Renal Failure, Acute

Renal Failure, Acute

DRG Category:674
Mean LOS:7 days
Description:SURGICAL: Other Kidney and Urinary Tract Procedures With CC
DRG Category:683
Mean LOS:4.7 days
Description:MEDICAL: Renal Failure With CC

Acute renal failure (ARF) is the abrupt deterioration of renal function that results in the accumulation of fluids, electrolytes, and metabolic waste products. It is usually accompanied by a marked decrease in urinary output. Although ARF is often reversible, if it is ignored or inappropriately treated, it can lead to irreversible kidney damage and chronic renal failure. Two types of ARF occur: community-acquired and hospital-acquired. Community-acquired ARF is diagnosed in about 1% of hospital admissions at the time of initial assessment. In comparison, hospital-acquired ARF occurs in up to 4% of hospital admissions and 20% of critical care admissions. There are many reasons for this increased incidence of hospital-acquired ARF, and they include an aging population, the use of nephrotoxic medications, and increasing severity of illness in hospitalized patients.

Approximately 70% of patients develop oliguric ARF with a urine output of less than 500 mL/day. The other 30% of patients never develop oliguria and have what is considered nonoliguric renal failure. Oliguric ARF generally has three stages. During the initial phase (often called the oliguric phase), when trauma or insult affects the kidney tissue, the patient becomes oliguric. This stage may last a week or more. The second stage of ARF is the diuretic phase, which is heralded by a doubling of the urinary output from the previous 24 hours. During the diuretic phase, patients may produce as much as 5 L of urine in 24 hours but lack the ability for urinary concentration and regulation of waste products. This phase can last from 1 to several weeks. The final stage, the recovery phase, is characterized by a return to a normal urinary output (about 1,500 to 1,800 mL/24 hr), with a gradual improvement in metabolic waste removal. Some patients take up to a year to recover full renal function after the initial insult.

Complications of ARF include severe electrolyte imbalances such as hyperkalemia and hypocalcemia. The patient is also at risk for secondary infections, congestive heart failure, and pericarditis. ARF that does not respond to treatment of the underlying cause can progress to chronic renal failure (see Renal Failure, Chronic, p. 967).

Causes

The causes of ARF can be classified as prerenal, intrarenal (intrinsic), and postrenal. Prerenal ARF results from conditions that cause diminished blood flow to the kidneys. Disorders that can lead to prerenal failure include cardiovascular disorders (dysrhythmias, cardiogenic shock, congestive heart failure, myocardial infarction), disorders that cause hypovolemia (burns, trauma, dehydration, hemorrhage), maldistribution of blood (septic shock, anaphylactic shock), renal artery obstruction, and severe vasoconstriction.

Intrarenal, or intrinsic, ARF involves the actual destruction of the renal parenchyma (functional cells). The most common cause of intrarenal failure is acute tubular necrosis, or damage to the renal tubules because of either a nephrotoxic or an ischemic injury. Nephrotoxic injuries occur when the renal tubules are exposed to a high concentration of a toxic chemical. Common sources of nephrotoxic injuries include antibiotics (aminoglycosides, sulfonamides), diuretics, NSAIDs (ibuprofen), and contrast media from diagnostic tests. Ischemic injuries occur when the mean arterial blood pressure is less than 60 mm Hg for 40 to 60 minutes. Situations that can lead to ischemic injuries include cardiopulmonary arrest, hypovolemic or hemorrhagic shock, cardiogenic shock, or severe hypotension.

Postrenal (postobstructive) ARF is caused by a blockage to urine outflow. One of the most common causes of postrenal ARF in hospitalized patients is an obstructed Foley catheter. Other conditions that can lead to postrenal ARF include ureteral inflammation or obstruction, accidental ligation of the ureters, bladder obstruction (infection, anticholinergic drug use, tumors, trauma leading to bladder rupture), or urethral obstruction (prostate enlargement, urethral trauma, urethral strictures).

Genetic considerations

Several heritable diseases that can lead to renal failure include the autosomal recessive condition Alport’s syndrome, which causes nephropathy that is often associated with sensorineural deafness and can be transmitted as X-linked recessive, autosomal recessive, and autosomal dominant forms. Renal hypouricemia, which is caused by mutations in the genes SLC2A9 or SLC22A12, can lead to exercise-induced ARF in about 10% of patients.

