LAUSR

Lactic acidosis, increased lactate levels N2 mmol/L with a high anion gapmetabolic acidosis, commonly occurs due to hypoperfusion/hypoxia (type A) but may also arise due to other causes, often overlooked, such as thiamine deficiency (type B) [1]. We report the perioperative occurrence of severe type B lactic acidosis with insulin-resistant hyperglycemia related to cadaveric kidney transplantation and its rapid resolution after intravenous thiamine administration. Written consent was obtained from the patient. A 62-year-old man with type 2 diabetes, hypertension, end-stage renal disease (ESRD), and chronic hemodialysis presented for cadaveric kidney transplantation. Patient had a preoperative random blood glucose of 112mg/dL andhis diabeteswas controlled bydiet only. Standard monitors were placed, anesthesia was then induced with propofol and maintainedwith sevoflurane. Baseline arterial blood gas (ABG) showed: pH, 7.41; PaCO2, 30 mmHg; PaO2, 196 mmHg; HCO3, 19 mmol/L; base excess, −6 mmol/L; Na, 136 mmol/L; K, 5.8 mmol/L; Cl, 111 mmol/L; glucose, 104 mg/dl; hematocrit, 33%; anion gap, 12. Following kidney perfusion, hyperkalemia (K 7.7 mg/dL) was noted and corrected with 25 g dextrose, 10 units insulin, 500 mg CaCl2, and 50 mEq/L NaHCO3. Vitals were stable throughout surgery (BP, 136/ 69 mmHg; heart rate, 109 beats per minute; temperature, 36.5 °C). Patient's totalfluid intakewas 2500mLnormal saline, 1500mL 5% albumin, and 250 mL pRBC. Estimated blood loss was 700 mL with 100 mL urine output. At the end of surgery, a repeat ABG showed worsening of lactic acidosis and hyperglycemia (Fig. 1). Patientwas kept intubated and admitted to the surgical intensive care unit (ICU). Examination of the abdomen and lower extremity pulseswas normal. Mesenteric ischemia, transplanted kidney ischemia, portal vein occlusion, lower extremity compartment syndrome, hepatic injury, and rhabdomyolysis were ruled out by normal duplex ultrasound, creatinine phosphokinase, troponins, and liver enzymes. Despite titrated insulin (10 units/h) and sodium bicarbonate infusions and boluses (30 mEq/h), there was no improvement in lactic acidosis and hyperglycemia after 6 h (Fig. 1). Suspecting thiamine deficiency, intravenous thiamine 50 mg was administered and continuous veno-venous hemofiltration (CVVH) was started to manage acid–base imbalance. Within 4 h, significant improvement inmetabolic acidosis occurred. A second dose of intravenous thiamine 50 mg was given. Lactate dropped from 14.5 to 2.3 mmol/L