Kidney Failure Management - Case Study Example

MR. EMERY KIDNEY FAILURE MANAGEMENT Briefly outline of how acute renal failure differs from chronic renal failure. Acute renal failure also known as acute kidney injury refers to a clinical syndrome characterized by a rapid decrease in renal excretory function, a rapid decline in glomerular filtration rate, retention of nitrogenous waste products, oliguria, proteinuria and creatinine. Other common clinical and laboratory manifestations include decreased urine output, accumulation of metabolic acids, and increased potassium and phosphate concentrations. (Mehta et al 2007) While the chronic kidney disease (CKD) was defined as the presence of kidney damage, which is indicated by decreased kidney function, presence of abnormal albumin excretion that is quantified by glomerular filtration rate that persists for more than 3 months and characterized by loss of renal cortex. (Abbas et al 2008) Pathophysiological links between Mr. Emery is past history and the development of Chronic Renal Failure. As Mr. Emery’s kidney function deteriorates, the secretion of erythropoietin becomes impaired, the red cell half-life decreases to control the reduction of erythropoietin exogenous Epoetinalfa was used. A number of other electrolyte abnormalities developed as the disease progressed Mr. Emery developed worsening chronic kidney disease, which leads to hypertension and the kidney secreted renin that exacerbate blood pressure. In addition, there is evidence, which suggest that renal nerves also, play a role in the increased blood pressure in patients with chronic kidney disease, the elevated blood pressure caused kidney damage and accelerated the decline in renal function. (Wuhl and Schaefer 2010) Because of the deterioration of 1-alpha-hydroxylase function Mr. Emery developed hypocalcemia because of the decreased absorption of calcium in the gut, which lead to secondary hyperparathyroidism that caused calcium to be mobilized on the bone. (Schmitt and Mehls 2011) The pathophysiological events underlying the inception of Mr. Emery’s chronic kidney failure progression characterized by a common renal phenotype of tissue destruction, inflammation and scarring, chemical such as urea and creatinine constantly attacking renal cells eventually activate inflammatory and fibrotic responses that not only interfere with the repair processes, but also redirect the renal tissue status through similar mechanisms of irreversible degeneration. The initial cellular damage eventually activates responses that finally damage other nephron structures leading to a vicious circle of malignancy where nephrons progressively disappear and are substituted by scar tissue. This cell damage and activation lead to inflammation and cytokine imbalance, which activates other cell type and contributes to unleashing fibrosis, mesangial and vascular contraction contributing to the reduced GFR, tubule degeneration and scarring. (José et al 2010) Relationship between his presenting symptoms and his disease process The relationship between the present symptoms and progress of recovery of Mr. Emery’s temperature is between the normal ranges of 37.0. Heart rate 96 is an indication of; pulmonary edema, which is increased vascular permeability to proteins resulting in protein-rich fluid accumulation in the alveolar air sacs. Respiration rate of 22.0 indicates that oxygenation is further hampered by decreased surfactant production secondary to cellular damage resulting in alveolar collapse, producing decreased pulmonary compliance, respiratory distress, increased work of breathing, and eventually respiratory failure. (Perina 2003) Part B Problems that Mr. Emery is facing, goals and nursing actions Anemia Mr. Emery has iron deficiency anemia therefore the nursing interventions would be to give him educate him the importance of lifestyle change and adopting a balance dietary regime. Because he lives alone and has no stable income, financial planning will be important to help him increase iron intake through proper diet and encouraging him to take small frequent meals during the day to increase his ability to maintain a nutritious diet. (Jones 2004) Medication for iron deficiency should be given about an hour before a meal, to increase the absorption of Iron ferrous fumarate in an acid environment and taking vitamin C to iron helps absorption. The interventions for anemia would involve evaluating Mr. Emery’s