* 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.
|Stage||Serum creatinine (SCr)||Urine output|
|1||Increase to 1.5 to 1.9 times baseline |
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 |
SCr ≥ 4 mg/dL (≥ 353.6 μmol/L)
Initiation of renal replacement therapy
eGFR < 35 mL/min/1.73 m 2 (< 18 years)
|< 0.3 mL/kg/h for ≥ 24 h |
Anuria for ≥ 12 h
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.
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 ).
Decreased renal perfusion
Decreased intravascular volume:
Absolute hypovolemia: bleeding, gastrointestinal losses
Relative hypovolemia: third-spacing, vasodilatation
Decreased cardiac output: cardiogenic shock, cardiac tamponade
Decreased renal perfusion pressure: sepsis, drugs
Increased renal outflow pressure: abdominal compartment syndrome
Ischemic acute tubular necrosis: hypotension, untreated prerenal oliguria
Nephrotoxic acute tubular necrosis: drugs (vancomycin, aminoglycosides), contrast media, rhabdomyolysis
Acute interstitial nephritis: nafcillin, furosemide
Urinary obstruction: bilateral renal calculus, prostate enlargement, Foley catheter obstruction
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.
Oliguria secondary to mechanical obstruction distal to the kidneys is traditional termed “postrenal” oliguria. This problem can result from tubular-ureteral obstruction (caused by stones, papillary sloughing, crystals, or pigment), urethral or bladder neck obstruction (secondary to prostatic enlargement), or simply a malpositioned or obstructed urinary catheter. Rarely, urine volume can be increased in cases of partial obstruction because of pressure-mediated impairment of urine concentration.
Evaluation of Patients With Oliguria
Detection of oliguria requires measurement of urine volume. In recent years, concern for catheter-associated urinary tract infections has resulted in the reduced use of catheters. However, in critically ill patients, close monitoring of urine output has been shown to be associated with improved detection of AKI, less fluid overload, and improved survival in patients developing AKI. While these observational results cannot establish a causal relationship, it seems prudent to monitor urine volume closely in critically ill patients and others at high risk of AKI.
Oliguria is an early manifestation of either reduced renal perfusion or impaired renal function. If the underlying cause of oliguria is not corrected, AKI usually results. However, merely reacting to oliguria, with “shotgun” therapy of either fluid and/or diuretics (which can be said to fix the chart while neglecting the patient) is no substitute for making a diagnosis and prescribing specific therapy. It is imperative that underlying pathologic mechanism(s) of oliguria are promptly identified and targeted therapy applied rapidly. Evaluation of a patient with oliguria includes focused history taking, chart review, and clinical examination. Supplementary urine testing, including examining the urinary sediment and measuring urinary electrolytes, may assist in the diagnosis. However, it is important to be alert to the possibility that oliguria may be postrenal, because identification and correction of this cause can be rapidly rewarding and avoid wasting time with ineffectual testing and interventions. Hence, it is worthwhile to rule out urinary obstruction as a cause of oliguria prior to embarking on any elaborate workup.
In the non-ICU setting, a prior history of prostatic hypertrophy, recent spinal anesthesia, bladder discomfort, and renal colic may provide some clues to the presence of distal obstruction. History of trauma and blood at the urethral meatus along with perineal ecchymoses and a “high-riding” prostate can suggest the diagnosis of urethral disruption. A rapid increase in serum blood urea nitrogen (BUN) concentration and creatinine concentration (especially a doubling every 24 hours) also suggests a diagnosis of urinary obstruction. The urine sediment in postrenal failure is often bland without casts or sediments. Renal ultrasonography is usually the test of choice to exclude urinary tract obstruction. This test is noninvasive and can be performed at the bedside. It carries the advantage of avoiding the potential allergic and toxic complications of radiocontrast media. However, under some circumstances, renal ultrasound may not yield good results. For example, in early obstruction or in obstruction associated with severe dehydration, hydronephrosis may not be seen on the initial ultrasound, although it may appear on a subsequent study. Computed tomographic scanning should be considered if the ultrasound results are equivocal or if the kidneys are not well visualized, or if the cause of the obstruction cannot be identified. In the ICU setting, distal obstruction appearing as oliguria is commonly caused by obstruction of the urinary catheter (especially in male patients). Hence, in patients with new-onset unexplained oliguria, the urinary catheter must be flushed or changed to rule out obstruction. Early diagnosis of urinary tract obstruction is important because many cases can be corrected and a delay in therapy can lead to renal injury.
