Practice nursing care for Clients
with Renal Disorders
Renal problems: infectious disorders
The urinary system is normally one in which a sterile body fluid (urine) is excreted. The unobstructed and complete passage of urine from the renal and urinary systems is critical to the sterility of the urinary tract. When a structural abnormality (either congenital or acquired) is present, the potential for degenerative changes from infection is dramatically increased. Urinary tract infection (UTI) usually refers to infections in this sterile system. Pyelonephritis is a bacterial infection within the kidney and renal pelvis—theupper urinary tract. Infections within the lower urinary tract are described in Chapter.
With improved diagnostic techniques and a better understanding of the inflammatory response, pyelonephritis has come to refer to active microorganisms or the effects of kidney infections. Acute pyelonephritis is the condition resulting from an active bacterial infection, whereas chronic pyelonephritis results from repeated or continued upper urinary tract infections or infectious sequelae. Chronic pyelonephritis is usually associated with an anatomic urinary tract anomaly, urinary obstruction or, most commonly,vesi-coureteral reflux. The vesicoureteral junction is the point at which the ureter joins the bladder. Reflux refers to the reverse (e.g., backward, upward, ascending) flow of urine toward the renal pelvis and kidney.
In pyelonephritis, microorganisms usually ascend from the lower urinary tract into the renal pelvis. Infection from organisms carried in the blood (hematogenous) may occur, but mey occur with much less frequency. Bacteria activate the in-matoryresponse, and local edema results.
Acute pyelonephritis involves acute interstitial inflammation, tubular cell necrosis, and a tendency for abscess formation. Abscesses, pockets of localized infection, can appear in the capsule, cortex, or medulla. The pattern of infection within the kidney is not uniform; normal tissue and tubules can lie next to infected areas. Fibrosis or scar tissue develops as the inflammatory process subsides. The calices become blunted, and scars develop in the interstitial tissue.
Vesicoureteral and intrarenal reflux of infected urine are the major mechanisms responsible for chronic pyelonephritis. Some papillae in the kidney do not close with increased in-tracaliceal pressure, causing intrarenal reflux. Refluxing papillae are most often located in the upper and lower poles of the kidney and therefore are more susceptible to chronic pyelonephritis. Inflammation, fibrosis, and deformity of the renal pelvis and calices are evident. Repeated or continuous infectious produce additional scar tissue. Vascular, glomeru-lar, and tubular changes within the scars can occur. Filtration, reabsorption, and secretion are eventually impaired, and renal function is diminished (Figure 71-3).
Single episodes of acute pyelonephritis may result from the entry of bacteria associated with pregnancy, obstruction, or reflux.Chronic pyelonephritis is usually associated with structural abnormalities and/or obstruction with reflux. Vesicoureteral reflux or obstruction leading to chronic pyelonephritis is often due to stones, obstruction, or neurogenic impairment involving the voiding mechanism. Reflux is more common in children, who as adults often have scarring associated with chronic pyelonephritis. Clients who develop chronic pyelonephritis without having reflux as a child are usually adults with a history of spinal cord injury, bladder tumor, prostatic hypertrophy, or urinary tract stones.
Acute or chronic pyelonephritis is more likely to occur in clients who have undergone manipulation of the urinary tract (e.g., placement of a urinary catheter), those who have diabetes mellitus or chronic renal calculi, or those who overuse analgesics. In clients with diabetes mellitus, the development and progression of bladder atony increase the tendency to develop pyelonephritis. In clients with chronic stone disease, j calculi provide a site for ongoing infection and resultant renal scarring. Nonsteroidal anti-inflammatory drug (NSAID) use has been associated with papillary necrosis, which then per- \ mits reflux.
The most common pyelonephritis-causing organism is Escherichia coli. Enterococcus faecalis is typical in hospitalized clients. Both are organisms of the gastrointestinal tract. Non-£. coli organisms such as Proteus mirabilis, Klebsiella and Pseudomonasaeruginosa and the more antibiotic-resistant organisms are also causes of pyelonephritis in hospitalized clients. When the infection is bloodborne, common infecting organisms include Staphylococcus aureus and the Candida and Salmonella species.
Theories of noninfectious or idiopathic causes of intrarenal scarring and the eventual outcome of pyelonephritis include an antibody reaction, cell-mediated immunity against the bacterial antigens, or an autoimmune reaction.
The exact incidence and prevalence of pyelonephritis are not known; this diagnosis is not separately reported from all urinary tract infections. Acute urinary conditions of the kidneys or urinary tract, nephritic syndrome, urethral stricture, and cystitis account for more than 7 million new cases annually in noninstutionalized Americans (NIDDK National Kidney and Urologic Diseases Information Clearinghouse, 1999). Women overall have more cases of pyelonephritis. After age 65, rates for men increase greatly because of the increased incidence of prostatitis.
The nurse asks about a history of urinary tract infections (UTIs), diabetes mellitus, stone disease, and other structural or functional abnormalities of the genitourinary tract. The nurse attempts to determine whether the UTIs were associated with pregnancy and asks the client about any previous experiences with pyelonephritis or similar symptoms. Recurrences are common and may lead to a deterioration of renal function.
PHYSICAL ASSESSMENT/CLINICAL MAN IFESTATIONS
The nurse asks the client about specific symptoms associated with acute pyelonephritis. Chronic pyelonephritis has a less dramatic clinical presentation; signs and symptoms are usually related to the infection or renal function. The nurse asks the client to describe any vague or nonspecific urinary. The nurse advises the client to complete all prescribed antibiotic regimens and instructs the client to report any side effects or unusual symptoms to the prescribing health team member rather than suspend the regimen. The client and family are referred for nutritional counseling as needed, because many clients have special nutritional requirements, such as those caused by diabetes mellitus or pregnancy.
HOME CARE MANAGEMENT
If no surgery is performed, the client may need assistance with self-care, nutrition, and medication administration at home. If surgical intervention is necessary, the client may require help with incision care, self-care, and transportation for follow-up medical appointments.
HEALTH CARE RESOURCES
The client may also briefly need a community health nurse to help administer medications or nutrition at home. Housekeeping services may also be helpful while the client is regaining strength.
• Evaluation: Outcomes
The nurse evaluates the care of the client with pyelonephritis on the basis of the identified nursing diagnoses and collaborative problems. Expected outcomes may include that the client will:
• Demonstrate methods of enhancing comfort
• Report that pain is controlled
• Express satisfaction with pain control
• Describe the role of antibiotics and self-administration of medications
• Explain and offer techniques to ensure adequate nutrition and hydration
• Describe the plan for posttreatment follow-up, including knowledge of recurrent symptoms
• Modify the prescribed regimen as directed by a health care professional
CRITICAL THINKING CHALLENGE
Your client is prescribed IV ciprofloxacin (Cipro) for pyelonephritis. She is also prescribed 25 mg meperidine every 3 hours prnfor her pain. Radiographic studies are deferred at this time because of her pregnancy. A urine culture indicates that the infecting organism is £ coli, and the sensitivity of the bacteria to ciprofloxacin is confirmed. After 3 days her pain is absent, her fever is resolved, and her urinary symptoms are clearing. She is to be discharged today and is to continue taking her antibiotic orally at home. A follow-up medical visit is scheduled in 7 days.
• What discharge planning and health care teaching are indicated at this time?
An abscess is a collection of fluid and cells caused by an inflammatory response to bacteria. An abscess may occur within the renal parenchyma (renal abscess), in the renal and Gerota's fascia (perinephric abscess), or in the flank. An abscess is suspected when fever and symptoms are not relieved promptly by antibiotic therapy.
A renal or perirenal abscess is readily diagnosed via sonogra-phy or a computed tomography (CT) scan. Arteriography andradionuclide scintillation methods (e.g., gallium scan) also may be useful for diagnosis. Symptoms of renal abscess include fever, flank pain, and general malaise. Local fl edema and erythema may be observed.
Drainage by surgical incision or needle aspiration is often necessary. Appropriate broad-spectrum antibiotics are "also prescribed.
The genitourinary tract is the most common extrapulmonary site of tuberculosis. Approximately 10% of new cases of tuberculosis are extrapulmonary (Tolkoff-Rubin, Cotran, & Rubin, 2000). Tuberculosis of the kidney is sometimes called granulomatousnephritis. After Mycobacterium tuberculosis invades the kidneys, usually by a bloodborne route, an inflammatory response is activated and forms scar tissue (granuloma) that replaces normal kidney tissue.
Clients may experience urinary frequency, dysuria, hematuria and/or proteinuria, flank pain or renal colic secondary to the passage of clots or stones, pyuria, and hypertension. Skin test (e.g., purified protein derivative [PPD]) or chest x-ray film evidence of tuberculosis may or may not be present.
Clients with current or previous pulmonary tuberculosis who show signs of unexplained fever, hematuria, and sterile pyuria are at high risk for renal tuberculosis. The diagnosis is made through a urine culture of three clean-catch, first-morning specimens. Other genitourinary sites for tuberculosis include the prostate, epididymis, ureters, testes, bladder, and seminal vesicles.
Antitubercular therapy is the primary treatment. Recommendations include a 2-month course of rifampin, isoniazid, andpyrazinamide followed by 4 months of rifampin and isoniazid. Three to six more months of rifampin and isoniazid may be recommended for men who may be harboring the organism in the prostate (Tolkoff-Rubin, Cotran, & Rubin, 2000).
Complications include the loss of renal function, nephro-lithiasis, obstructive uropathy, and bacterial superinfection of the urinary tract. Surgical excision of diseased tissue may be indicated to preserve renal function.
Renal disorders interfere with the ability of the kidney to filter wastes and to balance fluid and solutes. The kidneys work in an integrated way with so many other organ systems; therefore a renal disorder can significantly affect systemic health and lead to life-threatening outcomes. Renal disorders can be categorized as congenital, obstructive, infectious, glomerular, and degenerative. Renal tumors and renal trauma are also described in this chapter.
Polycystic Kidney Disease
Polycystic kidney disease (PKD) is one of the most common inherited disorders and affects 250,000 to 500,000 people in theUnited States. It can be inherited as either an autosomal dominant trait or, less commonly, as an autosomal recessive trait. People who inherit the recessive form of PKD usually die in early childhood. The 5% to 10% incidence of PKD in clients with no family history occurs as a result of a spontaneous genetic mutation. PKD is more common in Caucasians than in people of other races.
Fluid-filled cysts in the epithelial cells of the nephron characterize PKD. In the dominant form only 5% to 10% of nephronsmay be involved until the fourth decade of life, whereas in the autosomal recessive form nearly 100% of nephrons are involved at birth. Cysts develop as a result of kidney cell proliferation, altered secretion, and abnormal cell matrix biology (Avner, et al., 1999; Calvet& Grantham, 2001).
Cysts can develop anywhere in the nephron. Over time, small cysts become progressively larger (up to a few centimeters in diameter) and more widely distributed; the glomerular and tubular membranes are damaged. As the cysts become filled with fluid, thenephron functions of filtration, reabsorp-tion, and secretion become less effective.
The kidney tissue is eventually replaced by nonfunctioning cysts, which look like a cluster of grapes (Figure). The kidneys are grossly enlarged; each cystic kidney may enlarge to two or three times its normal size, becoming as large as a football. Other abdominal organs are displaced, and the client has considerable discomfort. The fluid-filled cysts are also prone to infection, rapture, and bleeding.
More than 60% of clients with PKD have high blood pressure. The cause of hypertension in this disorder is thought to be related to renal ischemia from the enlarging cysts. As the vessels are compressed and renal blood flow decreases, the renin-angiotensinsystem is activated, raising blood pressure. Control of hypertension is a top priority because proper treatment can interrupt the vasoconstriction that leads to renal ischemia.
Cysts may also occur in other tissues, such as the liver, blood vessels of the brain, and cardiac blood vessels. Cysts may alter liver function or result in spontaneous rapture of vascular cysts (berry aneurysms) in the brain, causing sudden death. For reasons as yet unknown, kidney stones occur in 8% to 36% of the clients with PKD. Heart valve abnormalities (e.g., mitral valve prolapse), left ventricular hypertrophy, and colonic diverticuli also are more prevalent in clients with PKD.
PKD has at least two inherited forms. Men and women have an equal chance of inheriting the disease because the gene responsible for PKD is not located on the sex chromosomes. The offspring of parents who have PKD have a 50% probability of inheriting the gene that causes the autosomal dominant form of the disease.
Manifestations of autosomal dominant polycystic kidney disease (ADPKD) usually do not appear until the fourth decade of life. Half of the affected people develop renal failure by age 50 years. ADPKD-1 is the most severe form both in disease progression and in mortality. ADPKD-2 involves a slower rate of cystic formation and growth, resulting in a delayed progression to renal failure and other complications.
At present, there is no way to prevent PKD, although early detection and management of hypertension may slow the progression of renal impairment. Genetic counseling and evaluation may be useful for adults who have one parent or both parents with PKD. For those whose clinical symptoms do not appear until after the childbearing years, offspring can be included in genetic counseling sessions.
nurse explores the family history of a client with suspected or actual PKD and asks whether either parent was known to have PKD or whether there is any family history of kidney disease.
The age at which signs and symptoms developed in the parent and any related complications may have prognostic
significance. The client is asked about constipation, abdominal discomfort, a change in urine color or frequency, high blood
pressure, headaches, and a family history of sudden death from a stroke.
PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS
Chart 71-1 lists key features of PKD. Pain is the presenting symptom in 20% to 30% of clients and islioted in at least 60%. The nurse inspects the abdomen. A protruding and distended abdomen is common as the cystic kidneys swell and push the abdominal contents forward. Polycystic kidneys are easily palpated because of their increased size. The nurse proceeds with gentle abdominal palpation because the cystic kidneys and nearby tissues may be tender, and palpation is uncomfortable.
The client also may have flank pain as a dull ache or as sharp and intermittent discomfort. Dull and aching pain is caused by increased kidney size with distention or from infection within the cyst. Sharp, intermittent pain occurs in response to a ruptured cyst or the presence of a stone. When a cyst ruptures, the client may notice bright red or cola-colored urine. The nurse suspects infection if the urine is cloudy or foul smelling or if there is dysuria (pain on urination).
Nocturia (the need to urinate excessively at night) may be an early disease sign and occurs because of decreased renal concentrating ability. As renal function further declines, the client experiences increasing hypertension, edema, and ure-micsymptoms such as anorexia, nausea, vomiting, pruritus, and fatigue. Because berry aneurysms often occur in clients with PKD, a severe headache with or without neurologic or vision alterations deserves particular attention.
As an inherited disorder, PKD may cause complex psychoso-cial responses. The client often has had direct experience with the effects and consequences of the disease in other close family members. He or she may have had a parent who died or other close relatives who required dialysis or transplantation. While obtaining the family history, the nurse listens carefully for spoken and unspoken feelings of anger, resentment, hostility, futility, sadness, or anxiety; such feelings may need further exploration. The focus may be one or both parents or the process of diagnosis and treatment. Feelings of guilt and concern for the client's own children may further complicate the adjustment.
Urinalysis usually reveals proteinuria (protein in the urine) once the glomerali are involved. Hematuria may be gross ormicroscopic. Bacteria in the urine suggest an infection, usually in the cysts. A urine sample for culture and sensitivity testing is obtained when there is clinical or laboratory evidence of infection. As kidney function deteriorates, serum creatinine and blood urea nitrogen (BUN) levels rise. With worsening kidney function, the 24-hour creatinine clearance decreases. Renal handling of sodium may cause either sodium losses or sodium retention.
Diagnostic studies include renal sonography, computed tomography (CT), and magnetic resonance imaging (MRI).
Small cysts are detectable by sonography, CT, or MRI. Renal sonography provides diagnostic evidence of PKD, with minimal risk in most cases.
Common nursing diagnoses for the client with polycystic kidney disease (PKD) include Acute Pain, Chronic Pain, and Constipation. Common collaborative problems include Potential for Infection, Hypertension, Stone Formation, or Renal Failure. Chart 71-2 lists some NIC interventions for clients with renal disorders. (See Chapter 70 for information on renal infections and stone formation. See Chapter 72 for care of the client with renal failure.)
PAIN MANAGEMENT; ANALGESIC ADMINISTRATION.
Comfort strategies include pharmacologic, physical, and inte-grative approaches. A combination may be most effective. Non-steroidal anti-inflammatory agents (NSAIDs) are used cautiously because of their tendency to adversely affect renal function. Aspirin-containing compounds are avoided to prevent an increased potential for bleeding.
If cyst infection is the cause of discomfort, the physician orders a lipid-soluble antibiotic such as trimethoprim/ sulfamethoxazole(Bactrim, Septra, Trimpex) or ciprofloxacin (Cipro), which penetrate the cyst wall. Monitoring serum cre-atinine levels is necessary because antibiotic therapy can be nephrotoxic. Applying dry heat to the abdomen or flank may promote comfort when renal cysts are infected. When pain is severe or debilitating, cysts can be decompressed with percutaneous needle aspiration and drainage.
The nurse teaches the client methods of enhancing relaxation and promoting comfort via deep breathing, guided imagery, or other relaxation strategies. The overall goal is client self-management.
BOWEL MANAGEMENT. The nurse also teaches the client how to prevent constipation. The teaching plan covers adequate fluid intake, the role of increased dietary fiber when fluid intake is more than 2500 mL/24 hr, and the need for regular exercise to achieve regular bowel elimination. The nurse explains that pressure on the large intestine may further impede peristalsis as the polycystic kidneys increase in size. Consequently, the client should know that these recommendations for bowel management might change, particularly if renal failure also develops. The nurse also advises about the appropriate use of stool softeners and bulk agents, including the careful use of laxatives, to prevent complications related to chronic constipation.
HYPERTENSION AND RENAL FAILURE
PROCESS; TEACHING: PRESCRIBED MEDICATION. Blood pressure control is necessary to minimize cardiovascular
complications and slow the progression of renal dysfunction. Nursing
interventions include education to promote
self-management and understanding (see Chapter 36
for more information on hypertension). When renal impairment is evident through
a decreased concentrating ability (e.g., nocturia, low urine specific gravity), the nurse
encourages the client to drink at least
Medications for blood pressure control include antihyper-tensive agents and diuretics. Antihypertensive agents include angiotensin-converting enzyme (ACE) inhibitors, calcium channel blockers, beta blockers, and vasodilators (see Chart 36-2). ACE inhibitors show promise in controlling the epithelial-proliferative aspects of PKD and in reducing mi-croalbuminuria (Torra, 1999). If PKD progresses to chronic renal failure or end-stage renal disease, treatment approaches are similar to those in Chapter 72.
The nurse teaches the client, family, or significant other how to measure and record blood pressure. The nurse also helps the client establish a schedule for self-administering medications, monitoring daily weights, and keeping blood pressure records (Chart 71-3). The potential side effects of the medications are explained. The nurse makes written materials, such as medication teaching cards and booklets, available.
A low-sodium diet is often prescribed to control the hypertension that usually accompanies PKD. However, some clients may experience salt wasting and do not require a sodium-restricted diet. As the disease progresses, the physician may limit the client's protein intake to slow the development of renal failure. The nurse assists the client, family, or significant other in understanding the recommended diet plan and clarifies its rationale. The nurse works closely with the dietitian to foster the client's understanding. The nurse may also initiate a referral for nutritional counseling.
Health Care Resources
The Polycystic Kidney Research Foundation conducts research and provides education about PKD. Many publications are available on request; there is a fee for some materials. Chapters of the National Kidney Foundation (NKF) and the American Association of Kidney Patients (AAKP) may also provide resources for client information and support.
Hydronephrosis, Hydroureter, and Urethral Stricture
Hydronephrosis and hydroureter are disorders usually associated with the obstruction of urine outflow. Urethral strictures also obstruct outflow. Prompt recognition and treatment are crucial to prevent permanent renal damage.
In hydronephrosis, the kidney becomes enlarged as urine accumulates in the pelvis and kidney tissue. Because the capacity of the renal pelvis is normally 5 to 8 mL, obstructions within it or at the ureteropelvic junction (UPJ) quickly result in renal pelvic distention. Kidney medullary pressure increases as the volume of urine increases. Over time, sometimes in only a matter of hours, the blood vessels and renal tubules can be damaged extensively.
