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CHRONIC RENAL FAILURE (END-STAGE RENAL DISEASE)
Chronic renal failure, or ESRD, is a progressive, irreversible de-terioration in renal function in which the body’s ability to main-tain metabolic and fluid and electrolyte balance fails, resulting in uremia or azotemia (retention of urea and other nitrogenous wastes in the blood).
The incidence of ESRD has increased by almost 8% per year for the past 5 years, with more than 300,000 patients being treated in the United States (USRDS, 2001).
ESRD may be caused by systemic diseases, such as diabetes mellitus (leading cause); hypertension; chronic glomerulonephri-tis; pyelonephritis; obstruction of the urinary tract; hereditary le-sions, as in polycystic kidney disease; vascular disorders; infections; medications; or toxic agents.
Autosomal dominant polycystic kidney disease accounts for 8% to 10% of cases of ESRD in the United States and Europe (Perrone, Ruthazer & Terrin, 2001). Comorbid conditions that develop during chronic renal insufficiency contribute to the high morbidity and mortality among patients with ESRD (Kausz et al., 2001).
Environmental and occupational agents that have been impli-cated in chronic renal failure include lead, cadmium, mercury, and chromium. Dialysis or kidney transplantation eventually be-comes necessary for patient survival. Dialysis is an effective means of correcting metabolic toxicities at any age, although the mor-tality rate in infants and young children is greater than adults in the presence of other, nonrenal diseases and in the presence of anuria or oliguria (Wood et al., 2001).
As renal function declines, the end products of protein metabo-lism (which are normally excreted in urine) accumulate in the blood. Uremia develops and adversely affects every system in the body. The greater the buildup of waste products, the more severe the symptoms. There are three well-recognized stages of chronic renal disease: reduced renal reserve, renal insufficiency, and ESRD (Chart 45-7).
The rate of decline in renal function and progression of chronic renal failure is related to the underlying disorder, the uri-nary excretion of protein, and the presence of hypertension. The disease tends to progress more rapidly in patients who excrete sig-nificant amounts of protein or have elevated blood pressure than in those without these conditions.
Because virtually every body system is affected by the uremia of chronic renal failure, patients exhibit a number of signs and symptoms. The severity of these signs and symptoms depends in part on the degree of renal impairment, other underlying condi-tions, and the patient’s age.
Hypertension (due to sodium and water retention or from activation of the renin–angiotensin–aldosterone system), heart failure and pulmonary edema (due to fluid overload), and peri-carditis (due to irritation of the pericardial lining by uremic toxins) are among the cardiovascular problems manifested in ESRD. Strict fluid volume control has been found to normalize hyper-tension in patients receiving peritoneal dialysis (Gunal, Duman, Ozkahya et al., 2001).
Cardiovascular disease is the predominant cause of death in patients with ESRD. In chronic hemodialysis patients, approxi-mately 45% of overall mortality is attributable to cardiac disease, and about 20% of these cardiac deaths are due to acute myocar-dial infarction (USRDS, 2001).
Severe itching (pruritus) is common. Uremic frost, the deposit of urea crystals on the skin, is uncommon today because of early and aggressive treatment of ESRD with dialysis.
GI signs and symptoms are common and include anorexia, nau-sea, vomiting, and hiccups. Neurologic changes, including al-tered levels of consciousness, inability to concentrate, muscle twitching, and seizures, have been observed. The precise mecha-nisms for many of these diverse signs and symptoms have not been identified. It is generally thought, however, that the accumu-lation of uremic waste products is the probable cause. Chart 45-8 summarizes the signs and symptoms often seen in chronic renal failure.
Decreased GFR can be detected by obtaining a 24-hour urinaly-sis for creatinine clearance. As glomerular filtration decreases (due to nonfunctioning glomeruli), the creatinine clearance value de-creases, whereas the serum creatinine and BUN levels increase. Serum creatinine is the more sensitive indicator of renal function because of its constant production in the body. The BUN is af-fected not only by renal disease but also by protein intake in the diet, catabolism (tissue and RBC breakdown), parenteral nutri-tion, and medications such as corticosteroids.
The kidney cannot concentrate or dilute the urine normally in ESRD. Appropriate responses by the kidney to changes in the daily intake of water and electrolytes, therefore, do not occur. Some pa-tients retain sodium and water, increasing the risk for edema, heart failure, and hypertension. Hypertension may also result from ac-tivation of the renin–angiotensin–aldosterone axis and the con-comitant increased aldosterone secretion. Other patients have a tendency to lose salt and run the risk of developing hypotension and hypovolemia. Episodes of vomiting and diarrhea may produce sodium and water depletion, which worsens the uremic state.