Gender, ethnic/racial, and life span considerations

Some experts report that the concentrating ability of the kidneys decreases with advancing age. Oliguria in the geriatric patient, therefore, may be diagnosed with urine production of as much as 600 mL/day. Elderly patients may have a decreased blood flow, decreased kidney mass, decreased filtering surface, and decreased glomerular filtration rate. The elderly, therefore, are more susceptible to insults that result in ARF, and their mortality rates tend to be higher. Older men have the added risk of preexisting renal damage because of the presence of benign prostatic hypertrophy. There are no known racial or ethnic considerations.

Global health considerations

ARF occurs around the globe, but no data are available on the international prevalence and incidence.

Assessment

History

When you elicit the patient’s history, look for a disorder that can lead to prerenal, intrarenal, or postrenal ARF. Question the patient about recent illnesses, infections, or injuries, and take a careful medication history with attention to maximum daily doses and self-medication patterns. Determine the patient’s urinary patterns and document information such as frequency of voiding, approximate voiding volume, and pattern of daily fluid intake. Evaluate the patient for a recent history of gastrointestinal (GI) problems, such as anorexia, nausea, and changes in bowel patterns. Some patients have a recent history of weight gain, edema, headache, confusion, and sleepiness.

Physical examination

The symptoms reflect the underlying disease process and may be nonspecific. The patient appears seriously ill and often drowsy, irritable, confused, and combative because of the accumulation of metabolic wastes. In the oliguric phase, the patient may show signs of fluid overload such as hypertension, rapid heart rate, peripheral edema, and crackles when you listen to the lungs. Patients in the diuretic phase appear dehydrated, with dry mucous membranes, poor skin turgor, flat neck veins, and orthostatic hypotension. The patient may have increased bleeding tendencies, such as petechiae, ecchymosis of the skin, and bloody vomitus (hematemesis).

Psychosocial

The patient with ARF may be highly anxious because of the unknown outcome of the problem. Anxiety may increase as symptoms such as hemorrhage or pain from an obstructing calculus appear. Because ARF may occur as an iatrogenic problem (a problem caused by the treatment of a disease), you may need to explain to the patient or significant others that the problem was not avoidable and is a potential complication of the underlying disorder.

Diagnostic highlights

TestNormal ResultAbnormality With ConditionExplanation
UrinalysisClear, hazy, colorless; straw, yellow, or amber coloredGranular muddy-brown casts suggest tubular necrosis; tubular cells or tubular cell casts suggest acute tubular necrosis; reddish-brown urine and proteinuria suggest acute glomerular nephritis; presence of red blood cells may indicate glomerular nephritis; and white blood cells may indicate pyelonephritisAcute damage to kidneys causes loss of red and white blood cells, casts (fibrous material or coagulated protein), or protein in the urine
Blood urea nitrogen5–20 mg/dLElevatedKidneys cannot excrete wastes
Serum creatinine0.5–1.1 mg/dLElevated; the RIFLE classification, based on a patient’s serum creatinine, is often used for ARF:
  • Risk (R): Increase in serum creatinine level by 1.5 or decrease in glomerular filtration rate (GFR) by 25%, or urine output (UO) < 0.5 mL/kg/hr for 6 hr
  • Injury (I): Increase in serum creatinine level by 2 or decrease in GFR by 50%, or UO < 0.5 mL/kg/hr for 12 hr
  • Failure (F): Increase in serum creatinine level by 3, decrease in GFR by 75%, or serum creatinine level > 4 mg/dL with acute increase of > 0.5 mg/dL; UO < 0.3 mL/kg/hr for 24 hr or anuria for 12 hr
  • Loss (L): Persistent ARF, complete loss of kidney function > 4 wk
  • End-stage kidney disease (E): Loss of kidney function > 3 mo
Kidneys cannot excrete wastes
24-hr urine creatinineFemales: 85–125 mL/min; males: 95–135 mL/min50% decreaseAcute damage to the kidney limits ability to clear creatinine
Urine sodium20–40 mEq/LPrerenal: < 20 mEq/L; intrarenal: < 20 mEq/L; postrenal: > 40 mEq/LPrerenal and sometimes intrarenal leads to sodium retention whereas postrenal leads to sodium loss in urine; fractional excretion of sodium (FENa) is calculated as: urine Na/plasma Na/urine creatinine/plasma creatinine; FENa < 1% is likely prerenal ARF; FENa > 1% is likely ATN

Other Tests: Complete blood count; cystatin C; erythrocyte sedimentation rate; hemodynamic monitoring; renal ultrasound; radionuclide scanning; magnetic resonance angiography; renal biopsy; serum levels of sodium, potassium, magnesium, and phosphorus; arterial blood gases