In clients with hydroureter, the pathophysiologic effects are similar but the obstruction is lower in the urinary tract. The ureter is most likely to become obstructed where the iliac vessels cross or at the ureterovesical entry. Dilation of the ureter above the point of obstruction results in enlargement as urine continues to accumulate.
In a client with a urethral stricture, the obstruction is very low in the urinary tract; this causes bladder distention to occur beforehydroureter and hydronephrosis. The problems and kidney damage are similar without prompt treatment.
A urinary obstruction can cause structural damage when pressure builds up directly on tissue. Tubular filtrate pressure also increases within the nephron as drainage through the collecting system is impaired. With this added pressure, glomeru-lar filtration decreases or ceases, and renal failure results. Nitrogenous waste products (urea, creatinine, and uric acid) and electrolytes (sodium, potassium, chloride, and phosphorus) are retained in the serum, and renal regulation of acid-base balance is impaired.
Disorders that can cause hydronephrosis or hydroureter include tumors, stones, trauma, congenital structural defects, and retroperitoneal fibrosis. Early treatment of the causes can prevent hydronephrosis and hydroureter and thus prevent permanent renal damage. The specific time needed to prevent permanent damage varies and depends on the client's underlying renal status. Permanent damage may occur in less than 48 hours in some clients and after several weeks in other clients.
The nurse obtains a history from the client, focusing on known renal or urologic disorders. A history of childhood urinary tract problems may signal the presence of previously unidentified structural defects. The nurse inquires about the client's pattern of urination, especially its amount, frequency, color, clarity, and odor. The client is asked about recent flank or abdominal pain. Chills, fever, and malaise may be present with a urinary tract infection (UTI).
The nurse inspects each flank to identify asymmetry, which may occur with a renal mass, and gently palpates the client's abdomen to identify any areas of tenderness. The urinary bladder is also palpated and percussed to detect distention. Gentle pressure on the abdomen may cause urine leakage, which reflects a full urinary bladder and possible obstruction of the bladder/urethral junction.
Urinalysis may show bacteria or white blood cells if infection is present. When urinary tract obstruction is prolonged, microscopic examination may reveal tubular epithelial cells. The chemical analysis of serum is normal unless decreased glomerularfiltration has occurred; serum creatinine and blood urea nitrogen (BUN) levels increase with a decreased glomerular filtration rate (GFR). Serum electrolyte levels may also be altered and indicate hyperkalemia, hyperphosphatemia, hypocalcemia, and metabolic acidosis (bicarbonate deficit).
Intravenous urography reveals ureteral or renal pelvis dilation. Urinary outflow obstruction may be revealed by sonog-raphy (renalechography) or computed tomography (CT).
FLUID MONITORING; URINARY RETENTION CARE; INFECTION PROTECTION. Urinary retention and potentialfor infection are the primary problems. Failure to treat the cause of urinary obstruction may lead to infection and renal failure. Surgery is usually required to remove or reduce the cause of the obstruction.
Degenerative disorders that cause changes in renal function are usually associated with the damage or effects caused by amultisystem disorder. Many of these degenerative disorders result from changes in kidney blood vessels.
Nephrosclerosis is a problem of changes in the nephron blood vessels. Vessel walls thicken, and the vessel lumen narrows. As a result, renal blood flow is decreased and kidney tissue is chronically hypoxic. Ischemia and fibrosis develop over time.
Nephrosclerosis is associated with all types of hypertension, atherosclerosis, and a history of diabetes mellitus. The more severe the hypertension, the greater the risk for extensive kidney damage. Nephrosclerosis is rarely seen when blood pressure is consistently below 160/110 mm Hg. The changes associated with hypertension may be reversible or within may progress to end-stage renal disease (ESRD) months or years.
Hypertension is the second leading cause of ESRD. Approximately 30% of clients requiring lifesaving renal replacement therapy (e.g., dialysis or transplantation) have hypertension as the cause of their renal failure (NIDDK).
Hypertension is more common in African Americans, and the risks of ESRD from hypertension are also greater for African Americans (Bakris et al., 2000). Between the ages of 25 and 45 years, the ratio of African Americans to Caucasians at risk for ESRD from hypertension is nearly 20:1 (Richardson & Piepho, 2000). These findings do not suggest that ESRD fromnephrosclerosis does not occur in Caucasians but rather that affected Caucasians are likely to be older.
Treatment aims to control high blood pressure and preserve renal function. Although many antihypertensive drags may lower blood pressure, the client's response is important in ensuring long-term adherence to the prescribed therapy. Factors promoting adherence include regimen simplicity (e.g., once-a-day dosing), low cost, and minimal side effects. Lack of basic knowledge or misinformation about hypertension poses additional challenges to nurses and all health care providers working with hypertensive clients. When evidence of renal disease occurs, adherence to therapy is even more important for preserving health.
Many medications can control high blood pressure (see Chart 36-2); more than one agent may be necessary. Angiotensin-converting enzyme (ACE) inhibitors are particularly useful in reducing hypertension and preserving renal function. Diuretics can maintain fluid and electrolyte balance in the presence of renal insufficiency. Caution is required to prevent hyperkalemia when potassium-sparing diuretics (e.g., triamterene or spironolactone) or combination agents containing a potassium-sparing diuretic are used for clients with known renal disease.
Pathologic processes affecting the renal arteries may result in severe lumen narrowing and drastically reduced blood flow to the renal parenchyma. Uncorrected renovascular disease, such as renal artery stenosis or thrombosis, causes ischemia and atrophy of renal tissue.
Renovascular disease is suspected with a sudden onset of hypertension, particularly in clients older than 50 years. Clients with high blood pressure but with a negative family history for hypertension may also be considered potential candidates for renal arterystenosis (RAS).
RAS from atherosclerosis or fibromuscular hyperplasia (increased amount of tissue) is the primary cause of renovascular disease. Other causes include thrombosis and renal aneurysms.
Atherosclerotic changes in the renal artery are often associated with sclerosis in the aorta and other major vessels. Changes in the renal artery are close to where the renal artery and aorta meet. Fibrotic changes of the vessel wall occur throughout the length of the renal artery.
Key features of renovascular disease are listed in Chart 71-8. The onset of hypertension is usually after age 40 to 50 years, and the family history is often negative for hypertension. Diagnosis is made by renal arteriography; measurement of renal vein renin levels provides additional evidence but may not be confirmatory. A renal arteriogram visualizes the renal vascu-lature and offers critical information for invasive treatment. The comparison of renal vein renin levels may reveal which kidney is producing more renin.
Visualization of the type of defect, extent of narrowing, and surrounding vasculature is critical to decide treatment intervention. The client's overall condition and the size of the atrophied kidney further influence decisions about intervention. RAS may be treated by drugs to control high blood pressure and by percutaneous transluminal balloon angioplasty or by surgical bypass procedures to restore the renal blood supply. Drugs may control high blood pressure but may not lead to long-term preservation of kidney function. In young and middle-aged adults, a lifetime of treatment with multiple agents for high blood pressure may make treatment difficult and the outcomes uncertain.
KEY FEATURES of Renovascular Disease
· Significant, difficult to control btood pressure
· Elevated serum creatinine
· Decreased creatinine clearance
Balloon angioplasty is considered less risky and requires much less time for recovery than does renal artery bypass surgery (see Chapter 36). Renal artery bypass surgery is a major procedure and involves at least 2 months for convalescence. A bypass may be performed for either one or both renal arteries. The surgeon inserts a synthetic graft that redirects blood flow from the abdominal aorta into the renal artery, beyond the area of stenosis. Increasingly, splenorenal bypass procedures can also restore renal blood flow. Technically, the process is similar to other arterial bypass procedures (see Chapter 36).
For clients with RAS, the diagnostic and treatment alternatives present tremendous decisional conflict. Clients often experience a deterioration of renal function, as noted by elevated serum creatinine levels and decreased creatinine clearance. These clients are at increased risk for acute renal failure from the administration of nephrotoxic agents such as ra-diopaque contrast media and from possible intraoperative hy-potensive episodes. However, no treatment probably means that dialysis is inevitable.
is the leading cause of end-stage renal disease (ESRD) among Caucasians in the
Immunologic response mechanisms have also been implicated in glomerular basement membrane thickening and other changes in clients with diabetic renal disease. Investigations continue to explore if defects are the result of genetic or metabolic disturbances.
Diabetic nephropathy is a microvascular complication of diabetes defined by persistent albuminuria (as shown by dipstick or a urinary albumin excretion rate above 0.3 g/dL), without evidence of other renal disease. A diagnosis of renal disease in clients with diabetes mellitus is made on the basis of the history and clinical examination. Diabetic renal disease is progressive (Table 71-4).Structural and functional changes occur in the kidneys of diabetic clients. Initially, kidney size is slightly increased and glomerularfiltration rates (GFR) are higher than normal. A radioimmunoassay of urine detects the microlevels of albumin associated withalbuminuria. Progressive renal damage occurs before dipstick procedures can detect protein in the urine. For most clients, proteinuria(albuminuria) indicates the need for a renal biopsy for further diagnosis. For the client with diabetes, observed microvascular changes in the retinacorrelate well with the renal microvascular changes. Examination of the retina showing capillary leakage, fibrosis, and the typical changes of diabetic retinopathy eliminates the need for a risky renal biopsy.
As with nephrotic syndrome, proteinuria may be mild, moderate, or severe. Clients with diabetes mellitus are always considered to be at risk for renal failure. If possible, nephrotoxic agents (e.g., radiopaque contrast media or aminoglycosides) and fluid volume deficit are avoided. Clients with worsening renal function may begin to have frequent hypoglycemic episodes and a decreased need for insulin or oral antihyperglycemic agents. The nurse explains to the client that the kidneys metabolize and excrete insulin. When renal function deteriorates, the insulin is available for a longer time and thus less of it is needed. Unfortunately, many clients believe this means their diabetes mellitus is improving. The result is accelerated progression to ESRD. (See Chapter 65 for more information on diabetic nephropathy.)
Care of the client with chronic renal insufficiency is thought to be more effective when a multidisciplinary case managementapproach is used. Research has not demonstrated a clear advantage to such an approach (see the Evidence-Based Practice forNursing box above).
Cysts and Benign Tumors
Benign urinary tract growths include cysts and tumors of the renal parenchyma or urinary bladder. Because malignant growths may occur within cystic structures, a thorough evaluation is essential. A simple renal cyst grows out of renal parenchymal tissue, usually the cortical tissue. The cyst is filled with fluid and can cause local tissue destruction as it enlarges. Many cysts cause no symptoms and are discovered accidentally during fluoro-scopic examination or autopsy.
Although the exact cause is unknown, cysts are usually considered a structural defect that occurs prenatally. The etiology and incidence of benign tumors is also unknown. Thus far there are no recognized methods of prevention.
Diagnosis of a simple renal cyst involves IV urography, sonography, and computed tomography (CT). If the cyst appears to be filled with fluid at urographic examination, a sonography is generally recommended; if the cyst appears denser, a CT scan is needed.
Treatment may consist of percutaneous aspiration of a fluid-filled cyst or surgical exploration with the potential for total or subtotalnephrectomy.
Renal Cell Carcinoma
Renal cell carcinoma is also referred to as adenocarcinoma of the kidney. As with other malignancies, the healthy tissue of the kidney is replaced and displaced by cancer cells. Although the exact mechanism is not known, the tumor cells are thought to originate in the proximal convoluted tubules of the nephron.
Systemic effects occurring with the cancer are called paraneoplastic syndromes and include anemia, erythrocy-tosis,hypercalcemia, liver dysfunction with elevated liver enzymes, hormonal effects, increased sedimentation rate, and hypertension.
Anemia and erythrocytosis may appear contradictory: There is some blood loss from hematuria, but the amount lost is not sufficient to cause anemia. Erythrocytosis may be caused by erythropoietin production in the tumor cells. Hypertension may result from increased renin.
Parathyroid hormone produced by tumor cells may be the cause of hypercalcemia; other hormone alterations include increasedrenin levels (causing hypertension) and increased human chorionic gonadotropin (hCG) levels, which are accompanied by decreased libido and changes in secondary sex characteristics. The cause of the increased sedimentation rate and changes in liver function studies is not known.
Renal tumors are categorized into four stages (Table 71-5). Complications include metastasis and urinary tract obstruction. Metastasis usually occurs via the blood or lymph to the adrenal gland, liver, lungs, long bones, or the other kidney. When the tumor surrounds a ureter, hydroureter and urinary tract obstruction may result.
The exact cause of renal cell carcinoma is unknown, but links to tobacco use and exposure to chemicals such as lead, phosphate, and cadmium have been observed. Other studies suggest the possibility of hereditary influences.
account for approximately 2% of reported
cancers, with about 28,800 new cases and 11,300 deaths annually in the
The nurse asks the client for specific information, including age, known risk factors (e.g., smoking or environmental exposures), history of weight loss, changes in urine color, abdominal or flank discomfort, and fever. The cause of fever is unknown, butpyrogens produced by the tumor cells have been implicated.
PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS
Presentations of renal carcinoma are seen only in 5% to 10% of clients and include flank pain, gross hematuria, and a palpable renal mass. The nurse asks about the nature of the flank or abdominal discomfort; clients typically describe the pain as dull and aching. The pain may be more intense if bleeding into the tumor occurs. The nurse inspects the flank, noting asymmetry or obvious protrusions. An abdominal mass may be detected through gentle palpation. A renal bruit may be heard on auscultation.
Hematuria is a late common sign. Blood in the urine may be grossly observable as bright red flecks or clots, or the urine may appear smoky or cola colored. Without gross hematuria, microscopic examination may or may not reveal red cells.
The skin is inspected for pallor, darkening of the nipples and breast enlargement (in men). Other findings may include muscle wasting, weakness, generally poor nutritional status, and weight loss. All tend to occur late in the disease.
Urinalysis may reveal red blood cells. Hematologic studies reveal decreased hemoglobin and hematocrit values, hypercalcemia, increased erythrocyte sedimentation rate, and increased levels of adrenocorticotropic hormone, human chorionic gonadotropin(hCG), cortisol, renin, and parathyroid hormone.
Renal masses may be detected by surgical exploration, IV urogram with nephrograms, or sonography. The mass and surrounding structures may be further delineated by CT with contrast or magnetic resonance imaging (MRI). Staging or determining the extent of tumor spread is best accomplished with renal arteriography and renal venography.
Interventions focus on controlling the cancer and preventing metastasis.
NONSURGICAL MANAGEMENT. Chemotherapy with a variety of agents has had limited effectiveness. The Food and Drug Administration (FDA) has approved expanded clinical trials for the study of interleukin-2 (IL-2), a biologic response modifier (see Chapters 20 and 25). Interferon (INF) and tumor necrosis factor (TNF) are also being used investigation-ally. Studies withlymphokine-activated killer (LAK) cells and tumor-infiltrating lymphocytes (TIL) are in the clinical trial stage.
SURGICAL MANAGEMENT. Renal cell carcinoma is usually treated surgically by nephrectomy (kidney removal) when pain, bleeding, or tumor spread cannot be controlled otherwise.
PREOPERATIVE CARE. The client is instructed about surgical routines (see Chapters 17, 18, and 19). The nurse explains the probable site of incision and the postoperative dressings, drains, or other equipment needed and reassures the client about pain relief. Preoperative care includes administering blood and fluids to achieve hemodynamic stabilization.
OPERATIVE PROCEDURE. The client is placed in the lateral position with the operative kidney uppermost; after positioning the arms and legs, the client's trunk area is flexed to increase exposure of the kidney area. Removal of the eleventh or twelfth rib is needed to provide better access to the kidney. The surgeon removes the entire kidney, renal artery and vein, and surroundingGerota's fascia after ligation of the ureter. The adrenal gland is left intact. A drain may be placed in the wound before closure.
When a radical nephrectomy is performed, the periaortic lymph nodes are also removed, the surgical approach may betransthoracic (as discussed in the previous paragraph), lumbar, or transabdominal depending on the size and location of the lesion.Radiation therapy may follow a radical nephrectomy. Studies are ongoing to identify the effectiveness of adjuvant therapy (e.g., chemotherapy).
POSTOPERATIVE CARE. Refer to Chapter 19 for postoperative care. Assessment of urologic and renal function is essential to determine function in the remaining kidney.
Monitoring. The nurse observes the client's abdomen for distention from bleeding and symptoms of adrenal insufficiency. The nurse observes the bed linens under the supine client, because bleeding may be present. Hemorrhage or adrenal insufficiency may be accompanied by hypotension, a decrease in urine output, and an altered level of consciousness.
A decrease in blood pressure is one of the earliest signs of both hemorrhage and adrenal insufficiency; in clients with hypotension, urine output also decreases immediately. Large water and sodium losses in the urine occur in clients with adrenal insufficiency; consequently, a large urine output is followed by hypotension and subsequent oliguria (<400 mL/24 hr or less than 25 mL/hr). The physician may prescribe IV replacement of fluids and the administration of packed red blood cells.
The second kidney is expected to provide adequate renal function. The nurse assesses urine output hourly for the first 24 hours postoperatively; a urine flow of 30 to 50 mL/hr is acceptable. Flow rates of less than 25 to 30 mL/hr suggest a decrease in renal perfusion. Initially, the postoperative hemoglobin level, hematocrit values, and white blood cell count may be measured every 6 to 12 hours.
The nurse monitors the client's temperature, pulse rate, and respiratory rate at least every 4 hours; careful measurement and recording of fluid intake and output are critical. The client is weighed daily.
The client may be in a special care unit for 24 to 48 hours postoperatively for monitoring of bleeding and/or adrenal insufficiency. A drain placed near the site of incision removes residual fluid. Because of the discomfort associated with lung expansion, the client is susceptible to atelectasis. Fever, chills, thick sputum, or decreased breath sounds suggest pneumonia.
Pain Management. After surgery, opioid analgesics (e.g., meperidine [Demerol], hydromorphone [Dilaudid], and morphine sulfate [Statex*^]) are given parenterally. The incision site, in which the major muscle groups associated with breathing and movement are involved, necessitates the liberal use of analgesic agents. These medications may be required for 3 to 5 days for pain management. Oral analgesic agents may be considered when the client is permitted to eat and drink.
Prevention of Complications. One or more antibiotics may be prescribed for intraoperative and postoperative prophylaxis. These agents are usually given as single-dose prescriptions. The need for additional antibiotics is based on clinical and laboratory evidence of infection. Steroid replacements may be necessary in adrenal insufficiency.
Trauma to one or both kidneys is always a concern in penetrating wounds or blunt injuries to the back, flank, or abdomen. Injury to the kidney can be minor, major, or pedicle. Strategies to prevent trauma are reviewed in Chart.
Minor injuries include contusions, small lacerations, and disruption of the integrity of the parenchyma and the calyx (forniceal disruption). In a person with a contusion, one or both kidneys sustained a bruise because of the major impact. Small blood vessels may be damaged, causing some hematuria. One or more small lacerations may result in small, localized hematomas. There may also be a small hematoma at the site of forniceal disruption. Common causes include falls, contact sports, and blows to the back and torso.
Major injuries involve lacerations to the cortex, medulla, or one of the segmental branches of the renal artery or vein. Deepparenchymal injuries may extend throughout the kidney and result in hematomas contained within or disrupting the capsule. Otherparenchymal injuries involve the cortex and cause shattering of tissue, resulting in either an intact or a disrupted capsule.
A major injury is most likely to follow a penetrating abdominal, flank, or back wound (such as seen with gunshot wounds, knife wounds, or motor vehicle accidents). Bleeding is extensive, and surgical exploration is often required. Because of the hemorrhage,hypoperfusion of renal parenchyma can produce short-term or long-term renin-induced hypertension
Pedicle injuries involve a laceration or disruption of the renal artery and/or renal vein. Hemorrhage is extensive and rapid, and death may ensue quickly unless diagnosis and intervention are prompt.
