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Oliguria
Oliguria is one of the most common problems faced by clinicians in the intensive care unit (ICU). The goal of this chapter is to understand the reasons for oliguria and provide an evidence-based, practical, physiology-based approach to diagnosing and treating it.
Definitions and epidemiology
An average person excretes 600 mOsm of solute/day, and the maximal urinary concentration that can be achieved is 1200 mOsm/L. Hence a urine output of at least 500 mL per day is obligatory for excreting the average daily solute load. Therefore oliguria has generally been defined as urine output less than 500 mL per 24 hours.
The incidence of oliguria has been variedly reported in the literature, mainly because of the different definitions used. Some studies have estimated that up to 18% of medical and surgical ICU patients with intact renal function exhibit episodes of oliguria. Furthermore, 88% of ICU patients who develop acute kidney injury (AKI) have a urine output of <0.5 mL/kg/h for 6 hours or more, and 18% have a urine output of <0.3 mL/kg/h for 24 hours or longer.
To standardize the definition across different studies and populations, the Acute Dialysis Quality Initiative (ADQI) adopted a definition of oliguria as urine output of less than 0.3 mL/kg/h for at least 24 hours ( www.ADQI.org ). For all practical purposes, however, urine output under 0.5 mL/kg/h is usually considered inadequate for most critically ill patients. This is in part because fluid input resulting from medications, nutrition, and other reasons typically exceeds this threshold in critically ill patients, and fluid overload may result if urine output is inadequate to maintain fluid balance. Hence any urine output <0.5 mL/kg/h should immediately be evaluated and therapy initiated to reverse the inciting mechanism when feasible.
Oliguria in acute kidney injury
Oliguria is often treated as an early marker of AKI. However, AKI need not manifest as oliguria in the intensive care setting, and oliguria is an insensitive and nonspecific clinical manifestation of AKI. Moreover, other factors, such as profound hypokalemia, hypothermia, hyperglycemia, and medications, can all lead to good urine output even in the presence of AKI, confounding the assessment of AKI severity. Although currently Kidney Disease: Improving Global Outcomes (KDIGO) definitions of AKI give equal weight to change in serum creatinine and reduction in urine output, these two measures differ significantly in terms of pathophysiology and their relationship to clinical outcomes. Although a rise in serum creatinine likely implies a true reduction in glomerular filtration, oliguria could just represent a stress response or imply an actual decrease in glomerular filtration. However, several studies have clearly demonstrated that even isolated oliguria (no creatinine criteria) is associated with significant short- and long-term adverse consequences, including death or permanent dialysis. When associated with increased serum creatinine, oliguria seems to denote worse prognosis and likely represents irreversible kidney injury. Ability of urine output to predict AKI also seems to vary across different patient cohorts, with better predictive ability in medical than surgical patients. When oliguria is prolonged, it almost always implies ongoing kidney injury, and the likelihood of reversibility of oliguria diminishes over time. Prowle et al. demonstrated that oliguria of longer than 12 hours’ duration predicted stage 2 AKI better, and oliguria of lesser duration, although common, did not lead to biochemical AKI. Hence although any oliguria (urine output <0.5 mL/kg/h) warrants a prompt assessment for risk of AKI, the presence of oliguria in itself does not imply occurrence of renal structural injury.
Pathophysiology of oliguria
Oliguria can occur because of decreased glomerular filtration rate (GFR), increased tubular reabsorption of filtrate, or a combination of both. Factors that decrease GFR in ICU patients include overt hypovolemia related to fluid losses, hemorrhage, third-spacing, low cardiac output states, and systemic vasodilatation, as seen commonly in patients with sepsis or secondary to sedatives. In hypovolemic patients, release of antidiuretic hormone (ADH) and activation of the renin–angiotensin system lead to increased reabsorption of water and oliguria with a high urine osmolality. Similarly, other stressors such as surgery, pain, and trauma also release ADH and along with sympathetic stimulation can lead to oliguria as a physiologic response. Under these circumstances, oliguria can be easily reversed with the timely resolution of the inciting stress and/or volume replacement.
