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Objectives: To report the prevalence of, and evaluate risk factors for, the development of hypertriglyceridemia (defined as a serum triglyceride level of > 400 mg/dL) in patients with coronavirus disease 2019 who received propofol. Design: Single-center, retrospective, observational analysis. Setting: Brigham and Women’s Hospital, a tertiary academic medical center in Boston, MA. Patients: All ICU patients who with coronavirus disease 19 who received propofol between March 1, 2020, and April 20, 2020. Interventions: None. Measurements and Main Results: The major outcome of this analysis was to report the prevalence of, and risk factors for, the development of hypertriglyceridemia in patients with coronavirus disease 19 who received propofol. Minor outcomes included the development of acute pancreatitis and description of propofol metrics. Of the 106 patients that were included, 60 (56.6%) developed hypertriglyceridemia, with a median time to development of 46 hours. A total of five patients had clinical suspicion of acute pancreatitis, with one patient having confirmatory imaging. There was no difference in the dose or duration of propofol in patients who developed hypertriglyceridemia compared with those who did not. In the patients who developed hypertriglyceridemia, 35 patients (58.5%) continued receiving propofol for a median duration of 105 hours. Patients who developed hypertriglyceridemia had elevated levels of inflammatory markers. Conclusions: Hypertriglyceridemia was commonly observed in critically ill patients with coronavirus disease 2019 who received propofol. Neither the cumulative dose nor duration of propofol were identified as a risk factor for the development of hypertriglyceridemia. Due to the incidence of hypertriglyceridemia in this patient population, monitoring of serum triglyceride levels should be done frequently in patients who require more than 24 hours of propofol. Many patients who developed hypertriglyceridemia were able to continue propofol in our analysis after reducing the dose.

Background: Phenobarbital offers several possible advantages to benzodiazepines including a longer half-life and anti-glutamate activity, and is an alternative for the treatment of alcohol withdrawal. The objective of this analysis was to evaluate the safety and efficacy of a phenobarbital protocol for alcohol withdrawal newly implemented at our institution. Methods: This was a single-center, retrospective analysis of adult patients admitted to the medical/surgical/burn/trauma intensive care unit (ICU) with or at risk of severe alcohol withdrawal. Patients who were admitted prior to guideline implementation and received scheduled benzodiazepines (PRE) were compared to those who received phenobarbital post guideline update (POST). The primary outcome was ICU length of stay (LOS). Results: Upon analysis, 68 patients in the PRE and 64 patients in the POST were identified for inclusion. The median APACHE II score was significantly higher in the POST (4.5 [3:9] vs 10 [5:13], P < 0.001). ICU (2 [1:2] vs 2 [2:5], P = 0.002) and hospital (4.5 [3:6] vs 8 [6:12], P < 0.001) LOS were significantly longer in the POST. There was no difference in mortality or duration of mechanical ventilation. More patients required propofol or dexmedetomidine on day one in the POST ( P < 0.001). Conclusion: Patients in the POST had significantly longer ICU and hospital LOS, and had a higher baseline severity of illness. Future research is needed to evaluate the efficacy and safety of phenobarbital compared to benzodiazepines for severe alcohol withdrawal.

Direct oral anticoagulants (DOACs), particularly direct factor Xa inhibitors, have been associated with prolongation of the prothrombin time and the international normalized ratio (INR). Although DOACs do not require monitoring, elevations in the INR have been reported in in vitro and observational studies. The literature surrounding the extent of elevation and the clinical significance is limited. The objective of this study was to quantify the degree of INR elevation in hospitalized patients receiving apixaban. This was a single-center, retrospective, observational analysis of adult patients who received at least 1 dose of apixaban during their hospital admission and had at least 1 INR sample collected prior to and following administration. The major end point of this study was to characterize the effect of apixaban on the INR by determining the percentage of patients with an INR higher than our laboratory defined normal (defined as INR > 1.1). Minor end point outcomes included the incidence of an INR increase >0.3 from baseline INR and additional patient-specific factors that may influence INR elevation. Seventy-nine patients were included in the analysis. On day 1 of therapy, the median (interquartile range, IQR) INR was 1.4 (1.3:1.6) with 84.5% of patients having an elevated INR. The median (IQR) INR increased to 1.5 (1.4:1.6) and 1.7 (1.5:1.9) on day 4 and day 7, respectively. Of patients whose INR increased by more than 0.3, the median (IQR) change in INR from baseline was 0.5 (0.4:0.6). Apixaban is associated with a notable increase in INR in hospitalized patients, although it is not clear the clinical impact of the increase. Although literature does not support monitoring INR as a marker of apixaban activity, it is important for clinicians to understand the association apixaban has on the INR to avoid inappropriate interpretation of routine coagulation assays.