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Abstract: PO1166

A Wide-Awake Patient with Severe Hypoglycemia and Lactic Acidosis

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Abdelsamad, Sarah, Wayne State University, Detroit, Michigan, United States
  • Mohanty, Madhumita J., Wayne State University, Detroit, Michigan, United States
  • Shah, Mili Jay, Wayne State University, Detroit, Michigan, United States
Introduction

Severe hypoglycemia is associated with altered mental status or loss of consciousness. We report an intriguing patient who had advanced liver disease and presented with severe hypoglycemia and lactic acidosis without any alteration in mental status.

Case Description

57-year-old female with severe decompensated alcoholic liver cirrhosis, ascites and recurrent hepatic hydrothorax presented to the Emergency Room with worsening shortness of breath. She had poor oral intake except for actively consuming ethanol. Chest X ray revealed worsening right hydrothorax. Routine blood tests revealed severe hypoglycemia (serum glucose 28mg/dL, severe anion gap metabolic acidosis (arterial pH 7.11, serum bicarbonate 6mmol/L, anion gap 40 mmol/L) and acute kidney injury with elevation of serum creatinine to 2.2 mg/dl. Subsequent laboratory investigation revealed serum lactic acid level of 23mmol/L. Serum ethylene glycol, methanol, salicylate and acetaminophen levels were undetectable. She had no seizures, malignancy or hypoxia. The patient was alert and oriented. She was hemodynamically stable. There was no evidence of sepsis, tissue hypoperfusion or bowel ischemia. She was not taking any medications which may have led to hypoglycemia or lactic acidosis. The patient was administered intravenous glucose with rapid improvement of her serum glucose and lactate level.

Discussion

This patient had no alteration in mental status despite severe hypoglycemia. Under normal circumstances, the brain primarily depends on glucose as the primary fuel. Studies have shown that under conditions of hypoglycemia and elevated serum lactic acid levels, lactate may serve as an alternative source of energy for the brain. We hypothesize that hyperlactatemia, by providing an alternate energy source, prevented mental status changes in this patient with severe hypoglycemia. Correction of hypoglycemia led to rapid correction of hyperlactatemia suggesting that perhaps lack of glucose may have contributed to hyperlactatemia. We did not identify any obvious cause of hypoglycemia or hyperlactatemia except for her end stage liver disease, continued ethanol use and perhaps also her oliguric acute kidney injury. This patient illustrates that hyperlactatemia may be neuroprotective in severely hypoglycemic patients.