Functional Oliguria versus AKI
A careful, targeted chart review and clinical examination can help identify the cause of oliguria. History suggestive of intravascular volume depletion such as history of vomiting and/or diarrhea, evidence of ongoing bleeding, perioperative fluid losses or deficits (e.g., gastric/ileostomy losses or vomiting), or extravascular fluid sequestration can point to a functional cause of oliguria with or without changes in serum creatinine or urea. Routine clinical examination for volume status including skin turgor, dry mucosa, and presence of pedal or sacral edema can help in decision making but are often insensitive and nonspecific. History of patient comorbidities, prior myocardial infarction, left ventricular systolic, or diastolic dysfunction can provide clues to impaired cardiac output as a cause of oliguria. Fever, increased white cell count, and a wide pulse pressure indicate sepsis-induced vasodilatation, leading to impaired renal perfusion and relative hypovolemia. A history of perioperative contrast administration for imaging, of intraoperative hypotension, or of administration of nephrotoxic agents can suggest an intrarenal cause of oliguria in an adequately volume-resuscitated patient.
Although traditional indicators of hydration status and tissue perfusion, such as heart rate, systemic blood pressure, capillary refill, jugular-venous pulsation, and peripheral edema can provide guidance for making appropriate interventions, they are neither sensitive nor specific. In the ICU, hemodynamic monitoring (measurements of central venous pressure [CVP], pulmonary artery occlusion pressure [PAOP], or mixed/central venous oxygen saturation) can provide some information about intravascular volume status. However, many of these traditional measures may be unreliable in the critically ill patient. The jugular-venous pulsation does not provide any information about left heart function and is not an accurate surrogate for right ventricular filling pressures in the presence of positive-pressure ventilation and positive end-expiratory pressure (PEEP). Similarly, peripheral edema is often caused by hypoalbuminemia and decreased oncotic pressure in critically ill patients. Thus patients may exhibit total body water overload and yet be intravascularly volume depleted. In addition, blood pressure and heart rate are affected by numerous physiologic and treatment variables in the ICU and are unreliable measures of volume status. In the ICU, increased CVP or PAOP does not ensure adequate preload and low values are not specific for fluid responsiveness. These parameters assume a linear pressure–volume relationship that is often not the case in sick patients with comorbidities. Moreover, studies have shown very poor correlation between these parameters and fluid responsiveness. Assessment for fluid responsiveness including the newer dynamic measures such as inferior vena cava (IVC) diameter and collapsibility, passive leg raise maneuver or changes in stroke volume variation (SVV) or cardiac output resulting from heart–lung interactions provide a more accurate estimate of whether a patient will benefit from a fluid bolus. These measures require continuous cardiac output monitoring using one of the newer pulse contour techniques. An arterial pulse pressure variation (PPV) greater than 13% in a patient who is not breathing spontaneously and who is on positive-pressure ventilation (TV 8 mL/kg or higher) is highly predictive of fluid responsiveness (reflecting the likelihood that a fluid challenge will increase cardiac output). In a spontaneously breathing patient or in a patient with arrhythmia, an increase in cardiac output by > 10% with passive leg raise is a strong indicator of fluid responsiveness. Although each of these dynamic measures has their fallacies, when two or three of them are combined at the bedside, they provide valuable information on whether a fluid bolus will improve the cardiac output.
Bedside hemodynamic assessment using ultrasound is now standard care in the hemodynamic optimization of a critically ill patient and hence should be incorporated with other parameters in deciding the appropriate intervention. Evaluation of IVC size and respiratory variation in diameter provide insight into the intravascular volume. Looking at the left and right ventricular size and contractility will help decide on the need of inotropes. Bedside ultrasound also enables the clinician to rule out quickly obstructive shock caused by pericardial tamponade, pneumothorax, and massive pulmonary embolism. In addition to assessment of fluid responsiveness, it is imperative that fluid tolerance be assessed. Although worsening hypoxemia or lung crackles may provide some clues, they are insensitive and nonspecific. B-lung profile on lung ultrasound suggests increasing fluid overload and when available, combining it with estimation of the extravascular lung water by one of the new commercially available pulse contour cardiac output monitors will help the clinician decide whether the patient can tolerate more fluids. When a patient is thought to be fluid responsive and fluid tolerant, a fluid challenge with 250 to 500 mL of isotonic crystalloid is necessary to assess the clinical response.