Primary nursing diagnosis

Diagnosis

Fluid volume deficit related to excessive urinary output, vomiting, hemorrhage

Outcomes

Fluid balance; Circulation status; Cardiac pump effectiveness; Hydration

Interventions

Bleeding reduction; Fluid resuscitation; Blood product administration; Intravenous therapy; Circulatory care; Shock management

Planning and implementation

Collaborative

Any nephrotoxic medications should be discontinued. During the oliguric-anuric stage, diuretic therapy with furosemide (Lasix) or ethacrynic acid (Edecrin) may be attempted to convert oliguric ARF to nonoliguric ARF, which has a better renal recovery rate. During the diuretic phase, fluid volume replacement may be ordered to compensate for the fluid loss and to maintain adequate arterial blood flow to the kidneys. A daily record of intake, output, and weights assists the physician in making treatment decisions. During fluid replacement, monitoring with central venous pressures or pulmonary artery catheters helps track the patient’s response to interventions. The physician should be notified if the patient’s urine output drops below 0.5 mL/kg per hour or if the daily weight changes by more than 2 kg (4.4 lb).

Electrolyte replacement is based on the patient’s serum electrolyte values. The physician attempts to limit hyperkalemia because of its potentially lethal effects on cardiac function. Note the excretory route for medications so that the already damaged kidneys are not further damaged by nephrotoxins. The patient’s response to medications is important; drug dosages may need to be decreased because of decreased renal excretion. In addition, timing of medications may need to be changed because of increased excretion during dialysis.

Renal replacement therapy includes intermittent hemodialysis (IHD), continuous venovenous hemodiafiltration (CVVHD), and peritoneal dialysis (PD). IHD is the most common and efficient way of removing extra volume from the blood but is associated with complications such as hypotension. CVVHD is a better choice when hypotension is a problem, such as in hemodynamically unstable patients who have critical illness. CVVHD is a continuous renal replacement technique that has increased risks of bleeding but leads to better control of uremia and cerebral perfusion. PD, while less expensive, does not remove the volume as efficiently as other methods. Indications for dialysis include fluid overload, hyperkalemia, metabolic acidosis, uremic intoxication, and the need to remove nephrotoxic substances such as metabolites or drugs. The diet for the patient with ARF is usually high in carbohydrates to prevent protein breakdown and low in protein to provide essential amino acids but to limit increases in azotemia (increased urea in the body). For patients who lose sodium in the urine, the diet is high in sodium; for patients with sodium and water retention, the diet is low in sodium and may also contain a fluid restriction. Potassium restrictions are frequently ordered based on laboratory values.

Pharmacologic highlights

Medication or Drug ClassDosageDescriptionRationale
DiureticsVaries by drugFurosemide (Lasix); bumetanide, ethacrynic acid (Edecrin); mannitolConvert oliguric ARF to nonoliguric
Dopamine1–3 mcg/kg/min IVVasodilatorLow-dose dopamine is a potent vasodilator, increasing renal blood flow and urine output
Phosphate binders15–30 mL with meals tidAluminum hydroxide (Basaljel, Amphojel)Enhance GI excretion of phosphorus

Other Drugs: Sodium polystyrene sulfonate (Kayexalate) can be administered orally or rectally to reduce potassium. Sodium bicarbonate may be ordered to correct metabolic acidosis. If the patient is receiving hemodialysis, supplements of water-soluble vitamins are needed because they are removed during dialysis. Other medications include antihypertensives to control blood pressure, antibiotics to manage secondary infections, diphenhydramine (Benadryl) to manage itching, and recombinant human erythropoietin to increase red blood cell production.

Independent

Rest and recovery are important nursing goals. By limiting an increased metabolic rate, the nurse limits tissue breakdown and decreases nitrogenous waste production. A quiet, well-organized environment at a temperature comfortable for the patient ensures rest and recovery. To help the patient deal with fluid restrictions, use creative strategies to increase the patient’s comfort and compliance. Give medications with meals or in minimal IV volumes to maximize the amount of fluid available for patient use.

Several factors place the patient with ARF at risk for impaired skin integrity. Uremia results in itching and dryness of the skin. If the patient experiences pruritus, help the patient clip the fingernails short and keep the nail tips smooth. Use skin emollients liberally, avoid harsh soaps, and bathe the patient only when necessary. Frequent turning and range-of-motion exercises assist in preventing skin breakdown. If the patient is taking medications that cause frequent stools, clean the perineum and buttocks frequently to maintain skin integrity.

