Renal failure results when the kidneys cannot remove the body’s metabolic wastes or perform their regulatory functions. The sub-stances normally eliminated in the urine accumulate in the body fluids as a result of impaired renal excretion, leading to a disrup-tion in endocrine and metabolic functions as well as fluid, elec-trolyte, and acid–base disturbances. Renal failure is a systemic disease and is a final common pathway of many different kidney and urinary tract diseases. Each year, the number of deaths from irreversible renal failure increases (U.S. Renal Data System, 2001).
ACUTE RENAL FAILURE
Acute renal failure (ARF) is a sudden and almost complete loss of kidney function (decreased GFR) over a period of hours to days. Although ARF is often thought of as a problem seen only in hos-pitalized patients, it may occur in the outpatient setting as well. ARF manifests with oliguria, anuria, or normal urine volume. Oliguria (less than 400 mL/day of urine) is the most common clinical situation seen in ARF; anuria (less than 50 mL/day of urine) and normal urine output are not as common. Regardless of the volume of urine excreted, the patient with ARF experiences rising serum creatinine and BUN levels and retention of other metabolic waste products (azotemia) normally excreted by the kidneys.
Three major categories of conditions cause ARF: prerenal (hypo-perfusion of kidney), intrarenal (actual damage to kidney tissue), and postrenal (obstruction to urine flow).
· Prerenal conditions occur as a result of impaired blood flow that leads to hypoperfusion of the kidney and a drop in the GFR. Common clinical situations are volume-depletion states (hemorrhage or GI losses), impaired cardiac perfor-mance (myocardial infarction, heart failure, or cardiogenic shock), and vasodilation (sepsis or anaphylaxis).
· Intrarenal causes of ARF are the result of actual parenchymal damage to the glomeruli or kidney tubules. Conditions such as burns, crush injuries, and infections, as well as nephrotoxic agents, may lead to acute tubular necrosis and cessation of renal function. With burns and crush injuries, myoglobin (a protein released from muscle when injury occurs) and he-moglobin are liberated, causing renal toxicity, ischemia, or both. Severe transfusion reactions may also cause intrarenal failure; hemoglobin is released through hemolysis, filters through the glomeruli, and becomes concentrated in the kidney tubules to such a degree that precipitation of hemo-globin occurs. Medications may also predispose a patient to intrarenal damage, especially nonsteroidal anti-inflammatory drugs (NSAIDs) and ACE inhibitors. These medications interfere with the normal autoregulatory mechanisms of the kidney and may cause hypoperfusion and eventual is-chemia. Other potential causes of intrarenal or intrinsic ARF include rhabdomyolysis, which results in accumula-tion of myoglobin in the glomeruli secondary to damage to skeletal muscle, and nephrotoxicity secondary to herbal remedies (Myhre, 2000).
· Postrenal causes of ARF are usually the result of an obstruc-tion somewhere distal to the kidney. Pressure rises in the kid-ney tubules; eventually, the GFR decreases.
Common causes of ARF are summarized in Chart 45-5. Although the exact pathogenesis of ARF and oliguria is not always known, many times there is a specific underlying problem. Some of the factors may be reversible if identified and treated promptly, before kidney function is impaired. This is true of the following conditions that reduce blood flow to the kidney and impair kidney function: (1) hypovolemia; (2) hypotension; (3) re-duced cardiac output and heart failure; (4) obstruction of the kidney or lower urinary tract by tumor, blood clot, or kidney stone; and (5) bilateral obstruction of the renal arteries or veins. If these conditions are treated and corrected before the kidneys are permanently damaged, the increased BUN and creatinine lev-els, oliguria, and other signs associated with ARF may be reversed.
Although not a common cause of ARF, some types of renal stones may increase the risk for ARF more than others. Heredi-tary stone diseases (cystinuria, primary hyperoxaluria, Dent’s dis-ease), primary struvite stones, and infection-related urolithiasis associated with anatomic and functional urinary tract anomalies and spinal cord injury may cause recurrent bouts of obstruction as well as crystal-specific effects on tubular epithelial cells and in-terstitial renal cells. This in turn may activate the fibrogenic cas-cade responsible for the loss of renal parenchyma (Gambaro, Favaro & D’Angelo, 2001).
