Extending surgeon response times in tier 2 traumas does not adversely affect patient outcomes.

BACKGROUND: The presence of a trauma surgeon during patient resuscitations is required at most American College of Surgeons-verified trauma centers despite little evidence showing improved patient outcomes in the less-than-critically injured (Tier 2) trauma patients. This study was designed to identify the impact of extending required surgeon response times on outcomes in tier 2 trauma patients. METHODS: An American College of Surgeons-verified level 2 trauma center extended the maximum allowed surgeon response time for tier 2 activations from 60 min to 120 min on November 1, 2011. Surgeon response time and patient outcomes of the retrospective control group (January 1, 2008-October 31, 2011) were then compared with the prospective test group (November 1, 2011-December 31, 2014). Primary outcomes included mortality and hospital length of stay (HLOS). Secondary outcomes were emergency department length of stay, and time from ED arrival to CT scan. A subset analysis of all patients evaluated by a surgeon within 60 min of arrival versus those evaluated by a surgeon after 60 min was also performed. RESULTS: The control and test groups were composed of 757 and 792 patients, and their mean injury severity score was 9.0 and 6.0, respectively. Emergency department length of stay showed a statistically significant increase of 12 min, whereas HLOS was unchanged throughout the study. Mortality was not significantly different between the groups. Subset analysis revealed a median surgeon arrival time of 15 min in the <60-min group and 85 min in the >60-min group, whereas the injury severity score, HLOS, and mortality were not significantly different between these subsets. No correlation existed between these outcomes and surgeon arrival time. CONCLUSIONS: Doubling required surgeon response time in tier 2 trauma patients does not produce negative outcomes in this patient group. Mandatory surgeon response times in similar patient groups can be re-evaluated to allow for greater flexibility of a limited surgeon workforce while still providing safe care.

Low-dose warfarin for prevention of symptomatic thromboembolism after orthopedic surgery.

BACKGROUND: Warfarin dosing with a target international normalized ratio (INR) range of 1.5-2.5 has not been reported as adequate for venous thromboembolism (VTE) prophylaxis after total knee (TKR) and total hip replacement (THR) surgery. OBJECTIVE: To evaluate the rate of symptomatic VTE after TKR and THR surgery using a low-dose (INR 1.5-2.5) warfarin protocol started the evening before surgery compared with a literature cohort treated with enoxaparin. METHODS: TKR/THR patients treated with a 21-day low-dose warfarin protocol were followed via a consecutive observational design. Main outcome measures were symptomatic VTE and pulmonary embolism (PE), with major bleeds and death as secondary outcomes. Low-dose warfarin was compared with a literature cohort of patients treated with enoxaparin who received enoxaparin for a similar length of time and was evaluated for the same outcomes. Cohort event rates were derived as a weighted average using the DerSimonian model. RESULTS: VTE, PE, bleeds, and deaths in the low-dose warfarin group were 8 (1.04%), 4 (0.52%), 8 (1.04%), and 4 (0.52%), respectively. The cohort weighted average values were 35 (1.33%), 19 (0.72%), 65 (2.46%), and 18 (0.67%), respectively. Odds ratios for low-dose warfarin for VTE, PE, and VTE plus PE were 0.778 (95% CI 0.36 to 1.68), 0.717 (0.24 to 2.11), and 0.754 (0.41 to 1.42), respectively, all nonsignificant. Odds ratios for bleeds and death were 0.420 (0.20 to 0.87; p = 0.02) and 0.756 (0.26 to 2.24; NS), respectively. CONCLUSIONS: For this evaluation, low-dose warfarin was comparable to the enoxaparin cohort for development of VTE, PE, and VTE+PE. Incidences of bleeds in the enoxaparin cohort were significantly higher than in patients receiving low-dose warfarin.

Rhabdomyolysis causing AV blockade due to possible atorvastatin, esomeprazole, and clarithromycin interaction.

OBJECTIVE: To report rhabdomyolysis (RML) causing third-degree atrioventricular block secondary to a possible interaction between atorvastatin, esomeprazole, and clarithromycin. CASE SUMMARY: A 51-year-old white woman presented to the emergency department with severe weakness, near syncope, shortness of breath, and chest pain. On admission, her electrocardiogram demonstrated bradycardia (40 beats/min) and third-degree heart block. A creatine kinase (CK) level was >7000 U/L. Her medication history was significant for long-term use of atorvastatin (>1 y), a 6-week history of esomeprazole use, and three 500-mg doses of clarithromycin just prior to admission. Her symptoms of weakness, shortness of breath, and chest pain coincided with starting the esomeprazole. During her hospitalization, the woman required pacemaker placement and her CK continued to rise to >40,000 U/L. Screening for other causes of RML, such as thyrotoxicosis, infection, and immune or hepatic diseases, was negative. She gradually improved over a 26-day hospitalization. DISCUSSION: This is a case of RML resulting in third-degree atrioventricular blockade. An objective causality assessment of the adverse reaction via the Naranjo probability scale revealed a probable association with atorvastatin and a possible association with esomeprazole and clarithromycin. The pharmacokinetic profiles of these agents suggest that a possible contribution to this reaction was P-glycoprotein (PGP) inhibition by esomeprazole altering atorvastatin's normally significant first-pass clearance. CONCLUSIONS: PGP drug interactions with atorvastatin and other hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) may be associated with unreported risks for RML. Further investigation into PGP impact on HMG-CoA appears warranted.