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Type A Lactic Acidosis Post-Cardiac — FRCA Final MCQ

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HardIntensive Care MedicineType A Lactic Acidosis Post-CardiacFRCA Final

Six hours after cardiac surgery with cardiopulmonary bypass, a 70-year-old man has a rise in arterial lactate from 2.8 to 12 mmol/L over 3 hours. His pH is 7.10, base excess is −18 mmol/L and urine output is less than 0.3 mL/kg/hour. Cardiac index is 3.0 L/min/m² and ScvO2 is 72%, but his noradrenaline requirement is increasing and he has developed abdominal distension with blood-stained rectal discharge. Bilirubin, alanine aminotransferase and INR are unchanged from baseline. He does not take metformin and has no history of intestinal resection or malnutrition. Which mechanism most likely accounts for his lactic acidosis?

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Correct answer: E — Type A lactic acidosis from regional splanchnic tissue hypoxia

The correct answer is E. The rapid early rise in lactate, oliguria, escalating vasopressor requirement and new abdominal signs indicate tissue hypoperfusion, with non-occlusive mesenteric ischaemia a critical possibility after cardiac surgery. A normal cardiac index and ScvO2 reflect global oxygen transport and do not exclude regional splanchnic or microcirculatory hypoxia; this is therefore type A lactic acidosis. Reduced hepatic clearance is less likely with unchanged hepatic indices and does not explain the abdominal findings. Metformin-associated lactic acidosis requires metformin exposure, usually with accumulation during renal deterioration. D-lactic acidosis occurs principally in short bowel syndrome and is not detected by routine L-lactate assays. Thiamine deficiency causes type B hyperlactataemia through impaired pyruvate dehydrogenase activity but is unsupported in a previously nourished patient with acute regional-ischaemic features.

Reference: Mothes H et al. Monitoring of the Progression of the Perioperative Serum Lactate Concentration Improves the Accuracy of the Prediction of Acute Mesenteric Ischemia Development After Cardiovascular Surgery. Journal of Cardiothoracic and Vascular Anesthesia. 2021;35:1792–1799. https://pubmed.ncbi.nlm.nih.gov/33663981/