Evaluation of levocarnitine, lactulose, and combination therapy for the treatment of valproic acid-induced hyperammonemia in critically ill patients.

INTRODUCTION: Critically ill patients treated with valproic acid are at risk for hyperammonemic encephalopathy. Both levocarnitine and lactulose, either alone or in combination, have been used for the treatment of hyperammonemia associated with valproic acid, however they have not been directly compared in the literature. The aim of this study was to compare the effect of levocarnitine, lactulose, and combination therapy for the treatment of valproic acid-induced hyperammonemia in critically ill patients. METHODS: This was a retrospective, system-wide, cohort study of critically ill patients who received valproic acid and levocarnitine, lactulose, or combination therapy from January 1, 2012 to October 31, 2019. The primary outcome of the study was the change in ammonia level from baseline to the lowest point within the first 48 h of treatment. Secondary outcomes included the change in ammonia levels within the first 7 days, the incidence of a clinically significant reduction, ICU length of stay, hospital length of stay, and hospital mortality. RESULTS: A total of 371 charts were reviewed and 114 patients (levocarnitine [n = 15], lactulose [n = 72], and combination [n = 27]) were included. No difference in the primary outcome was observed (levocarnitine [11umol/L] vs. lactulose [20 umol/L] vs. combination [23 umol/L], p = 0.605). The incidence of a clinically significant reduction in ammonia levels at 48 h did not differ between groups, nor did mortality. CONCLUSION: In critically ill patients with valproic acid-induced hyperammonemia, there was no significant difference in the reduction in ammonia levels in the first 48 h of treatment between levocarnitine, lactulose, and combination therapy.

Hemodynamic Adverse Effects of Dexmedetomidine and Propofol in a Critically Ill Trauma and Surgical Population: A Retrospective Cohort.

BACKGROUND: Propofol and dexmedetomidine may cause hemodynamic adverse effects (AEs) and more data are needed in a trauma and surgical population. OBJECTIVE: The objective of this study was to evaluate the rate of hemodynamic AEs requiring an intervention between dexmedetomidine and propofol in a critically ill trauma and surgical population. METHODS: This was a retrospective cohort study at a Level 1 trauma center. Intensive care unit patients admitted from October 1, 2017, through October 31, 2018, were divided into two groups: dexmedetomidine or propofol. The primary end point was the proportion of patients who required a therapeutic intervention for a hemodynamic AE within the first 24 hr of initiation of dexmedetomidine or propofol. RESULTS: A total of 800 charts were reviewed and 85 patients (dexmedetomidine [n = 35] and propofol [n = 50]) were included. The study population consisted of Caucasian (86%) males (61%) with a median age of 61 [interquartile range-IQR 48, 72], and 18% and 24% required antihypertensive and vasopressor agents, respectively. No difference in the primary outcome was observed (17 [49%] vs. 27 [54%], p = .624). There was no difference in the overall incidence of hemodynamic AE (18 [51%] vs. 30 [60%], p = .433). Dexmedetomidine patients had a greater decrease in median heart rate (HR) compared with the propofol (23 [IQR 16, 41] vs. 14 [IQR 5, 24] beats/min, p = .002). CONCLUSIONS: The rate of hemodynamic AEs requiring therapeutic interventions was similar between dexmedetomidine and propofol in a critically ill trauma and surgical population; however, dexmedetomidine may be associated with a larger decrease in HR.