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Background Bile duct injury (BDI) during cholecystectomy requiring biliary enteric reconstruction (BER) is associated with increased risk of postoperative mortality and substantive increases in costs of care. The impact of the timing of repair on overall costs of care is poorly understood. Materials and methods The Healthcare Cost and Utilization Project Florida State databases (2006-2015) were queried to identify patients undergoing BER within 1-y of cholecystectomy performed for benign biliary disease. Patients were then categorized by the time interval between cholecystectomy to BER: early (≤3 d), intermediate (4 d to 6 wk), or delayed (>6 wk). By repair timing strategy, 1-y outcomes were aggregated, including charges, inpatient costs, aggregate length of stay, and inpatient mortality. Results Of 563,887 patients undergoing cholecystectomy, 1168 required a BER (0.21%) within 1-y of cholecystectomy. Early BER was performed in 560 patients (47.9%), intermediate BER in 439 patients (37.6%), and delayed BER in 169 (14.5%) patients. On multivariable analysis adjusting for patient, procedure, and facility factors, intermediate BER demonstrated an increased risk of mortality (odds ratio 2.04, 95% confidence interval [CI]: 1.16-3.56) and increased aggregate inpatient cost (+$12,472; 95% CI: $6421-$18,524) relative to early BER. There was no notable difference in adjusted risk of inpatient mortality between the early and delayed BER cohorts (odds ratio 0.90; 95% CI: 0.32-1.25), but delayed BER was associated with increased aggregate inpatient costs (+$45,111; 95% CI: $36,813-$53,409). Conclusions When compared with delayed BER, early repair was associated with shorter aggregate inpatient hospitalization without increased postoperative mortality. Intermediate timing of repair is associated with increased costs and risk of mortality.

Background Atrial fibrillation (AF) with rapid ventricular rate (RVR; heart rate >100) in noncardiac postoperative surgical patients is associated with poor outcomes. The objective of this study was to evaluate the practice patterns of AF management in a surgical intensive care unit to determine practices associated with rate and rhythm control and additional outcomes. Materials and methods Adult patients (≥18 y) admitted to the surgical intensive care unit (SICU) from June 2014 to June 2015 were retrospectively screened for the development of new-onset AF with RVR. Demographics, hospital course, evaluation and treatment of AF with RVR, and outcome were evaluated and analyzed. Results Thousand seventy patients were admitted to the SICU during the study period; 33 met inclusion criteria (3.1%). Twenty-six patients (79%) had rate and rhythm control within 48 h of AF with RVR onset. β-Blockers were the most commonly used initial medication (67%) but were successful at rate and rhythm control in only 27% of patients (6/22). Amiodarone had the highest rate of success if used initially (5/6, 83%) and secondarily (11/13, 85%). Failure to control rate and rhythm was associated with a greater likelihood of comorbidities (100% versus 57%; P = 0.06). Conclusions New-onset AF with RVR in the noncardiac postoperative patient is associated with a high mortality (21%). Amiodarone is the most effective treatment for rate and rhythm control. Failure to establish rate and rhythm control was associated with cardiac comorbidities. These results will help to form future algorithms for the treatment of AF with RVR in the SICU.

Background The Advanced Surgical Skills for Exposure in Trauma (ASSET) course was developed to address limited experience of residents and practicing surgeons (PS) in rapid exposure of major blood vessels for trauma. This one day, case based, scenario driven, fresh cadaver dissection course emphasizes rapid surgical exposure of the vasculature of the neck, chest, abdomen, pelvis and extremities with additional focus on fasciotomies and pelvic packing. Contained herein are the results of the first 25 courses. Methods Data collected from 25 ASSET courses conducted between September 2010 and February 2012 included self-reported comfort level (5 point Likert scale) with each of 25 specific skills before and upon completion of the course, and evaluation of the course content. Statistical analysis was accomplished using the Student t -test with α set at P Results Ninety-one surgical trainees and 123 PS were taught at 11 ASSET sites. Self-assessed comfort levels for all 25 queried skills and exposures improved significantly over baseline with P values ranging from 1.6 × 10 −7 to 3.9 × 10 −41 . Participants gained new knowledge (4.83 on 5 point scale); learned new techniques (4.83), felt better prepared to expose traumatically injured vessels (4.88), and would recommend the course to a colleague (4.92). Conclusions The ASSET course was well received and significantly improved self-reported confidence in the exposures needed to care for trauma in both surgical trainees and PS. Ongoing experience with this course will enable more comprehensive psychometric analysis and further validation of this curriculum.

Background. Recent evidence suggests that hyperlactatemia in shock may reflect accelerated aerobic glycolysis linked to activity of the Na + , K + -ATPase rather than hypoxia. Epinephrine stimulates glycolysis in resting muscle largely by stimulating Na + , K + -ATPase activity. This study evaluates the effects of hemorrhagic shock, with and without combined α- and β-adrenergic receptor blockade, on lactate production, glycogenolysis, Na + –K + pump activity, and high-energy phosphates in rat skeletal muscle. Methods. Male Sprague–Dawley rats in four treatment groups were studied: unhemorrhaged control not receiving blockers (CN), controls receiving blockers (CB), shocked animals not receiving blockers (SN), and shocked rats receiving blockers (SB). Shocked rats (SN and SB) were bled to a MAP of 40 mm Hg, maintained for 60 min. Blocker groups (CB and SB) received propranolol and phenoxybenzamine. Arterial blood was drawn for plasma lactate, epinephrine, norepinephrine, and gas analysis. Lactate, glycogen, glucose 6-phosphate, ATP, phosphocreatine, and intracellular Na + and K + were determined in extensor digitorum longus and soleus muscles. For comparison, muscles were exposed to epinephrine and/or ouabain in vitro . Results. With the exception of P a CO 2 , HCO 3 , and base excess in the SN group, no significant differences in arterial blood gas parameters were noted. Adrenergic blockade significantly reduced plasma lactate concentration. In shocked rats, adrenergic blockade significantly reduced muscle lactate and glucose 6-phosphate accumulation. Intracellular Na + :K + ratio was decreased in SN rats, implying increased Na + –K + pump activity. Adrenergic blockade raised the intracellular Na + :K + ratio in shocked animals, implying decreased pump activity. Epinephrine exposure in vitro stimulated muscle lactate production, raised glucose 6-phosphate content, and significantly reduced soleus phosphocreatine stores. Conclusions. Neither hypoxia nor defective oxidative metabolism appeared responsible for increased glycolysis during hemorrhagic shock. Adrenergic blockade concurrently reduced plasma lactate, muscle levels of lactate and glucose 6-phosphate, and muscle Na + –K + pump activity during shock. Rapid skeletal muscle aerobic glycolysis in response to increased plasma epinephrine levels may be an important contributor to increased glycolysis in muscle and increased plasma lactate during hemorrhagic shock.