Algorithmic triage of acute oliguria (< 0.5 mL/kg/hr): urinary catheter patency check, volume responsiveness vs congestive nephropathy (VExUS Doppler), nephrotoxic drug review, and the furosemide stress test.
Acute oliguria (urine output < 0.5 mL/kg/hr for ≥ 6 consecutive hours, or sudden anuria < 50 mL/day) is an early, highly sensitive harbinger of Acute Kidney Injury (AKI) and renal hypoperfusion. Bedside management mandates an immediate mechanical rule-out of urinary catheter obstruction, distinguishing pre-renal hypoperfusion from venous congestive nephropathy and intrinsic tubular necrosis, and preventing indiscriminate fluid overloading.
Caution
Dangerous Diagnosis Not to Miss: Obstructed urinary catheter with bladder overdistension / rupture, Abdominal Compartment Syndrome (IAP > 20 mmHg directly compressing renal veins and parenchyma), Severe Cardiorenal Venous Congestion (VExUS Grade 3), and rapidly progressive glomerulonephritis / thrombotic microangiopathy.
Flush the Catheter: Flush the indwelling urinary catheter with 30–50 mL of sterile saline under sterile technique; check for blood clots, sediment, kinks, or airlocks in tubing.
Bladder POCUS: Perform bedside ultrasound of the bladder; a distended bladder (> 300–500 mL) despite an indwelling catheter indicates catheter obstruction or malposition (replace catheter immediately).
Assess systemic perfusion: use MAP together with capillary refill, mental status, lactate trend, cardiac function and the patient's baseline pressure; do not use one higher 'renal MAP' target solely because chronic hypertension is present.
Evaluate for a fluid-responsive perfusion deficit with history, examination and dynamic testing (for example passive-leg raise with a measured stroke-volume response when feasible) before giving repeated fluid.
Assess right-sided venous congestion with the whole hemodynamic picture. VExUS Doppler patterns can support clinically important systemic venous congestion, but the grade is not a stand-alone command to diurese or ultrafilter; decongest when congestion is contributing and perfusion can tolerate it.
Measure intra-abdominal pressure when abdominal compartment physiology is plausible. IAH is sustained/repeated IAP ≥12 mmHg; abdominal compartment syndrome is sustained IAP >20 mmHg with new organ dysfunction and requires urgent cause-directed decompression/resuscitation, often with surgical input rather than an oliguria-only rule.
Caution
Common Diagnostic Trap: Reflexively giving fluid boluses for every oliguric patient without assessing volume status or venous congestion. In sepsis and cardiorenal syndrome, excess fluid accumulates in the interstitial and venous beds, raising renal subcapsular pressure and directly causing congestive acute renal failure.
AKI: KDIGO staging, biomarkers, and renoprotective resuscitation.
CRRT: Modalities (CVVH/CVVHD/CVVHDF), filter anticoagulation, and dose delivery.
Shock & Septic Shock: Perfusion targets and dynamic fluid responsiveness.
Intra-Abdominal Hypertension: Bladder pressure monitoring and decompression.
RV Failure: Cardiorenal venous congestion and decongestion strategies.
Evidence status
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From recognizing hypoperfusion and initial crystalloid bolus to dynamic fluid responsiveness assessment and vasopressor targets.
From first-line norepinephrine titration to multi-agent vasopressor escalation and inotrope selection.
From multi-vasopressor failure to rescue non-adrenergic agents and mechanical circulatory support.
From confirming true hypotension to recognizing shock and its likely category.
Sepsis-AKI microcirculatory decoupling, KDIGO staging, Furosemide Stress Test (FST), urine microscopy, and the AEIOU dialysis threshold framework.
Principles of convection vs diffusion, filtration fraction, delivered effluent dosing (20–25 mL/kg/h), Regional Citrate Anticoagulation, and citrate toxicity.
Cellular dysoxia, DO2/VO2 physiology, the 4 shock phenotypes, dynamic fluid responsiveness (PLR/PPV) vs fluid tolerance (VExUS), and vasoactive pharmacology.
The subset of sepsis with profound circulatory and cellular/metabolic abnormality — clinically identified by a vasopressor requirement to maintain MAP ≥ 65 mmHg plus lactate > 2 mmol/L despite adequate fluid resuscitation.
RV anatomy and ischemia spiral, ventricular interdependence (D-sign), echocardiographic metrics (TAPSE, S', PAPi, VExUS), and the 4-pillar resuscitation strategy.
Primary pump failure, SCAI staging (A–E), PAC hemodynamics (CPO, PAPi), inotrope selection, emergent revascularization, and mechanical circulatory support.
Hemodynamic phenotypes (SCAPE vs ADHF vs Cardiogenic Shock), non-invasive positive pressure ventilation, high-dose vasodilator algorithms, loop diuretics, and sequential nephron blockade.
Phased energy and protein delivery, early enteral nutrition when safe, indirect calorimetry, refeeding prevention, feeding-intolerance troubleshooting, and individualized parenteral nutrition timing.