Abstract
A case of lactic acidosis in diabetes presumably induced by a large intake: of alcoholic beverage (whisky) and concomitant pneumonia is reported.
A 41-yr-old female was admitted to hospital due to disturbance of consciousness. She has had insulin dependent type diabetes for 5 years, following its detection by ketoacidosis coma.
On the day before admission, she had injected her usual dose of insulin and taken a bus trip. On the way, she drank a large amount of whisky. Nausea, vomiting, lethargy and general muscular pain ensued and she was taken to a local doctor's office. At that time her blood glucose was 676 mg/dl and her urine ketone was negative. In spite of an additional injection of insulin, her consciousness gradually deteriorated. She fell into an agitated state and was transferred to our ward. On admission, she was in a delirious condition. High fever and moist rales over the entire lungs were recognized. Her blood glucose was 340 mg/dl and blood gas analysis revealed the presence of hypoxia and metabolic acidosis, paO2 56.8, pCO2 14.2 mmHg, base excess -21.9 mEq/L, blood pH 7.182 and anion gap 26.6 mEq/L. Urine ketone was negative. Blood lactate was 5.27 mM, pyruvate O. 124 mM and the lactate/pyruvate ratio 42.6, indicating abnormal accumulation of lactate in the blood. In spite of oxygen supply, she rapidly fell into deep coma. Chest X-P revealed severe extensive pneumonia. Insulin, sodium bicarbonate, Tris buffer and antibiotics were administered and respiration was controlled with a respirator by the continuous positive pressure method. The patient recovered from the deep coma in 4 days. Abnormal elevation of blood urea nitrogen and creatinine persisted for 3 weeks, but finally normalized. LDH and amylase levels in the blood were elevated during the acute phase. After improvement, there was no impairment of renal and hepatic functions. Following the acute phase, her diabetes was found to be of the brittle type. There was virtually no response of blood C-peptide during the oral glucose tolerance test and the 24-hr urine C-peptide was almost undetectable.
Lactic acidosis in diabetes occurs mainly in patients treated with biguanide drugs. However, our patient did not take any biguanide. Her large intake of ethanol is thus considered likely as the precipitating cause of the lactic acidosis, and hypoxia due to severe pneumonia appears to have aggravated lactate accumulation.
