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Critical Care Medicine
Approach to the Critically Ill Patient
Oliguria
Etiology
Evaluation
History
Physical examination
Testing
Treatment
Key Points
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    Topics in Approach to the Critically Ill Patient
    • Introduction
    • Monitoring and Testing the Critical Care Patient
    • Critical Care Scoring Systems
    • Vascular Access
    • Oxygen Desaturation
    • Oliguria
    • Agitation, Confusion, and Neuromuscular Blockade
     
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    Oliguria

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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 3 categories:

    • Prerenal (blood-flow related)
    • Renal (intrinsic kidney disorders)
    • Postrenal (outlet obstruction)

    There are numerous such entities (see Acute Kidney Injury: Acute Kidney Injury (AKI)), but a limited number cause most cases of acute oliguria in hospitalized patients (see Table 7: Approach to the Critically Ill Patient: Some Causes of OliguriaTables).

    Table 7

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    Some Causes of Oliguria

    Mechanism

    Examples

    Prerenal*

    Hypovolemia

    Bleeding

    Fluid loss

    Inadequate fluid replacement

    Low cardiac output

    MI

    Heart failure

    Pulmonary embolism

    Decreased systemic vascular resistance

    Sepsis

    Renal

    Acute tubular necrosis

    Hypoperfusion (prolonged, eg, > 4 h)

    X-ray contrast dye

    Rhabdomyolysis

    Nephrotoxic drugs (eg, aminoglycosides and other antibiotics, NSAIDs)

    Postrenal

    Mechanical urinary obstruction

    Blocked urinary catheter

    Prostatic hypertrophy

    Urinary calculi

    Bladder or sphincter dysfunction

    Anticholinergic drug use

    Postoperative urinary retention

    Fecal impaction if severe

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

    Evaluation

    History: 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 (ATN) or a prerenal cause.

    Recent medical events are helpful; they include 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 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 (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 are also done. Prerenal conditions typically result in a 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

    Clinical Calculator

    Clinical Calculator

    Fractional Excretion of Sodium (FENa)

    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).

    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, BUN, and creatinine.
    • Measure urine Na and creatinine concentration, and calculate fractional Na excretion if it is unclear whether the cause is prerenal or renal; a ratio < 1 indicates the problem is prerenal, whereas a ratio > 3 indicates a probable renal cause.

    Last full review/revision October 2012 by Soumitra R. Eachempati, MD

    Content last modified November 2012

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