The nurse obtains a history of the client's usual health status and the events surrounding the trauma from the client, a witness, or emergency personnel. Critical assessment information includes a history of renal or urologic disease, surgical intervention, or systemic health problems (e.g., diabetes mel-litus or hypertension).
Ureteral and/or renal pelvic injury may cause diffuse abdominal pain, local collections of urine, and infection. The nurse asks the client about pain, specifically flank or abdominal pain, and solicits a description: Is the pain dull? Sharp? Constant? Intermittent?Aggravated by coughing?
The nurse measures the client's blood pressure and apical and peripheral pulse rates, respiratory rate, and temperature. The right and left flanks are inspected to determine asymmetry or penetrating injuries of the lower thorax or back. Similarly, the nurse inspects the abdomen for ecchymoses, percusses the abdomen for distention, and observes for penetrating wounds. The urethra is inspected for gross bleeding.
Urinalysis commonly reveals hemoglobin or red blood cells from the rupture of small or large renal blood vessels. Microscopic examination of the urine may also show red blood cell casts, which suggest tubular damage. Hemoglobin and hematocrit values decrease with blood loss; the white blood cell count is elevated with inflammation or infection.
Fluoroscopic procedures include IV urography, renal arte-riography, and computed tomography (CT). A urogram reveals the number of kidneys and the integrity and patency of the collecting system. Renal sonography is an alternative diagnostic procedure to a urogram that avoids radiopaque contrast media exposure to clients with elevated serum creatinine levels.
Renal arteriography reveals the number of kidneys and, more specifically, the blood supply to each. In clients with pedicle injuries, the contrast media used in arteriography extravasates from the ruptured vessels, and the renal parenchyma is not visualized. The CT scan shows the location of the injury and vascular and tissue integrity. Intracapsular and extracapsular hematomas are readily observable on the CT scan.
Nursing diagnoses for the client with renal trauma include Ineffective (Renal) Tissue Perfusion, Anxiety, Pain, Impaired Urinary Elimination, Post-Trauma Syndrome, and Risk for Infection. Interventions include medications for vascular support, fluids to restore fluid volume, and surgery when indicated.
DRUG THERAPY. Prescribed IV dopamine (Revimine4*1, others) supports renal perfusion. Coagulation factors such as vitaminÊ and platelets are assessed and administered as needed.
FLUID THERAPY. Fluid administration to restore circulating blood volume is critical for renal tissue perfusion. Crystalloidsolutions replace water and some electrolytes and include 0.9% sodium chloride (NSS), 5% dextrose in 0.45% sodium chloride, and Ringer's solution. When significant bleeding has occurred, whole blood or packed red cell replacement restores the oxygen-carrying capacity of hemoglobin. Plasma volume expanders, such as dextran or albumin, help re-establish plasma oncotic pressure and minimize fluid shift from the intravascular to the interstitial fluid space.
During fluid resuscitation or restoration, the nurse administers fluid at the prescribed rate and monitors the client for hemodynamicinstability. The nurse also monitors vital signs as often as every 5 to 15 minutes and measures and records urine output hourly. Urine output should be greater than 25 to 30 mL/hr.
SURGICAL MANAGEMENT. Surgical interventions may include nephrectomy and partial nephrectomy. For clients with major vascular tearing, the kidney may be surgically removed, repaired through revascularization techniques, and then reimplanted. The repair of kidney tissue outside the client is called bench surgery. Autotransplantation is transplantation of one's own kidney.
The nurse instructs the client, family, or significant other about the effects of the injury and how to assess for infection or other complications, such as the onset of bleeding or urinary retention. The client is instructed to observe the pattern and frequency of urination and to note whether the color, clarity, and amount appear normal. The nurse also instructs the client to seek medical attention if these characteristics change significantly and if a feeling of bladder distention or inadequate bladder emptying occurs, which suggests an obstruction. Chills, fever, lethargy, and/or cloudy, foul-smelling urine may suggest a urinary tract infection. The nurse warns the client not to ignore these symptoms and to seek medical care promptly if they occur.
ACUTE AND CHRONIC RENAL FAILURE
Acute and chronic renal failure have become
increasingly niore common in the
The functions of the kidney are excretion of waste, water and salt regulation, maintenance of acid balance, and hormone secretion. When renal function deteriorates gradually, as occurs with most causes of chronic renal failure, 90% to 95% of the nephrons must be destroyed before significant renal failure is evident. The client may have many years of decreased renal reserve and chronic renal insufficiency before the uremia of end-stage renal failure develops. During this time of decreased renal reserve and chronic renal insufficiency, the client is at increased risk for acute renal failure because of the diminished availability of functioning nephrons.
When renal deterioration is sudden, the capacity of the functioning nephrons is exceeded more quickly, and renal failure may develop with the loss of only 50% of functioning nephrons. Acute renal failure and chronic renal failure are compared in Table 72-1. Acute renal failure affects many body systems; chronic renal failure affects every body system. The abnormalities are primarily related to the effects of the following:
· Fluid volume excess
· Electrolyte and acid-base abnormalities
· Accumulated nitrogenous wastes
· Hormonal inadequacies
When renal function decreases to the point where the kidneys can no longer meet the body's homeostatic demands, renal replacement therapy is required to prevent death from potentially life-threatening consequences.
ACUTE RENAL FAILURE
Acute renal failure (ARF) is a rapid decrease in renal function, leading to the accumulation of metabolic waste in the body. ARF can result from conditions that cause inadequate kidney perfusion (prerenal failure); damage to the glomeruli, interstitium, or tubules (intrarenal failure); or obstruction (postrenal failure) (Kelly, 1997). ARF in clients with chronic renal insufficiency (CRI) may result in end-stage renal disease (ESRD) or may resolve to nearly the pre-ARF level of renal function. Many factors contribute to renal insults resulting in ARF, but the acute syndrome may be reversible.
The pathophysiologic process of ARF is related to the cause of the sudden decrease in kidney function and the involved site orsites of the kidney. Hypoperfusion, toxins, tubular ischemia, infections, and obstruction have different effects on the renal system. Any of these processes can result in a decreased glomerular filtration rate (GFR), alterations in renal tubular cell membrane integrity, and tubular lumen obstruction.
With acute hypoperfusion, autoregulatory responses (i.e., renal vasoconstriction, activation of renin-angiotensin-aldosterone, and release of antidiuretic hormone [ADH]) increase blood volume and improve renal perfusion. However, these compensatory mechanisms cause urine volume to fall, resulting in oliguria (urine output less than 400 mL/day). Tubular cell injury is more likely to occur from the increasing ischemia related to hypoperfusion. Toxins can cause vasocon-strictive responses in the kidney, leading to reduced renal blood flow and renal ischemia.
Interstitial inflammatory changes resulting from infection, drugs, or infiltrating tumors result in immune-mediated changes in renal tissue. With extensive tubular damage, sloughing of tubular cells and other formed elements (e.g., red blood cell [RBC] casts) may obstruct the tubular lumen and prevent the formation or outflow of urine. Obstruction anywhere within the genitourinary tract eventually results in full or partial obstruction to the formation and outflow of urine.
When intratubular pressure exceeds glomerular hydrostatic pressure, glomerular filtration ceases. This process causes a progressive elevation of the serum blood urea nitrogen (BUN) and creatinine levels. When the BUN rises faster than the serum creatinine level, the cause is usually related to protein catabolism or volume depletion. When both the BUN and creatinine levels rise and the ratio between the two remains constant, renal failure is present.
TYPES OF ACUTE RENAL FAILURE
Several syndromes describe the types of ARF. These include prerenal azotemia, intrarenal (intrinsic) ARF, and postrenal azotemia. Table 72-2 summarizes the pathologic changes and causes of ARF.
Prerenal azotemia can be reversed by establishing normal intravascular volume, increasing blood pressure and cardiac output. Prolonged, untreated hypoperfusion can lead to severe ischemic injury and intrarenal failure.
The term intrarenal ARF is often shortened to just ARF in the clinical setting. Other terms include acute tubular necrosis (ATN)and lower nephron nephrosis. Infections (bacteria, viral, fungal, or endotoxin), drugs (especially aminogly-coside antibiotics andnonsteroidal anti-inflammatory drugs [NSAIDs]), and infiltrating tumors (e.g., lymphomas or leukemias) can cause acute interstitial nephritis. Inflammation of the glomeruli (glomerulonephritis) or of the small vessels of the kidneys (vasculitis) or a major obstruction to blood flow can also cause intrarenal ARF.
Postrenal azotemia develops from obstruction to the outflow of formed urine anywhere within the genitourinary tract.
IPHASES OF ACUTE RENAL FAILURE
When a client's renal function has been compromised, the phases of ARF begin (Table 72-3). Increasing numbers of clients have anonoliguric form of ARF. The description of the phases of this form of ARF are similar to those described in Table 72-3 except for the references to urine output. In addition, the treatment of these clients is less complicated because renal replacement therapy is rarely needed. Interventions to restore circulating volume, improve cardiac output, or reestablish blood pressure may prevent progression of the phases when renal hypoperfusion is present.
Many types of renal insults can lead to reduced renal function. Severe hypotension from excessive blood loss or dehydrationresults in hypoperfusion of blood to the kidneys and can lead to prerenal ARF. Cardiac disease or heart failure also results in decreased renal perfusion. The client may be oliguric, or even anuric (less than 100 mL/24 hr), if the dehydration or renal blood flow obstruction is severe. The following are other conditions that precipitate ARF:
· Nephrotoxic agents (antibiotics, NSAIDs) (Table 72-4)
· Disseminated intravascular coagulation (DIC)
· Obstruction by thrombosis or stenosis
· Uric acid crystals or other obstructing precipitates
· Acute hemolytic transfusion reactions
· Complications of infection (e.g., endotoxins or sepsis)
· Acute glomerulonephritis
· Severe hypertension
· Hepatorenal syndrome of cirrhosis
ARF affects 20% of all critically ill clients and carries a 50% to 80% mortality rate (Stark, 1998). Eighty percent of ARF episodes are due to ATN and exacerbations of CRI. Volume depletion leading to prerenal azotemia is the most common cause of acute renal deterioration and is reversible in most cases with prompt intervention.
For clients surviving the precipitating event, the opportunity for return of renal function is good. Complications during the course of ARF can vastly increase mortality. Bloodstream infections associated with central and peripheral lines and the pulmonary system are most often involved in complications. However, the highest mortality occurs with trauma (70%) and surgery. ARF caused bynephrotoxic substances is associated with the lowest rates (10% to 26%) of recovery. The prognosis for ARF caused by obstruction or glomerulonephritis is much better.
Nurses have an essential role in the prevention of acute renal failure (ARF). The nurse notes the signs of impending renaldysfunction through careful physical assessment and close monitoring of laboratory values. Prompt recognition and correction ofextrarenal problems usually restore renal function before tissue damage can occur. Careful physical assessment is required to evaluate the client's fluid status. Intake and output records and body weights can assist in identifying trends in fluid balance. If vascular volume is depleted, decreased urine output, postural hypotension, and tachycardia will be present. Prompt fluid resuscitation for clients in the prerenal stage can prevent intrarenal problems that can lead to renal tissue damage and renal failure.
The nurse also monitors laboratory values for any changes that reflect compromised renal function. Decreased urine specific gravity indicates a loss of urine-concentrating ability and is the earliest sign of renal tubular damage. Other laboratory values that are helpful in monitoring renal function include serum creatinine, urine and serum electrolytes, and blood urea nitrogen (BUN).
The nurse is aware of nephrotoxic substances that the client may ingest or be exposed to (see Table 72-4). The nurse questions orders for potentially nephrotoxic drags, and the ordered dose is validated before the client receives the drag. Antibiotics are the most likely drag group to have nephrotoxic side effects. NSAIDs may cause or potentiate the risk for ARF. Combinations of drags can cause synergistic reactions, further increasing the risk for ARF. If a client must receive a potentially nephrotoxic drag, the nurse monitors laboratory values, including BUN, creatinine, and drag peak and trough levels, closely for indications of actual or potential renal dysfunction.
The accurate diagnosis of ARF, including its type and its cause, largely depends on a detailed history. The history must includequestions relating to the potential causes of ARF. The client is asked about exposure to nephrotoxins, recent surgery or trauma, transfusion, or other factors that might lead to renal ischemia. A medication history is also important, since treatment with certain anti-infectives, aminoglycoside antibiotics, angiotensin-converting enzyme (ACE) inhibitors, and NSAIDs can cause prerenal failure. Exposure to radiographic contrast medium can precipitate ARF, especially in older clients with reduced renal reserve. In some situations, ARF must be differentiated from chronic renal insufficiency (CRI). In these cases, the nurse asks about known renal diseases; systemic diseases, such as diabetes mellitus and systemic lupus erythematosus and other connective tissue diseases; and chronic hypertension.
To identify possible acute glomerulonephritis, questions about acute illnesses such as influenza, colds, gastroenteritis, and sore throats or pharyngitis, as well as the presence of cocoa-colored urine (hematuria), are included.
Reversible prerenal azotemia may be suspected after hypotension, hemorrhage or shock, burns, congestive heart failure (CHF), or any situation in which the client experiences in-travascular volume depletion. Phosphorus-containing bowel preparations and being allowed nothing by mouth (NPO) pre-operatively, in conjunction with the fluid losses of most surgical procedures, are sufficient to cause prerenal azotemia in many clients (Orias, Mahnensmith, & Perazella, 1999).
Postrenal azotemia can be identified by focusing on any history of obstructive disease processes that would be manifested as difficulty in starting the urine stream, changes in the amount or appearance of the urine, narrowing of the urine stream, nocturia, urgency, or symptoms of renal calculi. The nurse also notes any history of malignant carcinoma that may cause bilateral obstruction.
Because of the widely varied causes and the potentially reversible nature of the illness, the nurse obtains or validates a detailed history when ARF is suspected. In clients with postrenal azotemia, the nurse monitors for oliguria or intermittent anuria, symptoms of uremia, and lethargy. The nurse reports changes in the character of the urine stream or difficulty starting urination.
PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS
The clinical manifestations of ARF are related to azotemia, as well to as the underlying cause (Chart). Signs and symptoms ofprerenal azotemia are hypotension, tachycardia, decreased urine output, decreased cardiac output, decreased central venous pressure (CVP), and lethargy. The general clinical appearance of a client with prerenal azotemia is similar to that of a client with heart failure or dehydration, depending on the cause of the renal compromise.
Intrarenal (intrinsic) ARF usually involves damage to the glomeruli, interstitium, or tubules. Classic manifestations include oliguriaor anuria (absence of urine), edema, hypertension, tachycardia, shortness of breath, jugular venous disten-tion, elevated CVP, weight gain, rales or crackles, anorexia, nausea, vomiting, and lethargy or varying levels of consciousness. Clinical manifestations of electrolyte abnormalities, such as electrocardiographic (ECG) changes, may also be present.
The numerous alterations in laboratory values in the client with ARF are similar to those occurring in chronic renal failure (CRF). The nurse can expect to find rising BUN andcreatinine levels, and abnormalities in serum electrolytes. Table 72-5 shows the effects of renal failure on electrolyte values. Clients with ARF, however, typically do not experience the anemia associated with CRF un; less there is hemorrhagic blood loss. However,uremic hemolysis secondary to severe azotemia can develop and may be the cause of anemia in the early phase of ARF.
In the early phases of ARF, urinalysis and microscopic examination of urine may provide diagnostic information. Urine sodium levels are often less than 10 to 20 mEq/L in clients with prerenal azotemia. In prerenal azotemia, the urine is often concentrated, with a specific gravity greater than 1.020. The presence of urine sediment (red blood cells [RBCs], RBC casts, tubular cells), myoglobin, or hemoglobin; a urinary sodium level lower than 40 mEq/L; and a specific gravity of 1.010 are indicative of intrarenal failure. Inpostrenal failure, urinary sodium levels may be normal to 40 mEq/L, with a specific gravity of 1.000 to 1.010.
X-ray studies help to determine the cause of ARF. A flat-plate x-ray film of the abdomen is obtained to determine the size of the kidneys. In the absence of underlying renal disease, normal-size kidneys are expected. Enlarged kidneys, possibly due to obstruction, may result from hydronephrosis. This x-ray finding may also illustrate obstructing calculi in the renal pelvis, ureters, or bladder.
Renal ultrasonography is a noninvasive procedure using high-energy sound waves. It is useful in the diagnosis of urinary tract obstruction. Dilation of the renal calyces and collecting ducts, as well as calculi, can be detected.
Computed tomography (CT) scans without contrast dye can be obtained to identify obstruction or tumors. Contrast media are usually avoided to prevent further renal damage. A sonogram is generally preferred to the intravenous pyelogram (IVP) to determine kidney size and the patency of the ureters.
Aortorenal angiography may be used to examine renal blood vessels and blood flow. The procedure involves the necessary risk of using contrast media but can reveal any occlusion of major renal vessels by thrombus, embolus, or stenosis. Cystoscopy or retrograde pyelography may be indicated to identify possible obstructive lesions in the urinary tract.
OTHER DIAGNOSTIC ASSESSMENT
Renal biopsy may be performed if the primary cause is uncertain, an immunologic disease is suspected, or the reversibility of the renal failure needs to be determined after ARF has persisted for an extended period. The nurse assists with many of the diagnostic studies, prepares the client before the test, and provides follow-up care. The nurse must be aware of all test results and understand how they may affect the treatment regimen. (See Chapter 69 for a detailed discussion of renal diagnostic tests.)
The primary nursing diagnosis and collaborative problems for the client with acute renal failure (ARF) are Excess Fluid Volume, Potential for Pulmonary Edema, and Potential for Electrolyte Imbalances. The client with ARF may pass from the oliguric phase (in which fluid and electrolytes are retained) to the diuretic phase. If the client moves to the diuretic phase, hypovolemia and electrolyteloss are the primary problems. As a result, the client in the diuretic phase of ARF needs a plan of care that focuses on fluid and electrolyte replacement and monitoring.
These examples of output variation reflect the continually changing nature of ARF and the need for the plan of care to be constantly updated to reflect the client's movement through the stages of the disease process. Drug therapy, diet therapy, and renal replacement therapy (peritoneal dialysis [PD], hemodialysis [HD], or hemofiltration) are commonly employed in the management of ARF.
DRUG THERAPY. Clients with ARF receive numerous medications. As kidney function changes, the physician often modifies drug doses. The nurse is knowledgeable about the site of drug metabolism and is especially careful when administering medications. The nurse constantly monitors for possible side effects and interactions of the drags the client with ARF is receiving. Diuretics may be used to increase urine output.
In clients with prerenal azotemia, fluid challenges and diuretics are often used to promote renal perfusion. In clients without signs and symptoms of fluid volume excess, 500 to 1000 mL of normal saline may be infused over a 1-hour period. In prerenal azotemia, the client should respond to the fluid challenge by producing urine soon after the initial bolus. Diuretics such as furosemide (Lasix) may also be ordered in conjunction with a fluid bolus. If oliguric renal failure is diagnosed, the fluid challenges and diuretics are discontinued. The physician may prescribe low-dose (1 to 3 |xg/kg) dopamine in a continuous infusion to enhance renal perfusion and/or increase blood pressure (Zellner, 1999) (Chart 72-4). These clients often require central venous pressure (CVP) monitoring or measurement of pulmonary arterial pressure by means of a Swan-Ganz catheter for a more exact evaluation of their hemodynamicstatus. They also require constant nursing supervision for assessment of the response to fluid and drug administration. The nurse carefully monitors for signs of possible fluid overload.
Calcium channel blockers may be used to treat ARF resulting from nephrotoxic acute tubular necrosis (ATN) by preventing the influx of calcium into the kidney cells, thereby maintaining cell integrity and improving the glomerular filtration rate (GFR).
DIET THERAPY. Clients who have ARF often have a high rate of catabolism. The exact mechanism for this state is not well understood. Increases in catabolism may be related to the stress of a critical illness, causing an increase in levels of circulatingcatecholamines, cortisol, and glucagon, all of which stimulate catabolism. The rate of catabolism is correlated with the severity of uremia and azotemia. This hypercatabolic state causes the breakdown of muscle for protein, which leads to an increase in azotemiaand an even more elevated serum blood urea nitrogen (BUN) level.
