In a 45-year-old postoperative man with a colostomy, serum sodium 133 mmol/L, potassium 4.7 mmol/L, chloride 117 mmol/L, bicarbonate 8 mmol/L (normal anion‑gap metabolic acidosis), creatinine 1.12 mg/dL, mild hypomagnesemia, asymptomatic hypotension, and an ejection fraction of 20 %, what is the differential diagnosis for his metabolic acidosis?

Differential Diagnosis of Normal Anion-Gap Metabolic Acidosis in a Postoperative Colostomy Patient

In this 45-year-old postoperative colostomy patient with severe normal anion-gap metabolic acidosis (bicarbonate 8 mmol/L, chloride 117 mmol/L), the differential diagnosis includes: (1) high-output colostomy losses causing bicarbonate depletion, (2) iatrogenic hyperchloremic acidosis from excessive normal saline resuscitation, and (3) tissue hypoperfusion from cardiogenic shock given the severely reduced ejection fraction of 20%. 1, 2, 3

Immediate Diagnostic Priorities

Assess Tissue Perfusion

• Measure serum lactate immediately—a value >2 mmol/L signals inadequate tissue perfusion and ongoing shock, which would indicate a high anion-gap component superimposed on the hyperchloremic acidosis 1, 2
• The asymptomatic hypotension combined with EF 20% raises serious concern for cardiogenic shock with tissue hypoperfusion 1
• Failure of lactate to normalize within 24 hours predicts 77.8% survival, falling to 13.6% if elevated beyond 48 hours 1

Quantify Colostomy Output

• Document 24-hour colostomy output volume—high-output stomas (>1200 mL/day) cause massive bicarbonate losses leading to normal anion-gap metabolic acidosis 4, 5
• Colostomy effluent is rich in bicarbonate; excessive losses directly deplete systemic bicarbonate stores 5
• Measure stoma sodium concentration if output is high; sodium >90 mmol/L suggests significant electrolyte depletion 4

Calculate Anion Gap

• Anion gap = Na - (Cl + HCO₃) = 133 - (117 + 8) = 8 mmol/L, confirming normal anion-gap acidosis 3, 6
• This pattern excludes lactic acidosis, ketoacidosis, renal failure, and toxic ingestions as primary causes 6, 7
• The elevated chloride (117 mmol/L) with normal anion gap specifically identifies hyperchloremic acidosis 4, 3

Primary Etiologies in This Clinical Context

1. Iatrogenic Hyperchloremic Acidosis from Normal Saline

• Excessive intraoperative normal saline administration is the leading cause of postoperative metabolic acidosis 1, 2
• Normal saline contains 154 mEq/L chloride (supraphysiologic compared to plasma ~100 mEq/L), which lowers the strong ion difference and directly decreases pH 3
• Continuing normal saline infusion worsens existing acidosis and must be stopped immediately 1, 2
• The elevated chloride (117 mmol/L) strongly suggests this mechanism 4, 3

2. Gastrointestinal Bicarbonate Loss via Colostomy

• High-volume colostomy output causes direct bicarbonate loss, producing normal anion-gap metabolic acidosis 4, 5
• Patients with jejunostomy or high ileostomy can lose 2-4 L/day of bicarbonate-rich fluid 4
• Even moderate colostomy losses (>800-1000 mL/day) can precipitate significant acidosis 4
• This mechanism is independent of chloride elevation and represents true bicarbonate depletion 5

3. Tissue Hypoperfusion from Cardiogenic Shock

• EF 20% with asymptomatic hypotension indicates severe cardiac dysfunction with high risk of inadequate tissue perfusion 1
• Lactic acidosis from hypoperfusion would typically elevate the anion gap, but early or mild lactic acidosis can coexist with hyperchloremic acidosis 1, 6
• The combination of low cardiac output and fluid shifts postoperatively creates a perfect storm for mixed acidosis 1

4. Acute Kidney Injury (Less Likely but Consider)

• Creatinine 1.12 mg/dL may represent acute kidney injury in the postoperative setting, impairing renal acid excretion 6
• Early renal failure can present with normal anion-gap acidosis before uremic acids accumulate 7
• However, this creatinine level is only mildly elevated and less likely to cause bicarbonate 8 mmol/L 6

Critical Management Steps

Immediate Fluid Management

• Switch immediately to balanced crystalloids (lactated Ringer's or Plasma-Lyte) for all resuscitation and maintenance fluids 1, 2, 3
• Discontinue any ongoing 0.9% saline infusion immediately—this is a common iatrogenic contributor to worsening acidosis 1, 2
• Balanced crystalloids have physiologic chloride concentrations and do not precipitate hyperchloremic acidosis 2, 3

Optimize Cardiac Output

• With EF 20% and hypotension, consider vasopressor support (target MAP ≥65 mmHg) rather than aggressive fluid boluses that may worsen pulmonary edema 4, 1
• Ensure adequate analgesia, as uncontrolled pain worsens sympathetic stimulation and tissue perfusion 1
• Monitor for signs of cardiogenic shock: cool extremities, delayed capillary refill, oliguria 1

Colostomy-Specific Interventions

• If output >1200 mL/day, provide oral glucose-saline replacement solution with sodium ≥90 mmol/L 4
• Restrict hypotonic oral fluids (tea, coffee, juice) which worsen sodium and water losses 4
• Consider loperamide or other antimotility agents to reduce stoma output 4

Serial Monitoring Protocol

• Perform arterial blood gas every 1-2 hours initially to track pH, PCO₂, base excess, and lactate trends 1, 2
• Check serum electrolytes (Na, K, Cl, HCO₃) every 4-6 hours during active resuscitation 2
• Monitor magnesium closely—the current level of 1.5 mg/dL is low-normal and may worsen with ongoing losses 4, 2
• Target urine output >0.5 mL/kg/h as a perfusion marker 1, 2

Bicarbonate Therapy (Restrictive Approach)

• Do not administer sodium bicarbonate unless arterial pH falls below 7.15-7.20 with severe hemodynamic instability despite adequate volume resuscitation 2, 6
• Bicarbonate is not recommended for hypoperfusion-induced lactic acidosis unless pH is critically low, as it may worsen intracellular acidosis 2
• The primary treatment is addressing the underlying cause (stop saline, optimize cardiac output, reduce stoma losses) rather than buffering the acid 6, 7

Critical Pitfalls to Avoid

• Do not assume the acidosis is merely "dilutional" or benign—bicarbonate of 8 mmol/L represents severe acidosis requiring aggressive investigation 1
• Do not rely solely on blood pressure measurements—lactate concentration and base deficit are superior markers of tissue perfusion 1
• Rising lactate or worsening base deficit despite resuscitation indicates insufficient therapy or occult pathology (anastomotic leak, bowel ischemia, ongoing bleeding) and should prompt urgent imaging or return to the operating room 1, 2
• Do not continue normal saline "because the patient is hypotensive"—balanced crystalloids provide equal volume expansion without worsening acidosis 2, 3

Additional Rare Considerations

• If acidosis persists despite appropriate management, consider rare causes such as 5-oxoproline accumulation (especially if patient received prolonged acetaminophen), D-lactate from bacterial overgrowth, or propylene glycol toxicity 8, 7
• These diagnoses require specialized testing and should be considered only after common etiologies are excluded 8