From the Guidelines
The approach to oliguria (decreased urine output) begins with assessing the patient's volume status, vital signs, and medication history, and ensuring adequate fluid resuscitation with isotonic crystalloids at 10-20 mL/kg bolus, then reassessing, as recommended by recent guidelines 1. The initial assessment should include checking for obstruction by performing bladder ultrasound or placing a urinary catheter.
- Laboratory tests should include serum creatinine, BUN, electrolytes, urinalysis, and urine sodium.
- Calculate the fractional excretion of sodium (FENa) to differentiate prerenal (FENa <1%) from intrinsic renal causes (FENa >2%).
- Review and discontinue nephrotoxic medications such as NSAIDs, aminoglycosides, and ACE inhibitors/ARBs, as suggested by the Canadian Society of Nephrology commentary on the 2012 KDIGO clinical practice guideline for acute kidney injury 1. If the patient remains oliguric despite fluid resuscitation, consider diuretics like furosemide 20-40mg IV, as mentioned in the 2009 focused update incorporated into the ACC/AHA 2005 guidelines for the diagnosis and management of heart failure in adults 1. For persistent oliguria, nephrology consultation is warranted to evaluate for renal replacement therapy, as recommended by the Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016 1. The pathophysiology of decreased urine output typically involves prerenal causes (dehydration, heart failure), intrinsic renal damage (acute tubular necrosis), or post-renal obstruction (enlarged prostate, kidney stones), and early intervention is crucial as prolonged oliguria can lead to electrolyte imbalances, metabolic acidosis, and fluid overload, as highlighted in the recommendations for clinical trial design in acute kidney injury from the 31st Acute Disease Quality Initiative Consensus Conference 1.
From the FDA Drug Label
If increasing azotemia and oliguria occur during treatment of severe progressive renal disease, furosemide should be discontinued. The approach to oliguria is to discontinue furosemide if it occurs during treatment of severe progressive renal disease, as indicated by increasing azotemia and oliguria 2.
- Key points:
- Discontinue furosemide in cases of worsening renal function
- Monitor for signs of oliguria and azotemia
- Furosemide should be used with caution in patients with severe renal disease
From the Research
Approach to Oliguria
Oliguria, or decreased urine output, is a significant concern in critically ill patients. The approach to oliguria involves understanding the mechanisms of diuresis regulation and interpreting urine output in the context of the patient's condition 3.
Assessment of Urine Output
Urine output is a relevant marker of kidney function and an independent marker of serum creatinine 4. Assessing urine output is crucial in diagnosing and staging acute kidney injury (AKI). Frequent assessment of urine output can help in early detection of kidney injury and guide fluid resuscitation 4.
Treatment of Oliguria
The treatment of oliguria depends on the underlying cause. In some cases, low-dose diuretic challenge can help predict tolerance to negative fluid balance in mechanically ventilated patients 5. The urine output response to diuretic administration can be used to guide fluid removal treatment.
Prognostic Importance of Urine Output
Urine output is a prognostic indicator of mortality in critically ill patients 6. A urine output of less than 0.5 mL/kg/hr is associated with increased mortality, although the relative importance of urine output varies with admission diagnosis.
Key Considerations
- Urine output is a marker of kidney function and should be assessed frequently in critically ill patients 4.
- The approach to oliguria involves understanding the mechanisms of diuresis regulation and interpreting urine output in the context of the patient's condition 3.
- Low-dose diuretic challenge can help predict tolerance to negative fluid balance in mechanically ventilated patients 5.
- Urine output is a prognostic indicator of mortality in critically ill patients, with a threshold of less than 0.5 mL/kg/hr associated with increased mortality 6.