If the client with ARF has an adequate dietary intake (see Imbalanced Nutrition: Less Than Body Requirements [Chronic Renal Failure]), nutritional support may not be necessary. The health care provider may order a consultation with a dietitian, who will calculate the client's caloric requirements. In conjunction with the dietitian, the health care provider will order a diet with specific levels of protein and sodium and the amount of fluids required. If the client does not require dialysis, 0.6 g/kg of body weight or 40 g/day of protein is ordered. For clients needing dialysis, the protein level needed will range from 1 to 1.5 g/kg. The amount of dietary sodium ranges from 60 to 90 mEq. In the presence of hyperkalemia, dietary potassium is restricted to 60 to 70 mEq. The amount of fluid permitted is generally calculated to equal the urine volume plus 500 mL. The nurse continually assesses oral intake to make certain that sufficient calories are consumed.
Administering Renal-Dose Dopamine
Take an accurate weight because the dose is ordered according to the client's weight.
Know the hospital's policy regarding who is responsible for calculating the rate of infusion (i.e., physician, pharmacist, or nurse). Renal-dose dopamine is 1 to 5 //.g/kg body wt/min but is converted to mL/min for an IV infusion. Before hanging the dopamine infusion, double-check the amount of dopamine added to the solution, the total volume of solution (usually 250 mL), and the calculation mil-liliters per minute.
Do not hang the dopamine infusion until all questions about the calculation are clarified. If dopamine is to be infused into a peripheral vein, be sure that the line is intact and secured. Once the infusion is started, check the client's blood pressure and pulse per hospital policy or the physician's orders, usually at least every 2 hours. Notify the physician of changes in vital signs per policy or the physician's orders.
Monitor the IV site frequently for clinical manifestations of infiltration.
If infiltration occurs, stop the infusion but do not discontinue the IV catheter. Prepare for phentolamine (Regitine, Rogitine*) administration through the IV catheter and subcutaneously into the infiltrated tissue.
Many clients with ARF are too ill or too anorexic to eat sufficient food. For these clients, some form of nutritional support (e.g., total parenteral nutrition [TPN] or hyperalimen-tation) must be initiated to avoid catabolism. The goals of nutritional support in ARF are to provide sufficient nutrients to maintain or improve nutritional status, to preserve lean body mass, to restore or maintain fluid balance, and to preserve renal function.
If TPN is administered, the solutions may be formulated to meet the client's specific needs. Because kidney function is unstable in ARF, the nurse constantly monitors the serum electrolyte concentrations and facilitates revisions in the hy-peralimentation solution as needed. In addition to TPN, intravenous (IV) fat emulsion (Intralipid) infusions provide a non-protein source of calories. In uremicclients, fat emulsions can be used in place of glucose to avoid the problems associated with excessive sugars.
DIALYSIS THERAPIES. Hemodialysis (HD) and peritoneal dialysis (PD) may be implemented for clients with ARF if necessary. Until recently, intermittent hemodialysis (IHD) has been the most common treatment of ARF. The following are indications for dialysis in ARF:
• Persistent hyperkalemia
• Uncompensated metabolic acidosis
• Fluid volume excess unresponsive to diuretics
• Uremic pericarditis
• Uremic encephalopathy
Immediate vascular access for HD in clients with ARF is established by placement of a dual- or triple-lumen catheter specifically designed for HD. For HD that is expected to be necessary for several weeks, the catheter is usually placed into the subclavian or internal jugular vein. If only one or two treatments are expected to be necessary, as for removal of drugs or toxins by hemoperfusion, a femoral site may be selected. Longer use of the femoral site is generally discouraged because of positioning limitations (i.e., required immobility) and other potential complications, such as hematomas and infection. Repeated can-nulation of the femoral site also increases the risk for hematoma formation and makes repeated use of the vein impossible.
The subclavian vein is often preferred over femoral vein cannulation because the catheter can be left in place between dialysis treatments. This placement is also a disadvantage, however, because the longer the catheter is left in place, the greater is the chance for infection. The subclavian dialysis catheter (Figure 72-1) is inserted at the bedside. A physician performs the sterile procedure, and then the catheter is covered with a sterile dressing. Catheter placement is checked by chest x-ray examination before its use.
HD catheters have two lumens separating the outflow and inflow extensions of the catheter. Consequently, the continuous outflow of blood to be dialyzed is separated from the dialyzed blood returned through the inflow port and lumen. A triple-lumen catheter for HD is now available. The third lumen provides a port for drawing venous blood or administering medication and fluid without interruption of the dialysis lumens.
PD may also be used in the treatment of ARF, but its use may be limited in the critically ill, since mechanically ventilated clients may not be able to tolerate the accompanying abdominal distention, and since its use requires an intact, unin-fected abdominal cavity (Giuliano & Pysznik). PD uses the peritoneum as a semipermeable membrane for which dialysate is infused through a catheter implanted in the peritoneum. A more complete discussion of PD is provided later in this chapter under Chronic Renal Failure).
CONTINUOUS RENAL REPLACEMENT THERAPIES.
Currently, continuous renal replacement therapies (CRRTs) have become the standard treatment for ARF. Renal replacement therapies in the form of hemofiltration may be better tolerated than HD for clients who are critically ill, since rapid shifts of fluids and electrolytes associated with HD are avoided (Giuliano & Pysznik).
Continuous arteriovenous hemofiltration (CAVH) and continuous arteriovenous hemodialysis and filtration (CAVHD) provide additional renal replacement therapies for clients with ARF. These procedures share some similarities with HD, but their use and indications are specific and limited.
CAVH is indicated for clients who are fluid volume overloaded, resistant to diuretics, and hemodynamically unstable. The implementation of CAVH requires the placement of both arterial and venous catheters to provide adequate filtration sociated with the pump, but most pumps are equipped with alarms that detect air. These systems also require the use of anticoagulants, but at lower doses than needed for AV systems. These procedures are performed in a critical care unit, and clients require continuous nursing care.
POSTHOSPITAL CARE. The posthospital care for a client with ARF varies widely, depending on the status of the disease when the client is discharged. The course of ARF varies, with recovery lasting up to several months. If the renal failure is resolving, follow-up care is often provided by a nephrologist or by the family physician in consultation with the nephrologist. On occasion, however, ARF results in permanent renal damage and the need for chronic dialysis or even transplantation. In these cases, theposthospital care may be as extensive and multifaceted as it is for any other client with chronic renal failure (CRF) (see Community-Based Care [Chronic Renal Failure]).
If the ARF is in the process of resolving, the follow-up care may involve a variety of services. Frequent medical visits arenecessary, as are routine laboratory blood and urine tests to monitor renal function. Consultation with a dietitian may be needed to modify the client's diet according to the degree of renal function and ongoing nutritional requirements. Clients continuing dialysis after discharge must be taught to limit foods high in potassium and sodium and to observe protein restrictions. In addition, education concerning the need for limited fluid intake may be necessary.
Some clients may need some form of temporary dialysis until their kidneys can metabolize fluid and waste products independently. The dialysis begun while the client was hospitalized may be continued at an outpatient dialysis center for as long as necessary. Teaching concerning the type of dialysis, care of vascular access sites, dietary restrictions, fluid restrictions, and prevention of complications is ongoing throughout the recovery phase. Depending on their level of independence and family support, some clients may also need home care nursing or social work assistance.
CAVH removes large amounts of plasma water and solutes on a continuous basis. When large volumes of plasma water are removed, electrolytes are also removed. Electrolytes are replaced through prescribed amounts of IV electrolyte solution. The most significant disadvantage of arteriovenous (AV) filtration is the risk of bleeding associated with anticoagulants used to prevent membrane clotting (Craig, 1998).
A double-lumen dialysis catheter inserted into a large vein (subclavian, jugular) provides access for CAVHD. CAVHD uses adialysate (a solution composed of water, glucose, sodium chloride, potassium, magnesium, calcium, and bicarbonate) delivery system to remove nitrogenous or other waste products in addition to fluid in clients with limited cardiac output, those with significant hypotension, or those who have been unresponsive to diuretic therapy. The conventional form of HD would not be tolerated, and PD would probably be inadequate for the fluid removal required.
Continuous venovenous hemofiltration (CVVH) is often considered to be the treatment of choice for critically ill clients. CVVH requires only a double-lumen venous catheter for access and is powered by a pump, making the rate of filtration more reliable than that of the mean arterial pressure (Giuliano & Pysznik).
CHRONIC RENAL FAILURE
In contrast to the ability of the kidneys to regain function following acute renal failure (ARF), chronic renal failure (CRF) represents a clinical syndrome of progressive, irreversible kidney injury. When kidney function is inadequate for sustaining life, CRF is referred to as end-stage renal disease (ESRD). Terms associated with renal failure include azotemia (accumulation of nitrogenous waste products in the bloodstream), uremia (azotemia with clinical symptoms), uremic syndrome (the diverse systemic clinical and laboratory manifestations associated with ESRD), and renal replacement therapy (hemodialysis [HD], peritoneal dialysis [PD], renal transplantation; necessary to sustain life in clients with renal failure). ARF and CRF are compared in Table.
STAGES OF RENAL FAILURE
The kidneys tend to fail in an organized fashion. The client's progression toward ESRD usually begins with a gradual decrease in renal function of 30% to 50% (Table). Initially, there is a diminished renal reserve. A 24-hour urine specimen for monitoringcreatinine clearance is necessary to detect that renal reserve is less than normal. In this stage, reduced renal function occurs without any measurable accumulation of metabolic wastes in the serum because of the ability of the unaffected nephrons to compensate for the decreased functioning of the diseased nephrons. Renal damage is accompanied by an elevation in the systemic blood pressure, resulting in an increase in the pressure within the glomerular apparatus and the remaining unaffected nephrons. Eventually, the unaffected nephrons may be damaged by long-term exposure to this increased pressure, leading to the progressive renal damage characteristic of CRF. However, under stressful conditions, such as infection, fluid overload, or dehydration, renal function at this stage can appear compromised.
In the next stage, renal insufficiency, metabolic wastes begin to accumulate in the blood because the healthier kidney tissue can no longer compensate for the loss of nonfunction-ing nephrons. Levels of blood urea nitrogen (BUN), serum creatinine, uric acid, and phosphorus are increasingly elevated in relation to the degree of renal function loss. Careful nursing and medical management of fluid volume, blood pressure, electrolytes, dietary intake, and medication administration may slow the progression of renal failure.
Many clients ultimately progress to end-stage renal disease (ESRD). Excessive amounts of nitrogenous wastes, such as urea andcreatinine, accumulate in the blood, and the kidneys cannot maintain homeostasis. Initially, severe fluid overload and electrolyte and acid-base imbalances occur. Without renal replacement therapy, fatal complications are likely.
Renal dysfunction causes multiple pathologic situations, including disruptions in the glomerular filtration rate (GFR), abnormalities of urine production and water excretion, electrolyte imbalances, and metabolic abnormalities. The kidneys can maintain an effective GFR until 70% to 80% of renal function is lost. Homeostasis is maintained until late in the course of renal failure. When less than 20% of the nephrons are functional, the GFR is altered despite hypertrophy of the remaining nephrons. This alteration occurs because the hy-pertrophied nephrons can maintain the excretion of solutes or waste products only by decreasing water reabsorption. As a result, hyposthenuria (the loss of urine concentrating ability) and polyuria (increased urine output) occur. Both hyposthenuriaand polyuria are early signs of CRF and, if the problem is untreated at this stage, can cause severe dehydration.
As the disease progresses, the ability to dilute the urine is increasingly diminished, resulting in urine with a fixed osmo-lality(isosthenuria). As renal function continues to diminish, the concentration of urea is increased in the blood, and urine output decreases. When renal function deteriorates to this level, the client is at risk for fluid overload because of loss of adequate urine output.
UREA AND CREATININE. Renal failure also causes disturbances in urea and creatinine excretion. Creatinine is derived fromcreatine and phosphocreatine, which are present in skeletal muscle. The normal rate of creatinine excretion depends on muscle mass, physical activity, and diet. Without major alterations in the diet or physical activity, the serum creatinine level remains relatively constant. Creatinine is partially excreted by the renal tubules, and a decrease in renal function leads to a buildup of serum creatinine. Urea is the primary product of protein metabolism and is excreted by the kidneys. The BUN level normally varies directly with protein intake.
An important method for accurately estimating the GFR is to monitor the creatinine clearance of the kidneys. As renal function andglomerular filtration diminish, creatinine clearance decreases and the serum creatinine level rises (see Chapter 69).
SODIUM. In addition to decreased BUN and creatinine excretion, alterations in sodium excretion are common. Early in chronic renal failure (CRF), the client is particularly susceptible to hyponatremia (sodium depletion) because, although a diminishing number of nephrons are reabsorbing sodium at their maximal ability, there is an obligatory loss of sodium in urine production. Thus thepolyuria often seen in early renal failure also causes sodium depletion.
In the later stages of renal failure, the capacity of the kidneys to excrete sodium diminishes as urine production decreases. As a result, sodium retention can occur with only modest increases in dietary sodium intake and can lead to severe fluid and electrolyte imbalances. Sodium retention manifests as hypertension and edema. Despite the sodium retention, the concurrent retention of water results in an apparently normal serum sodium level; di-lutional hyponatremia is likely, since fluid volume excess develops (see Table).
POTASSIUM. The kidney is the primary organ responsible for potassium excretion. Any increase in potassium load during the later stages of renal disease can lead to hyper-kalemia (excessive potassium retention). Normal serum potassium levels of 3.5 to 5mEq/L are maintained until the 24-hour urine output falls below 500 mL with a decreased GFR. When hyperkalemia develops, serum levels are quickly elevated and may be 7 to 8 mEq/L or higher. Severe electrocardiographic (ECG) changes result from this elevation, increasing the risk of fatal dysrhythmias. Other factors contributing to hyperkalemia in renal failure include ingestion of potassium in medications, failure to restrict potassium in the diet, excessive tissue breakdown secondary to the hypercatabolic state, bloodtransfusions, and excessive bleeding or hemorrhage.
ACID-BASE BALANCE. In the early stages of renal disease, loss of functioning nephrons causes little change in blood pH because the remaining nephrons increase their rate of acid excretion. As the loss of nephrons continues, the kidneys cannot compensate and acid excretion is restricted; a bicarbonate deficit or metabolic acidosis results (see Chapter).
Many factors contribute to metabolic acidosis in renal failure. First, the kidney becomes unable to excrete excessive hydrogen ions. Normally, renal tubular cells secrete hydrogen ions into the tubular lumen for excretion, but ammonia and bicarbonate are required in order for excretion to take place. In clients with renal failure, the kidney's ability to produce ammonia is decreased, and the normal reabsorption of filtered bicarbonate does not occur. This process leads to a buildup of hydrogen ions for which the supply of bicarbonate and other buffering bases is inadequate. As a result, there is a base (bicarbonate) deficit in an environment with excess acid. In the presence of hyperkalemia, renal ammonium production and excretion are inhibited further.
As renal failure advances and acid retention increases, respiratory compensation is essential for maintenance of a blood pH compatible with life. The respiratory system compensates for the decreased pH by increasing the rate and depth of breathing to excrete carbon dioxide through the lungs. This pattern of breathing, called Kussmaul respiration, is increasingly apparent when worsening renal failure results in respiratory alkalosis. Serum bicarbonate measures the extent of metabolic acidosis (bicarbonate deficit). Individuals with CRF usually require treatment with alkali replacement to counteract acidosis.
CALCIUM AND PHOSPHATE. A complex, balanced reciprocal relationship between calcium and phosphate is influenced by vitamin D (see Chapter). Vitamin D facilitates calcium absorption in the intestines, and the kidney produces 1,25-dihydroxycholecalciferol, a hormone needed to create active vitamin D.
In renal failure, phosphate retention and a deficiency of active vitamin D contribute to the disruption in calcium and phosphate balance and metabolism. Normally, excessive dietary phosphate is excreted by the kidneys in the urine.
HYPERTENSION. Approximately 80% to 90% of clients with CRF have hypertension. Hypertension may be either the cause or the result of CRF. The elevation in blood pressure results from fluid and sodium overload and the malfunction of the renin-angiotensin-aldosterone system. The retention of sodium and water in renal disease causes circulatory overload, which leads to an elevated blood pressure. The kidneys respond to a decrease in renal blood flow or low serum sodium levels by trying to improve the renal blood flow. The release of renin further stimulates the production of angiotensin and aldosterone. Angiotensin causesvasocon-striction and an elevation in blood pressure. Aldosterone, a mineralocorticoid released by the adrenal glands, stimulates the distal convoluted tubule to reabsorb sodium and water. Consequently, plasma volume is expanded, and the blood pressure is elevated. As a result of this malfunction of the renin-angiotensin-aldosterone system, the blood pressure is elevated either by vasoconstriction or by volume expansion. The kidneys do not recognize the increase in blood pressure and continue to producerenin. The result is severe hypertension that is difficult to treat and that ultimately worsens renal function. Many clients with CRF also have cardiomyopathy and left ventricular hypertrophy as a consequence of prolonged hypertension.
HYPERLIPIDEMIA. CRF is associated with alterations in the metabolism of lipoproteins. Increased triglyceride, total cholesterol, and low-density lipoprotein levels are seen with a corresponding reduction in high-density lipoprotein levels. CRF renders individuals at increased risk for coronary artery disease and acute cardiac events.
CONGESTIVE HEART FAILURE. Many clients with renal failure have some form of myocardial dysfunction. CRF causes an increased workload on the heart because of anemia, hypertension, and fluid overload. Left ventricular hypertrophy and CHF are common manifestations of late end-stage renal disease (ESRD). Uremia itself may cause uremic cardiomyopathy, the uremic toxin effect on the myocardium. CHF is also common in these clients because of the presence of hypertension and coronary artery disease. Cardiac disease is the leading cause of death in clients with ESRD (U.S. Renal Data Systems, 1999).
UREMIC PERICARDITIS. Pericarditis also occurs in clients with CRF. If it is not treated effectively, this inflammation of the pericardium can lead to pericardial effusion, cardiac tamponade, and death. The pericardial sac becomes inflamed and irritated byuremic toxins or infection. Signs and symptoms include localized, severe chest pain, an increased pulse rate, a low-grade fever, and an intermittent and transient pericardial friction rub that can be heard on auscultation.
As the pericarditis continues and the pericardial effusion worsens, dysrhythmias may develop; heart tones become softer and less audible, the blood pressure decreases, and the client may experience shortness of breath. Progressive pericardial effusion results in cardiac tamponade, a medical and surgical emergency in which pulse pressure diminishes and bradycardia or asystole results.Treatment of pericardial tamponade involves removal of pericardial fluid by placement of a needle, catheter, or drainage tube into the pericardium or pericardiectomy with pericardial drainage. The incidence of uremic pericarditis has diminished with the initiation of early, aggressive dialysis.
Anemia is the primary hematologic abnormality in clients with CRF. Normochromic, normocytic anemia is a common manifestation of CRF and contributes to the client's symptoms. The causes include a decreased erythropoietin level with resulting decreased red blood cell (RBC) production, decreased RBC survival time resulting from uremia, iron and folic acid deficiencies, and impaired platelet function as a result of uremic toxins.
Uremia can affect all levels of the gastrointestinal (GI) system. The normal flora of the oral cavity is altered in uremia. The mouth normally contains the enzyme urease, which hy-drolyzes urea. The ammonia generated from this reaction contributes to uremichalitosis and may also cause uremic stomatitis (mouth inflammation).
Anorexia, nausea, vomiting, and hiccups are relatively common in clients with uremia. The specific cause of these symptoms is uncertain but may be related to increased nitrogenous waste levels (i.e., blood urea nitrogen [BUN] and creatinine levels) and metabolic acidosis.
