What is the possible etiology of severe metabolic acidosis, cardiac dysfunction, and hyperphosphatemia in a young vegetarian male with a history of protein supplement use?

Severe Metabolic Acidosis with Cardiac Dysfunction: Likely Acute Mesenteric Ischemia or Toxic Ingestion

This patient's presentation of profound shock, severe metabolic acidosis (lactate ~15), hyperphosphatemia (16 mg/dL), and refractory cardiac dysfunction despite ECMO most strongly suggests acute mesenteric ischemia (AMI), though toxic ingestion (particularly phosphate-containing compounds or protein supplement contamination) must be urgently excluded.

Primary Diagnostic Considerations

Acute Mesenteric Ischemia (Most Likely)

The constellation of sudden-onset vomiting/diarrhea, profound shock unresponsive to vasopressors, severe metabolic acidosis with elevated lactate, dilated bowel loops on CT, and extreme IL-6 elevation (>3000) is pathognomonic for AMI. 1

• Non-occlusive mesenteric ischemia (NOMI) is particularly likely given normal coronaries on angiography and the clinical context of a young patient in a hotel (possible dehydration, unusual food exposure) 1
• Severe metabolic acidosis and hyperkalemia result from bowel infarction and reperfusion injury 1
• The extreme cytokine storm (IL-6 >3000) reflects massive intestinal necrosis with bacterial translocation 1
• Dilated bowel loops on CT, while non-specific, support this diagnosis in the appropriate clinical context 1

Critical Pitfall: Delayed Recognition

Any negative changes in critically ill patients—including new organ failure, increased vasopressor requirements, and nutrition intolerance—should immediately raise suspicion for AMI, as classic symptoms are often absent in shocked patients. 1

Alternative Etiologies to Exclude Urgently

Severe Hyperphosphatemia as Primary Cause

Hyperphosphatemia (16.5 mg/dL) can independently cause high anion gap metabolic acidosis and must be considered. 2

• Possible sources in this patient:

  • Protein supplement contamination with phosphate compounds 2, 3
  • Rhabdomyolysis (CPK only 3K argues against this as primary cause) 2
  • Acute phosphate ingestion (accidental or intentional) 3

• Severe hyperphosphatemia causes metabolic acidosis through direct buffering effects and can precipitate cardiac dysfunction through hypocalcemia and direct myocardial toxicity 2, 3

Toxic Ingestion

Given the acute presentation in a hotel setting with friends/family denying self-harm:

• Metformin toxicity can cause severe lactic acidosis and biventricular cardiac dysfunction that persists despite correction of acidosis 4
• Hydroxyurea or other cytotoxic agents (though less likely given vegetarian lifestyle and no known malignancy) 5
• Contaminated protein supplements are a plausible source of phosphate or other toxins 2, 3

Diabetic Ketoacidosis with Complications

• GRBS 250 with positive ketones initially suggests DKA 1
• However, the severity of shock, cardiac dysfunction, and hyperphosphatemia are atypical for DKA alone 1
• DKA typically shows hypophosphatemia initially, not severe hyperphosphatemia 1

Immediate Diagnostic Steps Required

Laboratory Investigations

• Serum calcium (expect severe hypocalcemia with phosphate 16 mg/dL) 2, 3
• Beta-hydroxybutyrate levels (already elevated—quantify to assess DKA contribution) 1
• Metformin level if available 4
• Toxicology screen including heavy metals 3
• Analysis of protein supplement if available 2, 3

Imaging

• Repeat CT angiography specifically evaluating mesenteric vessels and bowel wall enhancement 1
• Consider diagnostic laparoscopy/laparotomy given high suspicion for bowel ischemia despite normal initial imaging 1

Management Priorities

Immediate Interventions

Prompt laparotomy is indicated if any signs of peritonitis develop or if clinical deterioration continues despite maximal support. 1

• Continue CRRT with aggressive phosphate removal 2
• Maintain broad-spectrum antibiotics (already initiated appropriately) 1
• Vasopressors should be used cautiously—dobutamine, low-dose dopamine, or milrinone are preferred over norepinephrine/epinephrine in suspected mesenteric ischemia 1

Metabolic Correction

• Severe hyperphosphatemia requires aggressive dialysis—CRRT is appropriate 2
• Calcium replacement will be needed if hypocalcemia is confirmed (likely with phosphate 16 mg/dL) 2, 3
• Continue bicarbonate therapy judiciously for pH <7.1, though primary treatment is addressing underlying cause 1

Surgical Consultation

Given the clinical picture, early surgical exploration should be strongly considered even with non-diagnostic imaging, as bowel infarction may be present and survival depends on prompt intervention. 1

Prognostic Considerations

• The combination of severe metabolic acidosis (lactate 15), refractory shock requiring ECMO/IABP, coagulopathy, and multi-organ failure carries extremely high mortality 1
• Survival depends on identifying and treating the underlying cause within hours 1
• If AMI with bowel infarction is confirmed, extensive resection may be required with potential for short bowel syndrome 1

Key Clinical Pearls

• Normal coronaries do not exclude cardiac dysfunction from metabolic causes (severe acidosis, hyperphosphatemia, hypocalcemia, toxins) 2, 4, 3
• The protein supplement history is critical—contamination with phosphate compounds or other toxins is possible 2, 3
• Persistent acidosis despite CRRT suggests ongoing tissue necrosis (bowel ischemia) or continued toxin absorption 1, 2
• Extreme hyperphosphatemia (16 mg/dL) is unusual even in renal failure and suggests exogenous source or massive tissue breakdown 2, 3