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Evaluation and Treatment of Acute Oliguria


* Previous edition author.

Oliguria is a one of the commonest clinical problems encountered by critically ill patients. The prevalence of the problem has been difficult to establish because of a wide variety of definitions used in the literature. Some studies have estimated that up to 18% of intensive care unit (ICU) patients with intact renal function exhibit episodes of oliguria. Furthermore, 69% of ICU patients who develop acute kidney injury (AKI) are oliguric. With the introduction of modern definitions of AKI ( Box 18.1 ), comparisons of urine output and creatinine criteria have shown that even isolated oliguria (no creatinine criteria) is associated with significant short- and long-term adverse consequences including death or permanent dialysis ( Box 18.2 ). A similar result has been reported in pediatric patients where use of plasma creatinine alone failed to identify AKI in 67.2% of patients with low urine output.

Box 18.1
Criteria for acute kidney injury.

Stage Serum creatinine (SCr) Urine output
1 Increase to 1.5 to 1.9 times baseline
OR
Increase of ≥ 0.3 mg/dL (≥ 26.5 μmol/L)		 < 0.5 mL/kg/h for 6 to 12 h
2 Increase to 2 to 2.9 times baseline < 0.5 mL/kg/h for ≥ 12 h
3 Increase greater than 3 times baseline
OR
SCr ≥ 4 mg/dL (≥ 353.6 μmol/L)
OR
Initiation of renal replacement therapy
OR
eGFR < 35 mL/min/1.73 m 2 (< 18 years)		 < 0.3 mL/kg/h for ≥ 24 h
OR
Anuria for ≥ 12 h

Box 18.2
Figures reused from Kellum JA, Sileanu FE, Murugan R, et al. Classifying AKI by urine output versus serum creatinine level. J Am Soc Nephrol 2015;26(9):2231-2238.
Panel A: AKI based on urine output and serum creatinine. Panel B: Clinical outcomes of AKI based on urine output and serum creatinine.

Age-adjusted 1-year survival rates by acute kidney injury (AKI) severity. Groups refer to combinations of urine output (UO) and creatinine (SC) criteria. Group 1 (green), no AKI by either criterion; group 2 (blue), stages 1–2 by UO criteria but no AKI by SC or stage 1 by SC and no AKI by UO; group 3 (yellow), stages 1–2 by UO plus stage 1 by SC or stages 2–3 by SC alone; group 4 (orange), stages 1–2 by UO plus stage 2 by SC or stage 3 by UO alone; group 5 (red), stage 3 by UO plus stages 1–2 by SC or stage 3 by SC plus stages 1–2 by UO; and group 6 (dark red) , stage 3 by both criteria.

Although numerous definitions for oliguria exist, most use a urine output of less than 200 to 500 mL in 24 hours to denote oliguria, whereas urine output of less than 50 to 100 mL/day is generally termed anuria. To standardize the use of the term across different studies and populations, the Acute Dialysis Quality Initiative (ADQI) proposed a definition of oliguria as urine output less than 0.5 mL/kg/h for at least 6 hours and this definition has been adopted by international guidelines (see Box 18.1 ). It has been convincingly demonstrated that AKI is associated with excess mortality even in the absence of the need for renal replacement therapy (RRT) and early identification of the cause of AKI and appropriate intervention may alter the progress of AKI. Hence oliguria being an early marker of AKI should be identified and evaluated with utmost urgency. Thus oliguria should warrant evaluation when the urine flow rate is less than 0.5 mL/kg/h for two consecutive hours.

However, oliguria is also context-specific and the 0.5/mL/kg/h threshold may not be appropriate for all. For example, it may be possible to excrete the daily solute load at a lower rate of urine production particularly if patients are not receiving nutrition and are at bed rest. The 0.5 mL/kg/h threshold was proposed by ADQI for patients in the ICU where average daily fluid administration often exceeds 3 L in an adult. In conditions where fluid use is far less, the threshold may not be as predictive. For example, Mizota and colleagues recently reported that intraoperative oliguria only predicts outcome when urine volume is less than 0.3 mL/kg/h. However, the approach outlined in this chapter is recommended when urine output is less than 0.5 mL/kg/h. Another issue is body composition. In comparison with adipose, muscle will generate more nitrogenous waste and therefore require a higher mean urine output per gram of tissue. We recommend using lean body mass (or similar approximations) to avoid over diagnosis of oliguria in obese patients.

One of the most common reasons for a fluid bolus in the ICU is oliguria. However, routine administration of a fluid bolus for oliguria has been shown to not improve the urine output in most cases and can potentially cause harm. A more thorough systematic approach is warranted to understand the pathophysiology of oliguria and implement the appropriate intervention. The goal of this chapter is to provide both a physiologic background and a practical clinical approach to evaluate and treat oliguria.

Pathophysiology

Urine output is a function of the glomerular filtration rate (GFR) and of tubular secretion and reabsorption. GFR is directly dependent on renal perfusion. Therefore oliguria generally indicates either a dramatic reduction in GFR or a mechanical obstruction to urine flow ( Box 18.3 ).

Box 18.3
Causes of oliguria.

Prerenal oliguria

  • 1.

    Decreased renal perfusion

    • a.

      Decreased intravascular volume:

      • i.

        Absolute hypovolemia: bleeding, gastrointestinal losses

      • ii.

