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 Acute Kidney Injury (AKI) Acute kidney injury is a rapid decrease in renal function over days to weeks, causing an accumulation of nitrogenous products in the blood (azotemia) with or without reduction in amount of urine... read more ), but a limited number cause most cases of acute oliguria in hospitalized patients (see table Some Causes of Oliguria Some Causes of Oliguria ).
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 Acute Tubular Necrosis (ATN) Acute tubular necrosis (ATN) is kidney injury characterized by acute tubular cell injury and dysfunction. Common causes are hypotension or sepsis that causes renal hypoperfusion and nephrotoxic... read more 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 Rhabdomyolysis Rhabdomyolysis is a clinical syndrome involving the breakdown of skeletal muscle tissue. Symptoms and signs include muscle weakness, myalgias, and reddish-brown urine, although this triad is... read more .
Vital signs are reviewed, particularly for hypotension, tachycardia, or both (suggesting hypovolemia Volume Depletion Volume depletion, or extracellular fluid (ECF) volume contraction, occurs as a result of loss of total body sodium. Causes include vomiting, excessive sweating, diarrhea, burns, diuretic use... read more or sepsis Sepsis and Septic Shock Sepsis is a clinical syndrome of life-threatening organ dysfunction caused by a dysregulated response to infection. In septic shock, there is critical reduction in tissue perfusion; acute failure... read more ) 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 End Point and Monitoring of Fluid Resuscitation Almost all circulatory shock states require large-volume IV fluid replacement, as does severe intravascular volume depletion (eg, due to diarrhea or heatstroke). Intravascular volume deficiency... read more ) or pulmonary artery occlusion pressure Pulmonary artery occlusion pressure (pulmonary artery wedge pressure) Some monitoring of critical care patients depends on direct observation and physical examination and is intermittent, with the frequency depending on the patient’s illness. Other monitoring... read more . 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.
If patients are taking diuretics, calculating the fractional excretion of urea (FEUrea) can help differentiate between prerenal state and acute tubular necrosis and is calculated using the following equation:
A FEUrea ratio> 50% usually indicates acute tubular necrosis.
A FEUrea ratio < 35% usually indicates a prerenal state.
A FEUrea between 35% and 50% is 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 renally dosed or 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 Overview of Renal Replacement Therapy Renal replacement therapy (RRT) replaces nonendocrine kidney function in patients with renal failure and is occasionally used for some forms of poisoning. Techniques include continuous hemofiltration... read more (eg, continuous venovenous hemofiltration or hemodialysis).
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.
For patients taking diuretics, measure urine and plasma urea as well as urine and plasma creatinine and calculate the fractional excretion of urea to determine if the cause is prerenal or renal; <35% indicates the problem is prerenal; >50% indicates the problem is acute tubular necrosis; and 35% to 50% indicates the etiology is indeterminate
Drugs Mentioned In This Article
|Drug Name||Select Trade|
|Aluvea , BP-50% Urea , BP-K50, Carmol, CEM-Urea, Cerovel, DermacinRx Urea, Epimide-50, Gord Urea, Gordons Urea, Hydro 35 , Hydro 40, Kerafoam, Kerafoam 42, Keralac, Keralac Nailstik, Keratol, Keratol Plus, Kerol, Kerol AD, Kerol ZX, Latrix, Mectalyte, Nutraplus, RE Urea 40, RE Urea 50 , Rea Lo, Remeven, RE-U40, RYNODERM , U40, U-Kera, Ultra Mide 25, Ultralytic-2, Umecta, Umecta Nail Film, URALISS, Uramaxin , Uramaxin GT, Urea, Ureacin-10, Ureacin-20, Urealac , Ureaphil, Uredeb, URE-K , Uremez-40, Ure-Na, Uresol, Utopic, Vanamide, Xurea, X-VIATE|