Anesthesiology APPLIED Exam › Critical care, resuscitation and trauma

Postoperative oliguria

Critical care, resuscitation and trauma·~5 min read· Physician-reviewed✓ Sourced · 3

Stem

A 71-year-old man, 80 kg, with hypertension treated with lisinopril (baseline blood pressure 155/88), is in the PACU after a 4-hour open right hemicolectomy. He received ketorolac at the end of the case. The nurse calls: urine output has been 15 mL/h for the last two hours. Blood pressure is 104/60, heart rate 98, and he is comfortable.

Question

The nurse asks whether to give a fluid bolus. How will you evaluate and manage his oliguria?

Ideal answer

HeadlineNo bolus over the phone; I go to the bedside and exclude post-renal first, the easiest to fix: flush or replace the Foley, bladder scan.

Define it, then act early: oliguria is less than 0.5 mL/kg/h for 6 hours by KDIGO,¹ but in PACU I act on two hours.
Volume status and perfusion: pressure versus baseline, heart rate, capillary refill, lactate, hemoglobin, the drains, and a dynamic test, passive leg raise or IVC ultrasound.
MAP within 10–20% of baseline, because his is well below usual. Fluid-responsive: a 250–500 mL balanced crystalloid bolus and reassess; if not, a vasopressor, not drowning him.
Stop the nephrotoxins: no more ketorolac, lisinopril held; electrolytes, creatinine and a urinalysis sent.
Keep the abdomen in mind: after a major abdominal case, intra-abdominal hypertension is on my list. No furosemide to make urine.

Breaking down the answer

Post-renal first — a kinked or clotted catheter is the most common and most embarrassing cause; a 5-minute check before anything else. A structured pre-renal, renal, post-renal approach shows organization.
Fluid only if fluid-responsive — a positive passive leg raise (stroke volume or cardiac output up about 10%, or pulse pressure over 15% without output monitoring)² or pulse-pressure variation over 13%. Otherwise fluid causes edema, including renal interstitial edema that worsens kidney function.
Perfusion pressure — chronic hypertension shifts renal autoregulation to the right, so a MAP of 65 may be too low for him.
Surgical context — after aortic cross-clamp, renal ischemia or embolism; after a long steep Trendelenburg case, rhabdomyolysis; after contrast, contrast nephropathy; after a big transfusion, hemolysis.
Bladder pressure — measured with no more than 25 mL of saline; 12 mmHg or more, sustained or repeated, is intra-abdominal hypertension, and sustained above 20 mmHg with new organ dysfunction is abdominal compartment syndrome;³ the treatment is decompression, not fluid.
No diuretics to treat a number — furosemide converts oliguric to non-oliguric renal failure without improving outcome; KDIGO suggests diuretics only for volume overload, recommends against low-dose dopamine and suggests against fenoldopam.¹
Nephrotoxins on my list — NSAIDs, aminoglycosides, ACE inhibitors and ARBs on the day of surgery, and IV contrast where avoidable.

Follow-up question

Overnight he bleeds from the anastomosis, returns to the operating room, and arrives in the ICU intubated after 3 L of crystalloid. Six hours later he has been oliguric for three hours, peak airway pressures are rising, the abdomen is tense, and the MAP is 60 on norepinephrine.

What is going on, and what do you do?

Follow-up answer

HeadlineAbdominal compartment syndrome until proven otherwise; bladder pressure through the Foley is 26 mmHg, which confirms it, and I tell the surgeon directly.

The treatment is decompressive laparotomy.³ Meanwhile I deepen sedation and trial neuromuscular block to improve abdominal wall compliance, decompress the stomach with a nasogastric tube,³ stop further fluid, maintain perfusion with norepinephrine, and ventilate with lower tidal volumes, accepting higher plateau pressures. After decompression I expect a reperfusion surge of potassium and acid and prepare calcium and bicarbonate, then reassess urine output, airway pressures and lactate.

Pitfalls that cost points

Giving furosemide to "see if the kidneys work."
Missing abdominal compartment syndrome in a ventilated patient whose airway pressures are rising.

Rapid-fire

Q: Why does the urine output fall in every surgical patient? A: Surgical stress raises ADH, aldosterone and catecholamines; some oliguria is normal physiology and does not mean kidney injury.

Q: Why is the fractional excretion of sodium less useful after surgery? A: Diuretics and saline load distort it; I use fractional excretion of urea below 35% if the patient received diuretics.

Q: What protects the kidney in high-risk surgery? A: Maintaining MAP and cardiac output, avoiding nephrotoxins and hyperchloremia, and limiting contrast; there is no proven pharmacologic protection.

Q: When do you call nephrology for dialysis? A: Refractory hyperkalemia, acidosis, volume overload, uremic complications, or certain toxins.

Numbers to know

Item	Value
Oliguria (KDIGO)	< 0.5 mL/kg/h for 6 h¹
AKI by creatinine	Rise ≥ 0.3 mg/dL in 48 h, or ≥ 1.5× baseline within 7 days¹
Fluid challenge	250–500 mL balanced crystalloid
Intra-abdominal hypertension	Bladder pressure ≥ 12 mmHg, sustained or repeated³
Abdominal compartment syndrome	> 20 mmHg with new organ dysfunction³
Diuretics in AKI	Only for volume overload¹

Sources

1.KDIGO Clinical Practice Guideline for Acute Kidney Injury · KDIGO, 2012 · kdigo.org
2.Surviving sepsis campaign: international guidelines for management of sepsis and septic shock 2021 · SCCM / ESICM, 2021 · pmc.ncbi.nlm.nih.govDynamic measures; passive leg raise with >15% pulse-pressure rise where output cannot be measured.
3.Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome · WSACS (Intensive Care Med), 2013 · ncbi.nlm.nih.gov

Facts on this page were checked against these sources on Oct 14, 2026. Guidelines change; confirm doses against current institutional protocols.