 2.0 to 3.0) is generally recommended. An exception to this recommendation applies to patients with "lone atrial fibrillation," defined as those who are younger than 65 years of age who have no history of stroke, transient ischemic attack, poor ventricular function, rheumatic heart disease, hypertension, or diabetes mellitus. In these patients, antiplatelet therapy may be just as effective as warfarin. Elderly patients with atrial fibrillation have a higher risk of serious hemorrhagic complications with warfarin, but they also have a greater reduction in the risk of embolic stroke.

Aspirin is recommended for atrial fibrillation in patients in whom warfarin is contraindicated and in those in whom warfarin would pose too high a risk for hemorrhagic complications. However, there is no evidence to support the use of antiplatelet agents in the primary prevention of noncardiac-related stroke. Although aspirin has been shown to reduce the incidence of first cardiac events, it has not been shown to affect the occurrence of first-time stroke.

For secondary prevention, antithrombotic therapy (either an antiplatelet or an anticoagulant) should be administered to all patients with ischemic stroke, barring a contraindication. Warfarin should be strongly considered for patients with stroke due to atrial fibrillation. The risk of recurrent stroke in these patients is extremely high: up to 12% during the first year.¹⁴ There is no evidence that warfarin is superior to aspirin in patients with noncardiac stroke. Ongoing studies are evaluating the efficacy of warfarin in other subgroups of stroke patients, such as those with intracranial stenoses, antiphospholipid antibodies, and PFO.

Intracerebral Hemorrhage

Blood pressure control is strongly recommended to prevent intracerebral hemorrhage (the current guidelines for blood pressure treatment can be found in the sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure).¹⁵ The AHA also recommends that patients with stroke (as well as those with acute myocardial infarction) be carefully considered for thrombolytic therapy to reduce the risk of intracerebral hemorrhage.¹⁶ Some evidence suggests that excessive alcohol consumption also increases a patient's risk for intracerebral hemorrhage, but this evidence is still incomplete; in the meantime, the AHA recommends that at-risk patients should be particularly conscious in avoiding heavy alcohol consumption.

OUTCOMES

As mentioned previously, stroke is the third-leading cause of death in the United States. The 30-day mortality rate is 7.6% for patients with ischemic stroke and 37.5% for those with hemorrhagic stroke.¹⁷ Most deaths within the first week are attributable to the severe nature of a stroke, while deaths that occur later are usually the result of complications of the stroke itself or of other comorbid conditions. Patients with stroke often have systemic vascular disease; the annual risk of vascular death in stroke patients is greater than 3%. Stroke survivors show significant functional improvement during the first 3 months of recovery. Further improvement can occur during the succeeding 3 months, especially in patients whose initial impairment was severe. Even so, most stroke survivors are left with some disability. For example, 48% are hemiparetic at 6 months and 22% cannot walk. As many as one-half of all stroke survivors are partially dependent on others to perform activities of daily living.¹⁸ The rate of recurrent noncardioembolic stroke is 3% to 7% per year.Return to Medicine Index

REFERENCES

The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group Tissue plasminogen activator for acute ischemic stroke. N Engl J Med. 1995; 333:1581-7.

Adams HP, Brott TG, Furlan AJ, et al. Guidelines for Thrombolytic Therapy for Acute Stroke: A supplement to the guidelines for management of patients with acute ischemic stroke, a statement for healthcare professionals from a special writing group of the stroke council, American Heart Association. Circulation. 1996;94:1167-1174.

International Stroke Trial Collaborative Group. The International Stroke Trial (IST): a randomised trial of aspirin, subcutaneous heparin, both, or neither among 19435 patients with acute ischaemic stroke. Lancet. 1997;349:1569-1581.

CAST (Chinese Acute Stroke Trial) Collaborative Group. CAST: randomised placebo-controlled trial of early aspirin use in 20,000 patients with acute ischaemic stroke. Lancet. 1997; 349:1641-9.