With advanced renal disease, metabolic acidosis occurs because the kidney cannot excrete increased loads of acid. Decreased acid secretion primarily results from inability of the kidney tubules to excrete ammonia (NH3−) and to reabsorb sodium bicarbonate (HCO3−). There is also decreased excretion of phosphates and other organic acids.
Anemia develops as a result of inadequate erythropoietin pro-duction, the shortened life span of RBCs, nutritional deficiencies, and the patient’s tendency to bleed, particularly from the GI tract. Erythropoietin, a substance normally produced by the kid-ney, stimulates bone marrow to produce RBCs. In renal failure, erythropoietin production decreases and profound anemia re-sults, producing fatigue, angina, and shortness of breath.
Another major abnormality seen in chronic renal failure is a dis-order in calcium and phosphorus metabolism. Serum calcium and phosphate levels have a reciprocal relationship in the body: as one rises, the other decreases. With decreased filtration through the glomerulus of the kidney, there is an increase in the serum phosphate level and a reciprocal or corresponding decrease in the serum calcium level. The decreased serum calcium level causes in-creased secretion of parathormone from the parathyroid glands. In renal failure, however, the body does not respond normally to the increased secretion of parathormone; as a result, calcium leaves the bone, often producing bone changes and bone disease. In addition, the active metabolite of vitamin D (1,25-dihydroxy-cholecalciferol) normally manufactured by the kidney decreases as renal failure progresses. Uremic bone disease, often called renal osteodystrophy, develops from the complex changes in calcium, phosphate, and parathormone balance (Barnas, Schmidt, Seidl et al., 2001).
Potential complications of chronic renal failure that concern the nurse and that necessitate a collaborative approach to care include the following:
· Hyperkalemia due to decreased excretion, metabolic acido-sis, catabolism, and excessive intake (diet, medications, fluids)
· Pericarditis, pericardial effusion, and pericardial tamponade due to retention of uremic waste products and inadequate dialysis
· Hypertension due to sodium and water retention and mal-function of the renin–angiotensin–aldosterone system
· Anemia due to decreased erythropoietin production, de-creased RBC life span, bleeding in the GI tract from irritat-ing toxins, and blood loss during hemodialysis
· Bone disease and metastatic calcifications due to retention of phosphorus, low serum calcium levels, abnormal vitamin D metabolism, and elevated aluminum levels
The goal of management is to maintain kidney function and homeostasis for as long as possible. All factors that contribute to ESRD and all factors that are reversible (eg, obstruction) are iden-tified and treated. Management is accomplished primarily with medications and diet therapy, although dialysis may also be needed to decrease the level of uremic waste products in the blood (Fink et al., 2001).
Complications can be prevented or delayed by administering pre-scribed antihypertensives, erythropoietin (Epogen), iron supple-ments, phosphate-binding agents, and calcium supplements.
Hyperphosphatemia and hypocalcemia are treatedwith aluminum-based antacids that bind dietary phosphorus in the GI tract. However, concerns about the potential long-term toxicity of aluminum and the association of high aluminum levels with neurologic symptoms and osteomalacia have led some physi-cians to prescribe calcium carbonate in place of high doses of aluminum-based antacids. This medication also binds dietary phosphorus in the intestinal tract and permits the use of smaller doses of antacids. Both calcium carbonate and phosphorus-binding antacids must be administered with food to be effective. Magnesium-based antacids must be avoided to prevent magnesium toxicity.
Hypertension ismanaged by intravascular volume control and a variety of anti-hypertensive agents. Heart failure and pulmonary edema may also require treatment with fluid restriction, low-sodium diets, diuretic agents, inotropic agents such as digitalis or dobutamine, and dialysis. The metabolic acidosis of chronic renal failure usu-ally produces no symptoms and requires no treatment; however, sodium bicarbonate supplements or dialysis may be needed to correct the acidosis if it causes symptoms (Tonelli et al., 2001).
Neurologic abnormalities may occur, so thepatient must be observed for early evidence of slight twitching, headache, delirium, or seizure activity. If seizures occur, the onset of the seizure is recorded along with the type, duration, and gen-eral effect on the patient. The physician is notified immediately. Intravenous diazepam (Valium) or phenytoin (Dilantin) is usu-ally administered to control seizures. The side rails of the bed should be padded to protect the patient.
Anemia associated with chronic renal failure istreated with recombinant human erythropoietin (Epogen). Ane-mic patients (hematocrit less than 30%) present with nonspecific symptoms, such as malaise, general fatigability, and decreased ac-tivity tolerance. Epogen therapy is initiated to achieve a hemat-ocrit of 33% to 38%, which generally alleviates the symptoms of anemia. Epogen is administered either intravenously or subcuta-neously three times a week. It may take 2 to 6 weeks for the hemat-ocrit to rise; therefore, Epogen is not indicated for patients who need immediate correction of severe anemia. Adverse effects seen with Epogen therapy include hypertension (especially during early stages of treatment), increased clotting of vascular access sites, seizures, and depletion of body iron stores (Fink et al., 2001).