Peptic ulcer disease is also common in clients with uremia; however, the exact cause is unclear. Uremic colitis with profound watery diarrhea or constipation may also be present in clients with uremia. Ulcerations may occur in the stomach or small or large intestine, causing erosion of blood vessels. The blood loss caused by these erosions may result in melena or, in more serious cases, may progress to hemorrhagic shock from severe GI bleeding.
The etiology of CRF is complex (Table). There are more than 100 different disease processes that can result in progressive loss of renal function (see also Chapter 71). However, diabetes and hypertension are the most common causes of CRF.
The number of
clients with CRF is continually increasing. The 1999 U.S. Renal Data Systems
annual report suggests that more than 307,000 people in the
There is a higher incidence of ESRD in men than in women (U.S. Renal Data Systems).
The greatest increase in ESRD is in those 65 years of age and older. More than
221,000 people were estimated to be receiving renal replacement therapy in the
When taking a history from a client with suspected chronic renal failure (CRF), the nurse focuses on the signs and symptoms of CRF. The client's age and gender are noted. The nurse obtains accurate weight and height measurements and inquires about usual weight and recent weight gain or loss. Weight gain may indicate cardiovascular overload and fluid retention caused by poorly functioning kidneys. Weight loss may be the result of anorexia associated with the uremic syndrome. The nurse also obtains a complete history of known renal or urologic disorders, long-term health problems, medication use, and current health conditions. The client is asked about knowledge of any existing renal disease or family history of renal disease, which might indicate a hereditary disorder. A history of kidney infection or renal calculi could imply past kidney damage. It is important to explore long-term healthproblems because illnesses such as hypertension, diabetes, systemic lupus erythematosus, arthritis, cancer, and tuberculosis can contribute to decreased renal function.
The nurse documents use of both prescription and over-the-counter medications because many medications are potentiallynephrotoxic and can cause renal damage.
The nurse examines the client's dietary or nutritional habits and discusses any present GI problems. A change in the taste of foods often accompanies renal failure. Clients may note that sweet foods are not as appealing or that certain foods, especially meats, leave a metallic taste in the mouth. The client is asked specifically about a history of GI problems, such as nausea, vomiting, anorexia, hiccups, diarrhea, or constipation. Any of these manifestations can be the result of the buildup of nitrogenous or other metabolic wastes that the body cannot excrete because of renal malfunction.
The nurse questions the client about his or her current energy level and any recent injuries or bleeding. Changes in the client's daily routine are explored as a possible result of physical fatigue. Weakness, drowsiness, and shortness of breath are typical and suggest impending pulmonary edema or neurologic degeneration. The nurse asks specifically about abnormal bruising or bleeding, which may be the result of hematologic changes associated with uremia.
The nurse discusses the client's urinary elimination in detail, including frequency of urination, appearance of the urine, and any difficulty starting or controlling urination. This information can help identify existing urologic disorders that may influence the preservation of existing renal function.
PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS
Chronic renal failure (CRF) results in many multisystem manifestations (Chart). Clinical manifestations of CRF or uremia are associated with changes in fluid volume and chemical composition. The specific causes of many of these manifestations are not known.
NEUROLOGIC MANIFESTATIONS. Neurologic manifestations of the uremic syndrome of CRF are numerous (see Chart) and vary widely, depending on nitrogenous waste products, acid-base imbalances, and electrolyte imbalances. The nurse observes for neurologic signs, ranging from lethargy to seizures or coma, indicating uremic encephalopathy. In addition, the nurse assesses for sensory changes that generally appear in a glove and stocking distribution over the lower extremities and examines for weakness in the upper or lower extremities (i.e., uremic neuropathy).
If untreated, uremic encephalopathy progresses to seizures and coma. Dialysis is the treatment of choice for neurologicdisturbances associated with CRF. The manifestations of uremic encephalopathy resolve with the initiation of dialysis. However, improvement in uremic neuropathy is limited if the neuropathy is severe and motor function is already impaired.
CARDIOVASCULAR MANIFESTATIONS. The clinical manifestations of CRF and uremia lead to specific cardiovascular abnormalities of fluid volume excess, hypertension, congestive heart failure (CHF), uremic pericarditis, and cardiac dysrhythmiasassociated with hyperkalemia. The nurse assesses for signs of a diminished ability to excrete salt and water. The resulting circulatory fluid overload, if untreated, can lead to CHF, pulmonary edema, peripheral edema, and hypertension.
The nurse assesses heart rate and rhythm, listening for extra beats (particularly an S3), irregular patterns, or a pericardial friction rub. Unless a hemodialysis (HD) vascular access has been previously created, blood pressure is measured in each arm. The nurse assesses the jugular veins for distention and assesses for the presence of pedal, pretibial, presacral, and peri-orbital edema. Shortness of breath with exertion and paroxysmal nocturnal dyspnea (PND) suggest fluid volume excess.
RESPIRATORY MANIFESTATIONS. Respiratory manifestations of CRF vary widely among clients (e.g., breath that smells like urine [uremic fetor or uremic halitosis], deep sighing, yawning, shortness of breath). The nurse notes the rhythm, rate, and depth of breathing. Tachypnea (increased rate of breathing) and hyperpnea (increased depth of breathing) are respiratory compensation mechanisms for worsening metabolic acidosis.
With severe metabolic acidosis, the nurse may observe extreme hyperventilation or Kussmaul respiration. A few clients have hilarpneumonitis, or uremic lung. In these clients, the nurse assesses for thick sputum, minimal coughing, an increased respiratory rate, and an elevated temperature. A pleu-ral friction rub may be heard with a stethoscope. Clients often have pleuritic pain with breathing. The nurse auscultates the lungs for crackles, which indicate fluid volume overload.
HEMATOLOGIC MANIFESTATIONS. Hematologic abnormalities include anemia and abnormal bleeding. The nurse notes indicators of anemia, including fatigue, pallor, lethargy, weakness, shortness of breath, and dizziness. The presence of abnormal bleeding is assessed by observing for bruising, petechiae, purpura, ecchymoses (confluent braises), mucous membrane bleeding in the nose or gums, abnormal vaginal bleeding, or gastrointestinal (GI) bleeding (often demonstrated by black tarry stools [melena]).
GASTROINTESTINAL MANIFESTATIONS. The nurse assesses for a foul odor to the breath, mouth ulceration, or mouth inflammation and notes any vomiting. Abdominal pain or cramping may be associated with uremic colitis. Stools may test positive for blood.
URINARY MANIFESTATIONS. The urinary findings in renal failure reflect the kidneys' decreasing functioning. At first, changes occur in the amount, frequency, and appearance of the urine. Many etiologic features of chronic renal disease result inproteinuria; some cause hematuria.
and composition of the urine change as renal function deteriorates. With the
onset of end-stage renal disease (ESRD), the urine may become more dilute and clearer,
reflecting a diminished glomerular filtration
rate (GFR). The nurse must be aware that the actual urine output in a client with CRF varies with the amount of remaining
renal function. The client with ESRD usually hasoligu-ria,
but some clients will remain relatively nonoliguric, producing
INTEGUMENTARY MANIFESTATIONS. There are several dermatologic manifestations of CRF. In clients with uremia, deposition of urochrome pigment in the skin results in a yellowish coloration. Some African Americans report a darkening of the skin. The anemia of CRF causes a sallowness to the quality of the color, which some people describe as a faded suntan. This is most noticeable in lighter-skinned clients.
Skin oils and turgor are decreased in clients with uremia. One of the most uncomfortable problems of uremia is severe pruritus(itching). The nurse also assesses for bruises (ecchymoses), purple patches (purpura), and occasionally, drug-induced rashes.
Uremic frost, a layer of urea crystals from evaporated perspiration, may appear on the face, eyebrows, axilla, and groin in clients with advanced uremic syndrome.
CRF and its treatment disrupt more aspects of a client's life than almost any other illness. Nurses are in a unique position to evaluate the client with newly diagnosed renal failure and to assist with these adjustments.
Psychosocial assessment and support are part of the nurse's role from the time that CRF is first diagnosed. Initially, the nurse asks about the client's understanding of the diagnosis and its implications for treatment regimens (e.g., diet, medication, and dialysis). The nurse assesses for any signs of anxiety and for the coping mechanisms used by the client or family members. Some of the psychosocial aspects altered by CRF include family relations, social activity, work patterns, body image, and sexual activity. Thechronicity of ESRD, the variety of treatment options, and the uncertainties surrounding the course of the disease and its treatment necessitate an ongoing psychosocial assessment.
CRF results in serious abnormalities in many laboratory values (see Chart). The following blood values are routinelymonitored in clients with CRF: creatinine, blood urea nitrogen (BUN), sodium, potassium, calcium, phosphate, bicarbonate, hemoglobin, and hematocrit.
Initially, a urinalysis is performed, and a 24-hour urine specimen for creatinine and urea clearance is obtained. In the early stages of renal insufficiency, urinalysis can reveal key indicators of kidney function. Urinalysis may show excessive protein, glucose, red blood cells (RBCs), white blood cells (WBCs), and decreased or fixed specific gravity. Urine osmo-lality is usually decreased. A 24-hourcreatinine clearance is calculated after serum and urinary creatinine levels are collected and quantified. These data, along with information on body weight and height, are used to calculate renal creatinine clearance. As renal failure progresses, the urine output may decrease dramatically.
Trends in renal function and progressive deterioration are typically monitored by measurements of the serum creatinine and BUN levels. Serum creatinine levels may increase gradually over a period of years, reaching levels of 15 to 30 mg/dL or more, depending on the client's muscle mass. Urea nitrogen levels are directly related to dietary protein intake. Without dietary protein restriction, BUN levels are typically 10 to 20 times the value of the serum creatinine level. As dietary protein is increasingly restricted in an attempt to slow the rate of progression of renal failure, BUN levels remain elevated but less than the 10:1 to 20:1 ratio of nonprotein-restricted clients. Other factors affect the level of BUN, and the nurse must consider these for a complete assessment. Chapter 69 describes the factors influencing BUN levels, as well as the interpretation of serum creatinine and creatinine clearance.
X-ray findings in clients with CRF
are few. Bone radiographs of the metacarpals and phalanges of the hand
can reveal the presence of renal osteodystrophy. With established ESRD,
the kidneys are atrophic and may be 8 to
CRITICAL THINKING CHALLENGEYou are gathering the initial history for a 67-year-old African-American client admitted to your unit with suspected CRF. The client tells you that he has a history of diabetes, gout, and peptic ulcer disease. He also states that he has noted a 7-pound weight gain over the last 4 weeks.
• What other questions should you ask this client regarding his symptoms?
• What risk factors for the development of CRF are noted in his past medical history?
• What cardiac and respiratory manifestations may you findon physical examination of this client?
The client with chronic renal failure (CRF) has usually experienced a progressive degeneration of renal function and is often hospitalized for evaluation and modification of the treatment plan. The focus of care is to control or manage symptoms and prevent complications.
COMMON NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS
The following are priority nursing diagnoses for clients with CRF:
1. Imbalanced Nutrition: Less Than Body Requirements related to nausea and vomiting, decreased appetite, effects of a catabolic state, decreased level of consciousness, altered taste sensations, or dietary restrictions
2. Excess Fluid Volume related to compromised regulatory mechanisms (inability of the kidneys to maintain body fluid balance)
3. Decreased Cardiac Output related to reduction in stroke volume as a result of electrical malfunction (dysrhythmias) and mechanical malfunction (increased preload [volume excess] and increased afterload [increased peripheral vascular resistance])
4. Risk for Infection related to inadequate primary defenses (broken skin), chronic disease, or malnutrition
5. Risk for Injury related to internal biochemical risk factors associated with renal failure (increased susceptibility to bleeding, falls, and pathologic fractures) and external risk factors, such as drugs
6. Fatigue related to altered metabolic energy production, imbalance between oxygen supply and demand, and anemia
7. Anxiety related to threat to or change in health status, socioeconomic status, relationships, role functioning, support systems, or self-concept; situational crisis; threat of death; lack of knowledge (procedures, diagnostic tests, disease process, renal replacement therapy); loss of control; feelings of failure; or disrupted family life
8. The primary collaborative problem is Potential for Pulmonary Edema.
ADDITIONAL NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS
In addition to the common nursing diagnoses and collaborative problems, clients with CRF may have one or more of thefollowing:
· Diarrhea related to chemical or electrolyte imbalances, ear, anxiety, or side effects of medications
· Impaired Oral Mucous Membrane related to parotid gland changes, limited fluid intake, malnutrition, and elevated levels ofuremic toxins
· Impaired Skin Integrity related to altered chemical balance and uremic toxins
· Social Isolation related to illness or alterations in physical appearance
· Interrupted Family Processes related to situational crisis, educed income, unemployment, or effects of chronicillness
· Sexual Dysfunction related to altered body function (decreased libido and/or impotence) from disease and/or effects of medications, depression, or disturbance in self-esteem or body image
· Disturbed Thought Processes related to irritation, centralnervous system (CNS) depression, side effects of medications, sleep deprivation, or clinical depression
· Deficient Knowledge (disease process, care regimen,and follow-up care) related to lack of informational resources and magnitude of the care issues
· Potential for Sepsis
· Potential for Malnutrition
· Potential for Electrolyte Imbalances
· Potential for Metabolic Acidosis
· Potential for Gastrointestinal (GI) Bleeding
Planning and Implementation
The Concept Map on p. 1683 addresses assessment and nursing care issues related to clients who have renal failure that has progressed to end-stage renal disease (ESRD).
IMBALANCED NUTRITION: LESS THAN BODY REQUIREMENTS
PLANNING: EXPECTED OUTCOMES. The client with CRF is expected to attain and maintain the following:
• Adequate nutritional status
• Ideal body weight for age, height, and body build
• Laboratory values within safe levels
The nutritional requirements and dietary restrictions for the client with renal failure vary according to the degree of decrease in renal function and the type of dialysis performed, if any (Table).
NUTRITION THERAPY. The purpose of nutrition therapy is the administration of food and fluids to support the metabolicprocesses of a client who is malnourished or at high risk of becoming malnourished. Clients begun on hemodialysis (HD) have an increase in catabolism and subsequent decrease in intake that often results in a loss of lean body mass. NIC interventions for nutrition therapy are summarized in Chart.
The client is referred to a registered dietitian for dietary teaching and planning. The nurse in collaboration with the dietitian instructs the client about alterations in the diet that are necessary as a result of CRF. Dietary alterations include control of protein intake; limitation of fluid intake; restriction of potassium, sodium, and phosphorus intake; administration of appropriate vitamin and mineral supplements; and provision of adequate calories to meet metabolic demand.
If adequate calories are not supplied, the body will use tissue protein for energy, which leads to a negative nitrogen balance and malnutrition. The dietitian assists in determining the number of calories and types of nutrients needed to meet nutritional requirements.
PROTEIN RESTRICTION. There is some evidence to suggest that early implementation of a protein-restricted diet prevents some of the symptoms associated with CRF and may preserve kidney function. Dietary protein is restricted on the basis of the degree of renal insufficiency and the severity of the symptoms in accordance with the belief that the accumulation of waste products from protein metabolism is the priàãó cause of uremia. However, recently the value of a low-protein diet has been debated. Malnutrition is often seen in clients undergoing maintenance HD, and at least one study suggests that a low-protein diet may not be necessary in renal failure. Some studies indicate that a prescription of
practice the glomerular filtration rate (GFR) is often used as an indicator of renal function and can be a guide to safe levels of protein consumption. A client with a severely reduced GFR who is not undergoing dialysis is usually permitted 0.55 to
The client receiving dialysis requires more protein because of protein loss through dialysis. HD clients have their protein requirements individually tailored according to their postdial-ysis, or "dry," weight. Typically, HD clients are allowed protein in the amount of 1 to 1.5 g/kg/day; peritoneal dialysis (PD) clients are allowed 1.2 to 1.5 g/kg/day because protein is lost with each exchange (Levine). Three fourths of the protein should be of high biologic value, such as milk, meat, or eggs. If protein intake is inadequate, a negative nitrogen balance develops and causes muscle wasting. Serum albumin and blood urea nitrogen (BUN) levels are used to monitor the adequacy of protein intake. Decreases in serum albumin levels indicate inadequate protein intake and malnutrition. Excessive protein intake can dramatically increase BUN levels in clients with renal failure.
SODIUM RESTRICTION. The nurse monitors fluid and sodium intake. In clients with little or no urine output, fluid and sodium retention can cause edema, hypertension, and congestive heart failure (CHF). Most clients with renal failure retain sodium; a few cannot conserve sodium.
status in terms of fluid and sodium retention can be estimated by monitoring body weight and blood pressure. Innondialyzed uremic clients, sodium is limited to 1 to
POTASSIUM RESTRICTION. The nurse monitors potassium intake because hyperkalemia can cause dangerous cardiacdysrhythmias. Cardiac rhythm is monitored for the tall, peaked T waves characteristic of hyperkalemia; the serum potassium level is also documented. The client with advanced CRF is instructed to limit potassium intake to 60 to 70 mEq/day. The labels of seasoning agents are carefully inspected for sodium and potassium content. Clients are instructed to avoid salt substitute agents, many of which are composed of potassium chloride, if oliguria is present. Clients receiving PD or who are producing urine may not need dietary potassium restrictions.
PHOSPHORUS RESTRICTION. Control of phosphate levels is begun early in renal failure to avoid osteodystrophy. The nurse monitors serum phosphate levels, and the physician may order dietary phosphorus restrictions and medications to assist with phosphate control. Phosphate binders must be taken at mealtime. Most clients with kidney disease already restrict their protein intake, and because high-protein foods are high in phosphorus, their phosphorus consumption is also reduced. Chapter 11 lists foods high in potassium, sodium, and phosphorus.
VITAMIN SUPPLEMENTATION. Most clients with renal failure require daily vitamin and mineral supplementation. Low-protein diets are usually deficient in vitamins, and water-soluble vitamins are removed from the blood during dialysis. In addition, anemia is a chronic problem in clients with renal failure because of the limited iron content of low-protein diets and decreased erythropoietin production by the kidneys. Thus supplemental iron is needed. Calcium and vitamin D supplements may also be required, depending on the client's serum levels and bone status.
INDIVIDUAUZATION OF THE DIET. Clients undergoing PD
require a slightly different diet from those undergoing HD. Because protein is lost with the dialysate in
PD, a major nutritional problem for these clients is replacing
lost protein. In many
cases, 1.2 to
The nurse plays a vital role in managing the client's diet. In collaboration with the dietitian, the nurse provides teaching and performs ongoing assessments of the client's comprehension of and compliance with dietary regimens. Written examples of the prescribed diet can be given to the client and family. The nurse and dietitian can help clients adapt the diet to their budget, ethnic background, and food preferences to maximize caloric intake within the diet's restrictions.
EXCESS FLUID VOLUME
PLANNING: EXPECTED OUTCOMES. The client with chronic renal failure (CRF) is expected to:
• Achieve and maintain an acceptable fluid balance
• Minimize the risk of complications from fluid imbalances
Management of the client with CRF includes drug therapy, diet therapy, fluid restriction, and dialysis. Diet therapy is discussed under Imbalanced Nutrition: Less Than Body Requirements.
FLUID MANAGEMENT. The purpose of fluid management is the promotion of fluid balance and the prevention of complications resulting from abnormal or undesired fluid levels. The nurse monitors the client's intake and output and hydration status. In addition, the nurse assesses for signs and symptoms indicative of fluid volume excess, such as crackles in the bases of the lungs, edema, and distended neck veins.
DRUG THERAPY. Diuretics are prescribed for clients with renal insufficiency when needed for treatment of fluid retention or to help control blood pressure. The diuresis produced from these drugs is useful in treating fluid overload in clients who still have some urine output. Diuretics are seldom used in clients with end-stage renal disease (ESRD) after dialysis has been initiated because, as kidney function diminishes, these drugs can have harmful side effects, including nephrotoxic and ototoxic effects.