The Publications Committee for the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) Investigators. Low molecular weight heparinoid, ORG 10172 (danaparoid), and outcome after acute ischemic stroke: a randomized controlled trial. JAMA. 1998;279:1265-1272.

Goldstein LB, Adams R, Becker K, et al. Primary prevention of ischemic stroke: a statement for healthcare professionals from the Stroke Council of the American Heart Association. Circulation. 2001;103:163-182.

Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA. 1995;273:1421-1428.

Biller J, Feinberg WM, Castaldo JE, et al. Guidelines for carotid endarterectomy: a statement for healthcare professionals from a Special Writing Group of the Stroke Council, American Heart Association. Circulation. 1998;97:501-509.

North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med. 1991;325:445-453.

Randomised trial of endarterectomy for recently symptomatic carotid stenosis: final results of the MRC European Carotid Surgery Trial (ECST). Lancet. 1998;351:1379-1387.

Mayberg MR, Wilson SE, Yatsu F, et al. Carotid endarterectomy and prevention of cerebral ischemia in symptomatic carotid stenosis. Veterans Affairs Cooperative Studies Program 309 Trialist Group. JAMA. 1991;266:3289-3294.

Barnett HJ, Taylor DW, Eliasziw M, et al. Benefit of carotid endarterectomy in patients with symptomatic moderate and severe stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med. 1998;339:1415-1425.

Albers GW, Hart RG, Lutsep HL, Newell DW, Sacco RL. AHA Scientific Statement. Supplement to the guidelines for the management of transient ischemic attacks: a statement from the Ad Hoc Committee on Guidelines for the Management of Transient Ischemic Attacks, Stroke Council, American Heart Association. Stroke. 1999;30:2502-2511.

EAFT (European Atrial Fibrillation Trial) Study Group. Secondary prevention in non-rheumatic atrial fibrillation after transient ischaemic attack or minor stroke. Lancet. 1993;342:1255-1262.

The sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med. 1997;157:2413-2446.

Broderick JP, Adams HP Jr, Barsan W, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: a statement for healthcare professional from a special writing group of the Stroke Council, American Heart Association. Stroke. 1999;30:905-915.

Rosamond WD, Folsom AR, Chambless LE, et al. Stroke incidence and survival among middle-aged adults: 9-year follow-up of the Atherosclerosis Risk in Communities (ARIC) cohort. Stroke. 1999;30:736-743.

Post-Stroke Rehabilitation. Rockville, Md: US Dept of Health and Human Services; 1995. Agency for Health Care Policy and Research publication 95-0662.

Disclaimer

Definition Prevalence Pathophysiology Signs and Symptoms Diagnosis Therapy Prevention Outcomes References

National Guidelines Thrombolytic therapy for acute stroke (AHA) Guidelines for carotid endartertectomy (AHA-Stroke Council) Sixth report of Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure National Cholesterol Education Program Third Report on the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III)

http://www.acnp.org/Docs/G5/CH92_1317-1326.pdf

http://www.basp.ac.uk/3_STROKE.PDF

Stroke reference

Bruno A, Biller J, Adams HP, et al: Acute blood glucose level and outcome from ischemic stroke. Trial of ORG 10172 in Acute Stroke Treatment (TOAST) Investigators. Neurology 1999;52:280-284

Toole JF. Brain Infarction: Pathophysiology, Clinical Feature and Management Cerebrovascular disorders. In: Toole JF (Editor) 5^th edition. Philadelphia, PA: Lippincott Williams & Wilkins; 1999

Hakim AM: Ischemic penumbra, the therapeutic window. Neurology. 1998;51(supp 3):S44-46

Barnett, Henry JM, Mohr JP, Stein BM, Yatsu FM (eds), Stroke Pathophysiology, Diagnosis and Management. Third edition, Philadelphia, PA: Churchill Livingston; 1998

http://www.ferne.org/Lectures/pathophysiology%200501.htm#CP

This assignment will discuss and critical analysis how nursing skills can be safely utilized to deliver effective nursing care and assessment, planning and evaluation of care to influences the patient experience. The pathphysiology of fluid and electrolyte balance, effect of severe dehydration on and management of fluid and electrolyte imbalance will be discussed.

