ABSTRACT
We have experienced two patients with alcoholic lactic acidosis complicated with liver disease and diabetes mellitus who were successfully treated. They developed hypoglycemia, dehydration, lactic acidosis, and renal failure after drinking a large volume of alcohol without eating for 1 week before onset. Acidosis was thought to be directly related to excessive alcoholic intake, because it was no associated with severe liver failure and rhabdomyolysis. During monitoring of respiratory and circulatory functions, a rapid infusion of fluids adjusting to water and electrolyte imbalance was performed. A mixture of physiological saline and 5% glucose solution was thought to be effective in these cases. Patients recovered from renal failure and lactic acidosis without hemodialysis. Our experience will hopefully provide a key to successful treatment of fatal alcoholic lactic acidosis.
Subject(s)
Acidosis, Lactic/etiology , Alcoholism/complications , Diabetes Mellitus, Type 2/etiology , Liver Diseases, Alcoholic/etiology , Acidosis, Lactic/physiopathology , Acidosis, Lactic/rehabilitation , Aged , Alcoholism/physiopathology , Alcoholism/rehabilitation , Combined Modality Therapy , Critical Care , Diabetes Mellitus, Type 2/physiopathology , Diabetes Mellitus, Type 2/rehabilitation , Fluid Therapy , Glucose Solution, Hypertonic/administration & dosage , Humans , Insulin/administration & dosage , Liver/physiopathology , Liver Diseases, Alcoholic/physiopathology , Liver Diseases, Alcoholic/rehabilitation , Liver Function Tests , Male , Middle Aged , Water-Electrolyte Balance/physiologyABSTRACT
During an incremental exercise test, three consequences of the onset of anaerobic metabolism can be observed: rise in blood lactate (lactate threshold, LT); fall in standard bicarbonate (lactic acidosis threshold, LAT); nonlinear increase in CO2 output (V-slope gas exchange threshold, GET). We compared these thresholds in 31 patients with COPD. We found that the GET and LAT overestimated the LT. A better relationship was found between LAT and GET, even though GET was significantly higher than LAT (by 124 ml/min; p < 0.0001). However, since the bias is appreciably greater at lower LAT values (likely because VCO2 kinetics are slower than VO2 kinetics), we separated the studies into two groups: (A) tests where LAT occurred within the first 2 min of the increasing work rate period, and (B) tests where LAT occurred after 2 min. For Group A, there was a substantial bias between LAT and GET (323 ml/min, p < 0.0001), whereas the bias was much smaller (only 5.4%, though statistically significant) for Group B (57 ml/min, p < 0.01). We conclude that when lactic acidosis occurs after the first 2 min of incremental exercise, the GET closely approximates the point at which blood bicarbonate begins to fall.