Finally, ACS should be suspected in any patient with a tensely distended abdomen, progressive oliguria, or an increased airway pressure (transmitted across the diaphragm). The mainstay of the diagnosis is measurement of intra-abdominal pressure. The most common measure of intra-abdominal pressure is by bladder pressure, which is easily accessible. Bladder pressure has been shown to correlate well with intra-abdominal pressure over a wide range of pressures.
Although the yield may be low, examining the urine sediment may provide some important insight into the cause of oliguria. The presence of tubular epithelial casts increases the likelihood of AKI. However, the discriminating ability of this finding is very limited. The main usefulness of examining the urine sediment is for detecting red cell casts, which indicate glomerular disease (rare in the ICU setting). Urine eosinophilia is neither sensitive nor specific for acute interstitial nephritis and should not be relied on.
Urine sodium and urea concentrations can be of value in assessing oliguria. A fractional excretion of sodium (FE Na ) is more accurate, and a value less than 1% has traditionally been used as a marker for a prerenal cause of oliguria, whereas a value greater than 1% generally suggests a loss of tubular function and hence AKI. Importantly, conditions such as rhabdomyolysis, contrast nephropathy, and sepsis are all causes of AKI in which FE Na can be low. Furthermore, these indices are unreliable once the patient has received diuretic or natriuretic agents (including dopamine and mannitol) and may also be confounded by endogenous osmolar substances such as glucose or urea. In patients who have received diuretics, fractional excretion of urea (FE urea ) may be useful. The FE urea is 50% to 65% in normal subjects and usually below 35% in settings where oliguria is not caused by tubular damage per se. A recent study concluded that a low FE urea (≤ 35%) was a more sensitive and specific index than FE Na in identifying intact tubular function especially if diuretics were administered.
Several biomarkers have been evaluated in AKI and their utility in predicting progression of AKI in critically ill patients explored. Biomarkers in AKI can be stratified into those that primarily correspond to GFR (Cystatin C) and those that reflect tubular damage (e.g., neutrophil gelatinase-associated lipocalcin [NGAL], kidney injury molecule-1 [KIM-1]) or stress (tissue inhibitor of metalloproteinases-2 [TIMP-2] and insulin-like growth factor binding protein 7 [IGFBP 7]). NGAL is a 25 kDa protein of the lipocalcin family that is produced at the thick ascending loop of Henle and the intercalated cells of the collecting duct. NGAL has been detected as early as 3 hours after injury and it remains elevated up to 5 days based on AKI severity. Several studies have found NGAL to be a useful marker in predicting AKI onset and progression in a varied population.
Few biomarkers have been tested against full AKI criteria including urine output. One exception is the combination of TIMP-2 and IGFBP 7, which has been validated to predict moderate to severe (stages 2–3) AKI using serum creatinine and urine output criteria. The test has been validated using expert adjudication and has been approved by the US Food and Drug Administration. Importantly, biomarkers may have a role in evaluating oliguria. Koyner et al. found that death or dialysis at 9 months after ICU admission was lowest for patients without AKI but significantly increased in biomarker-positive patients (using TIMP-2 and IGFBP 7) with AKI compared with those with AKI who were biomarker negative.
In addition to biomarkers, there is an increasing number of published studies on the use of furosemide in the evaluation of oliguria. In a recent study, Koyner et al. used a furosemide stress test (FST) to evaluate renal tubular functional integrity and its ability to predict progression of AKI and compared its performance with traditional biomarkers. In this study, a standard intravenous dose of furosemide (1 mg/kg for furosemide naive patients and 1.5 mg/kg for furosemide exposed patients) was administered to patients with stage 1 or 2 AKI and the authors found a cut-off 2-hour urine output of < 200 mL to be highly predictive of progression to stage 3 AKI (area under the curve [AUC]: 0.87) and need for RRT (AUC: 0.86). In a recent randomized control trial, FST nonresponse was used as a strategy to identify patients who might need RRT and these patients were randomized to early versus standard RRT. Although this small study did not find any differences between treatment groups, it is one of the first studies to utilize a clinically applicable functional marker of AKI to select a population that may potentially need and benefit from RRT. Importantly, authors have cautioned that FST should not be attempted on hypovolemic patients and ample care should be exercised when using it.