Also, it will highlight possible causes and the effect of vomiting and diarrhoea on the fluid and electrolyte balance, plus wound management around sacral and peri-anal areas, which are excoriated. Finally, care of patient in isolation and management of Alan Cole’s care would include monitoring of his general wellbeing and the importance of effective communication role of the nurse will be viewed.

Alan Coles is admitted to a side room because it is not yet clear whether profuse episode of diarrhoea is infectious or not. Every episode of unknown origin of diarrhoea should be assumed communicable and precaution must be taken (Alexandra et al 2000). It is important for the nurses to practice universal precaution which, is a measure taken to protect health workers when they have or may have contact with blood or other bodily fluid from anyone, regardless of whether that individual is know to have an infection or not (DoH 1998). Therefore, nurses caring for Alan Coles must practise good hand washing technique before and after attending to him, safe disposal of clinical waste and wearing disposable gloves and apron in order to protect themselves against any spillage and to prevent the risk of spreading any communicable diseases from Alan to other patients, staff and visitors to the ward (Heath 2001).

To make appropriate assessment and give adequate correct treatment to Alan Coles, it is important for the nurse to understand the anatomy and physiology of fluid and electrolyte balance and how severe dehydration from diarrhoea and vomiting can affect the balance of body fluid and electrolyte.

Body fluid is made up of water and certain dissolved substances called electrolytes. The body fluid is divided into two major compartments know as the cellular and extracellular fluids. The cellular fluid represents the fluid contained within the body cells while the extracellular fluid surrounds the cells. The body cells feed themselves and excrete waste by constantly exchanging material with their environment (Jevon & Ewens 2002).

However, the fluid in body is maintained by osmotic pressure within each compartment. Osmosis is the passage of fluid from a high concentration to a low concentration through a semi permeable membrane and is determined by the electrolyte concentration of the fluid in each compartment. Just as the cellular and extra cellular fluid each has its own characteristic chemical composition, so does each secretion or excretion exhibit a composition that is relatively during health but which may deviate widely from normal during an illness (Kumar 2003).

Total body fluid is maintained when input equal output. For an average adult, this is roughly 2 ½ litres per day in and 2 ½ per day out. When the secretions and excretions are depleted, they deplete the extracellular fluid, which in turn deplete the cellular fluid. The time it takes a depleted secretion or excretion to affect the extracellular fluid to affect cellular fluid varies widely and depend, in general, upon the level of the inequality between gains and losses (Phipps et al 2003).

On the other hand, according to Speakman and Weldy (2001) the term electrolyte means salt, specifically ions; this ion is electrically charged and moves to either a negative or positive electrode. Electrolytes are important because they are what the cells especially nerve, heart and muscle use to maintain voltages across their cell membranes and to carry electrical impulses such as nerve impulses and muscle contractions across themselves and to other cells.

Electrolyte balance must be maintained by oral intake and hormonal

regulation, generally with the kidneys as effectors. Measurement of electrolytes is a commonly performed by diagnostic procedure, done as a blood test or as part of urinalysis. As part of assessment, Alan blood sample will be taken for laboratory test to find out what electrolytes are imbalances and they should be replaced accordingly. The kidneys work to keep the electrolyte concentrations in the blood constant despite changes in the body. Electrolyte imbalance therefore occurs when imbalance of certain ionized salts such as bicarbonate, calcium, chloride, magnesium, phosphate, potassium, and sodium in the blood (Heath 2001).