There are four clinical phases of ARF: initiation, oliguria, diure-sis, and recovery. The initiation period begins with the initial in-sult and ends when oliguria develops. The oliguria period is accompanied by a rise in the serum concentration of substances usually excreted by the kidneys (urea, creatinine, uric acid, or-ganic acids, and the intracellular cations [potassium and magne-sium]). The minimum amount of urine needed to rid the body of normal metabolic waste products is 400 mL. In this phase ure-mic symptoms first appear and life-threatening conditions such as hyperkalemia develop.
Some patients have decreased renal function with increasing nitrogen retention, yet actually excrete normal amounts of urine (2 L/day or more). This is the nonoliguric form of renal failure and occurs predominantly after nephrotoxic antibiotic agents are administered to the patient; it may occur with burns, traumatic injury, and the use of halogenated anesthetic agents.
In the diuresis period, the third phase, the patient experiences gradually increasing urine output, which signals that glomer-ular filtration has started to recover. Laboratory values stop rising and eventually decrease. Although the volume of urinary output may reach normal or elevated levels, renal function may still be markedly abnormal. Because uremic symptoms may still be pres-ent, the need for expert medical and nursing management con-tinues. The patient must be observed closely for dehydration during this phase; if dehydration occurs, the uremic symptoms are likely to increase.
The recovery period signals the improvement of renal func-tion and may take 3 to 12 months. Laboratory values return to the patient’s normal level. Although a permanent 1% to 3% re-duction in the GFR is common, it is not clinically significant.
Almost every system of the body is affected when there is failure of the normal renal regulatory mechanisms. The patient may appear critically ill and lethargic, with persistent nausea, vomit-ing, and diarrhea. The skin and mucous membranes are dry from dehydration, and the breath may have the odor of urine (uremic fetor). Central nervous system signs and symptoms in-clude drowsiness, headache, muscle twitching, and seizures. Table 45-1 summarizes common clinical findings for all three categories of ARF.
Urine output varies (scanty to normal volume), hematuria may be present, and the urine has a low specific gravity (1.010 or less, compared with a normal value of 1.015 to 1.025). Patients with prerenal azotemia have a decreased amount of sodium in the urine (below 20 mEq/L) and normal urinary sediment. Patients with intrarenal azotemia usually have urinary sodium levels greater than 40 mEq/L with casts and other cellular debris. Uri-nary casts are mucoproteins secreted by the renal tubules when-ever inflammation is present.
Ultrasonography is a critical component of the evaluation of both acute and chronic renal failure. Although many sonographic find-ings are nonspecific, their diagnostic utility is greatly enhanced by a familiarity with the clinical presentation and a thorough under-standing of renal pathophysiology (O’Neill, 2000).
The BUN level rises steadily at a rate dependent on the degree of catabolism (breakdown of protein), renal perfusion, and protein intake. Serum creatinine rises in conjunction with glomerular damage. Serum creatinine levels are useful in monitoring kidney function and disease progression.
With a decline in the GFR, the patient cannot excrete potassium normally. Patients with oliguria and anuria are at greater risk for hyperkalemia than those without oliguria. Protein catabolism re-sults in the release of cellular potassium into the body fluids, caus-ing severe hyperkalemia (high serum K+ levels). Hyperkalemia may lead to dysrhythmias and cardiac arrest. Sources of potas-sium include normal tissue catabolism, dietary intake, blood in the GI tract, or blood transfusion and other sources (intravenous infusions, potassium penicillin, and extracellular shift in response to metabolic acidosis).
Patients with acute oliguria cannot eliminate the daily metabolic load of acid-type substances produced by the normal metabolic processes. In addition, normal renal buffering mechanisms fail. This is reflected by a fall in the serum CO2-combining power and blood pH. Thus, progressive metabolic acidosis accompanies renal failure.
