Practice nursing care for Clients with Renal Disorders

Practice nursing care for Clients with Renal Disorders

 

 

Acute and chronic renal failure have become increasingly niore common in the United States, resulting in considerable morbidity and mortality. Acute renal failure is responsible for 7% of all hospital admissions, and the prevalence of end-stage renal disease has virtually doubled in the last decade (Stark, 1998; U.S. Renal Data Systems, 1999). There are many causes of renal failure, but complications related to poorly controlled diabetes remain the most common cause.

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 cao longer meet the body’s homeostatic demands, renal replacement therapy is required to prevent death from po­tentially life-threatening consequences.

 

ACUTE RENAL FAILURE

OVERVIEW

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.

Pathophysiology

The pathophysiologic process of ARF is related to the cause of the sudden decrease in kidney function and the involved site or sites 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 nephroephrosis. Infections (bacte­ria, viral, fungal, or endotoxin), drugs (especially aminogly-coside antibiotics and nonsteroidal 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.

PHASES 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 a nonoliguric 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.

Etiology

Many types of renal insults can lead to reduced renal function. Severe hypotension from excessive blood loss or dehydration results 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

·        Vasculitis

·        Severe hypertension

·        Hepatorenal syndrome of cirrhosis

 

 Incidence/Prevalence

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 by nephrotoxic substances is associated with the lowest rates (10% to 26%) of recovery. The prognosis for ARF caused by obstruction or glomerulonephritis is much better.

 COLLABORATIVE MANAGEMENT

  Prevention

Nurses have an essential role in the prevention of acute renal failure (ARF). The nurse notes the signs of impending renal dysfunction through careful physical assessment and close monitoring of laboratory values. Prompt recognition and cor­rection of extrarenal 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.

Assessment

 HISTORY

The accurate diagnosis of ARF, including its type and its cause, largely depends on a detailed history. The history must include questions 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 72-1). Signs and symp­toms of prerenal 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 oliguria or 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.

 LABORATORY ASSESSMENT

The numerous alterations in laboratory values in the client with ARF are similar to those occurring in chronic renal fail­ure (CRF) (Chart 72-2; see also Laboratory Assessment [Chronic Renal Failure], p. 1681). The nurse can expect to find rising BUN and creatinine 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. In postrenal failure, urinary sodium levels may be normal to 40 mEq/L, with a specific gravity of 1.000 to 1.010.

 

  RADIOGRAPHIC ASSESSMENT

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.)

 

Interventions

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 electrolyte loss 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 (Chart 72-3; see also Drug Therapy un­der Chronic Renal Failure, p. 1685). 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 hemodynamic status. 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 cir­culating catecholamines, 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 azotemia and 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] , p. 1682), 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.

 

 

 

BEST PRACTICE/or

Administering Renal-Dose Dopamine

 

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 uremic clients, 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:

•  Uremia

•  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, 1998). 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, pp. 1694-1697).

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, 1998).

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 thaeeded for AV sys­tems. These procedures are performed in a critical care unit, and clients require continuous nursing care.

 

F i g u r e 72-1 Subclavian dialysis catheters. These catheters are radiopaque tubes that can be used for hemodialysis access. The Y-shaped tubing allows arterial outflow and venous return through a single catheter.

A, Mahurkar catheters, made of polyurethane and used for short-term access.

B, A PermCath catheter, made of silicone and used for long-term access. (Courtesy Kendall Company, Bothell, WA.)

 

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, the posthospital care may be as extensive and multifac-eted as it is for any other client with chronic renal failure (CRF) (see Community-Based Care [Chronic Renal Failure], p. 1700).

If the ARF is in the process of resolving, the follow-up care may involve a variety of services. Frequent medical visits are necessary, 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.

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 a dialysate (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.

 

CHRONIC RENAL FAILURE

OVERVIEW

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 [Chart 72-5]), ure-mic 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 72-1.

 

Pathophysiology

 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 72-6). Initially, there is a diminished renal reserve. A 24-hour urine specimen for monitoring creatinine 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 cao 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 and creatinine, 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.

 PATHOLOGIC ALTERATIONS

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 hypos­thenuria and 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.

 METABOLIC ALTERATIONS

UREA AND CREATININE.

 Renal failure also causes disturbances in urea and creatinine excretion. Creatinine is de­rived from creatine 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 and glomerular 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 the polyuria 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 (see Chapters 12 and 13). 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 72-5).

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 5 mEq/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, blood transfusions, and excessive bleeding or hemorrhage. (See Chapter 13 for further discussion of hyperkalemia.)

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 16).

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 13). 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 causes vasocon-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 produce renin. 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 by uremic 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.

HEMATOLOGIC ALTERATIONS

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.

GASTROINTESTINAL ALTERATIONS

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 uremic halitosis 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.

Etiology

The etiology of CRF is complex (Table 72-7). 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.

Incidence/Prevalence

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 United States are re­ceiving treatment for ESRD. In 1999 the reported incidence of renal disease (i.e., new clients requiring renal replacement therapy) was 79,102. There were more than 57,000 deaths in 1999 related to ESRD. Three primary causes of ESRD in­clude diabetes mellitus  (40%), hypertension (27%), and

glomerulonephritis (11%). There is a higher incidence of ESRD in men than in women (U.S. Renal Data Systems, 1999). 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 United States in 1999 (U.S. Renal Data Systems, 1999). Chart 72-6 addresses prevention of renal and urinary problems.