When nursing patients with fluid and electrolyte imbalance and those receiving infusions, the nurse must understand how the role of electrolytes in the body fluids, the reason why and how their levels are maintained within homeostatic limits, and the problem that can arise as a result of the imbalance

When fluid imbalance occurs between cellular and extracellular compartments, it is usually caused by a change in the sodium or potassium concentration and the fluid compartments in the body exchange fluid to compensate for losses, consequently the fluid lost initially from one compartment inevitably results in a loss from all compartment. It is important to give immediate attention and treatment to patients who have fluid and electrolyte imbalance as delay in treatment could be fatal and lead to death (Hand 2001).

The medical intervention aim for Alan’s care while in the ward would be the application of intravenous therapy to replace losses, correct and maintain fluid and electrolyte imbalance thus allowing normal cells and organ function, and treat the underlining causes of fluid and electrolyte imbalance.

The cause of Alan’s fluid and electrolyte imbalance is severe dehydration. Severe dehydration is accompanied by a deficiency of electrolytes because as more water is lost, the sodium level rises. When electrolytes in the bloodstream are also deficient, water moves less readily from inside cells. If the amount in the bloodstream were not replenished as it would normally be, Alan‘s blood pressure could fall, causing him light-lightheadness or faintness, particularly upon standing a condition called orthostatic hypotension. If Alan continues to loss water and electrolyte, his blood pressure can fall dangerously low, resulting in shock and severe damage to many internal organs especially the kidney, liver and the brain eventually leading to death (Smeltzer and Bare 2004).

Replacing and maintaining the correct fluid balance is an important part of treating Alan. To do this the nurse not only need to be able to assess how much fluid a patient needs but what type of fluid to give (Mallet and Dougherty 2000). Intravenous fluids may be classified into crystalloids, colloids and blood products. If fluid loss is under- corrected then Alan may develop hypovolaemia, which may lead to renal impairment and other complications. Also, over correction can lead to pulmonary oedema and heart failure (Saddler 2001).

Crystalloids, such as normal saline and dextrose 5%, are substances that form a true solution and pass freely through a semi permeable membrane. They contain water and electrolytes and stay in the intravascular compartment for a shorter time than colloids. However, crystalloid solutions are convenient to use and have no side effect. Colloids, on the other hand, are substances that do not dissolve into a true solution and do not pass through a semi permeable memebrane. Colloid solutions tend to stay in intravascular compartment for longer than crystalloids, and therefore less volume is needed. Colloids also increase colloidal osmotic pressure, draining water out of the interstitial spaces into the intravascular compartment (Shami & Davidson 1997).

Shami & Davidson (1997) explains further that when capillary permeability is increased colloids may leak across the capillary membrane and increases interstitial oncotic pressure, causing oedema. This may also happen if too much colloid is given and pulmonary oedema may occur and interfere with gas exchange.

Colloid solutions such as plasma expander will be given to Alan to improve the cardiovascular function and transport oxygen to severe dehydrated tissue through an indwelling catheter positioned in large vein. Further fluid resuscitation with crystalloid will be given as required.

Nurses in the United Kingdom have a professional responsibility to ensure that patients in their care are given the right information about their condition and understand the risks and implications of any intervention required. Nurses also have the responsibility to gain the consent of patients for whom they have duty of care Alan needs to be reassured and supported in order to keep him less anxious and co-operate with nurse (MNC 2002).

However, before intravenous fluid therapy procedure is carried out full vital signs assessment has to be done. Alan’s temperature, pulse respiration rate and blood pressure will be taken as a baseline and use as an assessment to justify his response to treatment. The nurse will explain to Alan the purpose of intravenous fluid procedure, the amount and frequency of fluid and at the same time obtaining his consent to pass the intravenous catheter to replace and correct his fluid and electrolyte imbalance (NMC 2000).

Sullivan (1999) emphasis that intravenous therapy plays an important in the treatment regime for many hospital patients, when use correctly, fluid therapy can be beneficial and life saving. Although, just as with any other medication, the inappropriate use of fluid therapy can lead to detrimental and even tragic circumstances. Therefore fluid therapy should be approach with caution.

