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
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
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.
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.
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*|
|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|
|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|
|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|
|*Confidence intervals omitted for clarity|
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.
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:
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
Competing interests: None declared.
References w1-w27 are on studentbmj.com.
K A L Carroll, fifth year medical student, Imperial College, London Email: email@example.com J Chataway, consultant neurologist, St Mary's Hospital, London
studentBMJ 2006;14:309-352 September ISSN 0966-6494
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.
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.
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. 4th 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 5th London: Saunders
Mallett J. and Dougherty L. (2000) The Royal Marsden Hospital Manual of Clinical Nursing Procedures 5th 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 7th 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.10th Ed. Philadelphia: Lippincott Williams & Wilkins
Tortora, J G. & Grabowski, R.S. (2001) Introduction to the Human Body, The Essentials of Anatomy and Physiology. 5th New York: John Wiley and Sons, INC.