In a patient with arterial blood gas pH 7.38, bicarbonate 13 mmol/L, potassium 3 mmol/L, creatinine 5.3 mg/dL, urea 17.8 mmol/L, base excess –3, and lactate 0.7 mmol/L, what is the impression (diagnosis) and appropriate management?

Severe Metabolic Acidosis with Acute Kidney Injury and Hypokalemia

This patient has severe metabolic acidosis (bicarbonate 13 mmol/L, pH 7.38) driven by acute kidney injury (creatinine 527 µmol/L ≈ 6.0 mg/dL, urea 17.8 mmol/L) with a mild elevation in β-hydroxybutyrate (3 mmol/L) indicating starvation ketosis, complicated by dangerous hypokalemia (K⁺ 3 mmol/L), requiring immediate aggressive potassium replacement before any other intervention, followed by urgent renal replacement therapy and cautious bicarbonate administration only if pH falls below 7.1. 1

Immediate Diagnostic Assessment

Calculate the anion gap to characterize the acidosis: Anion gap = [Na⁺] – ([Cl⁻] + [HCO₃⁻]). A value >12 mEq/L indicates high anion-gap metabolic acidosis. 1 The elevated creatinine (527 µmol/L ≈ 6.0 mg/dL) and urea (17.8 mmol/L) confirm acute or acute-on-chronic kidney injury as the primary driver of uremic acidosis. 1

Interpret the β-hydroxybutyrate level: At 3 mmol/L, this is elevated above the normal threshold of <0.5 mmol/L but falls short of diabetic ketoacidosis criteria (which requires glucose >250 mg/dL, pH <7.3, bicarbonate <15 mEq/L, and moderate-to-severe ketonemia). 2 This mild ketonemia likely represents starvation ketosis in the setting of poor oral intake and renal failure. 2

Assess respiratory compensation: The pH of 7.38 (within normal range 7.35–7.45) despite a bicarbonate of 13 mmol/L indicates robust respiratory compensation. 1 The patient is hyperventilating to lower PaCO₂ and maintain near-normal pH. 1

Verify lactate is not elevated: Lactate 0.7 mmol/L is normal (<2 mmol/L), ruling out lactic acidosis as a contributor. 1

Critical Priority: Hypokalemia Management

Potassium 3 mmol/L is dangerously low and represents the most immediate life-threatening abnormality. 2 Severe hypokalemia (<3.3 mEq/L) can precipitate fatal cardiac arrhythmias, especially in the setting of acidosis and renal failure. 2

Potassium Replacement Protocol

• Do not administer any insulin or bicarbonate until potassium is ≥3.3 mmol/L, as both drive potassium intracellularly and can worsen hypokalemia. 2
• Aggressively replace potassium first: Administer 20–40 mEq potassium chloride intravenously over 1–2 hours via central line (peripheral administration should not exceed 10 mEq/hour). 2
• Recheck serum potassium every 2 hours until it reaches ≥3.3 mmol/L, then maintain at 4–5 mmol/L throughout treatment. 2
• Once potassium is ≥3.3 mmol/L, add 20–30 mEq/L potassium to all IV fluids (using approximately 2/3 potassium chloride and 1/3 potassium phosphate to prevent hypophosphatemia). 2

Fluid Resuscitation

Initiate isotonic saline (0.9% NaCl) at 15–20 mL/kg/hour to restore intravascular volume and improve renal perfusion, as volume depletion commonly accompanies acute kidney injury. 2 However, monitor closely for fluid overload given the severe renal impairment (creatinine 6.0 mg/dL), as these patients cannot excrete excess volume. 2

Renal Replacement Therapy

Urgent continuous renal replacement therapy (CRRT) or intermittent hemodialysis is indicated for:

• Severe uremia (urea 17.8 mmol/L, creatinine 527 µmol/L) 1
• Metabolic acidosis refractory to medical management 1
• Inability to safely administer fluids due to volume overload risk 2

Use bicarbonate-buffered dialysate or replacement fluid rather than lactate-buffered solutions, as lactate metabolism may be impaired in critically ill patients with renal failure and can worsen acidosis. 3 Bicarbonate fluids provide more rapid correction of base excess and lactate clearance. 3

Bicarbonate Therapy Considerations

Bicarbonate is NOT indicated at this pH (7.38). 1, 2 The American Diabetes Association and British Thoracic Society guidelines are clear: bicarbonate therapy should only be considered when pH <7.1 (and specifically <6.9 in DKA), as it provides no benefit in acidosis resolution and may cause harm. 2, 4

• Base excess of –3 mEq/L does not meet the threshold (BE <–10 with pH <7.1) for bicarbonate administration. 1
• If pH were to fall below 7.1 despite renal replacement therapy, then consider intravenous sodium bicarbonate 50–100 mEq (one to two 50 mL vials) slowly over 30–60 minutes, with repeat arterial blood gas in 30 minutes. 4
• Avoid rapid bicarbonate infusion, as it can cause paradoxical intracellular acidosis, hypernatremia, hyperosmolality, and overshoot alkalosis. 4

Starvation Ketosis Management

The mild ketonemia (β-OHB 3 mmol/L) requires carbohydrate administration to suppress hepatic ketogenesis. 2 Once the patient can tolerate oral intake:

• Provide 150–200 grams of carbohydrate daily to reduce ketone production. 2
• If unable to eat, add 5–10% dextrose to IV fluids to provide substrate and suppress ketosis. 2
• Monitor blood glucose to avoid hyperglycemia and osmotic diuresis. 2

Monitoring Strategy

• Arterial or venous blood gas every 2–4 hours to track pH, bicarbonate, and base excess. 2 Venous pH is adequate for monitoring after initial arterial sample (venous pH typically 0.03 units lower than arterial). 2
• Serum electrolytes (Na⁺, K⁺, Cl⁻, HCO₃⁻) every 2–4 hours to calculate anion gap and monitor potassium. 2
• Renal function (creatinine, urea) daily to assess response to therapy. 2
• β-hydroxybutyrate every 4–6 hours until it normalizes to <0.5 mmol/L. 2 Do not rely on urine ketones, as they do not measure β-OHB and can be misleading. 2
• Continuous cardiac monitoring given the severe hypokalemia and acidosis. 2

Differential Diagnosis to Exclude

• Diabetic ketoacidosis: Ruled out by normal pH, glucose not provided but β-OHB only mildly elevated, and bicarbonate 13 (not <15). 2
• Lactic acidosis: Ruled out by normal lactate 0.7 mmol/L. 1
• Toxic ingestion (salicylate, methanol, ethylene glycol): Consider if anion gap is markedly elevated and history suggests exposure. 2
• Rhabdomyolysis: Check creatine kinase if muscle injury suspected. 2

Critical Pitfalls to Avoid

• Do not give bicarbonate at pH 7.38—it is contraindicated and provides no benefit. 1, 2
• Do not administer insulin or bicarbonate before correcting hypokalemia to ≥3.3 mmol/L—this can precipitate fatal arrhythmias. 2
• Do not withhold renal replacement therapy in severe uremic acidosis with creatinine 6.0 mg/dL—dialysis is the definitive treatment. 1
• Do not use lactate-buffered dialysate in critically ill patients with renal failure—bicarbonate-buffered solutions are superior. 3
• Do not rely on urine ketones to monitor ketosis—measure blood β-hydroxybutyrate directly. 2
• Do not assume the patient is stable because pH is normal—the underlying metabolic acidosis (bicarbonate 13) and severe renal failure indicate critical illness requiring intensive monitoring. 1