UNLABELLED: Propofol infusion syndrome (PIS) is defined by arrhythmia, rhabdomyolysis, lactic acidosis, and unrecognized leads to death. We sought to determine the incidence of PIS in trauma patients and evaluate the efficacy of a prospective screening protocol in this patient population. MATERIALS AND METHODS: In Phase I of the before-and-after study (1st January, 2005-31st December, 2005), trauma patients who received propofol were evaluated. Records were reviewed for demographics, injury severity, propofol time, dose, and rates, laboratory values, and adverse events. Patients were identified with PIS based on two of the following criteria: (1) cardiac arrhythmia/collapse, (2) metabolic acidosis, (3) rhabdomyolysis, and (4) acute kidney injury. Phase II (1st January, 2006-31st December, 2011) consisted of a prospective screening protocol (elevated lactate or creatine phosphokinase (CPK)) to identify patients at risk for PIS. RESULTS: 207 patients were identified in Phase I. 6 (2.9%) developed PIS with a 50% mortality. No differences were seen in age, gender, or mechanism. PIS patients were more injured (median ISS 44 vs 26, p=0.04; median head AIS 5 vs 4, p=0.003) and received more propofol (median 50,350 vs 9770 mg, p=0.001) with longer infusion times (413 vs 65 h, p=0.001). Sodium, creatinine, and CPK levels were higher in those that developed PIS (160 vs 145 mmol/L, p=0.001; 4.3 vs 1.1mg/dL, p=0.005; 59,871 vs 520 U/L; p=0.002). Pre-screening PIS incidence was 2.9% (6/207), but after screening (January 2006) the incidence dropped to 0.19% (2/1038, p<0.001). CONCLUSIONS: PIS is a morbid and lethal entity associated with sedation of critically injured patients. A simple screening procedure utilizing serum CPK (<5000 U/L) can essentially eliminate the development of PIS.
UNLABELLED: Propofol infusion syndrome (PIS) is defined by arrhythmia, rhabdomyolysis, lactic acidosis, and unrecognized leads to death. We sought to determine the incidence of PIS in traumapatients and evaluate the efficacy of a prospective screening protocol in this patient population. MATERIALS AND METHODS: In Phase I of the before-and-after study (1st January, 2005-31st December, 2005), traumapatients who received propofol were evaluated. Records were reviewed for demographics, injury severity, propofol time, dose, and rates, laboratory values, and adverse events. Patients were identified with PIS based on two of the following criteria: (1) cardiac arrhythmia/collapse, (2) metabolic acidosis, (3) rhabdomyolysis, and (4) acute kidney injury. Phase II (1st January, 2006-31st December, 2011) consisted of a prospective screening protocol (elevated lactate or creatine phosphokinase (CPK)) to identify patients at risk for PIS. RESULTS: 207 patients were identified in Phase I. 6 (2.9%) developed PIS with a 50% mortality. No differences were seen in age, gender, or mechanism. PIS patients were more injured (median ISS 44 vs 26, p=0.04; median head AIS 5 vs 4, p=0.003) and received more propofol (median 50,350 vs 9770 mg, p=0.001) with longer infusion times (413 vs 65 h, p=0.001). Sodium, creatinine, and CPK levels were higher in those that developed PIS (160 vs 145 mmol/L, p=0.001; 4.3 vs 1.1mg/dL, p=0.005; 59,871 vs 520 U/L; p=0.002). Pre-screening PIS incidence was 2.9% (6/207), but after screening (January 2006) the incidence dropped to 0.19% (2/1038, p<0.001). CONCLUSIONS: PIS is a morbid and lethal entity associated with sedation of critically injured patients. A simple screening procedure utilizing serum CPK (<5000 U/L) can essentially eliminate the development of PIS.