The nurse uses
daily weight measurements and intake and output records as important sources of
assessment data. Daily weight gain generally indicates fluid retention rather
than true body weight gain. The nurse estimates the amount of fluid retained:
FLUID RESTRICTION. The amount of fluid restriction ordered is discussed under Sodium Restriction, p. 1684. The nurse considers all forms of intake, including oral, intravenous, and fluid or medication administration through gastrointestinal (GI) tubes, when calculating fluid intake. The nurse assists the client in distributing fluid intake by mouth over a 24-hour period. The client's response to fluid restriction is monitored, and the health care provider is notified if signs and symptoms of fluid volume excess persist or worsen.
DECREASED CARDIAC OUTPUT
PLANNING: EXPECTED OUTCOMES. The client with CRF is expected to attain and maintain normal sinus rhythm, adequate cardiac output, and blood pressure in expected ranges.
INTERVENTIONS. Many clients with long-standing hypertension have renal insufficiency, and some progress to CRF and ESRD. Therefore the control of hypertension is an essential factor in preserving renal function. To control hypertension, the physician may order calcium channel block-ers, angiotensin-converting enzyme (ACE) inhibitors, alpha-adrenergic and beta-adrenergic blockers, and vasodilators. Recent studies have documented the effectiveness of ACE inhibitors, as compared with otherantihypertensives, in slowing the progression of renal failure (Levine, 1997). More inforation on the specific medications can be found in Chapter 36. Indications vary, depending on the client, and these drags are used carefully to avoid hyperkalemia and hypotension. Various combinations and doses may be tried until blood pressure control is adequate and side effects are minimized. Calcium channel blockers seem to improve the GFR and renal blood flow.
The client and family or significant others are instructed to measure blood pressure. The nurse evaluates the client's ability to measure and record blood pressure accurately using the client's own equipment. The nurse periodically rechecks measurement accuracy. In addition to accurate measurement of blood pressure, the client and family must understand the relationship of blood pressure control and regulation to diet and medication therapy. The nurse further instructs the client to measure weight daily and to bring records of blood pressure measurements and weights for discussion with the physician, nurse, or dietitian.
The nurse assesses and monitors, on an ongoing basis, for signs and symptoms of decreased cardiac output, heart failure, congestive heart failure (CHF), and dysrhythmias. These topics are discussed in Chapters.
RISK FOR INFECTION
PLANNING: EXPECTED OUTCOMES. The client with CRF is expected to remain free of infection.
INTERVENTIONS. The nurse or assistive nursing personnel provides meticulous care to any areas where skin integrity has been broken (incisions, site of drains, puncture sites, cracked or excoriated skin, pressure sores) and provides good basic preventive skin care. For clients undergoing dialysis, the nurse also inspects the vascular access site or PD catheter insertion site. These areas are assessed on an ongoing basis for redness, swelling, pain, and drainage. Vital signs are monitored for any signs or symptoms of infection.
RISK FOB INJURY
PLANNING: EXPECTED OUTCOMES. The client with chronic renal failure (CRF) is expected to remain free of injury (will not fall or experience injury from a fall and will not experience pathologic fractures, bleeding, or toxic effects of medications administered in the presence of CRF).
INTERVENTIONS. Managing drag therapy in clients with CRF is a complex and ongoing clinical problem. Many over-the-counter drags contain ingredients that may affect renal function. Therefore it is important to obtain a detailed drag history. The nurse must be aware of the use of each drag, its side effects, and the site of metabolism. The nurse, in conjunction with the physician and pharmacist, monitors the client closely for drag-related complications and adjusts dosages accordingly.
Certain medications must be avoided, and the dosages of others must be adjusted according to the degree of remaining renal function. As the client's renal function decreases, repeated dosage adjustments are necessary. The nurse assesses for side effects and signs of drug toxicity and notifies the physician as appropriate.
A number of medications are routinely administered to clients with renal failure. The nurse giving these medications understands the rationale for administration and the nursing interventions for each drag. Many clients have some degree of cardiac disease and may require cardiotonic drags, such as digoxin. Clients with decreased renal function are particularly susceptible to digoxin toxicity because the drug is excreted by the kidneys. The nurse caring for clients with CRF who are receiving any digitalis derivative, including digoxin, monitors for signs of toxicity, such as nausea, vomiting, anorexia, visual disturbances, restlessness, headache, fatigue, confusion, cardiac irregularities (particularly bradycardia [pulse rate, 50 to 60 beats/min] and tachycardia [pulse rate, 100 beats/min]), and serum drag levels above therapeutic range. In addition, serum levels of potassium are monitored closely in any client receiving cardiotonic medications.
Drags to control an excessively high phosphate level include phosphate-binding compounds. Calcium acetate, calcium carbonate, and aluminum hydroxide are used as phosphate-binding agents in clients with renal failure. These drags treat the metabolic complications that if untreated may lead to renal osteodystrophy and related injuries. To prevent further complications, the nurse stresses the importance of these and all medications.
Hypercalcemia (excessively high serum calcium levels) is a possible complication for clients taking calcium-containing compounds to control phosphate excess. Hypophosphatemia (low serum phosphoras levels) is also a possible outcome of phosphate binding but is typically also associated with phosphate depletion in clients who are not eating adequately but are continuing to take phosphate-binding medications. In clients taking aluminum-based phosphate binders for prolonged periods, retention and deposition of aluminum may cause bone disease or neurologic manifestations that may not be reversible. The nurse monitors the client for evidence of muscle weakness, anorexia, malaise, tremors, or bone pain.
Clients with renal disease should avoid antacid compounds containing magnesium. Clients with renal failure cannot excrete magnesium and thus should avoid additional intake.
In addition to the drugs used to treat renal failure, the use of other medications requires special consideration. These medications include antibiotics, opioids, antihypertensives, diuretics, insulin, and heparin.
Many antibiotics are safe for clients with renal failure, but those excreted primarily by the kidneys require dose modification. To prevent complications of bloodstream infections from oral cavity bacteria, prophylactic antibiotic treatment is routinely given to clients with CRF before any dental procedures. The antibiotic and protocol used vary with the client's needs and the physician's preference.
The nurse administers opioid analgesics cautiously in clients with renal failure because the effects often last much longer than in people with healthy kidneys. Clients with uremia are particularly sensitive to the respiratory depressant effects of these drags. Because opioids are metabolized by the liver and not the kidneys, the dose recommendations are often the same regardless of the level of renal function. The nurse monitors these clients closely after opioid administration and evaluates the need for additional administration on the basis of the client's reaction to the drag.
As renal disease progresses, the client with diabetes melli-tus often requires modification of an insulin or oral antidia-betic drag dose because of decreased insulin metabolism by ailing kidneys. Frequent blood glucose determinations are obtained to evaluate the client's insulin or oral agent needs. Urine glucose measurements are less accurate when renal disease is present.
Because of poor platelet function and capillary fragility in renal failure, heparin and other anticoagulants are used cautiously.
HI PLANNING: EXPECTED OUTCOMES. The client with chronic renal failure (CRF) is expected to conserve energy by balancing activity and rest in order to be able to perform self-care and activities of daily living.
INTERVENTIONS. All clients with renal dysfunction are given some type of vitamin and mineral supplement. Because of diet restrictions and vitamin losses associated with both peritoneal dialysis (PD) and hemodialysis (HD), water-soluble vitamins must be replaced. The nurse avoids giving the client these vitamin supplements before HD treatment because they will be dialyzed out of the body and the client will receive no benefit.
The anemic client with CRF is treated with recombinant erythropoietin (erythropoietin alfa [Epogen, Procrit]). The goal of erythropoietin therapy is to achieve a hematocrit of 30% to 35%. For erythropoietin to stimulate bone marrow to produce red blood cells (RBCs), clients must have adequate iron stores. In addition, chronic administration of erythropoietin can deplete iron stores, necessitating iron supplementation. Many who receive epoetin alfa report improved appetite and sexual function along with decreased fatigue; in some clients, hypertension associated with a rise in hematocrit has been reported. The improved appetite may challenge clients in their attempts to maintain dietary protein, potassium, and fluid restrictions and necessitates additional education.
PLANNING: EXPECTED OUTCOMES. The client with CRF is expected to eliminate or reduce feelings of apprehension and tension from an unidentified source as evidenced by:
Seeking information to reduce anxiety
• Using effective coping strategies
• Reporting an absence of physical manifestations of nxiety
INTERVENTIONS. The nurse has the most frequent contact with the client with CRF when the client is hospitalized or undergoing in-center dialysis treatments. Thus nurses perform an ongoing assessment of the client's anxiety level to determine the level of nursing intervention required. The nurse observes the client's behavior for physical cues indicating anxiety (e.g., an anxious facial expression or gestures and an increased pulse rate). In addition, the nurse evaluates the support systems, as evidenced by the involvement of family and friends with the client's care.
Unfamiliar settings and situations, and lack of knowledge about treatments and tests can increase the client's anxiety level. The nurse explains all procedures, tests, and treatments. The client's knowledge deficits concerning normal renal function and renal failure are identified. Evaluating the client's current knowledge avoids needless repetition during teaching sessions. The nurse provides instruction appropriate to the client's needs and ability to understand. By explaining the disease process, the nurse enhances the client's acceptance and decreases anxiety.
The nurse provides continuity of care, whenever possible, to establish a consistent nurse-client relationship to decrease anxiety and promote discussions of client and family concerns. As the nurse-client relationship develops, the client is encouraged to discuss current problems or concerns. A multi-disciplinary team of professionals participates to provide support and counseling for the client and family, often over many years of treatment.
The nurse encourages the client to ask questions and discuss fears about the diagnosis of renal failure. An open atmosphere that allows for discussion can decrease anxiety level. Nurses also facilitate discussions with family members or significant others concerning the prognosis and the potential impact on the client's lifestyle.
POTENTIAL FOR PULMONARY EDEMA
PLANNING: EXPECTED OUTCOMES. The client with CRF is expected to remain free of pulmonary edema. A secondary outcome is to maintain optimal fluid volume balance through dialysis and pharmacologic measures, thus preventing the onset of pulmonary edema.
INTERVENTIONS. In the client with CRF, pulmonary edema can result from either of two distinct mechanisms: left-sided heart failure or microvascular injury. In left-sided heart failure, the heart is unable to adequately eject blood from the left ventricle, leading to an increase in hydrostatic pressure. The increased pressure allows fluid to cross the capillaries into the pulmonary interstitium. Pulmonary edema can also occur from injury to the vascular endothelium or alveolar epithelial cells secondary to uremia. Fluids then leak into the interstitial space and ultimately into the alveoli.
The nurse assesses the client for early signs of pulmonary edema, such as restlessness, heightened anxiety, tachycardia, dyspnea, and crackles that begin at the base of the lungs. As pulmonary congestion worsens, the level of fluid in the lungs rises. Auscultation will reveal increased rales, decreased air exchange, and dullness to percussion at the upper limits of fluid collection. The client may expectorate frothy, blood-tinged sputum. With further cardiac and respiratory compromise, the client can become diaphoretic and cyanotic.
The client who develops pulmonary edema is often admitted to the intensive care unit for aggressive treatment, which includes continuous cardiac monitoring. The client is placed in a high Fowler's position and given oxygen to maximize lung expansion and improve gas exchange. Drug therapy with renal failure and pulmonary edema is difficult at best because of the potential adverse effects of drugs on the kidneys. Treatment of pulmonary edema involves the administration of potent loop diuretics, such asfurosemide (Lasix). Furosemide dosing usually begins at 40 mg, administered intravenously over a 1- to 2-minute period. This dose may be repeated in 30 minutes if no response is elicited. For clients already receiving maintenance doses of furosemide, an IV dose equivalent to the oral maintenance dose is given; it is doubled in 30 minutes if no response is seen (Johnson & Lalonde, 1997). Renalimpairment multiplies the risk of ototoxicity with the use of furosemide; thus IV doses are given cautiously.
Morphine sulfate 1 to 2 mg administered intravenously is usually prescribed to reduce myocardial oxygen demand by reducing ventricular preload and to provide vasodilation and sedation. The dose is adjusted to achieve the desired response, but the potential for respiratory depression exists. Therefore the nurse monitors the client's respiratory rate and blood pressure closely. To further decrease hydrostatic pressure, a continuous infusion pump may administer a vasodilator, such as nitroglycerin. Vital signs are monitored vigilantly, since these drugs in combination may result in severe hypotension.
Nursing interventions include Foley catheter placement and frequent assessment of urine output to gauge the effectiveness of diuretic therapy. Diuresis usually begins within 5 minutes of administration of IV furosemide. Urine output is measured every 15 to 30 minutes during the acute episode and every hour thereafter until the client is stabilized. In addition, the nurse assesses breath and heart sounds for improvement in crackles and for the presence of an S3, indicating fluid overload.
The nurse monitors serum chemistry results for electrolyte imbalances and reports abnormalities to the appropriate health care provider so that correction of imbalances can be initiated. Continuous cardiac monitoring is initiated to identify potentialdysrhythmias. Oxygen saturation levels are monitored by pulse oximetry and arterial blood gas values. The oxygen delivery system is adjusted to maintain adequate oxygen saturation levels. The nurse monitors the client for deterioration, manifested as increasing pulmonary congestion and hypoxemia. It may be necessary to intubate the client and mechanically ventilate the lungs at this point to prevent death.
Clients with CRF are at increased risk for developing pulmonary edema, since they may present with precipitating fluid volume overload and existing cardiac compromise secondary to hypertension and volume overload. Such clients are less likely to respond quickly to treatment and are more likely to develop adverse effects from pharmacologic agents as a result of renal impairment. Occasionally, ultrafiltration may be used to further reduce fluid volume.
Renal Replacement Therapies
Renal replacement therapy is required only when the clinical and laboratory manifestations of renal failure present complications that are potentially life threatening or that pose continuing discomfort to the client. When the client can no longer be managed with conservative therapies, such as diet, medication, and fluid restriction, dialysis is indicated. Transplantation may be discussed at any time.
Hemodialysis (HD) is one of several renal replacement therapies used for the treatment of renal failure (Table 72-9). Dialysis removes excess fluids and waste products and restores chemical and electrolyte balance. HD involves the extracorporeal (outside of the body) passage of the client's blood through a semipermeable membrane that serves as an artificial kidney.
CLIENT SELECTION. Any client may be considered for HD therapy. Initiation of renal replacement therapy depends on the symptoms of the client, not on the creatinine clearance. Dialysis is initiated immediately for clients who exhibit the following: fluid overload refractory to diuretics, presence of pericarditis, uncontrolled hypertension, neurologic manifestations, and development of bleeding diathesis. More commonly, dialysis is started when clients have signs of symptom progression, such as nausea and vomiting, decreased attention span, decreased cognition, worsening anemia, and pruritus (Levine, 1997).
The duration of survival after HD depends on the client's age, the cause of renal failure, and the presence of other diseases, such as coronary artery disease, hypertension, or diabetes. The following are general guideline requirements for appropriate client selection:
· Presence of fatal, irreversible renal failure when other therapies are unacceptable or ineffective
· Absence of illnesses that would prevent or seriously complicate HD
· Expectation of rehabilitation
· The client's acceptance of the regimen
DIALYSIS SETTINGS. Clients may receive HD treatments in any of several settings, depending on specific needs. They may be dialyzed in an acute care (hospital-based) center if they have recently begun treatment or have complicating conditions that require close nursing or medical supervision. Stable clients with chronic renal failure (CRF) may be he-modialyzed in a freestanding HD center in the community hen they no longer require intensive supervision. Stable clients may participate in complete or partial self-care in an outpatient center or with in-home HD.
In-home HD offers the least disruptive form of therapy and allows for the most adaptation of the regimen to the client's lifestyle. Unfortunately, many clients cannot participate in in-home dialysis because they lack a reliable and consistent partner to administer the therapy and manage the dialysis machine. For some clients and partners, the responsibilities of in-home dialysis are extremely stressful, so that this option is less desirable. In addition, a water treatment system must be installed in the home to provide a safe, clean water supply for the dialysis process.
Regardless of the setting for therapy, the client needs ongoing nursing support and intervention to maintain this complex and lifesaving treatment.
PROCEDURE. The principles of HD are based on the passive transfer of toxins, which is accomplished by diffusion. Diffusionis the movement of molecules from an area of higher concentration to an area of lower concentration. The rate of diffusion is affected by numerous factors. Diffusion during dialysis occurs more rapidly when the membrane pores are large, there is a large surface area of membrane, the temperature of the solutions is higher, and there is a greater difference in the solute concentrations. Molecules that are too large, such as RBCs and plasma proteins, cannot pass through the membrane.
When HD is initiated, blood and dialysate flow in opposite directions from their respective sides of an enclosed semiper-meablemembrane. The dialysate is a balanced mix of electrolytes and water that closely resembles human plasma. On the other side of the membrane is the client's blood, which contains metabolic waste products, excess water, and excess electrolytes. During HD, the waste products move from the blood into the dialysate because of the difference in their concentrations (diffusion). Excess water is also removed from the blood into the dialysate (osmosis). Electrolytes can move in either direction, as needed, and take some fluid with them. Potassium and sodium typically move out of the plasma into the dialysate, whereas bicarbonate and calcium move from the dialysate into the plasma. This process continues as the blood and the dialysate are circulated past the membrane for a presetlength of time. Water volume may be removed from the plasma by applying positive or negative pressure to the system.
The components of an HD system include a dialyzer, dialysate, vascular access routes, and an HD machine. The artificial kidney,or dialyzer (Figure 72-3), has four components: a blood compartment, a dialysate compartment, a semi-permeable membrane, and an enclosed structure to support the membrane.
Dialysate is made from clear water and chemicals and is free of any metabolic waste products or drugs. Because bacteria and other microorganisms are too large to pass through the membrane, dialysate does not need to be sterile. The water used in dialysate must meet specific standards, and water treatment systems are used to ensure a safe water supply. The dialysate composition may be altered according to the client's needs for treatment of electrolyte imbalances. During HD, the dialysate is warmed to approximately 100° F (37. 8° C) to increase the efficiency of diffusion and to prevent a decrease in blood temperature.
An essential function of an HD machine is the monitoring for potential problems, including the following:
· Changes in dialysate temperature
· Presence of air in the blood tubing
· A blood leak in the dialysate compartment
· Changes in the pressure or composition within the blood and the dialysate compartments
If any of these problems are detected, an alarm alerts the nurse. The monitoring systems protect the client from life-threatening complications that can result if these technical problems are not corrected.
All models of HD machines function, in principle, as illustrated in Figure 72-4. Figure 72-5 shows one type of machine. The duration and frequency of HD treatments depend on the amount of metabolic waste to be cleared, the clearance capacity of thedialyzer, and the amount of fluid to be removed. Most dialyzers provide sufficient clearance to limit the total number of hours of dialysis to about 12 hours a week. This time is usually divided into three 4-hour treatments a week. For clients with less muscle or more ongoing urine production, two 5- to 6-hour treatments a week may be adequate. If the client gains large amounts of fluid weight, a longer treatment time may be needed to remove the fluid without hypotension or severe side effects.
ANTICOAGULATION. To prevent blood clots from forming within the dialyzer membrane and the blood tubing, anticoagulation with heparin is necessary during HD treatments. Heparin, a short-acting anticoagulant, inhibits the tendency of blood to clot when it comes in contact with foreign surfaces. There is considerable variability among clients intheir anticoagulation response and elimination of heparin. The heparin dose must be adjusted on the basis of each client's need. Clients receiving erythropoietin may need more heparin. Heparin remains active in the body for 4 to 6 hours after administration, making the client at risk for hemorrhage during and immediately after HD treatments. The client must avoid any invasive procedures during that time. Thus the nurse monitors closely for any signs of bleeding or hemorrhage. Clotting tendencies can be monitored during HD with a bedside machine (such as the Hemochron), by whole-blood clotting times (Lee-White clotting test), or by activated partial thromboplastin times (aPTT) during and after HD. Protamine sulfate is given as an antidote to neutralize heparin's anticoagulant activity when necessary.
VASCULAR ACCESS. For hemodialysis (HD) to be performed, a vascular access route is required (Table 72-10). Dialysis treatments necessitate the easy availability of a large amount of blood flow—at least 250 to 300 mL/min, usually for a period of 3 to 4 hours. Normally, the body cannot provide this type of circulatory access without surgical revision of blood vessels.