Note that one of the most common sources of postrenal ARF is an obstructed urinary catheter drainage system. Before contacting the physician about a decreasing urinary output in an acutely or critically ill patient, make sure that the catheter is patent. If institutional policy permits, irrigate the Foley catheter using sterile technique with 30 mL of normal saline to check for obstruction. Note any kinks in the collecting system. If institutional policy permits, replace the indwelling Foley catheter with a new catheter and urinary drainage system to ensure it is functioning adequately. Signs that postrenal ARF is caused by obstruction in the urinary catheter include a sudden cessation of urinary output in a patient whose urinary output has previously been high or average and a urinary output with normal specific gravity and normal urinary sodium.

The patient with ARF is often irritable and confused. Recognize that the irritability is part of the disease process. Keep the environment free of unnecessary clutter to reduce the chance of falls. If the patient is on bedrest, maintain the bed in the low position and keep the side rails up. Keep the patient’s call light within easy reach and the patient’s belongings on a bedside table close to the bed. The patient with ARF is anxious not only because of the ambiguity of the prognosis, but also because he or she may be in an acute care environment for treatment. Provide the patient with ongoing, repeated information about what is happening and why. Ongoing reassurance for both the patient and the significant others is essential.

Evidence-Based Practice and Health Policy

Carl, D.E., Grossman, C., Behnke, M., Sessler, C.N., & Gehr, T.W. (2010). Effect of timing of dialysis on mortality in critically ill, septic patients with acute renal failure. Hemodialysis International, 14(1), 11–17.

  • Investigators hypothesize that early initiation of renal replacement therapy (RRT) in patients with blood urea nitrogen (BUN) < 100 mg/dL compared to late initiation of RRT in patients with BUN > 100 mg/dL will facilitate better outcomes.
  • In a retrospective study among 147 patients being treated for ARF secondary to sepsis, RRT was initiated early in 57.8% of patients and initiated late in 42.2% of patients. Compared to early initiation of RRT, late initiation increased the odds of mortality at 14 days by 3.6 times (95% CI, 1.7 to 7.6; p = 0.001) and 2.6 times at 28 days (95% CI, 1.2 to 5.7; p = 0.01).
  • Patients in the early RRT initiation group had a mean BUN of 66 mg/dL (SD, ± 20.2 mg/dL) compared to 137 mg/dL in the late RRT initiation group (SD, ± 28.4 mg/dL) (p < 0.001). However, mean urine output 24 hours prior to initiation of RRT was also significantly lower among the early initiation group compared to the late initiation group (653 mL/day versus 1,258 mL/day; p = 0.001).
  • Survival at 28 days was higher among patients with an increased mean arterial pressure (p = 0.01), an increased initial platelet count (p = 0.02), and absence of acute liver failure (p = 0.002).

Documentation guidelines

  • Physical findings: Urinary output and description of urine, fluid balance, vital signs, findings related to original disease process or insult, presence of pain or pruritus, mental status, GI status, and skin integrity
  • Condition of peritoneal or vascular access sites
  • Nutrition: Response to dietary or fluid restrictions, tolerance to food, maintenance of body weight
  • Complications: Cardiovascular, integumentary infection

Discharge and home healthcare guidelines

All patients with ARF need an understanding of renal function, signs and symptoms of renal failure, and how to monitor their own renal function. Patients who have recovered viable renal function still need to be monitored by a nephrologist for at least a year. Teach the patient that she or he may be more susceptible to infection than previously. Advise daily weight checks. Emphasize rest to prevent overexertion. Teach the patient or significant others about all medications, including dosage, potential side effects, and drug interactions. Explain that the patient should tell the healthcare professional about the medications if the patient needs treatment such as dental work or if a new medication is added. Explain that ongoing medical assessment is required to check renal function.

Explain all dietary and fluid restrictions. Note if the restrictions are lifelong or temporary. Patients who have not recovered viable renal function need to understand that their condition may persist and even become chronic. If chronic renal failure is suspected, further outpatient treatment and monitoring are needed. Discuss with significant others the lifestyle changes that may be required with chronic renal failure.

References in periodicals archive ?
Medical evaluation conducted in June also revealed that the OFW suffers from an acute renal failure, acute respiratory failure and stage 3 chronic kidney disease.
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Severe renal adverse events with Immune Globulin Intravenous (Human) have included acute renal failure, acute tubular necrosis, proximal tubular nephropathy, and osmotic nephrosis.
In another case the accidental rectal administration of 50 ml of 9% acetic acid in a 5-year-old child caused necrosis of the colon, acute renal failure, acute liver dysfunction and disseminated intravascular coagulation (6).