In a 70‑year‑old intubated man with stage III acute kidney injury, oliguria, rising creatinine (~326 µmol/L, eGFR ≈ 17 mL/min), refractory volume overload, severe ARDS on 100% FiO₂, mixed respiratory acidosis, and a do‑not‑resuscitate (DNR) order, should renal replacement therapy (preferably continuous renal replacement therapy) be initiated?

Yes, Initiate Renal Replacement Therapy Immediately

This patient requires urgent initiation of continuous renal replacement therapy (CRRT) based on multiple absolute indications: refractory volume overload with severe ARDS on 100% FiO₂, oliguria unresponsive to diuretics, rising creatinine (326 µmol/L), and mixed acid-base disturbance in the setting of hemodynamic instability. 1, 2

Absolute Indications Present

Your patient meets multiple life-threatening criteria that mandate RRT initiation:

• Refractory fluid overload with cumulative negative balance of -5037 mL despite furosemide, combined with severe ARDS requiring 100% FiO₂ and bilateral pulmonary infiltrates on chest X-ray 1, 3
• Persistent oliguria (260 mL output on most recent day) despite diuretic therapy in the context of Stage III AKI 2, 3
• Severe respiratory compromise with oxygen saturation of only 85-88% on maximal ventilatory support (FiO₂ 100%), where further volume removal is critical but cannot be achieved medically 4, 1
• Mixed acid-base disturbance (respiratory acidosis pH 7.32, pCO₂ 58, with metabolic alkalosis) that will worsen with aggressive diuretic therapy 5

Why CRRT Over Intermittent Hemodialysis

CRRT is the mandatory modality for this patient, not intermittent hemodialysis:

• Hemodynamic instability requiring norepinephrine 15 cc/hr makes intermittent hemodialysis poorly tolerated 4, 1
• Severe ARDS with impaired gas exchange benefits from the gradual, continuous fluid removal that CRRT provides, avoiding rapid intravascular volume shifts that worsen pulmonary edema 4, 1
• Cerebral pathology (subarachnoid hemorrhage) is a specific indication for CRRT over intermittent dialysis to avoid rapid osmotic shifts and increased intracranial pressure 1, 6

The Futility of Escalating Diuretics

Increasing furosemide to BID will fail and delay necessary intervention:

• The patient is already oliguric on furosemide 40 mg with only 260 mL output on the most recent day, demonstrating diuretic resistance 3
• In ARDS with severe volume overload, the FACTT-lite protocol recommends aggressive diuresis only when patients are not in shock and off vasopressors ≥12 hours – this patient is on continuous norepinephrine 4
• Further diuretic escalation in the setting of Stage III AKI (eGFR 17 mL/min, creatinine 326 µmol/L) risks worsening renal injury without achieving adequate decongestion 3

CRRT Prescription Specifics

Initiate CRRT with the following parameters:

• Modality: Continuous venovenous hemodiafiltration (CVVHDF) to address both volume overload and metabolic derangements 1
• Dose: 20-25 mL/kg/hour effluent volume (approximately 1400-1750 mL/hour for a 70 kg patient) 1, 2
• Access: Right internal jugular vein preferred, with ultrasound guidance and post-placement chest X-ray confirmation 1
• Anticoagulation: Regional citrate anticoagulation as first-line, but given the mixed acid-base disturbance and potential for citrate accumulation, consider no anticoagulation initially or heparin if bleeding risk permits 1
• Buffer: Bicarbonate-based replacement fluid (NOT lactate) given the respiratory acidosis and potential for impaired lactate clearance in shock 1, 5

Goals of CRRT in This Patient

Target the following endpoints:

• Fluid removal: Aim for net negative 1-2 liters over first 24 hours to improve oxygenation while monitoring hemodynamics 4, 1
• Acid-base correction: Gradual normalization of pH toward 7.35-7.40 through continuous bicarbonate buffering 5
• Electrolyte management: Maintain potassium 4.0-5.0 mEq/L, correct hypernatremia (147 mmol/L) gradually 1
• Azotemia control: Reduce BUN (43.5 mmol/L) and stabilize creatinine 3

Critical Pitfall to Avoid

Do not delay RRT initiation waiting for "traditional" absolute indications like severe hyperkalemia (K+ 6.5) or uremic pericarditis:

• The combination of refractory volume overload with severe ARDS on maximal support is itself an absolute indication 1, 2
• Mortality in septic AKI requiring RRT exceeds 70%, and delays in initiation worsen outcomes 7
• The patient's DNR status does not contradict CRRT initiation – CRRT is a supportive measure that may allow recovery, and can be discontinued if goals of care change or renal recovery occurs 2

Monitoring During CRRT

Assess the following parameters every 4-6 hours:

• Hemodynamics (MAP, vasopressor requirements) – CRRT may improve hemodynamics by removing inflammatory mediators 1
• Oxygenation (FiO₂ requirements, oxygen saturation) – expect improvement with volume removal 4
• Acid-base status (arterial blood gases) – target pH >7.30 initially 5
• Electrolytes (especially potassium, calcium, phosphate) – CRRT causes rapid shifts 1
• Filter circuit pressures and blood flow – to detect clotting and ensure adequate dose delivery 1

Prognosis and Renal Recovery

Realistic expectations for this critically ill patient:

• Septic AKI requiring RRT has 70% in-hospital mortality, but survivors show trends toward renal recovery and RRT independence (91% in one series) 7
• Urine output is the most reliable predictor of successful CRRT discontinuation (sensitivity 66%, specificity 74%) – currently this patient has minimal output 2
• Given subarachnoid hemorrhage, severe ARDS, and multiorgan failure, the overall prognosis is guarded, but CRRT provides the only opportunity for renal and volume status stabilization 6, 7

The decision to prime the family for possible hemodialysis is appropriate, but CRRT should be initiated emergently rather than waiting for further deterioration. 1, 2