It is important for the nurse administering intravenous solution to have knowledge for therapy, side effect and potential adverse reaction and appropriate intervention particularly related to the management of anaphylaxis (Hand 2001).

Prior to the administration of intravenous solutions, the nurse will appropriately label all containers vials and syringes, identifying Alan as the correct patient needing the solution and verify the contents, dose, rate, route, expiry date and integrity of the solution, check the syringe size and brand displayed before starting the infusion (Dougherty and Lamb (2002).

In addition aseptic technique is vital in the prevention of intravenous related infections, thus asepsis will be maintained at the insertion of catheter and also at removal of the device. Adequate care will be taken making sure that bruising did not occur at any time during episode of intravenous therapy (Mallet and Dougherty 2000).

Furthermore, once infusion is set up, the nurse will check the volume delivered by examining the barrel of syringe routinely and finally store medical devices carefully and always report faulty devices. Accurate fluid is crucial to infusion device performance because incorrect infusion rates can arise from prescription errors, incorrect infusion rate setting, failure to set the flow and lack of understanding of the device operation. Errors can also occur when using incorrect administration sets with volumetric pumps because of subtle differences in cross-sectional areas of tubing in different brands of administration sets. Damage to the backing plate against which the pumping action squeezes the administration tubing can lead to errors in infusion rates (Amoore and Adamson 2003).

The nurse will be accountable for evaluating and monitoring effectiveness of prescribed fluid replacement therapy; documenting Alan’s response to treatment, recognising adverse effects and achieving effective delivery of prescribed rehydration therapy. The nurse has the responsibility to report any adverse event as per organisational policies and procedures. Also, Alan will be monitored for side effects such as infiltration and phlebitis, which is the inflammation of the intima of the vein wall that can be caused by physical access to the vein. Regular monitoring of infusion sites, choice of correct access device, intravenous dressing and the use of in-line pressure monitors may help to reduce the extent to which infiltration and phlebitis occurs (Dougherty and Lamb 1999).

Fluid balance chart will commence immediately to record intake of all oral fluids including medicines, recording any intravenous and oral intake. The nurse will measure all fluid output losses such as urine, diarrhoea and vomiting as accurately as possible. Nurses must be aware of the many ways in which the accuracy of fluid intake / output calculation may be comprised, for example, duplication or omission of items, use of estimation rather than measurement arithmetical errors, shift change errors that is, in carrying calculation forward from previous shifts, recording wrong intravenous bag and failure to observe patterns in consecutive daily balance (Smeltzer and Bare 2004).

Alan would need to be continuously assessed and monitor to check that his blood pressure does not become too low. His pulse rate, respiratory rate and body temperature will be monitor initially at every hour. Furthermore, Alan will be monitor for signs of a satisfactory response to rehydration which are return of a strong radial pulse, improved level of consciousness, increased ability to drink, much skin turgor and passage of urine. When these are seen, the interval of between reassessments will be lengthened from very hour to four hourly.

Also Alan will be place on a daily weight chart and note any decrease or increase weight as an accurate daily weight is an important indicator of fluid balance in the body (Brooker and Nicol 2003).

The cause of Alan’s fluid and electrolyte imbalance is by severe dehydration from ongoing profuse diarrhoea and vomiting which has now stopped. Once the drip is in progress, the next course of action is to address the profuse diarrhoea.

On admission to the ward one of the main nursing goal in caring for Alan will be to prevent and minimise the spread of any communicable disease and maintain safe environment. As recommended by the Alexandra et al (2000), acute diarrhoea of unknown origin should be assumed to be communicable and precautions taken.

Universal precaution measure must be carried out as stated earlier. Nurse must remember to wash their hands using hand wash technique with bactericidal soap and running water, dry hand properly and disposable gloves and apron must worn and dispose off appropriately. A sterile jug must be use for urinary collection. All used soiled linens must be bagged and properly in red linen bag (Malik et al 2002).