The patient receiving Epogen may experience influenza-like symptoms with initiation of therapy; these tend to subside with repeated doses. Management involves adjustment of heparin to prevent clotting of the dialysis lines during hemodialysis treat-ments, frequent monitoring of hematocrit, and periodic assess-ment of serum iron and transferrin levels. Because adequate stores of iron are necessary for an adequate response to erythropoietin, supplementary iron may be prescribed. In addition, the patient’s blood pressure and serum potassium level are monitored to detect hypertension and rising serum potassium levels, which may occur with therapy and the increasing RBC mass. The occurrence of hy-pertension requires initiation or adjustment of the patient’s anti-hypertensive therapy. Hypertension that cannot be controlled is a contraindication to recombinant erythropoietin therapy.
Patients who have received Epogen have reported decreased levels of fatigue, an increased feeling of well-being, better tolerance of dialysis, higher energy levels, and improved exercise tolerance. Additionally, this therapy has decreased the need for transfusion and its associated risks, including bloodborne infectious disease, antibody formation, and iron overload (Fink et al., 2001).
Dietary intervention is necessary with deterioration of renal func-tion and includes careful regulation of protein intake, fluid intake to balance fluid losses, sodium intake to balance sodium losses, and some restriction of potassium. At the same time, adequate caloric intake and vitamin supplementation must be ensured. Pro-tein is restricted because urea, uric acid, and organic acids—the breakdown products of dietary and tissue proteins—accumulate rapidly in the blood when there is impaired renal clearance. The allowed protein must be of high biologic value (dairy prod-ucts, eggs, meats). High-biologic-value proteins are those that are complete proteins and supply the essential amino acids necessary for growth and cell repair.
Usually, the fluid allowance is 500 to 600 mL more than the previous day’s 24-hour urine output. Calories are supplied by car-bohydrates and fat to prevent wasting. Vitamin supplementation is necessary because a protein-restricted diet does not provide the necessary complement of vitamins. Additionally, the patient on dialysis may lose water-soluble vitamins from the blood during the dialysis treatment.
Hyperkalemia is usually prevented by ensuring adequate dialysis treatments with potassium removal and careful monitoring of all medications, both oral and intravenous, for their potassium con-tent. The patient is placed on a potassium-restricted diet. Occa-sionally, Kayexalate, a cation-exchange resin, administered orally, may be needed. The patient with increasing symptoms of chronic renal failure is referred to a dialysis and transplantation center early in the course of progressive renal disease. Dialysis is usually initiated when the patient cannot maintain a reasonable lifestyle with conservative treatment.
The patient with chronic renal failure requires astute nursing care to avoid the complications of reduced renal function and the stresses and anxieties of dealing with a life-threatening illness. Ex-amples of potential nursing diagnoses for these patients include the following:
· Excess fluid volume related to decreased urine output, dietary excesses, and retention of sodium and water
· Imbalanced nutrition: less than body requirements related to anorexia, nausea and vomiting, dietary restrictions, and altered oral mucous membranes
· Deficient knowledge regarding condition and treatment regimen
· Activity intolerance related to fatigue, anemia, retention of waste products, and dialysis procedure
· Low self-esteem related to dependency, role changes, changes in body image, and sexual dysfunction
Nursing care is directed toward assessing fluid status and iden-tifying potential sources of imbalance, implementing a dietary program to ensure proper nutritional intake within the limits of the treatment regimen, and promoting positive feelings by en-couraging increased self-care and greater independence. It is ex-tremely important to provide explanations and information to the patient and family concerning ESRD, treatment options, and potential complications. A great deal of emotional support is needed by the patient and family because of the numerous changes experienced. Specific interventions, along with rationale and evaluation criteria, are presented in more detail in the Plan of Nursing Care.
The nurse plays an extremely im-portant role in teaching the patient with ESRD. Because of the extensive teaching needed, the home care nurse, dialysis nurse, and nurse in the outpatient setting all provide ongoing education and reinforcement while monitoring the patient’s progress and compliance with the treatment regimen.
A nutritional referral and explanations of nutritional needs are helpful because of the numerous dietary changes required. The patient is taught how to check the vascular access device for pa-tency and how to take precautions, such as avoiding venipunc-tures and blood pressure measurements on the arm with the access device.