There may be an increase in serum phosphate concentrations; serum calcium levels may be low in response to decreased ab-sorption of calcium from the intestine and as a compensatory mechanism for the elevated serum phosphate levels.
Anemia inevitably accompanies ARF due to reduced erythropoi-etin production, uremic GI lesions, reduced RBC life span, and blood loss, usually from the GI tract. With use of the parenteral form of erythropoietin (Epogen), anemia is not the major prob-lem it once was.
A careful history is obtained to determine whether the patient has been taking potentially nephrotoxic antibiotic agents or has been exposed to environmental toxins. The kidneys are especially sus-ceptible to the adverse effects of medications because the kidneys are repeatedly exposed to substances in the blood. They receive a large blood flow (25% of the cardiac output at rest; the entire blood volume circulates through the kidneys about 14 times a minute). In addition, the kidney is the major excretory organ for many toxic substances, and during the normal urine concentra-tion process, these substances increase in concentration and can be toxic to the kidneys. Therefore, in patients taking potentially nephrotoxic medications (aminoglycosides, gentamicin, tobramy-cin, colistimethate, polymyxin B, amphotericin B, vancomycin, amikacin, cyclosporine), renal function should be monitored closely. Serum BUN and creatinine levels should be obtained at baseline by 24 hours after initiation of these medications and at least twice a week while the patient is receiving them.
Any agent that reduces renal blood flow (eg, chronic analgesic use) may cause renal insufficiency. Chronic analgesic use, partic-ularly with NSAIDs, may cause interstitial nephritis and papil-lary necrosis. Patients with heart failure or cirrhosis with ascites are at particular risk for NSAID-induced renal failure. Increased age, preexisting renal disease, and the administration of several nephrotoxic agents simultaneously increase the risk for kidney damage.
Management of ARF is expensive and complex, and even when optimal, the mortality rate remains high. Therefore, pre-vention of ARF is key (Chart 45-6).
The kidney has a remarkable ability to recover from insult. Therefore, the objectives of treatment of ARF are to restore nor-mal chemical balance and prevent complications until repair of renal tissue and restoration of renal function can take place. Any possible cause of damage is identified, treated, and eliminated. Prerenal azotemia is treated by optimizing renal perfusion, whereas postrenal failure is treated by relieving the obstruction. Treatment of intrarenal azotemia is supportive, with removal of causative agents, aggressive management of prerenal and postrenal failure, and avoidance of associated risk factors. Shock and infection, if present, are treated promptly. Overall, medical management in-cludes maintaining fluid balance, avoiding fluid excesses, or pos-sibly performing dialysis.
Maintenance of fluid balance is based on daily body weight, serial measurements of central venous pressure, serum and urine concentrations, fluid losses, blood pressure, and the clinical sta-tus of the patient. The parenteral and oral intake and the output of urine, gastric drainage, stools, wound drainage, and perspira-tion are calculated and are used as the basis for fluid replacement. The insensible fluid lost through the skin and lungs and produced through the normal metabolic processes is also considered in fluid management.
Fluid excesses can be detected by the clinical findings of dys-pnea, tachycardia, and distended neck veins. The lungs are auscultated for moist crackles. Because pulmonary edema may be caused by excessive administration of parenteral fluids, extreme caution must be used to prevent fluid overload. The development of gen-eralized edema is assessed by examining the presacral and pre-tibial areas several times daily. Mannitol, furosemide, or ethacrynic acid may be prescribed to initiate a diuresis and prevent or mini-mize subsequent renal failure.
Adequate blood flow to the kidneys in patients with prerenal causes of ARF may be restored by intravenous fluids or blood product transfusions. If ARF is caused by hypovolemia secondary to hypoproteinemia, an infusion of albumin may be prescribed. Dialysis may be initiated to prevent serious complications of ARF, such as hyperkalemia, severe metabolic acidosis, pericardi-tis, and pulmonary edema. Dialysis corrects many biochemical abnormalities; allows for liberalization of fluid, protein, and sodium intake; diminishes bleeding tendencies; and may help wound healing. Hemodialysis, peritoneal dialysis, or any of the new continuous renal replacement therapies may be performed.