Sometimes a good rule is “don’t just do something; stand there.” Telephone orders from the on-call room for fluids and then for diuretics, or for both at the same time, are far too common an occurrence in modern ICUs, and such practices are inherently dangerous. Oliguria is a clinical sign, not a diagnosis. There is no single therapeutic strategy for oliguria; there are only treatments for conditions that cause it. Augmenting urine output with forced diuresis only masks the problem and may actually worsen fluid depletion. Conversely, the assumption that all oliguria is fluid responsive until proven otherwise leads to fluid overload. Always evaluate first and treat the underlying cause of oliguria, not the urine output.
Hypovolemia and Shock
Although hypovolemia is a common contributing factor in the development of oliguria, it is important that careful assessment of fluid status, preload responsiveness, and fluid tolerance be performed and thoughtful decision taken before a fluid bolus is given. Routine empiric fluid therapy for every episode of oliguria should be strongly discouraged. Both the type of fluid and the volume of fluid given have important therapeutic implications. When fluid therapy is needed, 500 mL of crystalloid with physiologic amounts of chloride such as Ringer lactate or one of the newer balanced crystalloids should be administered. Hyperoncotic colloids such as 20% albumin and several starch preparations have been shown to cause AKI and to increase the need for RRT and mortality and hence should be avoided. Although 5% albumin has been shown to be equivalent to normal saline, its relatively short intravascular half-life (only slightly longer than crystalloids) and higher cost make it less preferred fluid compared with crystalloids. Importantly, 0.9% saline should be avoided except in select cases (e.g., acute hyponatremia with hypochloremic alkalosis) because it can potentially worsen AKI.
Fluid overload caused by repeated overzealous fluid boluses has been consistently shown to worsen AKI and mortality. Fluid overload increases renal intracapsular and renal venous pressures leading to renal hypoperfusion. Hence fluid boluses for oliguria should be done only when the patient is hypotensive, with a low cardiac output, and there is clear evidence of preload responsiveness and fluid tolerance. Renal hypoperfusion is quite common in critically ill patients since the autoregulatory mechanisms that maintain GFR despite fluctuations in MAP are disrupted in patients with sepsis or other causes of AKI. Hence, in these patients, renal perfusion is directly related to systemic arterial pressure. Therefore rapid correction of hypotension with fluid resuscitation when indicated and often with vasoactive drugs is paramount. Vasoactive drugs should be initiated once adequate intravascular volume has been ensured. In critically ill patients, vasoactive drugs may be initiated concurrently with volume expansion when life-threatening hypotension exists. Vasoactive drugs, once initiated, should be titrated to maintain adequate mean arterial pressures. The ideal blood pressure to aim for in patients with oliguria must be individualized on the basis of factors such as premorbid blood pressure or presence of vascular disease but rarely below MAP of 65 mmHg. Similarly, in patients with chronic hypertension and renal vascular disease, the autoregulation curves are shifted to the right and therefore a higher MAP may be required to ensure adequate renal perfusion. Hemodynamic monitoring devices may provide important information to guide assessment of intravascular volume status and may enable a more streamlined, goal-directed approach to therapy.
Cardiac Dysfunction and ACS
Some patients may have impaired cardiac contractility (left- or right-sided) despite adequate intravascular volume. These patients may require treatment with an inotrope to improve renal perfusion. Finally, if ACS is diagnosed, prompt measures to decrease intra-abdominal pressure including operative decompression of the abdominal cavity with maintenance of an open abdomen through use of temporary abdominal wall closure techniques should be considered to improve renal perfusion.
Low-dose dopamine (< 5 μg/kg/min) is not recommended to augment renal perfusion in patients with oliguric AKI. Dopamine increases urine output because it is a natriuretic agent mediated by inhibition of Na + – K + – ATPase at the tubular epithelial cell level and not by increasing renal perfusion. There is abundant evidence that low-dose dopamine does not afford any renal protection in oliguria. One multicenter randomized controlled trial and two comprehensive meta-analyses of dopamine in critically ill patients have shown that dopamine does not prevent the onset of AKI, decrease mortality, or reduce the need for RRT.
