Salbutamol induced lactic acidosis; A retrospective analysis of an emergency department

Salbutamol Induced Lactic Acidosis; A Retrospective Analysis of an Emergency Department Introduction: Many studies have shown that serum lactate levels are elevated in circumstances such as hemorrhagic shock, sepsis, acute lung injury, acute liver failure, MODS or ARDS, and there is a relationship between hyperlactatemia and prognosis. Although there are case series and low-participation clinical studies that salbutamol causes lactic acidosis, there are no well-designed clinical studies involving a large number of patients. In our study, we aimed to determine whether there is a change in the lactate level of the patients given salbutamol for treatment. Materials and Method: In our study, the patients who admitted to the Emergency Department of Dokuz Eylül University between 30.10.2016 and 30.04.2017 and the first and second arterial blood gas analysis and serum lactate, pH, pCO2, pO2, HCO3-, BE and K + levels were studied also who were given inhaled salbutamol treatment for any reason within the period blood gas analysis were done were included. Patients who underwent at least 2 arterial blood gas sampling and given a drug with salbutamol active substance were evaluated by means of HBYS. Results: 396 patients were included in the study. Of the patients, 217 (54%) were male and the median age was 75 (IQR 65-83) years. The median value of salbutamol administered for each patient was 15 mg (CAG 10-22.5). Conclusion: There was no difference between lactate levels, before and after the treatment in the patients who were admitted to the emergency department and who were given inhaled salbutamol treatment for any reason. The median time between the two measured arterial blood gases was 352 (CAG 167-776) minutes. The causes of salbutamol administration were as follows; pneumonia (46.2%), COPD exacerbation (29.8%), congestive heart failure (10.9%), hyperkalemia (4.8%), asthma (3%) and other causes (5.3%). The median value of lactate level before treatment with salbutamol was 1.8 mmol / L (1.2-2.7) and after treatment was 1.8 mmol / L (1.1-2.9). Before and after treatment, increase in O2 value (61.7 mmHg, 70.9 mmHg, p <0.01) and decrease in K + value (4.1 mmol / L, 4.1 mmol / L, p <0.01) were observed. There was no difference between the lactate levels and dose of salbutamol more than 25 mg (1.8 mmol / L, 1.8 mmol / L, p = 0.78) or 25 mg and less (1.7 mmol / L, 1.9 mmol / L, p = 0.71). Patients who used metformin (2.5 mmol / L, 2.0 mmol / L, p = 0.02) had a decrease in lactate levels after salbutamol administration, but no difference was found between the patients' lactate values (1.7 mmol / L, 1.8 mmol / L, p = 0.43) who didn't use metformin. When the time elapsed between the evaluation of two blood gases was less than 2 hours (1.7 mmol / L, 1.8 mmol / L, p = 0.65) and the time elapsed between two blood gases was 2 hours or more (2.2 mmol / L, 2.4 mmol / L, p = 0.20) no difference between the lactate values of the patients were seen. Keywords: Salbutamol, lactic acidosis, emergency departments, lactic acid