Additionally, the patient and family require considerable as-sistance and support in dealing with the need for dialysis and its long-term implications. For instance, they need to know what problems to report to the health care provider, including the following:
· Worsening signs and symptoms of renal failure (nausea, vomiting, change in usual urine output [if any], ammonia odor on breath)
· Signs and symptoms of hyperkalemia (muscle weakness, diarrhea, abdominal cramps)
· Signs and symptoms of access problems (clotted fistula or graft, infection)
These signs and symptoms of decreasing renal function, in ad-dition to increasing BUN and serum creatinine levels, may indi-cate a need to alter the dialysis prescription. The dialysis nurses also provide ongoing education and support at each treatment visit.
The importance of follow-up examinationsand treatment is stressed to the patient and family because of changing physical status, renal function, and dialysis require-ments. Referral for home care provides the home care nurse with the opportunity to assess the patient’s environment, emotional status, and the coping strategies used by the patient and family to deal with the changes in family roles often associated with chronic illness.
The home care nurse also assesses the patient for further dete-rioration of renal function and signs and symptoms of complica-tions resulting from the primary renal disorder, the resulting renal failure, and effects of treatment strategies (eg, dialysis, medica-tions, dietary restrictions). Many patients need ongoing education and reinforcement on the multiple dietary restrictions required, including fluid, sodium, potassium, and protein restriction. Reminders about the need for health promotion activities and health screening are an important part of nursing care for the patient with renal failure.
Changes in kidney function with normal aging increase the sus-ceptibility of elderly patients to kidney dysfunction and renal fail-ure. Because alterations in renal blood flow, glomerular filtration, and renal clearance increase the risk for medication-associated changes in renal function, precautions are indicated with all medications.
This is because of the frequent use of multiple-prescription and over-the-counter medications by elderly patients. The incidence of systemic diseases, such as atherosclerosis, hyper-tension, heart failure, diabetes, and cancer, increases with advanc-ing age, predisposing older adults to renal disease associated with these disorders. Therefore, nurses in all settings need to be alert for signs and symptoms of renal dysfunction in elderly patients.
With age, the kidney is less able to respond to acute fluid and electrolyte changes. Therefore, acute problems need to be pre-vented if possible or recognized and treated quickly to avoid kid-ney damage. When the elderly patient must undergo extensive diagnostic tests, or when new medications (eg, diuretic agents) are added, precautions must be taken to prevent dehydration, which can compromise marginal renal function and lead to ARF.
The elderly patient may develop atypical and nonspecific signs and symptoms of disturbed renal function and fluid and elec-trolyte imbalances. Recognition of these problems is further ham-pered by their association with preexisting disorders and the misconception that they are normal changes of aging.
The incidence of ARF is increasing in older, hospitalized patients. About half of patients who develop ARF during hospitalization for a medical or surgical problem are older than 60 years of age. Evidence also demonstrates that ARF is often seen in the com-munity setting. Nurses in the ambulatory setting need to be cog-nizant of the risk for ARF in their elderly patients, especially those undergoing diagnostic testing or procedures that can result in de-hydration. The mortality rate is slightly higher for ARF in elderly patients than for their younger counterparts.
The etiology of ARF in older adults includes prerenal causes, such as dehydration, and intrarenal causes, such as nephrotoxic agents (medications, contrast agents). Diabetes mellitus increases the risk for contrast agent-induced renal failure because of pre-existing renal insufficiency and the imposed fluid restriction needed for many tests. Suppression of thirst, enforced bed rest, lack of drinking water, and confusion all contribute to the older patient’s failure to consume adequate fluids and may lead to dehydration and compromise of already decreased renal function.
Historically, the age of patients developing ESRD steadily rose each year, but it appears to have stabilized since 1993 at a mean age of 60 years. In the past, rapidly progressive glomerulonephri-tis, membranous glomerulonephritis, and nephrosclerosis were the most common causes of chronic renal failure in the elderly. Today, however, diabetes mellitus and hypertension are the lead-ing causes of chronic renal failure in the elderly (Bakris et al., 2000). Other common causes of chronic renal failure in the el-derly population are interstitial nephritis and urinary tract ob-struction. The signs and symptoms of renal disease in the elderly are commonly nonspecific. The occurrence of symptoms of other disorders (heart failure, dementia) can mask the symptoms of renal disease and delay or prevent diagnosis and treatment. The patient often develops signs and symptoms of nephrotic syn-drome, such as edema and proteinuria.
Hemodialysis and peritoneal dialysis have been used effec-tively in treating elderly patients (Carey et al., 2001). Although there is no specific age limitation for renal transplantation, con-comitant disorders (ie, coronary artery disease, peripheral vascu-lar disease) have made it a less common treatment for the elderly.
The outcome, however, is comparable to that of younger pa-tients. Some elderly patients elect not to participate in these treatment strategies. Conservative management, including nutri-tional therapy, fluid control, and medications, such as phosphate binders, may be considered in patients who are not suitable for or elect not to participate in dialysis or transplantation.
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