Chapter 45 Low Urine Output (Case 30)
Postoperative context: A 58-year-old male with a past medical hx of coronary artery disease has a 1-day hx of low urine output after open cholecystectomy for acute cholecystitis.
| Prerenal (Hypoperfusion) | Renal (Intrinsic) | Postrenal (Obstructive) |
|---|---|---|
| Hypovolemia | Acute tubular necrosis (ATN) | Urinary retention |
| Shock syndromes | Acute interstitial nephritis (AIN) | Benign prostatic hypertrophy (BPH) and ureteral ligature |
PATIENT CARE
Clinical Thinking
• Since the kidney receives 20% of cardiac output, urine output is in part a reflection of that cardiac output. Similarly, it is an indirect measure of intravascular volume status. Decreased urine output is not a dx, but rather a symptom of hypoperfusion, intrinsic renal injury, or postrenal obstruction.
• The causes of decreased urine output fall into one of three categories: prerenal, intrarenal, and postrenal pathology.
• The most common prerenal etiology is hypovolemia, diagnosed clinically in the setting of oliguria, hypotension, tachycardia, and dry mucous membranes. Oliguria due to hypovolemia should correct with appropriate volume replacement. Typically creatinine increases less than 0.1 to 0.3 mg/dL/day.
• The most common intrarenal etiology is ATN, usually due to ischemia or toxin exposure. ATN is usually sudden in onset and worrisome because of its severity and potential for irreversible damage. Typically creatinine increases greater than 0.5 mg/dL/day.
• The most common postrenal etiology is obstruction, either mechanical or physiologic, and is usually due to urinary retention, prostate disease, and/or nephrolithiasis.
History
• Inquire about suprapubic fullness, which may suggest a bladder etiology such as retention, and dysuria or difficulty voiding, which may suggest prostate disease or UTI.
• A relevant PMH searches for coronary disease, previous infarction, hypertension, previous renal disease, autoimmune disease, prostate and bladder problems, allergies to medications, and recent dye studies in preoperative and intraoperative radiographic studies.
• Review the medications received prior to the oliguric state. Determine exposures to medications such as NSAIDs, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers, and general anesthetics.
• Assess intake and output. Regarding intake: Is the patient NPO? Poor appetite? Has volume been inefficiently maintained? Regarding output: Did the patient undergo a bowel prep? Has there been vomiting, diarrhea, sweating? Is the patient on diuretics?
Physical Examination
• VS and intake/output: Temperature, pulse, BP, central venous pressure (CVP), pulmonary capillary wedge pressure (PCWP), if available, for signs of hypovolemia.
• Appearance: Suspect hypovolemia if pale, sunken eyes, dry mucous membranes, decreased skin turgor, and dry axilla.
• Chest: Jugular venous distention (JVD), crackles and peripheral edema for congestive heart failure.