 

COLLABORATIVE MANAGEMENT

   Assessment

    HISTORY

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 health problems 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 po­tentially nephrotoxic 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 72-7). 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 72-7) and vary widely, depending oitrogenous 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 neurologic disturbances 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 dysrhythmias associated 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 hilar pneumonitis, 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 in proteinuria; some cause hematuria.

The quantity 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 has oligu-ria, but some clients will remain relatively nonoliguric, producing 1 L or more per 24 hours. Urine volume pro­duced per day will probably change again after dialysis is initiated.

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.

 PSYCHOSOCIAL ASSESSMENT

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. The chronicity of ESRD, the variety of treatment options, and the uncertainties surrounding the course of the disease and its treatment neces­sitate an ongoing psychosocial assessment.

LABORATORY ASSESSMENT

CRF results in serious abnormalities in many laboratory val­ues (see Chart 72-2). The following blood values are routinely monitored 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-hour creatinine 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.

 RADIOGRAPHIC ASSESSMENT

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 9 cm or less. This diminished size is usually the result of renal tubu­lar atrophy and fibrosis. If obstructive uropathy is a possible factor contributing to deterioration of renal function that is more rapid than expected, a renal ultrasound or computed tomography (CT) scan without contrast media may be ob­tained. (See Chapter 69 for a complete description of renal diagnostic tests.)

CRITICAL THINKING CHALLENGE

You 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?

Analysis

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 commoursing diagnoses and collabora­tive problems, clients with CRF may have one or more of the following:

·        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 of uremic 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

INTERVENTIONS.

 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 72-8).

 NUTRITION THERAPY. The purpose of nutrition therapy is the administration of food and fluids to support the metabolic processes 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 72-8.

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 priагу 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 1.5 g of protein/kg of body weight per day may be necessary for weight gain and improvement iutritional status in clients undergoing maintenance HD (Kuhlmann, Schmidt, & Kohler, 1999; Mehrotra & Nolph, 1999).

In clinical 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 0.60 g of protein per kilogram of body weight (e.g., 40 g of protein daily for a 150-pound [70-kg] adult). If proteinuria is present, protein is added to the diet in amounts equal to that lost in the urine, as determined by a 24-hour urine collection. The calculation for the protein requirement is based on actual body weight (corrected for edema), not ideal body weight.

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, 1997). 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.

The client’s status in terms of fluid and sodium retention can be estimated by monitoring body weight and blood pressure. In nondialyzed uremic clients, sodium is limited to 1 to 3 g daily, and fluid intake depends on urine output. In oliguric clients re­ceiving dialysis, the sodium restriction is 2 to 4 g daily; fluid in­take is limited to 500 to 700 mL plus the amount of any urine output. The client is instructed not to add salt at the table or dur­ing food preparation. Foods high in sodium (processed foods, fast foods, potato chips, pretzels, pickles, ham, bacon, and sausage) are permitted in moderation. Herbs and spices can be used as an alternative to salt for enhanced flavoring of food.

POTASSIUM RESTRICTION. The nurse monitors potas­sium intake because hyperkalemia can cause dangerous cardiac dysrhythmias. 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 1.5 g of protein per kilogram of body weight per day is recommended. The anorexia that often ac­companies advanced renal disease requires clients to consume a diet with sufficient protein that includes high-calorie enteral supplements. The amount of sodium restriction varies with fluid weight gain and blood pressure. There is usually no need to restrict dietary potassium because the dialysate is potas­sium free. The potassium restriction, if any, is determined by the serum potassium level.

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

iNTERVENTIONS.

 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, p. 1682, and dialysis is dis­cussed under Renal Replacement Therapies, p. 1688).

 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 (see Chart 72-8). 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 wheeeded 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: 1 kg of weight equals approximately 1 L of fluid re­tained. Daily weights are taken at the same time each day, on the same scale, with the client wearing the same amount of clothing, and after the bladder has been emptied if the client is not anuric. The weight is monitored for changes before and after dialysis.

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 maintaiormal 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 other antihypertensives, 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 33 through 35.

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 FOR 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 (see Chart 72-3). 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.

 FATIGUE

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.

 ANXIETY

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 as furosemide (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). Renal impairment 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 potential dysrhythmias. 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 cao longer be managed with conservative therapies, such as diet, med­ication, and fluid restriction, dialysis is indicated. Transplan­tation may be discussed at any time.

 HEMODiALYSiS

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.

Diffusion is 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-meable membrane. 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 preset length 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 the dialyzer, 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 wheecessary.

 

 

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. The polytetrafluoroethylene (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 of hemorrhage during dialysis and for 1 hour after dialysis (Chart 72-10).

 

Figure 72-6 9 Options for long-term vascular access for hemodialysis.

A, A surgically created venous fistula. The increased pressure from the artery forces blood into the vein. This process causes the vein to dilate enough for fistula needles to be placed for hemodialysis. When the vein dilates in this matter, the fistula is said to be “developed.”

B, A surgically placed straight vascular graft in the upper arm. The graft creates a shunt between arterial and venous blood.

 

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 and barbiturates 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 В 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).