Because hyperkalemia is the most life-threatening of the fluid and electrolyte disturbances, the patient is monitored for hyper-kalemia through serial serum electrolyte levels (potassium value more than 5.5 mEq/L [5.5 mmol/L]), electrocardiogram changes (tall, tented, or peaked T waves), and changes in clinical status.
The elevated potassium levels may be reduced by administering cation-exchange resins (sodium polystyrene sulfonate [Kayexalate]) orally or by retention enema. Kayexalate works by exchanging a sodium ion for a potassium ion in the intestinal tract. Sorbitol is often administered in combination with Kayexalate to induce a diarrhea-type effect (it induces water loss in the GI tract).
If a retention enema is administered (the colon is the major site for potassium exchange), a rectal catheter with a balloon may be used to facilitate retention if necessary. The patient should re-tain the resin 30 to 45 minutes to promote potassium removal. Afterward, a cleansing enema may be prescribed to remove the Kayexalate resin as a precaution against fecal impaction.
Because many medications are eliminated through the kidneys, medication dosages must be reduced when a patient has ARF. Ex-amples of commonly used medications that require adjustment are antibiotic agents (especially aminoglycosides), digoxin, ACE inhibitors, and medications containing magnesium.
Many medications have been used in patients with ARF in an attempt to improve patient outcomes. Diuretic agents are often used to control fluid volume, but they have not been shown to hasten the recovery from ARF.
Low-dose dopamine (1 to 3 g/kg) is often used to dilate the renal arteries through stimulation of dopaminergic receptors; however, research has not definitely demonstrated that dopamine prevents ARF or improves outcome in patients with established renal failure.
Atrial natriuretic peptide (ANP), an endogenous hormone synthesized by the cardiac atria, has been shown to improve renal function in multiple animal models of ARF. It has also decreased the need for dialysis in patients with oliguric acute tubular necro-sis in a multisite clinical trial of patients. Patients with nonoliguric acute tubular necrosis did not benefit (Lewis, Salem, Chertow et al., 2000). Further research on ANP use is underway.
In patients with severe acidosis, the arterial blood gases or serum bicarbonate levels (CO2-combining power) must be mon-itored because the patient may require sodium bicarbonate therapy or dialysis. If respiratory problems develop, appropriate ventilatory measures must be instituted. The elevated serum phosphate level may be controlled with phosphate-binding agents (aluminum hy-droxide). These agents help prevent a continuing rise in serum phosphate levels by decreasing the absorption of phosphate from the intestinal tract.
ARF causes severe nutritional imbalances (because nausea and vomiting contribute to inadequate dietary intake), impaired glu-cose use and protein synthesis, and increased tissue catabolism. The patient is weighed daily and can be expected to lose 0.2 to 0.5 kg (0.5 to 1 lb) daily if the nitrogen balance is negative (ie, the patient’s caloric intake falls below caloric requirements). If the patient gains or does not lose weight or develops hypertension, fluid retention should be suspected.
Dietary proteins are limited to about 1 g/kg during the oliguric phase to minimize protein breakdown and to prevent accumula-tion of toxic end products. Caloric requirements are met with high-carbohydrate meals because carbohydrates have a protein-sparing effect (ie, in a high-carbohydrate diet, protein is not used for meeting energy requirements but is “spared” for growth and tissue healing). Foods and fluids containing potassium or phos-phorus (bananas, citrus fruits and juices, coffee) are restricted. Potassium intake is usually restricted to 40 to 60 mEq/day, and sodium is usually restricted to 2 g/day. The patient may require parenteral nutrition.