LONG-TERM VASCULAR ACCESS. An internal access is preferred for most clients undergoing long-term HD (see Table 72-10). There are two common choices: an internal arte-riovenous (AV) fistula or an AV graft (Figure 72-6). AV fistulas are formed by connecting (anastomosis) an artery to a vein. The most commonly used vessels are the radial or brachial artery and the cephalic vein of the nondominant arm. This process increases the blood flow through the vein to 250 to 400 mL/min, the amount required for dialysis to be effective.
Some time is necessary for an AV fistula to develop, and the amount of time required for the fistula to "mature" varies. Primary AV fistulas may not be suitable for use for as long as 4 months. Therefore vascular access must be planned accordingly. As the fistula matures, the increased pressure of the arterial blood flow into the vein causes the vessel walls to thicken. This thickening increases their strength and suitability for repeated cannulation.
To obtain access to a fistula, the nurse cannulates it or inserts two needles, one toward the venous blood flow and one toward the arterial blood flow. This procedure allows the HD machine to draw the blood out through the arterial needle and return it through the venous needle. The client may require a temporary vascular access (AV shunt or HD catheter) for HD treatments until the fistula is ready for use.
AV grafts are used when the AV fistula does not develop or when complications of the AV fistula limit continued use. Thepolytetrafluoroethylene (PTFE) graft is a synthetic material (Gore-Tex). This type of graft is commonly used in older clients undergoing HD.
PRECAUTIONS. Several precautions must be observed to ensure the functioning of an internal AV fistula or AV graft. First, the nurse assesses for adequate circulation in the fistula or graft, as well as in the distal portion of the extremity. The nurse then checks for a bruit or a thrill by auscultation or palpation over the access site. Repeated compression can result in the loss of the vascular access; therefore the nurse avoids taking the blood pressure in the arm with the vascular access unless absolutely necessary. The AV fistula or graft is not used for administration of IV fluids; venipuncture is avoided anywhere in the arm used for HD access. Chart 72-9 lists best practices for care of the client with an HD access.
COMPLICATIONS. Complications can occur regardless of the type of access. The most common problems include thrombosis or stenosis, infection, aneurysm formation, ischemia, and high-output heart failure.
Thrombosis, or clotting, is the most frequent complication. Some clients are more susceptible to clotting than are others and may be given anticoagulants. Surgical declotting or revision of stenotic areas is typically performed in the surgical suite with the use of local anesthesia.
Most infections that occur in clients undergoing long-term HD involve the vascular access. The most common organism causing infection is Staphylococcus aureus, which can be introduced by punctures for dialysis access. The nurse limits the incidence of infections by using careful sterile technique before needle cannulation (Table 72-11).
Aneurysms can form in any internal fistula and are caused by repeated needle punctures at the same site. Aneurysms that appear to be increasing in size may cause loss of the fistula's function and require surgical repair.
Ischemia occurs in a few clients with vascular access when the formation of the fistula causes a decrease in arterial blood flow to areas distal to the fistula. Ischemic symptoms (steal syndrome) vary from cold or numb fingers to gangrene. If the collateral circulation is inadequate, the existing fistula may need to be ligated and a new fistula created in another area for circulation to be preserved in the extremity.
The shunting of blood directly from the arterial system to the venous system, through the fistula, can cause high-output heart failure in clients with a limited cardiac reserve (see Chapter 35). This complication occurs rarely, but if it does, the fistula may need to be revised to decrease the blood flow from the arterial supply.
TEMPORARY VASCULAR ACCESS. The first type of vascular access developed was the external arteriovenous (AV) shunt(Figure 72-7; see also Table 72-10), but it is rarely
used today. To create a shunt, the surgeon places a piece of sil-icone rubber (Silastic) tubing into an artery and a second piece into an adjacent vein. The tubings are connected externally to provide a readily available vascular access. The arterial limb is used to obtain the blood for passage through the artificial kidney (dialyzer membrane), and the venous limb is used to return the blood to the client's body after each pass through the dialyzer.
Temporary vascular access with special catheters has replaced the use of the AV shunt for most clients requiring immediate HD. A catheter designed for HD may be inserted into the subclavian, internal jugular, or femoral vein if no permanent vascular access is available for use (see Dialysis Therapies, pp. 1674 and 1675). The lumens of these devices are considerably smaller than the permanent accesses, and the duration of each dialysis session is increased (usually requires 4 to 8 hours).
POSTDIALYSIS NURSING CARE. The nurse closely monitors the client immediately after dialysis and for several hours afterward for any side effects from the treatment. The more common clinical manifestations of complications include hypotension, headache, nausea, malaise, vomiting, dizziness, and muscle cramps.
The nurse obtains vital signs and weight for comparison with predialysis measurements. Blood pressure and weight are expected to be reduced as a result of fluid removal. Excessive hypotension may require rehydration with IV fluids, such as normal saline. The client's temperature may also be elevated, because the dialysis machine warms the blood slightly. If the temperature is elevated excessively, sepsis is suspected and a blood sample is obtained, as ordered, for culture and sensitivity determinations.
The heparinization required for hemodialysis (HD) increases the clotting time and thus the risk for excessive bleeding. All invasive procedures must therefore be avoided for 4 to 6 hours after dialysis, and the nurse continually monitors the client for signs ofhemorrhage during dialysis and for 1 hour after dialysis (Chart 72-10).
COMPLICATIONS. A variety of fluid-related and infectious complications can occur from HD. The most common complications include disequilibrium syndrome and acquisition of viral infections.
Dialysis disequilibrium syndrome may develop during HD or after HD has been completed. The cause is unknown but may be due to the rapid decrease in blood urea nitrogen (BUN) levels during HD. These changes in urea levels can cause cerebral edema, which leads to increased intracranial pressure. Neurologic complications can result (headache, nausea, vomiting, restlessness, decreased level of consciousness, seizures, coma, or death).
Early recognition by the nurse of the signs of the syndrome and appropriate treatment with anticonvulsant medications andbarbiturates may prevent a life-threatening situation. Dialysis disequilibrium syndrome may be avoided, or minimized, by introducing HD for short periods initially with low blood flows so that rapid changes in plasma composition are avoided.
Infectious diseases transmitted by blood transfusion are another serious complication associated with long-term HD. Two of the most serious blood-transmitted infections are hepatitis and human immunodeficiency virus (HIV).
Hepatitis infection in clients with chronic renal failure (CRF) has decreased in recent years, paralleling the decrease in blood transfusion requirement for these clients because of the availability of erythropoietin therapy. Yet, because of the blood access and the risk of microscopic exposure, hepatitis continues to be a problem for clients undergoing HD. The hepatitis Â virus can be transmitted through the use of contaminated needles or instruments, by entry of contaminated blood through open wounds in the skin or mucous membranes, or through transfusion of blood contaminated with the virus.
The incubation period for acute hepatitis is 6 weeks to 6 months. Thus the nurse continually monitors the client undergoing HD who is receiving frequent transfusions for signs of hepatitis virus infection (see Chapter 59).
HIV is a bloodborne and body fluid-borne virus with some potential threat to clients undergoing HD. Fortunately, the risks of HIV transmission are minimized by the consistent practice of standard precautions (blood and body fluids), routine screening of donated blood for HIV, and decreased numbers of blood transfusions for clients with end-stage renal disease (ESRD). Despite this progress, however, an unknown number of clients may have already been infected with the HIV virus. Clients who have been undergoing HD and who received frequent transfusions during the early to mid-1980s are at risk for acquired immunodeficiency syndrome (AIDS) (see also Chapter).
Peritoneal dialysis (PD) takes place within the peritoneal cavity. PD is slower than hemodialysis (HD), however, and more time is needed for the same effect to be obtained.
CLIENT SELECTION. Most clients with chronic renal failure (CRF) can select either HD or PD. For clients who arehemodynamically unstable and for those who cannot tolerate systemic anticoagulation, PD is less hazardous than HD. The lack of vascular access due to inadequate vessels may eliminate HD as an option. In addition, some clients with a new arteriovenous (AV) fistula receive PD while waiting for the access to mature for HD. PD is also often the treatment of choice in the older adult and pediatric populations because it offers more flexibility if the client's status changes frequently.
In some relatively rare situations, PD cannot be performed, usually because of peritoneal adhesions or intra-abdominal surgery in the peritoneal cavity. In these cases, the peritoneal membrane's surface area has been reduced too much to allow for adequate dialysis exchange. In other cases, peritoneal membrane fibrosis may occur after repeated infections, which decreases membrane permeability despite adequate surface area.
PROCEDURE. The surgical insertion of a siliconized rubber (Silastic) catheter into the abdominal cavity
is required to allow the infusion of dialyzing fluid (dialysate)
(Figure). According to the physician's order,
PROCESS. PD occurs through diffusion and osmosis across the semipermeable peritoneal membrane and adjacent capillaries. The peritoneal membrane is large and porous. It allows solutes, which carry fluid with them, to move by an osmotic gradient from an area of higher concentration in the body (blood) to an area of lower concentration in the dialyzing fluid.
The peritoneal cavity is rich in capillaries and provides a ready access to the blood supply. The fluid and waste products dialyzed from the client move through the blood vessel walls, the interstitial tissues, and the peritoneal membrane and are removed when the dialyzing fluid is drained from the body.
The efficiency of PD can be affected by numerous situations, such as changes in the peritoneal membrane's permeability caused by infection or irritation, and changes in the capillary blood flow resulting from vasoconstriction, vascular disease, or decreased perfusion of the peritoneum. Excess water removal (ultrafiltration) in HD is accomplished by use of hydrostatic positive pressure ortransmembrane negative pressure on the dialysis machine. In PD, the amount of water removed from the client depends on theconcentration of the dialysate. Increasing the glucose concentration of the dialysate makes the solution increasingly more hypertonic. The more hypertonic the solution, the greater the osmotic pressure for ultrafiltration and thus the greater the amount of fluid removed from the client during an exchange. The physician orders the dialysate concentration on the basis of the client's fluid status.
MEDICATION ADDITIVES. Heparin may be added to the dialysate to prevent fibrin clot formation in the catheter or tubing; this intraperitoneal (IP) heparin administration is necessary only after new catheter placement or with the occurrence of peritonitis. There is no systemic absorption of heparin with IP administration, so clotting studies are not needed.
Other agents that may be administered by the IP route include potassium chloride and antibiotics. Commercially prepared dialysatedoes not contain potassium chloride. Some clients will need potassium chloride added to the dialysate so that the dialysate does not excessively deplete potassium from the plasma. Oral potassium supplements may be prescribed in selected clients. The physician may order IP administration of antibiotics (e.g., gentamicin, vancomycin, cephalosporins) when peritonitis is present or suspected. The combination of potassium chloride and antibiotics in the same bag of dialysate is not recommended, because chemical interactions may limit effectiveness.
TYPES OF PERITONEAL DIALYSIS. Many types of PD are available, including continuous ambulatory PD, multiple-bag continuous ambulatory PD, automated PD, intermittent PD, and continuous-cycle PD. The selection of the type depends on the client's ability and lifestyle.
CONTINUOUS AMBULATORY PERITONEAL DIALYSIS.
In continuous ambulatory peritoneal dialysis (CAPD), the client performs self-dialysis by infusing four 2-L exchanges of dialysateinto the peritoneal cavity, where the dialysate remains for 4 to 8 hours, 7 days a week. During the dwell period, the client can choose a continuous connect system or a disconnect system.
With the continuous connect system (straight transfer set), the dialysate bag is usually attached to the catheter by 48-inch (122-cm) tubing; the empty bag and tubing are folded and worn beneath the clothing until they are used for outflow. After draining, the client removes the bag and connects a new bag to repeat the process.
With the disconnect system (Y-transfer set), the client removes the connecting tubing and empty dialysate bag after inflow and attaches a protective cap to the PD catheter junction. The disconnect system eliminates the need to wear the tubing and bag but requires opening the system two extra times with each exchange. This opening of the system increases the potential for contamination and infection.
With CAPD treatment, no machine is necessary, and client independence is encouraged. Theoretically, no partner is required. However, many home training programs suggest that a partner be trained in CAPD as a support for the client should illness or temporary disability occur. Devices to assist in the safe, uncontaminated connection of the tubing spike with the dialysate bag are increasingly in use. These devices can be considered for clients with impaired vision, limited manual dexterity, or decreased upper extremity strength. CAPD offers the advantage of constant removal of fluid and wastes and more nearly resembles renal function than does HD. Some clients continue to perform their own exchanges while hospitalized.
MULTIPLE-BAG CONTINUOUS AMBULATORY PERITONEAL DIALYSIS. For those who are unable to perform self-CAPD in the acute care setting, a multiple-bag CAPD (MB-CAPD) system allows continuation of CAPD. With MB-CAPD, a manifold of tubing connected to the dialysate and hanging on a portable pole is attached to the PD catheter by connecting tubing (see Figure 72-8). The nurse inflows the dialysate at the prescribed time, allows the dwell, and initiates the outflow for each exchange. The MB-CAPD system permits mobility for the ambulatory client and provides for continuous PD.
AUTOMATED PERITONEAL DIALYSIS. An automated cycling machine that provides for dialysate inflow, dwell, and outflow according to preset times and volumes may be used. A warming chamber for dialysate is part of the machine. Automated peritoneal dialysis (APD) may be used in the acute care setting, the outpatient dialysis center, or the client's home. The functions are performed in response to machine programming that can be individualized for the client's specific needs. A typical prescription calls for 30-minute exchanges (10/10/10 for inflow, dwell, and outflow) for a period of 8 to 10 hours. The machines have numerous safety monitors and alarms and are relatively simple to learn to use.
APD has several distinct advantages. It permits the performance of in-home dialysis while the client sleeps, allowing him or her to be dialysis free during waking hours. Also, because the number of connections and disconnections are fewer with APD, the incidence of peritonitis has been reduced. Finally, APD provides a means by which increased volumes of dialysis solution can be administered to clients who require higher clearances (Levine, 1997).
PERITONEAL DIALYSIS. Intermittent peritoneal
dialysis (IPD) combines the principles of an osmotic pressure gradient and true dialysis. The client usually requires exchanges of
CONTINUOUS-CYCLE PERITONEAL DIALYSIS. Continuous-cycle peritoneal dialysis (CCPD) also uses an automated cycling machine. Exchanges occur at night while the client sleeps. The final exchange of the night is left to dwell through the day and is drained the next evening as the process is repeated. CCPD offers the advantage of 24-hour dialysis, as in CAPD, but the sterile catheter system is less often violated.
COMPLICATIONS. Complications are possible with PD, but many can be treated or prevented with careful nursing care.
PERITONITIS. The major complication of PD is peritonitis. The most common cause of peritonitis is contamination of the connection site during an exchange. This infection of the peritoneum is manifested by cloudy dialysate outflow (effluent), fever, rebound abdominal tenderness, abdominal pain, general malaise, nausea, and vomiting.
When peritonitis is suspected, the nurse sends a specimen of the dialysate outflow for culture and sensitivity study, Gram stain, and cell count to identify the infecting organism so that an appropriate antibiotic can be ordered. Procedures for routine or periodic culturing of PD effluent vary with institutional practice. In today's era of cost containment, routine practices are less likely to be the norm. Cloudy or opaque effluent is the earliest sign of peritonitis. Thus nursing observations are key to the detection and identification of peritonitis. The best treatment of peritonitis is prevention. The nurse must maintain meticulous sterile technique when caring for the PD catheter and when hooking up or clamping off dialysate bags (Chart 72-11).
PAIN. Pain during the inflow of dialysate is common during the first few exchanges because of peritoneal irritation; however, it disappears after a week or two. Cold dialysate aggravates discomfort. Thus the dialysate bags should be warmed before instillation by use of a heating pad to wrap the bag or by use of the warming chamber of the automated cycling machine. Microwave ovens are not recommended for the warming of dialysate because of their unpredictable warming patterns and temperatures.
EXIT SITE AND TUNNEL INFECTIONS. The normal exit site from a PD catheter should be clean, dry, and without pain or evidence of inflammation. Exit site infections (ESIs) are associated with all types of PD catheters. Such infections can be difficult to treat and can become chronic. Exit site and tunnel infections cause increased morbidity, since they can lead to peritonitis, catheter failure, and hospitalization. Dialysate leakage and pulling or twisting of the catheter can predispose the client to ESIs. A Gram stain and culture should be performed when exit sites have purulent drainage.
Tunnel infections occur in the path of the catheter from the skin to the cuff. Signs of infection include redness, tenderness, and pain. ESIs are treated with antimicrobials; however, deep cuff infections usually require catheter removal.
INSUFFICIENT FLOW OF THE DIALYSATE. Constipation is the primary cause of inflow or outflow problems. To prevent constipation, the physician orders a bowel preparation before placing the PD catheter.
Because outflow drainage is by gravity, the nurse ensures that the drainage bag is lower than the client's abdomen. The nurse inspects the connection tubing and PD system for kinking or twisting and rechecks to make sure that clamps are open. If inflow or outflow drainage is still inadequate, the nurse attempts to stimulate inflow or outflow by repositioning the client. Turning the client to the other side or making sure that he or she is in good body alignment may help. Having the client in a supine low-Fowler's position seems to minimize the buildup of intra-abdominal pressure. Increased intra-ab-dominal pressure that occurs in the sitting or standing position, or with coughing, contributes to leakage at the PD catheter site.
Fibrin clot formation may occur after PD catheter placement or with the onset of peritonitis. Careful milking of the tubing may dislodge the fibrin clot and facilitate inflow and outflow. Radiographic examination is needed to identify PD catheter migration out of the pelvic area. If migration has occurred, the physician repositions the PD catheter.
DIALYSATE LEAKAGE. When dialysis is initiated, small volumes of dialysate are used. It may take clients 1 to 2 weeks to tolerate a full 2-L exchange without leakage around the catheter site. Leakage tends to occur most often in obese or diabetic clients, older adults, and those on long-term steroid therapy (Levine, 1997). Dialysate leakage presents as clear fluid emitting from the catheter exit site. During this time, clients may require hemodialysis (HD) support.
OTHER COMPLICATIONS. The PD effluent (outflow drainage) is expected to be relatively clear and light yellow. The nurse notes any change in the color of the outflow. With the initial exchanges, the outflow may be bloody. The physician may order several in-and-out exchanges of unwarmed dialysis solution in an effort to clear the dialysate of blood. In these cases, the client's hematocrit, pulse, and blood pressure are closely monitored. If the drainage return is brown, a bowel perforation must be suspected. Similarly, if the outflow is the same color as urine and has the same glucose concentration, a possible bladder perforation should be investigated. If the drainage is cloudy or opaque, an infection is suspected.
NURSING CARE DURING PERITONEAL DIALYSIS. In the hospital setting, peritoneal dialysis (PD) is routinely initiated and monitored by the nursing staff. Before the treatment, the nurse evaluates baseline vital signs, including blood pressure, apical and radial pulse rates, temperature, quality of respirations, and breath sounds. The client is weighed, always on the same scale, before beginning the procedure and at least every 24 hours while receiving treatment. Baseline laboratory value determinations, such as electrolyte and glucose levels, are also essential and are repeated at least daily during the PD treatment.
During PD, the nurse continually monitors the client. Vital signs are taken regularly and recorded on a flow sheet. For the first few exchanges, the nurse records the vital signs every 15 minutes. The nurse also performs an ongoing assessment of the client for signs of respiratory distress, pain, or discomfort. The abdominal dressing around the catheter exit site is checked frequently for wetness. The nurse monitors dwell time and initiates outflow. The physician orders dwell time according to the client's needs for fluid removal and electrolyte balance.