The selective dopamine-1 agonist fenoldopam was evaluated in a multicenter trial that randomized 315 patients with baseline creatinine clearance less than 60 mL/min to fenoldopam mesylate or placebo and found no difference between the groups in the incidence of contrast nephropathy. Furthermore, fenoldopam has been shown to cause hypotension and therefore can predispose patients to AKI by reducing renal perfusion pressure. On the basis of these data, we strongly recommend against the use of dopamine and fenoldopam to augment renal perfusion in patients with oliguria.
Oliguria Secondary to AKI
Continued maintenance of adequate intravascular volume, maintenance of an adequate MAP, and avoidance of nephrotoxic agents are the only interventions shown to impact outcome once AKI has occurred. The use of diuretic agents in oliguric renal failure is widespread despite the convincing lack of evidence supporting efficacy. Traditionally, diuretics have been used in the early phases of oliguria in an attempt to convert oliguric AKI to nonoliguric AKI. Presumably, the absence of oliguria makes it easier to regulate volume status and prevent fluid overload. Many small trials have evaluated the efficacy of loop diuretics in preventing AKI and have provided inconsistent results. One systematic review compared fluids alone with diuretics in people at risk of AKI from various causes. This study failed to show any benefit from diuretics with regard to incidence of AKI, the need for dialysis, or mortality. Two extensive observational studies have been published on diuretic use in AKI and have provided conflicting results. The first was a cohort study (PICARD study) of patients with AKI in the ICU, in which patients were characterized by the use of diuretics on or before the day of renal consultation. In this study, with adjustments for relevant covariates and propensity scores, diuretic use was associated with significantly increased risk for death or nonrecovery of renal function (odds ratio [OR], 1.77; 95% confidence interval, 1.14–2.76). Although this association does not establish a causal link between diuretic use and harm in the setting of oliguric AKI, it does suggest that this therapy does not afford any benefit to the kidney. Subsequently, a recent multinational observational study of 1743 patients evaluated the effect of loop diuretics on clinical outcomes. The study investigators created three multivariate models to assess the relationship between diuretics and mortality and found that diuretic use was not significantly associated with increased mortality in any of the three models (OR for death was about 1.2 in all three models). However, no benefit was seen. On the basis of the current evidence, diuretics should never be considered a treatment for oliguria but may be necessary to prevent and manage volume overload in critically ill patients.
Finally, oliguric patients with fluid overload not responding to a diuretic trial should be considered for early RRT. Although there is little dispute about the necessity of renal replacement therapy for the treatment of fluid overload refractory to diuretic therapy, there is no consensus on the degree of azotemia or duration of renal failure warranting initiation of therapy in the absence of this absolute indication. When oliguria persists and AKI progresses despite optimization of volume, maintenance of adequate MAP, improved hemodynamics or a diuretic trial, RRT should be considered sooner rather than later. Current available evidence does not allow recommendation of the optimal timing of the initiation of renal replacement therapy. The FST discussed previously may have a role in identifying patients who are likely to recovery quickly and for whom early RRT is not indicated.
Oliguria Secondary to Obstruction
The definitive treatment for obstructive oliguria is to relieve the obstruction. This might be as simple as flushing or changing the urinary catheter. Other patients require more invasive procedures such as a percutaneous nephrostomy or a suprapubic decompression of the bladder. Prompt management is the key to avoiding renal injury.
Oliguria is one of the most common clinical problems encountered by physicians caring for perioperative patients in the ICU. Any delay in its recognition and treatment can lead to the progression to AKI, which in turn carries significant morbidity and mortality. Hence, the presence of oliguria should alert the clinician to undertake a diligent search for any correctable underlying causes ( Box 18.3 ). Ensuring adequate renal perfusion through optimization of volume status, cardiac output, and MAP together with avoidance of nephrotoxins is key. Diuretic use may not alter the need for RRT or outcomes. Diuretics may be required to treat fluid overload, but they are not treatments for oliguria. Early renal replacement therapy should be considered in patients with oliguria secondary to AKI and fluid overload especially if they fail to respond to diuretics.