        Relative hypovolemia: third-spacing, vasodilatation

    • b.

      Decreased cardiac output: cardiogenic shock, cardiac tamponade

    • c.

      Decreased renal perfusion pressure: sepsis, drugs

  • 2.

    Increased renal outflow pressure: abdominal compartment syndrome

Intrarenal oliguria

  • 1.

    Ischemic acute tubular necrosis: hypotension, untreated prerenal oliguria

  • 2.

    Nephrotoxic acute tubular necrosis: drugs (vancomycin, aminoglycosides), contrast media, rhabdomyolysis

  • 3.

    Acute interstitial nephritis: nafcillin, furosemide

Postrenal oliguria

  • 1.

    Urinary obstruction: bilateral renal calculus, prostate enlargement, Foley catheter obstruction

Prerenal Oliguria

When the cause of oliguria is impaired renal perfusion, it is often termed “prerenal oliguria.” However, renal perfusion is a function of circulating volume, cardiac output, mean arterial pressure, renal vascular resistance, and venous pressure (back pressure on the renal veins). Hence so-called prerenal oliguria can occur as the result of an absolute or a relative decrease in circulating volume, decreased cardiac output, decreased mean arterial pressure, vascular disease, or high pressures in the abdomen or right heart. In short, the term has probably outlived its usefulness as a counterpoint to urinary tract obstruction (postrenal) and it would be better to focus on the specific pathophysiology that is occurring.

An absolute decrease in circulating volume can be caused by hemorrhage or volume losses from a variety of sources. A relative decrease in circulating volume can be caused by fluid sequestration after surgery or an increase in the capacitance of the vasculature that results from vasodilatation (e.g., as a result of sepsis). Perioperative cardiac ischemia or underlying impaired left-ventricular function can lead to decreased cardiac output and impaired renal perfusion. A less frequent but serious cause of decreased cardiac output after major abdominal surgeries is abdominal compartment syndrome (ACS) in which an acute rise in intra-abdominal pressure both decreases venous return to the heart and increases renal venous congestion, dramatically impairing renal perfusion. Right-heart failure and fluid overload also commonly lead to AKI by increasing venous pressure and thus reducing renal perfusion pressure. Massive postoperative pulmonary thromboembolism and pneumothorax can cause obstructive shock and decreased cardiac output. Systemic vasodilation leading to decreased mean arterial pressure (MAP) and renal hypoperfusion may occur as a result of the inflammatory response triggered by the surgery itself, sepsis, or medications (sedative and analgesics).

Finally, other rare causes of decreased renal perfusion and oliguria include aortic dissection and inflammation (vasculitis, especially scleroderma), affecting either the intrarenal or extrarenal circulation. Renal atheroemboli (usually caused by cholesterol emboli) generally affect older patients with a diffuse erosive atherosclerotic disease. This condition is most often seen after manipulation of the aorta or other large arteries during arteriography, angioplasty, or surgery. This condition may also occur spontaneously or after treatment with heparin, warfarin, or thrombolytic agents.

Rarely, decreased renal perfusion may occur as a result of an outflow problem such as renal vein thrombosis or ACS. ACS is defined as organ dysfunction that results from an increase in intra-abdominal pressure. Normal intra-abdominal pressure is 5–7 mmHg. Abdominal perfusion pressure (APP) is the pressure difference between the MAP and intra-abdominal pressure (IAP) (APP = MAP–IAP). Sustained intra-abdominal pressure > 12 mmHg is called intra-abdominal hypertension. When the IAP is sustained > 20 mmHg with or without APP > 60 mmHg, it is called ACS. ACS can be seen in a wide variety of medical and surgical conditions, most often after major abdominal operations requiring administration of a large volume of fluid (e.g., ruptured abdominal aortic aneurysm repair), emergent laparotomies with tight abdominal wall closures, acute severe pancreatitis, and abdominal-wall burns with edema. ACS leads to acute oliguria and AKI mainly via increasing renal outflow pressure, and thereby reducing renal perfusion. Other possible mechanisms in ACS include direct renal parenchymal compression and renin-mediated arterial vasoconstriction. However, evidence suggests that the rise in renal venous pressure, rather than the direct effect of parenchymal compression, is the primary mechanism of kidney injury. Generally, these changes occur in direct response to the increase in intra-abdominal pressure, with oliguria developing at a pressure of greater than 15 mmHg and anuria at a pressure of greater than 30 mmHg.

Oliguria as a Consequence of Renal Tubular Injury

The most common cause of oliguria in the ICU is AKI. For many years the term acute tubular necrosis (ATN) was used to describe AKI caused by an ischemic and/or nephrotoxic insult. So-called ischemic ATN was thought to result from untreated “prerenal factors,” while nephrotoxic ATN was understood to occur as a consequence of the direct nephrotoxicity of agents such as antibiotics, heavy metals, solvents, contrast agents, and crystals (uric acid or oxalate). However, we now understand that most cases of AKI are caused by a variety of insults affecting the renal tubules and the microcirculation and that most AKI is in fact a “toxic nephropathy” whether caused by endogenous mediators (e.g., cytokines, hemoglobin), bacterial toxins (e.g., endotoxin), or medications. Uncommonly, drugs (e.g., nafcillin, pantoprazole, sulfamethoxazole-trimethoprim, furosemide) can also cause an acute interstitial nephritis leading to oliguria and AKI.

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