Use of Iatrogenic Lipid Emulsion and Subsequent Plasmapheresis for the Treatment of Amitriptyline Overdose.

Plasmapheresis for the treatment of hypertriglyceridemia is relatively uncommon and mostly reported either in patients experiencing hypertriglyceridemia-induced acute pancreatitis or patients with therapy-resistant familial hypercholesterolemia. Standard therapies for hypertriglyceridemia include dietary modification and lipid-lowering medication. For severe hypertriglyceridemia, the risk of pancreatitis increases significantly as triglyceride levels increase above 1000 mg/dL, and current therapies are unable to reduce triglyceride levels rapidly enough. Here, we report a case of a 48-year-old male patient who presented to the emergency department due to an amitriptyline overdose. In addition to being started on IV sodium bicarbonate therapy, an intravenous 20% fat emulsion bolus at 1.5 mL/kg was administered followed by 0.25 mL/kg/min infusion for 4 hours as a strategy to absorb lipophilic amitriptyline. Two days posttreatment, he was noted to have substantial hypertriglyceridemia (serum triglycerides: 6,475 mg/dL). His amylase was within the normal range at 37 U/L (reference range: 20-100 U/L), his lipase was low at 40 U/L (reference range: 75-390 U/L), and he was without evidence of any clinical sequelae secondary to hypertriglyceridemia (e.g., pancreatitis). Due to the severity of his hypertriglyceridemia, plasmapheresis was initiated urgently for rapid reduction in serum triglyceride levels to prevent pancreatitis and end-organ damage. He underwent a 1-plasma volume exchange with 5% albumin as the replacement fluid. This reduced his triglyceride levels to 185 mg/dL (reference range: 3-149 mg/dL). His symptoms secondary to his amitriptyline overdose were also resolved. Here, we report a 2-step process of intravenous lipid emulsion followed by plasmapheresis for amitriptyline overdose.

Five-Year Outcomes After Implementing a Pain, Agitation, and Delirium Protocol in a Mixed Intensive Care Unit.

Objective: Assess for continued improvements in patient outcomes after updating our institutional sedation and analgesia protocol to include recommendations from the 2013 Society of Critical Care Medicine (SCCM) Pain, Agitation, and Delirium (PAD) guidelines. Methods: Retrospective before-and-after study in a mixed medical/surgical intensive care unit (ICU) at an academic medical center. Mechanically ventilated adults admitted from September 1, 2011 through August 31, 2012 (pre-implementation) and October 1, 2012 through September 30, 2017 (post-implementation) were included. Measurements included number of mechanically ventilated patients, APACHE IV scores, age, type of patient (medical or surgical), admission diagnosis, ICU length of stay (LOS), hospital LOS, ventilator days, number of self-extubations, ICU mortality, ICU standardized mortality ratio, hospital mortality, hospital standardized mortality ratio, medication data including as needed (PRN) analgesic and sedative use, and analgesic and sedative infusions, and institutional savings. Results: Ventilator days (Pre-PAD = 4.0 vs. Year 5 post = 3.2, P < .0001), ICU LOS (Pre-PAD = 4.8 days vs. Year 5 post = 4.1 days, P = .0004) and hospital LOS (Pre-PAD = 14 days vs. Year 5 post = 12 days, P < .0001) decreased after protocol implementation. Hospital standardized mortality ratio (Pre-PAD = 0.69 vs. Year 5 post = 0.66) remained constant; while, APACHE IV scores (Pre-PAD = 77 vs. Year 5 post = 89, P < .0001) and number of intubated patients (Pre-PAD = 1146 vs. Year 5 post = 1468) increased over the study period. Using the decreased ICU and hospital LOS estimates, it is projected the institution saved $4.3 million over the 5 years since implementation. Conclusions: Implementation of an updated PAD protocol in a mixed medical/surgical ICU was associated with a significant decrease in ventilator time, ICU LOS, and hospital LOS without a change in the standardized mortality ratio over a five-year period. These favorable outcomes are associated with a significant cost savings for the institution.

Propylene glycol-associated renal toxicity from lorazepam infusion.

OBJECTIVES: Using data from patients who developed elevations in serum creatinine concentrations while receiving continuous-infusion lorazepam, we sought to determine the correlations between the magnitude of serum creatinine concentration rise and each of the following variables: serum propylene glycol level, cumulative lorazepam dose, and duration of lorazepam administration. An additional objective was to identify clinical markers for propylene glycol toxicity. DESIGN: Retrospective chart review. SETTING: Medical-surgical intensive care unit and burn unit at a university hospital. PATIENTS: Eight patients who developed elevations in serum creatinine concentrations while receiving continuous-infusion lorazepam (range 2-28 mg/hr). MEASUREMENTS AND MAIN RESULTS: The mean cumulative dose of lorazepam was 4305 mg (range 1200-10,920 mg), and the mean propylene glycol level determined at the time of peak serum creatinine concentration was 1103 microg/ml (range 186-3450 microg/ml). Serum creatinine concentrations increased in all eight patients during lorazepam infusion and decreased in seven within 3 days after stopping infusion. A weak-to-moderate correlation existed between the magnitude of the rise in serum creatinine concentration and propylene glycol level (r=0.53). A weak-to-moderate correlation also was identified between cumulative lorazepam dose and magnitude of serum creatinine concentration rise (r=0.43), and a strong-to-moderate correlation was found between duration of lorazepam infusion and magnitude of serum creatinine concentration rise (r=0.60). Propylene glycol levels were strongly correlated with both serum osmolality and osmol gap. CONCLUSION: The patients' increased serum creatinine concentrations are likely to have resulted from exposure to propylene glycol as a result of lorazepam infusion. Serum osmolality and osmol gap may be useful markers for propylene glycol toxicity.