Diarrhoea, according to Cohen and Wood (2000) is three or more watery stools on more than three occasions; this may be accompanied with vomiting or fever. Diarrhoea is caused by bacteria, viruses, protozoa and algae-like organisms Since Alan is returning from India, poor hygiene, contaminated food or water and general change in climate could have caused his diarrhoea episode or he could have contracted travellers’ diarrhoea or it could have been triggered simply by a change in his diet while in India (Hinchiff et al 2003).

According to Tortora and Grabowski (2001) the most common organism responsible for traveller’s diarrhoea is Escherichia coli, which can be transmitted mainly through the faecal route, where organisms are carried from hand to mouth, or by contaminated food and drink. Alan may have contracted this organism through food and drink when partying on the beach in India

Identification of underlying cause is imperative because the treatment and expected outcome depend on it.

Thus laboratory examination of stool samples to check if there is infection will be done and blood tests will be carried out. Alan’s stool specimen will be collected in a clear plastic container and placed in a self sealing bag and accompanied with request form containing accurate information about Alan such as diagnosis, symptoms and the fact that he has just returned from India. The stool specimen will then be sent for culture to the department of Microbiology as soon as possible to determine the cause of diarrhoea and vomiting (Hillingdon Hospital 1996).

If the episode of the diarrhoea continues and frequency increases, it might be necessary to give Alan anti-motility medication such as loperimade which relax the muscles of the small intestine and/or the colon and slow down the intestines but their side effect includes tummy cramps and dizziness. Should Alan experience and cramp due to spasm of the intestinal muscles, he will be given non steroid anti inflammatory drug such as paracetamol tablets, because Alan did not have underlying disease, therefore it will not be necessary to use antibiotic in treating the diarrhoea unless there is a culture proven bacterial infection that requires antibiotics (British National Formulary 2005).

Alan Coles is under weight; this may be due to eating sparing while in India. Alan will refer to the hospital dietician, who will assess Alan’s nutritional needs and make appropriate recommendation on what Alan should be eating.

Nurses have a duty as an educator to educate their patients about risk associated hygiene and traveller diarrhoea. In addition Alan will be advice and educate on healthy eating habits that may reduce the risk of significant weight loss and prevent fluid and electrolyte imbalance in the future. Calories intake should be adequate and he should eat more properly washed fruits and vegetables (Hinchiff et al 2003).

There is potential problem of dry and cracked lips and formation of sordes in Alan mouth due to severe dehydration. Alan will be given regular mouth care encourage him to drink fluid to stimulate the flow of salvia which will help keep his mouth clean and moist (Cohen and Wood 2000).

Hinchilff et al (2003) recommended the use of Vaseline to be applied patients lips to keep them moist. The use of strong solutions of glycerine should be avoided as they absorb moisture from mucosa causing drying by osmotic action.

Alan sacral and peri anal areas are excoriated as a result of excessive passing of liquid stool and frequent wipe or cleaning of the sacral and peri anal area. The excoriated areas need to be kept clean and thoroughly dry, as often as necessary to protect the areas from moisture. This will be accomplished by the use of moisture barriers, such as Cavilon Durable Barrier Cream, applied to the skin after each episode of diarrhoea. The goal is to keep the area dry. To prevent any pressure sore Alan will be nurse on air mattress to encourage even distribution of his body weight and relieve pressure areas to prevent more damage or tissue breakdown (Simon et al 2002)

Finally as Alan is nurse in side room, the nurse will spend time with Alan and encourage him to read books and newspapers, watch television or listen to radio and most importantly explain the reason of isolation to Alan so that he can have an understanding of why he is isolated to reduce psychological effects of isolation (Hinchiff et al 2003)

In conclusion, this assignment has discussed the pathophysiology of body fluid and electrolytes balance, how fluid and electrolytes imbalances occurs in body and the effects on Alan general well begin. Also it identified intravenous fluid therapy treatment side effects and caution to be taken by the nurses looking after Alan. The purpose of fluid therapy management has been highlighted and the importance of universal precaution when handling diarrhea and vomiting of unknown origin.