The oliguric phase of ARF may last 10 to 20 days and is fol-lowed by the diuretic phase, at which time urine output begins to increase, signaling that kidney function is returning. Blood chem-istry evaluations are made to determine the amounts of sodium, potassium, and water needed for replacement, along with assess-ment for overhydration or underhydration. After the diuretic phase, the patient is placed on a high-protein, high-calorie diet and is encouraged to resume activities gradually.
The nurse has an important role in caring for the patient with ARF. In addition to directing attention to the patient’s primary disorder (which may be a factor in the development of ARF), the nurse monitors for complications, participates in emergency treatment of fluid and electrolyte imbalances, assesses progress and response to treatment, and provides physical and emotional support. Additionally, the nurse keeps family members informed about the patient’s condition, helps them understand the treat-ments, and provides psychological support. Although the devel-opment of ARF may be the most serious problem, the nurse must continue to include in the plan of care those nursing measures in-dicated for the primary disorder (eg, burns, shock, trauma, ob-struction of the urinary tract).
Because of the serious fluid and electrolyte imbalances that can occur with ARF, the nurse monitors the patient’s serum electrolyte levels and physical indicators of these complications during all phases of the disorder. Hyperkalemia is the most immediate life-threatening imbalance seen in ARF. Parenteral fluids, all oral in-take, and all medications are screened carefully to ensure that hidden sources of potassium are not inadvertently administered or consumed. Intravenous solutions must be carefully selected ac-cording to the patient’s fluid and electrolyte status. The patient’s cardiac function and musculoskeletal status are monitored closely for signs of hyperkalemia.
The nurse monitors fluid status by paying careful attention to fluid intake (intravenous medications should be administered in the smallest volume possible), urine output, apparent edema, distention of the jugular veins, alterations in heart sounds and breath sounds, and increasing difficulty in breathing. Accurate daily weights, as well as intake and output records, are essential.
Indicators of deteriorating fluid and electrolyte status are re-ported immediately to the physician, and preparation is made for emergency treatment. Hyperkalemia is treated with glucose and insulin, calcium gluconate, cation-exchange resins (Kayexalate), or dialysis. Fluid and other electrolyte disturbances are often treated with hemodialysis, peritoneal dialysis, or other continu-ous renal replacement therapies.
The nurse also directs attention to reducing the patient’s meta-bolic rate during the acute stage of renal failure to reduce catab-olism and the subsequent release of potassium and accumulation of endogenous waste products (urea and creatinine). Bed rest may be indicated to reduce exertion and the metabolic rate during the most acute stage of the disorder. Fever and infection, both of which increase the metabolic rate and catabolism, are prevented or treated promptly.
Attention is given to pulmonary function, and the patient is as-sisted to turn, cough, and take deep breaths frequently to prevent atelectasis and respiratory tract infection. Drowsiness and lethargy may prevent the patient from moving and turning without en-couragement and assistance.
Asepsis is essential with invasive lines and catheters to minimize the risk of infection and increased metabolism. An indwelling uri-nary catheter is avoided whenever possible because of the high risk for UTI associated with its use.
The skin may be dry or susceptible to breakdown as a result of edema; therefore, meticulous skin care is important. Additionally, excoriation and itching of the skin may result from the deposit of irritating toxins in the patient’s tissues. Massaging bony promi-nences, turning the patient frequently, and bathing the patient with cool water are often comforting and prevent skin breakdown.
The patient with ARF requires treatment with hemodialysis, peri-toneal dialysis, or continuous renal replacement therapies to pre-vent serious complications; the length of time that these treatments are necessary varies with the cause and extent of damage to the kidneys. The patient and family need assistance, explanation, and support during this time. The purpose and ra-tionale of the treatments are explained to the patient and family by the physician. High levels of anxiety and fear, however, may necessitate repeated explanation and clarification by the nurse. The family members may initially be afraid to touch and talk to the patient during the procedure but should be encouraged and assisted to do so.
Although many of the nurse’s functions are devoted to the technical aspects of the procedure, the psychological needs and concerns of the patient and family cannot be ignored. Continued assessment of the patient for complications of ARF and of its pre-cipitating cause is essential.
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