Although oliguria is simplistically perceived as a decline in glomerular filtration, multiple mechanisms have been implicated for oliguria in the critically ill patient with AKI, including overall reduction in renal blood flow, regional intrarenal variation in blood flow and redistribution, alteration in glomerular hemodynamics, direct glomerular injury, ischemia to the proximal tubule (S3 segment), renal interstitial edema, inflammatory insult, and tubular obstruction. Not uncommonly, increased abdominal pressure decreases GFR by direct compression on the kidneys, leading to increased renal venous pressures. Fluid overload has been consistently shown to worsen renal functions in critically ill patients by increasing renal intracapsular and renal venous outflow pressures and is strongly associated with worsening of AKI and mortality.
Mechanical obstruction to urine flow is common and usually caused by obstruction or malposition of a urinary catheter, urethral or bladder neck obstruction from an enlarged prostate or malignancy, or tubuloureteral obstruction as seen in papillary necrosis.
Diagnostic approach to oliguria
The diagnosis of oliguria necessitates an integrated approach as outlined in Fig. 14.1 . Accurate monitoring of intake and output is required, usually with a urinary catheter in place. Intensive urine output monitoring has been shown to improve the detection of AKI and improve outcomes. The risks of urinary catheter–associated urinary tract infections must be balanced against the benefit of hourly urine output monitoring in patients with high risk for the development of AKI. In general, patients in stage 1 KDIGO AKI or higher will benefit from accurate urine output monitoring and warrant a urinary catheter. Transient oliguria is common and may not be an independent risk factor for morbidity and mortality in critically ill or injured patients, but sustained oliguria (at least 6 hours’ duration) often indicates AKI and has been shown to be independently associated with hospital mortality. Oliguria mandates immediate evaluation for reversible causes and a risk assessment for AKI. The main goal of managing oliguria is to rapidly determine and correct the underlying cause(s), to halt the progression of kidney injury. Merely reacting to every oliguria with either fluid and/or diuretic therapy should be condemned, and efforts should be taken to understand and address the underlying pathophysiology. Targeted therapy to reverse the inciting events should be applied rapidly.
Clinical history and examination
Evaluation of a patient with oliguria should start with a focused history taking, chart review, and clinical examination. A history suggestive of overt 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. History of patient comorbidities, prior or present myocardial infarction, or left ventricular systolic or diastolic dysfunction can provide clues to impaired cardiac output as a cause of oliguria. History of fever with localizing symptoms with or without hypotension makes septic AKI likely. A history of recent contrast administration for imaging, of intraoperative hypotension, or administration of nephrotoxic agents can suggest an intrarenal cause of oliguria in an adequately volume-resuscitated patient. Chart review should involve capturing of episodes of hypotension, duration of any hemodynamic instability, cumulative fluid balance, previous use of diuretics, use of nephrotoxic agents, and dosing of medications.
Routine clinical examination for volume status, including skin turgor, dry mucosa, and the presence of pedal or sacral edema, are insensitive and nonspecific and can be misleading. In critically ill patients, functional hemodynamic monitoring has become the standard for assessment of fluid responsiveness (see later). A tense abdomen can be a very early and important clue for the onset of abdominal compartment syndrome (ACS) and should trigger frequent measurements of intraabdominal pressure (IAP) and hourly urine output monitoring.
Rule out urinary obstruction
Acute oliguria in the ICU with no obvious inciting event should prompt an evaluation for postrenal obstruction. Elderly men with a prior history of prostatic hypertrophy/malignancy and elderly women with bladder neck obstruction are at high risk for such obstruction. Clinical palpation for a distended bladder and bladder ultrasound to determine residual urine volume should be immediately performed and the need for urinary catheterization decided. In critically ill patients with a urinary catheter already in place, obstruction of the urinary catheter by clots or sediments should be ruled out by flushing the catheter. Although uncommon in the acute setting, complete or severe partial bilateral ureteral obstruction may also lead to acute, “acute on chronic” failure.
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