Oliguria

A cardinal sign of renal and urinary tract disorders, oliguria is clinically defined as urine output of less than 400 ml/24 hours. Typically, this sign occurs abruptly and may herald serious — possibly life-threatening — hemodynamic instability. Its causes can be classified as prerenal (decreased renal blood flow), intrarenal (intrinsic renal damage), or postrenal (urinary tract obstruction); the pathophysiology differs for each classification. (See How oliguria develops, page 470.) Oliguria associated with a prerenal or postrenal cause is usually promptly reversible with treatment, although it may lead to intrarenal damage if untreated. However, oliguria associated with an intrarenal cause is usually more persistent and may be irreversible.

History

Begin by asking the patient about his usual daily voiding pattern, including frequency and amount. When did he first notice changes in this pattern and in the color, odor, or consistency of his urine? Ask about pain or burning on urination. Has the patient had a fever? Note his normal daily fluid intake. Has he recently been drinking more or less than usual? Has his intake of caffeine or alcohol changed drastically? Has he had recent episodes of diarrhea or vomiting that might cause fluid loss? Next, explore associated complaints, especially fatigue, loss of appetite, thirst, dyspnea, chest pain, or recent weight gain or loss (in dehydration).

Check for a history of renal, urinary tract, or cardiovascular disorders. Note recent traumatic injury or surgery associated with significant blood loss, as well as recent blood transfusions. Was the patient exposed to nephrotoxic agents, such as heavy metals, organic solvents, anesthetics, or radiographic contrast media? Next, obtain a drug history.

Physical assessment

Begin the physical assessment by taking the patient’s vital signs and weighing him. Assess his overall appearance for edema. Palpate both kidneys for tenderness and enlargement, and percuss for costovertebral angle (CVA) tenderness. Also, inspect the flank area for edema or erythema. Auscultate the heart and lungs for abnormal sounds, and the flank area for renal artery bruits. Assess the patient for edema or signs of dehydration such as dry mucous membranes.

Obtain a urine specimen, and inspect it for abnormal color, odor, or sediment. Use reagent strips to test for glucose, protein, and blood. Also, use a urinometer to measure specific gravity.

Medical causes

Acute tubular necrosis

An early sign of acute tubular necrosis, oliguria may occur abruptly (in shock) or gradually (in nephrotoxicity). Usually, it persists for about 2 weeks, followed by polyuria. Related features include signs of hyperkalemia (muscle weakness and cardiac arrhythmias), uremia (anorexia, confusion, lethargy, twitching, seizures, pruritus, and Kussmaul’s respirations), and heart failure (edema, jugular vein distention, crackles, and dyspnea).

Calculi

Oliguria or anuria may result from calculi lodging in the kidneys, ureters, bladder outlet, or urethra. Associated signs and symptoms include urinary frequency and urgency, dysuria, and hematuria or pyuria. Usually, the patient experiences renal colic — excruciating pain that radiates from the CVA to the flank, the suprapubic region, and the external genitalia. This pain may be accompanied by nausea, vomiting, hypoactive bowel sounds, abdominal distention and, occasionally, fever and chills.

Glomerulonephritis (acute)

Acute glomerulonephritis produces oliguria or anuria. Other features are mild fever, fatigue, gross hematuria, proteinuria, generalized edema, elevated blood pressure, headache, nausea and vomiting, flank and abdominal pain, and signs of pulmonary congestion (dyspnea and productive cough).

Heart failure

Oliguria may occur in left-sided heart failure as a result of low cardiac output and decreased renal perfusion. Accompanying signs and symptoms include dyspnea, fatigue, weakness, peripheral edema, distended jugular veins, tachycardia, tachypnea, crackles, and a dry or productive cough. In advanced heart failure, the patient may also develop orthopnea, cyanosis, clubbing, ventricular gallop, diastolic hypertension, cardiomegaly, and hemoptysis.

Hypovolemia

Any disorder that decreases circulating fluid volume can produce oliguria. Associated findings in hypovolemia include orthostatic hypotension, apathy, lethargy, fatigue, gross muscle weakness, anorexia, nausea, profound thirst, dizziness, sunken eyeballs, poor skin turgor, and dry mucous membranes.

Pyelonephritis (acute)

Accompanying the sudden onset of oliguria in acute pyelonephritis are high fever with chills, fatigue, flank pain, CVA tenderness, weakness, nocturia, dysuria, hematuria, urinary frequency and urgency, and tenesmus. The urine may appear cloudy. Occasionally, the patient with acute pyelonephritis also experiences anorexia, nausea, diarrhea, and vomiting.

