Acute Kidney Injury, Urinary Tract Obstruction
1. Description of the problem
What every clinician needs to know
Oliguria is usually defined as urine output of less than 0.5 ml/kg/hour. However, the Acute Dialysis Quality Initiative (ADQI) has suggested a standardized definition of urine output less than 0.3 ml/kg/hour for at least 24 hours. Although neither sensitive nor specific, oliguria usually implies impaired renal perfusion and the onset of acute kidney injury (AKI) and hence needs immediate attention, evaluation and intervention. Oliguria not intervened appropriately in a timely manner will lead to irreversible AKI which adds significantly to the mortality of the acutely ill intensive care unit (ICU) patients. Diuretic use just to improve urine output without proper evaluation of oliguria and treatment of the underlying cause is not recommended and may even be harmful.
Oliguria is itself a clinical manifestation of AKI. However persistent oliguria can lead to a fluid overload state that presents as tachypnea and hypoxemia. Oliguria can present with other clinical manifestations of AKI including tachypnea (from metabolic acidosis), arrhythmias (from metabolic acidosis and hyperkalemia) and altered mentation and coagulopathy (from uremia).
Key management points
Important principles of management of oliguria include:
Aggressive correction of hypovolemia.
Maintenance of adequate perfusion pressures ( target mean arterial pressure [MAP] >70mmHg).
Withdrawal or minimization of offending agents if any.
Evaluating and relieving obstructed urinary system.
Identification and treatment of underlying problem ( e.g. sepsis, hemorrhage, cardiogenic shock, etc.).
Avoidance of diuretics to improve urine output unless clear signs of fluid overload present.
2. Emergency Management
Stabilizing the patient
In any acutely ill patient with oliguria, a quick clinical examination to look for other signs of impaired organ perfusion (altered mentation, mottled extremities, cold and clammy skin, poor capillary refill, etc.) should be undertaken first. The severity of hypotension if any and the degree of compensatory response (tachycardia) should be assessed. After ensuring a patent airway and adequate breathing, aggressive fluid resuscitation with isotonic crystalloids should be initiated in all patients with clinical evidence of intravascular hypovolemia.
Intravenous fluid bolus of 250-500 ml aliquots of isotonic crystalloid (0.9% saline or Lactated Ringer’s) should be rapidly given over 15-30 minute intervals with careful assessment of response and tolerance. In patients with refractory or life-threatening hypotension, vasopressor infusion (dopamine or norepinephrine) should be started as an intravenous infusion. In patients with clinical evidence of cardiogenic shock, infusion of epinephrine or a combination of dobutamine and norepinephrine should be initiated. In patients suspected to have severe sepsis or septic shock, the first dose of antibiotic appropriate for the suspected source of sepsis should be administered within 1 hour of care initiation in the ICU.
Management points not to be missed
After above emergency measures have been carried out, the following tasks should be routinely done in all ICU patients with acute oliguria:
If no urinary catheter, place a new urinary catheter.
Ensure patency of existing urinary catheter by clinically or sonographically examining for a full bladder.
Change urinary catheter if existing catheter not patent.
Order ultrasound of kidneys, ureters and bladder to rule out an obstructed urinary system and assess size of kidneys.
Order spot urine sodium, urea and creatinine.
Check intra-abdominal pressure in patients with acute onset of abdominal distension.
If oliguria persists, check arterial blood gas and serum potassium (looking for metabolic acidosis and hyperkalemia).
Review medication chart and consider discontinuation of all potential nephrotoxic drugs.
Review medication chart and adjust doses of all renally excreted drugs based on calculated creatinine clearance.
Drugs and dosages
Norepinephrine: 0.01-0.1 mcg/kg/min
Epinephrine: 0.01-0.1 mcg/kg/min
Dobutamine: 2.5-15 mcg/kg/min
Diagnostic criteria and tests
Oliguria itself is diagnosed based on patient’s intake and output chart. However, the cause of oliguria may warrant further investigations. A thorough clinical examination and review of patient’s medical records should be undertaken prior to ordering of any tests. Although a good history and clinical examination can distinguish between a pre- and an intra-renal mechanism for the oliguria, in some patients measurement of serum and urine sodium, urea and creatinine may assist in identifying the pathophysiologic reason. Fractional excretion of sodium (FENa) and urea (FEUrea) can be calculated and if FENa is more than 1% and FEUrea under 25% it usually but not always points to a pre-renal mechanism for the oliguria. Renal ultrasound to rule out obstruction should be considered in all patients with history suggestive of prostatic hypertrophy, renal colic or urosepsis.
