Endocrine Abstracts

Lactic acidosis defined by a lactate >4 mmol/l, pH <7.35 and bicarbonate <20mmol/l is the commonest cause of metabolic acidosis in hospitalised patients. It is grouped into type A (hypoperfusion) and type B (non-hypoperfusion). Alcoholic lactic acidosis is a rare type B form. We report an obfuscated severe case in a patient with a history of alcohol abuse.

Case report: 36 year old female presented with myalgia, collapse and impaired conscious level. Examination: cachectic, dehydrated, sinus tachycardia 120/minute, blood pressure 100/60 mmHg, tachypnoeic 28 per minute. Alcohol consumption was denied. Investigations: pH 6.76, bicarbonate 3.1 mmol/l, lactate 23.7 mmol/l, ketones 2.3 mmol/l, glucose 5.9 mmol/l, sodium 142 mmol/l, chloride 103 mmol/l, potassium 5.7 mmol/l, urea 3.6 mmol/l, creatinine 111 umol/l, eGFR 48 ml/per min, osmolality 317 mmol/Kg, CRP 2 mg/l, amylase 411 U/l, corrected anion gap 33 mmol/l, toxicology screen negative for ethanol, ethyl alcohol and methanol. The initial diagnosis was antifreeze ingestion (latter two results not available at that time). Intensive fluid resuscitation with Hartmann’s, 10% dextrose and fomeprizole resulted in correction of clinical and laboratory abnormalities within 48 hours. Endocrine opinion was sought on the aetiology of the lactic acidosis. The patient confirmed chronic and acute (3 days prior to admission) consumption of whisky with subsequent anorexia.

Discussion: Metabolism of ethanol is to acetaldehyde and then acetate by the NAD+ cofactor enzymes alcohol dehydrogenase and aldehyde dehydrogenase respectively. The conversion results in increased generation of NADH which alters the redox reaction catalysed by lactic dehydrogenase to favour pyruvate to lactate conversion. The half-life of ethanol (4-5h), resulting in its absence on toxicology screen, plus initial denial of its consumption confounded the diagnosis. The rapid recovery was attributed to the absence of co-pathologies.