For hourly exchanges, dwell time usually ranges from 20 to 40 minutes. Glucose absorption may occur in some clients, and blood glucose assessment is necessary. The outflow should be a continuous stream after the clamp is completely open. The total amount of outflow is recorded accurately after each exchange. Accurate inflow and outflow records are maintained when hourly PD exchanges are done. When outflow is less than inflow, the difference is equal to the amount absorbed or retained by the client during dialysis and should be counted as intake. For clients performing self-CAPD, or when the MB-CAPD system is used, a daily weight is used to monitor fluid status. A visual inspection of the outflow bag and daily weights may be sufficient to note the adequacy of the return.
transplantation are life-sustaining treatments for end-stage renal disease
(ESRD); transplantation is not considered a "cure." It is
up to each client, in consultation with nephrology personnel, to determine which type of
therapy is best suited to that client's physical condition and lifestyle. In
2001, 13,290 kidney transplants were performed. Currently, more than 48,000 people are awaiting renal transplantation in the
CANDIDATES. Candidates for transplantation must be free of medical problems that might increase the risks associated with the procedure. The usual age range for clients undergoing transplantation is 2 to 70 years of age. In clients older than 70 years of age, the risk of complications increases, but clients older than 70 years of age are considered on an individual basis. A thorough body systems assessment of the client is performed before the client is considered for transplantation (see the Legal/Ethical Issues in Health Care box at right). The process of transplantation can place a life-threatening stress on the cardiac system in clients with advanced, uncorrectable cardiac disease. Thus these clients are usually excluded from consideration for transplantation. Contraindications for transplantation include metastatic malignant neoplasms, chronic infection, severe cardiovascular disease unresponsive to treatment, and severe psychosocial problems such as chemical dependency (Bartucci, 1999). In addition, longstanding disease of the pulmonary system increases the risk of morbidity and mortality owing to respiratory tract infections after transplantation. Clients with diseases of the gastrointestinal (GI) system may require treatment before consideration for transplantation. Such problems as peptic ulcer and diverticulosis can be severely aggravated by the large doses of steroids used after transplantation.
The urinary system must be completely evaluated to ensure its ability to manage normal urine flow. Many clients with ESRD have not used their lower urinary tract for extended periods, and ureteral or bladder abnormalities may require surgical correction before renal transplantation.
Metabolic diseases, such as diabetes mellitus, gout, and hyperparathyroidism, cause even greater risks. These clients can still accept a renal transplant, but careful observation and management are necessary to limit complications. Other conditions that may complicate transplantation include malignant neoplasm and inflammatory disease. Clients with a recent history of a malignant tumor are usually treated with dialysis because of the shortage of donor organs, the possibility that the cancer could attack the transplanted kidney, and the limited life expectancy of these clients. In addition, the immunosup-pressive agents used after transplantation increase the risk for cancer recurrence. If more than 2 to 5 years have passed since eradication of the cancer, the client can be considered for a transplant.
Other complicating conditions are considered on an individual basis, depending on the client's current health status. Renaltransplantation can be considered for most of those with ESRD and may prove to be the optimal therapy for many people (see the Evidence-Based Practice for Nursing box on p. 1698).
DONORS. The sources of donor kidneys are living donors, non-heart-beating donors (NHBDs), and cadaveric donors. The available kidneys are matched on the basis of immunologic similarity between the donor and the recipient. Living donors are most often blood relatives, but in recent years, unrelated donors have been used. NHBDs are persons declared dead by cardiopulmonary criteria. Kidneys from NHBDs are harvested immediately after death in cases where clients have previously given consent for organ donation and no longer seek active treatment or by in situ preservation in which a cool preservation solution is infused via a catheter inserted into the abdominal aorta after death is declared. Cadaveric donors are usually individuals who suffered irreversible brain injury, typically as a result of trauma. This type of donor must be maintained on a ventilator and have sufficient cardiovascular functioning in order for the kidneys to remain transplantable (Bartucci, 1999).
The size of the kidney is seldom a problem in adults. Pe-diatric cadaveric kidneys hypertrophy to accommodate adult needs within a few months.
Organs from living related donors (LRDs) provide the highest rates of renal graft survival (90%). Donors are usually at least 18 years old because of legal requirements and are seldom older than 65 years of age. General physical criteria for donors include the following:
· Absence of systemic disease and infection
· No history of cancer
· Absence of hypertension and renal disease
· Adequate renal function as evidenced by diagnostic studies
In addition, LRDs must express a clear understanding of the associated surgery and a willingness to give up a kidney. Some transplant centers also require a psychiatric evaluation to determine the motivation of the donor.
advances in immunosuppressant therapy and medical management, the United
Network of Organ Sharing (UNOS) reported 1-year renal transplant graft survival
to be 90% for all
centers in the
PREOPERATIVE CARE. Many issues must be decided before transplantation. Some issues are related to client health and others to the actual transplant procedure. The Clinical Pathway on pp. 1848-1851 highlights care needs for the client undergoing renal transplantation.
IMMUNOLOGIC STUDIES. The major barrier to successful renal transplantation after a suitable donor kidney is available is the body's ability to identify and reject tissue that is not its own. This immunologic process attacks the transplanted kidney and renders it nonfunctional. For immunologic contraindications to be overcome, in-depth tissue typing is done on all candidates for transplantation. These studies include simple ABO blood group typing for compatible blood transfusions and human leukocyte antigen (HLA) studies, as well as other tests. The HLAs have become the principal histo-compatibility system used to match transplant recipients with compatible donors. The more similar the antigens of the donor are to those of the recipient, the more likely it is that the transplant will be successful and immunologic rejection will be avoided. Research is ongoing in immunology, and new information in this area could increase the success rate of organ transplantations in the future (see Chapter 20).
SURGICAL TEAM. The surgical team is a group of specialists trained in transplantation procedures. The team includes operating room nurses (circulating and scrub nurses), clinical nurse specialists, and preoperative nurses, as well as transplant surgeons, anesthesiologists, and nephrologists. The role of the preoperative nurse includes the following:
· Teaching about the procedure and postoperative care
· In-depth client assessment
· Coordination of diagnostic tests
· Development and implementation of treatment plans
The transplant recipient usually requires dialysis within 24 hours of the surgery. In addition, the recipient often receives a blood transfusion before surgery. Current research favors donor-specific transfusions, in which blood from the kidney donor is transfused into the recipient. This procedure has resulted in increased graft survival, especially of organs from LRDs.
OPERATIVE PROCEDURES. The donor nephrec-tomy procedure varies depending on whether the donor is an NHBD,cadaveric donor, or living donor. The NHBD or cadaveric donor nephrectomy is conducted as a sterile autopsy in the operating room. All arterial and venous vessels and as long a piece of ureter as possible are carefully preserved. After removal, the kidneys are preserved until time for implantation into the recipient. The technique for kidney removal from living donors requires greater surgical care and is a delicate procedure lasting 3 to 4 hours. A flank incision is used, and care is taken to avoid scarring. Donors usually experience more pain than do recipients. They also need special nursing care and support for the psychologic adjustment to loss of a body part.
The transplantation surgery usually takes 4 to 5 hours. The transplanted kidney is usually placed in the right anterior iliac fossa(Figure 72-9) instead of the usual anatomic position. This placement allows easier anastomosis of the ureter and the renal artery and vein, and it also allows for assessment by palpation. The recipient's own nonfunctioning kidneys are not usually removed unless chronic infection in one or both kidneys would compromise overall recovery. The client is then taken to the postanesthesia unit and then, when stable, to a designated surgical unit in the transplant center or to a critical care unit.
POSTOPERATIVE CARE. Postoperative care of the kidney transplant recipient requires that nurses be knowledgeable about the expected clinical findings and potential complications unique to this population. Nursing care includes ongoing physical assessment with an emphasis on evaluation of renal function. The transplant recipient requires particularly close attention because the immunosuppressive drug therapy to prevent tissue rejection causes impaired healing and an increased susceptibility to infection. Careful uro-logic management is essential to graft success. These clients always have a large indwelling (Foley) catheter for accuratemeasurements of urine output and decompression of the bladder and to prevent stretch on suture and anastomosis sites on the bladder. An abrupt decrease in urine output is significant, since it can herald the onset of complications such as rejection, acute tubular necrosis (ATN), thrombosis, or obstruction. The urine color is carefully monitored (usually hourly). The urine is initially pink and bloody, but it gradually returns to normal over a period of several days to several weeks, depending on renal function. A continuous bladder irrigation is occasionally prescribed to decrease the formation of blood clots, which could increase pressure in the bladder and jeopardize the graft. Routine catheter care is performed to minimize contamination of the catheter; the nurse adheres to the agency's policy. The catheter is removed as soon as possible to avoid infection, usually 3 to 7 days postoperatively. The nurse is also responsible for obtaining daily urine tests, including urinalysis, glucose determinations, tests for the presence of acetone, culture, and specific gravity measurement.
During the postoperative period, the function of the transplanted kidney (renal graft) can result in either oliguria or diuresis. Oliguriamay occur as a result of ischemia and ATN, rejection, or other complications. To increase urine output, the physician may order diuretics and osmotic agents, such as mannitol. The nurse and the physician carefully monitor the client's fluid status because fluid overload can cause hypertension, congestive heart failure (CHF), and pulmonary edema. Daily weight measurement, frequent blood pressure readings, and careful intake and output measurements are required to evaluate fluid status.
Instead of oliguria, the client may have diuresis, especially with a transplanted kidney from a living related donor (LRD). The nurse carefully monitors fluid intake and output and observes for electrolyte imbalances, such as hypokalemia and hyponatremia.Hypovolemia from excessive diuresis may cause hypotensive episodes. The nurse strives to prevent this situation because decreased blood pressure also decreases the oxygen and blood supply to the new kidney, which can threaten graft survival.
COMPLICATIONS. Unfortunately, numerous potential complications are associated with transplantation surgery.
REJECTION. The most common and the most threatening complication of renal transplantation is rejection. Rejection is the leading cause of graft loss. A reaction occurs between the antigens in the transplanted kidney and the antibodies and cy-totoxic T-cells in the recipient's blood. These immunologic substances treat the new kidney as a foreign invader and cause tissue destruction, thrombosis, and eventual necrosis of the kidney. The three types of rejection are hyperacute, acute, and chronic. Acute rejection is the most common type in the transplant client. It is treated with increased immunosuppressive therapy and can be reversible. Rejection can be diagnosed by clinical manifestations, a renal scan, and renal biopsy. Table 72-12 summarizes the characteristics of the three types of rejection; Chapter 20 discusses their pathophysiology and treatment.
ACUTE TUBULAR NECROSIS. Prolonged preservation of cadaveric kidneys before transplantation can result in isch-emicdamage that is manifested as acute tubular necrosis (ATN). These clients usually need to be dialyzed until urine output becomes sufficient and the blood urea nitrogen (BUN) and creatinine normalize. Because ATN is often difficult to distinguish from acute rejection, clients need to undergo weekly biopsies to assess the need for further immunosup-pression if rejection is occurring.
THROMBOSIS. Thrombosis may occur during the first 2 to 3 days following transplantation. A sudden decrease in urine production or output may signal impaired perfusion resulting from thrombosis. Ultrasound examination of the kidney will reveal decreased or absent blood supply, and emergency surgery is required to prevent further ischemic damage or loss of the graft (Bartucci, 1999).
RENAL ARTERY STENOSIS. Stenosis of the renal artery is detected by identification of hypertension, a bruit over the arteryanastomosis site, and decreased renal function. The involved artery must be surgically resected and the kidney anastomosed to another artery. Clients with vascular complications nearly always require surgical intervention. Other vascular problems include vascular leakage or thrombosis, both of which require an emergency transplant nephrectomy.
OTHER COMPLICATIONS. Other complications may involve the wound or genitourinary tract. Wound complications, such ashematomas, abscesses, and lymphoceles, can become a medium for infection and can place external pressure on the new kidney. Infection is a significant cause of morbidity and mortality in the transplant recipient. Prevention of infection is paramount. Strict aseptic technique and handwashing must be rigorously enforced. Because of immunosuppression, transplant recipients may not present with typical signs of infection. Low-grade fevers, mental status changes, and vague complaints of discomfort may be present before sepsis. Nurses play a pivotal role in the early detection of infection.
Genitourinary tract complications include ureteral leakage, fistula, or obstruction; calculus formation; bladder neck con-tracture; scrotal swelling; and graft rupture. Surgical intervention may be required.
IMMUNOSUPPRESSIVE DRUG THERAPY. The success of renal transplantation depends on changing the client's immunologic response so that the new kidney is not rejected as a foreign organ. The nurse administers and is aware of the immunosuppressive drugs that protect the transplanted organ. These drugs include corticosteroids, antilym-phocyte preparations, monoclonal antibodies, and cy-closporine (Cyclosporin A). Chapter 20 discusses the mechanisms of action for these agents and the associated client responses. Clients who must take immunosuppressant medications are vulnerable to infection secondary tomyelo-suppression. Clients are at risk for developing a number of fatal viral, fungal, bacterial, or protozoal infections (Giuliano & Sims, 1999).
HOME CARE MANAGEMENT
Because of the complex nature of chronic renal failure (CRF), its progressive course, and multiple treatment modalities, a case manager may be useful in the planning, coordination, and evaluation of care. As the renal disease progresses, the client is seen by a physician or nurse practitioner regularly and may have frequent hospitalizations. The nurse, in conjunction with the dietitian and social worker, evaluates the home environment and determines special equipment needs before discharge. Once the client is discharged, home care nurses may direct care and monitor progress Chart 72-12 provides a focused assessment guideline for the client after renal transplantation.
The nurse provides ongoing health teaching about the diet in renal disease and the pathophysiologic process of renal disease. As CRF approaches end-stage renal disease (ESRD), one of the following courses of treatment is chosen: he-modialysis (HD), peritoneal dialysis (PD), or transplantation. For each form of treatment, the client must learn the relevant information and procedures and consider his or her personal lifestyle, support systems, and methods of coping. Decision making about the treatment modality, or even whether to pursue treatment, is very difficult for many clients and their families. Nurses provide information and emotional support to assist clients with these decisions.
Treatment with HD necessitates a working knowledge of the dialysis machine and the care of the client's vascular access. If the client chooses in-home HD, the home care nurse makes preparations for installation of the appropriate equipment, including a water treatment system. Regardless of whether the treatment is provided at home or in a center, the nurse provides ongoing physical assessment and health teaching to promote maximal independence at home.
The client receiving PD needs extensive training in the procedure. The client also needs assistance in obtaining equipment and the numerous supplies involved. Home care nurses perform physical assessments, monitor vital signs, assess compliance with drug and diet regimens, and carefully monitor for signs and symptoms of peritonitis.
The nurse plays a vital role in the long-term care of the client with a renal transplant. This client is usually discharged 3 to 4 weeks after surgery. Meticulous maintenance of prescribed immunosuppressive drug therapy is essential for the survival of the renal graft. Thus the nurse facilitates acceptance and understanding of this regimen as a part of daily life. The nurse also carefully monitors for signs of graft rejection and for complications, such as infection.
Health teaching is a primary function of nurses caring for clients with any form of renal disease. The home care nurse collaborates with other members of the health care team, especially the dietitian, pharmacist, and physician, to instruct clients and family members or significant others in all aspects of diet therapy, necessary drag therapy, and associated renal pathologic changes. Clients and family members are taught to report signs and symptoms of complications, such as fluid overload and infection. When a client requires a more advanced form of therapy, such as dialysis or transplantation, the teaching focuses on the chosen therapeutic intervention.
HD is the most complex form of therapy for the client and family to understand. Even if clients receive HD in a dialysis center instead of at home, they are usually expected to have some knowledge of the HD machine. The client or a family member or other caregiver must be taught to care for the vascular access and to report signs of infection and stenosis. The client who plans to have in-home HD will need a partner. Both the client and the partner must be completely educated in the entire process of HD and must be able to perform it independently before the client is discharged from the HD center or hospital HD unit.
PD involves extensive health teaching. This instruction can be given to the client alone or to the client and a family member or other caregiver if the client cannot perform the procedure. The nurse emphasizes sterile technique because peritonitis is the most common complication of PD performed at home. The nurse instructs clients to report the signs and symptoms associated with peritonitis. They should report the presence of cloudy effluent and abdominal pain, especially when accompanied by rebound tenderness. Clients are taught that cloudy effluent needs to be analyzed promptly. A specimen is sent by the home care nurse for culture and sensitivity, cell count, and Gram stain to identify the causative organism. Clients are taught that peritonitis is treated with antimicrobial therapy, usually given by the intraperitoneal (IP) route. To prevent peritonitis, they are taught how breaks in aseptic technique can occur, resulting in peritonitis. In addition, to eradicate the infection, nurses must educate clients about the importance of completing the antibiotic regimen. Nurses need to teach that repeated episodes of peritonitis can result in diminished ultrafiltrationcapability, which may necessitate transfer to HD.
The client receiving a renal transplant also needs extensive health teaching. The nurse provides instruction about drug regimens, home monitoring, immunosuppression, signs and symptoms of rejection, infection, and prescribed changes in the diet and activity level.
The nurse provides psychologic support for the client and family or significant others. The nurse facilitates the client's adjustment to the diagnosis of renal failure and eventual acceptance of the treatment regimens.
For many clients, the reduction of uremic symptoms in the initial weeks and months of dialysis treatment creates a sense of euphoria and well-being (the "honeymoon" period). They feel better physically, their mood may be happy and hopeful, and they tend to overlook the inconvenience and discomfort of frequent dialysis treatments. The nurse realizes that this mood is temporary and uses the time to initiate health care teaching. The nurse stresses that although the client's uremic symptoms have diminished, the client will not return completely to the previous state of well-being. The client and the family may have looked on dialysis as a cure instead of a required lifelong treatment. Many clients enter a phase of discouragement and disillusionment sometime during the first year of treatment; this may last a few months to a year or longer. The difficulties of incorporating dialysis into daily life are staggering, and clients often become disappointed and depressed as the problems become apparent. During this time, they may struggle against the idea of having to be permanently dependent on a disruptive therapy. The fear of rejection by health staff and family members or significant others reinforces feelings of helplessness and dependence. Some people retreat into complete or partial denial of the disease and the need for treatment. They may deny the need for dialysis or may not comply with medication administration and dietary restrictions. Nurses who work with these clients need to monitor any maladaptive behaviors that may contribute to non-compliance and suggest psychiatric referrals. Nurses and family members should focus on the positive aspects of the treatments. The nurse continues health care education with clients as active participants and decision makers.
Most clients with chronic renal failure (CRF) eventually enter a phase of acceptance or, at least, resolution. The prospect of a chronic illness may be devastating for some people, and each person reacts differently. To make this long-term adaptation, the client must adjust to continuous change, but specific concerns depend on the current physical status and particular treatment method.
After clients have accepted or become resigned to the chronicity of their disease, they usually attempt to return to their previous activities. Resuming the previous level of activity, however, may not be possible. The nurse and other health care professionals can help clients to establish realistic goals that allow them to lead active, productive lives.
HEALTH CARE RESOURCES
Professionals from various disciplines are valuable resources for the client with renal failure. Home care nurses are often required to monitor the client's status and evaluate maintenance of the prescribed treatment regimen (HD or PD). A client with advanced renal failure may need the assistance of a home care aide in performing the activities of daily living. Social services personnel are usually involved because of the complex process of applying for financial aid to pay for the required medical care (see the Cost of Care box above). To increase the functional capacity of the client, a physical therapist may be beneficial. Consultation with a dietitian will assist the client and family members in understanding the special dietary needs. A psychiatric evaluation may be needed to assist with depressive symptoms and maladjustment. Clergy and pastoral care specialists offer spiritual support.
Clients with CRF are routinely observed by a physician, usually a nephrologist. Such organizations as the National Kidney Foundation (NKF), the American Kidney Fund, and the National Association of Patients on Hemodialysis and Transplantation (NAPHT) may be helpful to clients and families.
The nurse evaluates the care of the client with chronic renal failure (CRF) on the basis of the identified nursing diagnoses and collaborative problems. The expected outcomes are that the client will:
· Achieve and maintain appropriate fluid volume
· Maintain serum electrolyte levels in expected ranges
· Maintain heart rate and blood pressure in expected ranges
· Comply with the prescribed dietary regimen
· Maintain an adequate nutritional status
· Seek information to reduce anxiety
· Use effective coping strategies
· Report an absence of physical manifestations of anxiety