Establishing a diagnosis
The following steps done sequentially can usually identify the cause of oliguria in the majority of patients:
Clinical examination to assess intravascular volume status, including heart-rate, blood-pressure, capillary refill, skin turgor, presence or absence of elevated jugular venous pressure, and edema.
Clinical and or sonographic evaluation for a distended urinary bladder.
Sonography of the kidneys, ureter and bladder to rule out obstructed system.
Urine routine to look for urine osmolality and presence or absence of casts, pigments and crystals.
Serum and urine sodium, urea and creatinine to distinguish pre-renal from intra-renal mechanisms causing the oliguria.
Measurement of intra-abdominal pressure in patients with acute onset abdominal distension.
Key diagnostic tests usually will be:
Serum urea, creatinine and electrolytes.
Arterial blood gas analysis if the clinical picture warrants it.
Urine output is a function of glomerular filtration, tubular secretion and tubular reabsorption. Glomerular filtration rate (GFR) is dependent on cardiac output and renal perfusion. Cardiac output in turn is determined by stroke volume and heart-rate. The determinants of stroke volume include preload (intravascular volume status), contractility of the heart and the afterload against which the heart has to pump blood. Renal perfusion is mainly driven by mean arterial pressure. Hence any decline in intravascular volume, cardiac contractility or mean arterial pressure leads to decreased GFR. Oliguria occurs due to decreased GFR, increased tubular re-absorption or both. Not uncommonly, oliguria can be merely due to mechanical obstruction of urine flow.
The exact incidence of oliguria in the ICU is unclear due to various definitions used in the past. Two-thirds of ICU patients with AKI are oliguric. The incidence of oliguria in ICU patients in one study was about 18%. Patients with AKI who have oliguria have a poorer outcome compared to patients who are non-oliguric. However, converting oliguric AKI to non-oliguric AKI using diuretics does not seem to improve the prognosis of oliguric AKI. In one recent study, the presence of less than 4 hours of oliguria provided a sensitivity of 50% and a specificity of 86% for the prediction of AKI.
Special considerations for nursing and allied health professionals.
What's the evidence?
Description of the problem
Zaloga, GP, Highes, SS. “Oliguria in patients with normal renal function”. Anesthesiology. vol. 72. 1990. pp. 598-602. (An observational study evaluating incidence and etiology of oliguria in patients with normal creatinine.)
Power, JR, Liu, JL. “Oliguria as predictive biomarker of acute kidney injury in critically ill patients”. Crit Care. vol. 15. 2011;Jul 19. pp. R172(An observational study evaluating the value of oliguria as a biomarker in predicting AKI in ICU patients.)
Uchino, S, Doig, GS. “Diuretics and mortality in acute renal failure”. Crit Care Med. vol. 32. 2004 Aug. pp. 1669-77. ( A large multicenter, multinational observational study that examined the impact of diuretic therapy on outcome of AKI and suggested no benefit.)
Bersten, AD, Holt, AW. “Vasoactive agents and the role of renal perfusion pressure”. New Horiz.. vol. 3. 1995. pp. 650-1. (A brief article discussing the effect of vasoactive agents on renal perfusion pressure.)
Bagshaw, SM, Langenberg, C, Bellomo, R. “Urinary biochemistry and microscopy in septic acute renal failure: systematic review”. Am J Kid Dis. vol. 48. 2006; Nov. pp. 695-705. (Systematic review that evaluates the scientific basis of the use of urinary indices in septic acute renal failure.)
Muffarej, FA, Abel, LM, Chawla, LS. “Understanding intra-abdominal hypertension: From bench to bedside”. J of Intensive Care Med. 2011. April 27. (A good review on the physiologic effects of intra-abdominal hypertension on various organs.)
Copyright © 2017, 2013 Decision Support in Medicine, LLC. All rights reserved.
No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC. The Licensed Content is the property of and copyrighted by DSM.
- 1. Description of the problem
- 2. Emergency Management
- 3. Diagnosis
- Special considerations for nursing and allied health professionals.
- What's the evidence?