understanding of nutritional issues contributing to the anemia with the help of a 24-hour food log, which assist in evaluate the intake of protein, iron, calories, and other nutrients needed for hematopoiesis. Carry out regular monitoring of the laboratory data of Mr. Emery to determine the status of the anemia by monitoring the vital signs at rest and during the goal of these interventions is to assess whether Mr. Emery is free of complications from the anemia (Smeltzer et al 2008) Diabetic neuropathy Establish rapport with Mr. Emery to take and record his vital signs, monitor his temperature, assess skin turgor and mucous membranes for signs of dehydration and encourage him to increase fluid intake. Mr. Emery taught how to care for his foot through proper foot inspection to reinforce the need for regular self-care, provide him with regular foot examinations to reduce rates of ulceration and even amputation. (Callaghan at el 2012) Edema The intervention for edema, advice Mr. Emery to keep his swollen limbs elevated above the level of the heart to assist venous return and to avoid tight or restrictive clothing on the affected limbs. If the edema is in the legs, advise the patient to avoid compression of the abdomen and suggest weight loss regimens and to maintain his skin clean. Educate the patients how to gently and carefully wash his skin daily with soap substitutes, moisturize it gently with creams and how to inspect the skin for any signs of breakdown or infection. Take regular, gentle exercise that activates the skeletal muscle pump that will be of use to patients with lower-limb edema. For edema of a single limb caused by venous hypertension, the underlying cause must be treated by restricted sodium intake and adherence to the prescribed diuretic regimen. (Penzer 2003) The medications and rationale of the chosen interventions for Mr. Emery The National Kidney Foundation recommends that anemic patients should undergo annual and compulsory complete blood count. It is advisable that those patients who have anemia associated with chronic kidney failure to undergo further evaluation to determine the exact cause of anemia (National Kidney Foundation 2002) (TREAT) trail of patients anemia associated with chronic kidney failure recommended that a target of 13.5g/dl or rescue with Epoetinalfa when the level drops below 9.0 g/dl to activate the erythropoiesis on the bone barrow, with an aim of increase circulating red blood cells. (Pfeffer et al 2009) Strict blood pressure control was adhered to as a priority in the care of Mr. Emery, ARBs inhibitors or ACE were recommended as the initial medications to achieve blood pressure control, a multidrug regimen was preferred because of the other conditions Mr. Emery had such as anemia and iron deficiency. (Segura and Ruilope 2009) When the glomerular membrane was damaged, the first protein spilled into the urine was albumin. Therefore, screening for the presence of microalbuminuria was the most sensitive analysis of confirmation early kidney damage. Microalbuminuria was considered positive when the level was greater than 30.5 mg/g and when the level of proteinuria exceeds 500.0 mg/g, using a spot urine protein or creatinine ratio was recommended to assess the severity of the proteinuria and its response to interventions. (ADA 2008) Mode of action, adverse effects and key nursing considerations Epoetinalfa (Eprex) The progression of chronic kidney injury, the kidney’s ability to secrete erythropoietin decreases and Mr. Emery could become anemic to slow down the progression of damage erythropoietin-stimulating agent was considered to improve their quality of life. The mode of action of Epoetin stimulates the proliferation and differentiation of the erythroid stem cell as well as the proliferation and maturation of the erythron, by binding to the erythropoietin receptor on the red cell progenitor surface, which lead to an increase in hemoglobin formation and an associated acceleration of cell maturation with reduction in the cell cycle time. (European Medicines Agency 2007) The rationale of administering epeotinalfa was to increase hemoglobin level and sustain a normal level of hemoglobin. Cholecalciferol Mode of action of vitamin D, vitamin D suppresses renin secretion, which has been indicated as a beneficial to the management of chronic kidney disease. Adverse effects of vitamin D include anorexia, nausea, vomiting, diarrhea, weight loss, sweating, thirst, headache, vertigo, raised