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Oliguria is urine output < 500 mL in 24 h in an adult or < 0.5 mL/kg/h in an adult or child (< 1 mL/kg/h in neonates).
Etiology
Causes of oliguria are typically divided into three categories:
There are numerous such entities (see Renal Failure: Acute Renal Failure (ARF)), but a limited number cause most cases of acute oliguria in the hospitalized patient (see Table 7: Approach to the Critically Ill Patient: Some Causes of Oliguria ).
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Table 7
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Some Causes of Oliguria
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Mechanism
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Examples
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Prerenal*
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Hypovolemia
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Bleeding
Fluid loss
Inadequate fluid replacement
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Low cardiac output
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MI
Heart failure
Pulmonary embolism
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Decreased systemic vascular resistance
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Sepsis
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Renal
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Acute tubular necrosis
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Hypoperfusion (prolonged, eg, > 4 h)
X-ray contrast dye
Rhabdomyolysis
Nephrotoxic drugs (eg, aminoglycosides and other antibiotics, NSAIDs)
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Postrenal
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Mechanical urinary obstruction
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Blocked urinary catheter
Prostatic hypertrophy
Urinary calculi
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Bladder or sphincter dysfunction
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Anticholinergic drug use
Postoperative urinary retention
Fecal impaction (if severe)
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*These prerenal conditions often coexist and rapidly (ie, < 1 h) reduce urine output.
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Evaluation
History:
In communicative patients, 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 clot, kinking) or displacement, whereas a gradual decrease is more likely due to acute tubular necrosis (ATN) or a prerenal cause.
Recent medical events are helpful, including review of recent BP 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.
Testing:
In all catheterized patients (and those with an ileal conduit), patency should be ascertained by irrigation before further testing; this may solve the problem. In many remaining patients, etiology is clinically apparent (eg, shock, sepsis). In others, particularly those with multiple disorders, testing is needed to differentiate prerenal from renal (ATN) 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 Shock and Fluid Resuscitation: End point and Monitoring) or pulmonary artery occlusion pressure (see Approach to the Critically Ill Patient: Pulmonary artery occlusion pressure (PAOP)). 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.
Laboratory tests should be done. Serum electrolytes, BUN, and creatinine are standard; often urine Na and creatinine concentration also are done. Prerenal conditions typically result in BUN/creatinine ratio > 20, vs ≤ 10 in both normal states and ATN. In prerenal conditions, urine Na is < 20 mEq/L as the kidney attempts to retain maximum Na to preserve intravascular volume. In ATN, urine Na is usually > 40 mEq/L. The fractional Na excretion (FENa) is a more accurate representation of the kidney's ability to retain Na and is defined as
A ratio < 1 indicates the kidney is able to reabsorb Na, and hence the problem is prerenal. A ratio > 3 indicates a probable renal cause.
Treatment
Identified causes are treated; outflow obstruction is corrected, volume is replaced, 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).
Last full review/revision March 2009 by Soumitra R. Eachempati, MD
Content last modified March 2009
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