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Cherisse Berry

, MD, New York University School of Medicine

Last full review/revision Nov 2020| Content last modified Nov 2020
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Oliguria is urine output < 500 mL in 24 hours in an adult or < 0.5 mL/kg/hour in an adult or child (< 1 mL/kg/hour in neonates).

Etiology of Oliguria

Causes of oliguria are typically divided into 3 categories:

  • Prerenal (blood-flow related)

  • Renal (intrinsic kidney disorders)

  • Postrenal (outlet obstruction)

There are numerous such entities (see Acute Kidney Injury), but a limited number cause most cases of acute oliguria in hospitalized patients (see table Some Causes of Oliguria).


Some Causes of Oliguria






Fluid loss

Inadequate fluid replacement

Low cardiac output

Decreased systemic vascular resistance


Hypoperfusion (prolonged, eg, > 4 hours)

X-ray contrast agent

Nephrotoxic drugs (eg, aminoglycosides and other antibiotics, nonsteroidal anti-inflammatory drugs)


Mechanical urinary obstruction

Blocked urinary catheter

Bladder or sphincter dysfunction

Anticholinergic drug use

Postoperative urinary retention

Fecal impaction if severe

* These prerenal conditions often coexist and rapidly (ie, in < 1 hour) reduce urine output.

Evaluation of Oliguria


In communicative patients, a marked urge to void suggests outlet obstruction, whereas thirst and no urge to void suggest volume depletion. In obtunded (and presumably catheterized) patients, a sudden decrease in urine flow in a normotensive patient suggests catheter occlusion (eg, caused by a clot or kinking) or displacement, whereas a gradual decrease is more likely due to acute tubular necrosis or a prerenal cause.

Recent medical events are helpful; they include review of recent blood pressure readings, surgical procedures, and drug and x-ray contrast administration. Recent surgery or trauma may be consistent with hypovolemia. A severe crush injury, deep electrical burn, or heatstroke suggests rhabdomyolysis.

Physical examination

Vital signs are reviewed, particularly for hypotension, tachycardia, or both (suggesting hypovolemia or sepsis) and fever (suggesting sepsis). Signs of focal infection and cardiac failure should be sought. Palpable bladder distention indicates an outlet obstruction. Dark brown urine suggests myoglobinuria.


In all catheterized patients (and those with an ileal conduit), patency should be ascertained by irrigation before further testing; this approach may solve the problem. In many of the remaining patients, etiology (eg, shock, sepsis) is clinically apparent. In others, particularly those with multiple disorders, testing is needed to differentiate prerenal from renal (acute tubular necrosis) causes. In patients without a urinary catheter, placement of a catheter should be considered; this will diagnose and treat obstruction and provide continuous monitoring of output.

If a central venous or pulmonary artery catheter is in place, volume status (and with a pulmonary artery catheter, cardiac output) can be determined by measuring central venous pressure (see End Point and Monitoring) or pulmonary artery occlusion pressure. However, many physicians would not insert such a line for acute oliguria unless other indications were present. An alternative in the patient without signs of volume overload is to rapidly give a test bolus of IV fluid, 500 mL 0.9% saline (20 mL/kg in children); an increase in output suggests a prerenal cause. Serum electrolytes such as sodium, blood urea nitrogen and creatinine should be measured to assist in determining the cause of oliguria. A high ratio of serum BUN to creatinine (eg, > 20:1) suggests a prerenal cause.

Calculating the fractional excretion of sodium (FENa) from the plasma and urine concentrations of sodium can help to differentiate between the prerenal state and acute tubular necrosis using the following equation:

  • A FENa ratio > 2% usually indicates acute tubular necrosis.

  • A FENa ratio < 1% usually indicates a prerenal state such as dehydration or other forms of prerenal azotemia.

  • FENa ratios between 1% and 2% are compatible with acute tubular necrosis or a prerenal state.

Treatment of Oliguria

Identified causes are treated; outflow obstruction is corrected, volume is replaced, and cardiac output is normalized. Nephrotoxic drugs are stopped, and another drug is substituted. Hypotension should be avoided to prevent further renal insults. Patients with renal failure that cannot be reversed may require renal replacement therapy (eg, continuous venovenous hemofiltration or hemodialysis).

Key Points

  • Categories of causes of oliguria include decreased renal blood flow, renal insufficiency, and urinary outflow obstruction.

  • History and physical examination often suggest a mechanism (eg, recent hypotension, nephrotoxic drug use).

  • Measure serum electrolytes, blood urea nitrogen, and creatinine.

  • Measure urine sodium and creatinine concentration, and calculate fractional sodium excretion if it is unclear whether the cause is prerenal or renal; a ratio < 1 indicates the problem is prerenal, a ratio > 2 indicates acute tubular necrosis, and ratios between 1% and 2% are indeterminate.

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