Renal artery occlusion (bilateral)

Renal artery occlusion may produce oliguria or, more commonly, anuria. Other features include severe, constant upper abdominal and flank pain, nausea and vomiting, and hypoactive bowel sounds. The patient also develops a fever 1 to 2 days after the occlusion, as well as diastolic hypertension.

Renal failure (chronic)

Oliguria is a major sign of end-stage chronic renal failure. Associated findings reflect progressive uremia and include fatigue, weakness, irritability, uremic fetor, ecchymoses and petechiae, peripheral edema, elevated blood pressure, confusion, emotional lability, drowsiness, coarse muscle twitching, muscle cramps, peripheral neuropathies, anorexia, metallic taste in the mouth, nausea and vomiting, constipation or diarrhea, stomatitis, pruritus, pallor, and yellow- or bronze-tinged skin. Eventually, seizures, coma, and uremic frost may develop.

Renal vein occlusion (bilateral)

Renal vein occlusion occasionally causes oliguria accompanied by acute low back and flank pain, CVA tenderness, fever, pallor, hematuria, enlarged and palpable kidneys, edema and, possibly, signs of uremia.

Sepsis

Any condition that results in sepsis may produce oliguria, along with fever, chills, restlessness, confusion, diaphoresis, anorexia, vomiting, diarrhea, pallor, hypotension, and tachycardia. The patient may exhibit signs of local infection, such as dysuria and wound drainage. In severe infection, he may develop lactic acidosis marked by Kussmaul’s respirations.

Toxemia of pregnancy

In severe preeclampsia, oliguria may be accompanied by elevated blood pressure, dizziness, diplopia, blurred vision, epigastric pain, nausea and vomiting, irritability, and severe frontal headache. Typically, the oliguria is preceded by generalized edema and sudden weight gain of more than 3 lb (1.4 kg) per week during the second trimester or more than 1 lb (0.5 kg) per week during the third trimester. If preeclampsia progresses to eclampsia, the patient develops seizures and may slip into coma.

Urethral stricture

Urethral stricture produces oliguria accompanied by chronic urethral discharge, urinary frequency and urgency, dysuria, pyuria, and diminished urine stream. As obstruction worsens, urine extravasation may lead to formation of urinomas and urosepsis.

Other causes

Diagnostic studies

Radiographic studies that use contrast media may cause nephrotoxicity and oliguria.

Drugs

Oliguria may result from drugs that cause decreased renal perfusion (diuretics), nephrotoxicity (most notably, aminoglycosides and chemotherapeutic drugs), urine retention (adrenergics and anticholinergics), or urinary obstruction associated with precipitation of urinary crystals (sulfonamides and acyclovir).

Special considerations

Monitor vital signs, intake and output, and daily weight. Depending on the cause of the oliguria, fluids are normally restricted to between 600 ml and 1 L more than the patient’s urine output for the previous day. Provide a diet low in sodium, potassium, and protein.

Laboratory tests may be necessary to determine if the oliguria is reversible. Such tests include serum blood urea nitrogen and creatinine levels, urea and creatinine clearance, urine sodium levels, and urine osmolality. Abdominal X-rays, ultrasonography, computed tomography scan, cystography, and a renal scan may be required.

Pediatric pointers

In the neonate, oliguria may result from edema or dehydration. Major causes include congenital heart disease, respiratory distress syndrome, sepsis, congenital hydronephrosis, acute tubular necrosis, and renal vein thrombosis. Common causes of oliguria in children between ages 1 and 5 are acute poststreptococcal glomerulonephritis and hemolytic-uremic syndrome. After age 5, causes of oliguria are similar to those in adults.

Geriatric pointers

In elderly patients, oliguria may result from gradual progression of an underlying disorder. It may also result from overall poor muscle tone secondary to inactivity, poor fluid intake, and infrequent voiding attempts.

Patient counseling

Explain applicable fluid restrictions or increases to the patient. For example, the patient with renal calculi may require increased fluids, whereas the patient with renal failure may need to restrict fluid intake. Review the prescribed diet with the patient, and obtain a nutritional consult, if necessary.

Pictures

Book Source Details

• Book Title: Signs & Symptoms: A 2-in-1 Reference for Nurses
• Author(s): Springhouse
• Year of Publication: 2007
• Copyright Details: Signs & Symptoms: A 2-in-1 Reference for Nurses, Copyright © 2007 Lippincott Williams & Wilkins.

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Copyright Details: Signs & Symptoms: A 2-in-1 Reference for Nurses, Copyright © 2008 Williams & Wilkins.

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More About This Book: Title: Signs & Symptoms: A 2-in-1 Reference for Nurses Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2007 ISBN: 1-58255-318-1

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