concentrations of calcium and phosphate in plasma and urine. (Zhang et al p 800) Vitamin D is administered to improve bone mineral density, decrease the risk of falls fractures in people older people like Mr. Emery who is 65 years Ferrous Fumarate Mode of action of ferrous fumarate Fe3+ is used to supplement iron in the red blood cells, the iron is used to activate erythropoiesis at the pro-erythroblast stage and later in the red cell maturation cycle. The Fe3+ is then bound to transferrin and transported to the bone marrow where it is incorporated into hemoglobin. The adverse effects of ferrous fumarate are flushing, sweating, and chills, fever Chest, and back pain. Atenolol The mode of action of atenolol is a class of beta-blockers and works by relaxing blood vessels, slowing heart rate and decrease blood pressure to improve blood flow, Its adverse effects are dizziness, tiredness, lightheadedness, depression, drowsiness, nausea, diarrhea and the rare ones are shortness of breath, swelling of the hands, feet, ankles, or lower legs, unusual weight gain, fainting. (American Society of Health-System Pharmacists 2011) The disease from a GP’s nurse perspective there was a need to have had good communication between the general practitioner and the nephrologist. It will improve the Mr. Emery’s care the nurse could provide some of the local support such as monitoring his blood pressure and when changes need to be made should be discussed with the nephrologist. The nurse needs to educate Mr. Emery on the importance of maintaining a balance dietary intake, maintain a constant time interval of eating to keep blood glucose level constant, take regular exercise, and take his medication as prescribed by his doctor. Educate the patient no how to care for his foot and maintain proper skin hygiene. The nurse must keep in mind; the common causes of proteinuria that include orthostatic proteinuria, transient proteinuria that can occur during many illnesses are too screened and ruled out. It is important to monitor the blood pressure, sugar and the nurse should serve as a great resource to coordinate all of Mr. Emery care. Reference list Abbas K, Robert T, John R. S, (2008) Chronic Kidney Disease and Its Complications Prim Care Clin Office Pract 35, 329–344 American Diabetic Association(ADA) (2008) standards of medical care in diabetes. Diabetes Care 31(1), S12–54. American Society of Health-System (2011) Medication Information for consumers. Bethesda, Maryland. Callaghan B C, Little A A, Feldman E L, Hughes R A. (2012) Enhanced glucose control for preventing and treating diabetic neuropathy. Cochrane Database Syst Rev. European Medicines Agency. (2007) Epoetins and cardiovascular risks in patients with chronic kidney disease. London: EMEA; Available at: Jones, K.J. (2004). Nursing management hematologic problems. Medical-surgical nursing 705-75) José M L, Martínez-Salgado C, Ana B. Rodríguez-Peña, Francisco J L H. (2010) pathophysiological mechanisms of chronic kidney disease: Pharmacology & Therapeutics 128, 61–81 Peyerl F W, Joy M S, Karagiannis P C, (2007) Outcomes of hyperparathyroidism in chronic kidney disease. Management Care Pharm J 13, 397–411. Melamed ML, Astor B, Michos ED (2009) 25-hydroxyvitamin D levels, race, and the progression of kidney disease. J Am Soc Nephrol 20, 2631–2639. Penzer R (2003) Lymphoedema. Nursing Standard. 17, 35, 45-53. Perina G D (2003) Noncardiogenic pulmonary edema, Emerg Med Clin N Am 21, 385–393 Pfeffer M A, Chen C Y and Burdmann E A (2009) A trial of epoetin alfa in type 2 diabetes and chronic kidney disease. N Engl Med J 361, 2019–2032 Phrommintikul A, Elsik M, Haas SJ, Krum H. (2007) haemoglobin concentrations in anaemic patients with chronic kidney disease treated with erythropoietin. Lancet 369(9559), 381-8. Schmitt C. Pand O. Mehls, (2011) Mineral and bone disorders in children with chronic kidney disease, Nature Reviews Nephrology, 7(11), pp. 624–634. Segura J, Ruilope L M. (2009) should diuretics always be included as initial antihypertensive management in early-stage CKD? Curr Opin Nephrol Hypertens 18, 392–6. Wuhl E and F. Schaefer, (2010) Can we slow the progression of chronic kidney disease? Current Opinion in Pediatrics, 22(2), pp. 170–175 Zhang Y, Kong J, Deb D K. Vitamin D receptor attenuates renal fibrosis by suppressing the renin-angiotensin system. J Am Soc Nephrol 21, 966–973. 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