The assignment has also discussed the significance of communication skill and the how effective it is in the delivery of Nursing Care. It continues to identify how important it is to involve patient in his own care.

This assignment has heightened the importance of continuous education and the fact that the nurses have a duty to gain evidence base knowledge to help in providing the best care possible.

Reference List:

Alexandra, M. F., Fawcett, J. N.; Runciman, P. J. (2000) Nursing Practice: Hospital and Home. The Adult. London: Churchill Livingstone

Amoore, J. and Adamson, L. (2003) Infusion device: characteristic, limitations and risk management. Nursing Standard. 17, 28, pp 45-52

BNF British National Formulary 50, September 2005

Brooker, C. & Nicol, M. (2003) Ed Nursing Adults the Practice of Caring London: Mosby.

Cohen, B.J. and Wood, D. L. (2000) Memmler’s The Human body in health and Disease. Philadelphia: Lippincott Williams & Wilkins

Department of Health (2003) Winning ways working together to reduce healthcare associated infection in England. London: Department of Health.

Dougherty, L. & Lamb, J. (1999) Intravenous Therapy in Nursing Practice. UK: Churchill.

Hand, H. (2001) The use of Intravenous Therapy. Nursing Standard [http://gateway2.uk.ovid.com/ovidweb.cgi]. Volume 15 (43), pages 47-55 [Accessed on 09/10/2003]

Heath, H. B. M. (2001) Potter & Perry’s Foundation in Nursing Theory and Practice. China: Mosby

Hinchiff, S. M., Norman, S. E., Schober, J. E. (2003) Nursing Practice and Healthcare. 4^th ed. London: Edward Arnold

Jevon, P. & Ewens, B. (2002) Monitoring the Critically Ill Patient (Essential Clinical Skills for Nurses) United Kingdom: Blackwell Science

Krujver, I. (2000) Evaluation of Communication Training Programs in Nursing Care. Patient Education and Counseling. 39 (1) 129-145.

Kumar, P. & Clark, M. (2003) Clinical Medicine 5^th London: Saunders

Mallett J. and Dougherty L. (2000) The Royal Marsden Hospital Manual of Clinical Nursing Procedures 5^th England: Blackwell Science.

Nursing and Midwifery Council (2002) Professional Code of Conduct. London: NMC.

Plumer, A. L. and Weinstein, S (1996) Plumer’s Principles and Practice of Intravenous Therapy. USA: Lippincott William & Wilkins

Phipps, J. W., Monaham, D. F. Sands, K. J. Marek, F. J. &Neighbors, M. (2003) Medical and Surgical Nursing, Health and illness Perspectives 7^th ed. London: Mosby.

Sadler, T. (2001) Fluids and Electrolytes Made Incredibly Easy (Incredibly Easy). Springhouse Publishing

Simon C, Everitt H, Birtwistle J, & Stevenson B. (2002) Oxford Handbook of General Practice. Oxford: Oxford University Press

Speakman, E. and Weldy, N. J. (2001) Body Fluids and Electrolytes. 8th ed. London: Mosby Inc.

Sullivan, A. (1999) "Hydration for Adults. Nursing Standard: Vol.14, (8). pages 44-46.

Smeltzer, S. and Bare, B. G. (2004) Brunner and Suddarth's Textbook of Medical-surgical Nursing.10^th Ed. Philadelphia: Lippincott Williams & Wilkins

Tortora, J G. & Grabowski, R.S. (2001) Introduction to the Human Body, The Essentials of Anatomy and Physiology. 5^th New York: John Wiley and Sons, INC.