Achieving Mastery of General Surgery Operative Skill in the Army Healthcare System.

INTRODUCTION: Operative case volumes for military surgeons are reported to be significantly lower than civilian counterparts. Among the concern that this raises is an inability of military surgeons to achieve mastery of their craft. MATERIAL AND METHODS: Annual surgical case reports were obtained from seven Army military treatment facilities (MTF) for 2012-2016. Operative case volume and cumulative operative time were calculated for active duty general surgeons and for individual MTFs. Subgroup analyses were also performed based upon rank. Results were extrapolated to calculate the amount of time it would take to reach a cumulative of 10,000 hours of operative time (the a priori definition for achieving mastery). RESULTS: One hundred and two active duty general surgeons operated at the seven MTFs during the study period and met the inclusion criteria. The average surgeon performed 108 ± 68 cases/year. The average surgeon operated 122 ± 82 hours/year. At this rate, it would take over 80 years to reach mastery of surgery. When stratified based upon rank, Majors averaged 113 ± 75 hours/year, Lieutenant Colonels averaged 170 ± 100 hours/year, and Colonels averaged 136 ± 101 hours/year (p < 0.05). When stratified based upon individual MTF, surgeons at the busiest facility averaged 187 ± 103 hours/year and those at the least busy facility averaged 85 ± 56 hours/year (p < 0.05). CONCLUSIONS: Obtaining mastery of general surgery is a nearly impossible proposition given the current care models at Army MTFs. Alternative staffing and patient care models should be developed if Army surgeons are to be masters at their craft.

Hydrogen sulfide improves resuscitation via non-hibernatory mechanisms in a porcine shock model.

BACKGROUND: Hydrogen sulfide (H2S) has been demonstrated to induce a "suspended animation-like" state in rodent models by reversible inhibition of cellular respiration and marked metabolic suppression and has been proposed as a potential pharmacologic adjunct to resuscitation from shock states. There are few data currently available about the mechanisms and efficacy of H2S in larger animals or humans. We examined H2S as a pharmacologic adjunct to resuscitation in a porcine model of severe traumatic shock. METHODS: Twenty-one adult swine were assigned to three study arms: sham, H2S, and saline vehicle controls (SC). All pigs underwent laparotomy and instrumentation, and the two study arms then underwent a 35% controlled hemorrhage followed by 50 min of truncal ischemia via aortic cross-clamp. H2S (5 mg/kg) or saline was administered immediately before reperfusion, followed by 6 h of resuscitation. Resuscitation requirements, laboratory parameters, end-organ histology, and inflammatory product gene expression (by reverse transcription-polymerase chain reaction) were measured and compared between groups. RESULTS: All animals survived to the 6-h postresuscitation time point. Both treatment arms demonstrated severe shock characterized by fluid and vasopressor requirements, metabolic acidosis, and hypotension compared with sham animals. Animals treated with H2S demonstrated significantly lower resuscitative requirements (total epinephrine 727 versus 3052 µg; P < 0.05), decreased fluid requirements, and lower serum lactate levels (7 versus 10 mmol/L) versus SC. Cardiac output was slightly decreased with H2S treatment but all other hemodynamic and metabolic parameters were equivalent between H2S and C groups. Serum liver and kidney biomarkers were unchanged, but administration of H2S was associated with a significant improvement in histopathologic liver and kidney injury scores compared with SC (both P < 0.05). Both study groups demonstrated significantly increased gene expression of hypoxia-inducible factor 1α and nitric oxide synthase (endogenous nitric oxide synthase, inducible nitric oxide synthase [iNOS]2, iNOS3) relative to sham animals. However, H2S was associated with increased expression of hypoxia-inducible factor 1α and decreased iNOS2 levels compared with SC. CONCLUSIONS: Administration of H2S in a large-animal model of severe traumatic shock resulted in a significant decrease in resuscitative requirements, decreased metabolic acidosis, and less end-organ histologic injury compared with standard resuscitation. H2S did not induce profound metabolic suppression as seen in rodents, and appears to have alternative mechanisms of action in large animals.

Flutamide fails to reduce resuscitation requirements in a porcine ischemia-reperfusion model.

BACKGROUND: Hemorrhagic shock and subsequent resuscitation can lead to ischemia-reperfusion injury, followed by multiorgan failure and death. Flutamide, a vasoactive nonsteroidal antiandrogen compound, is thought to improve tissue and organ perfusion. We tested whether administration of flutamide-cyclodextrin (FLU-CYD) alters physiologic parameters or resuscitation requirements in a porcine model of severe acidosis and shock secondary to combined hemorrhage + ischemia-reperfusion injury. METHODS AND MATERIALS: Fifteen male pigs underwent a 35% blood-volume hemorrhage. Ischemia was induced by cross-clamping the supraceliac aorta for 50 min followed by reperfusion and resuscitation. FLU-CYD complex was administered during aortic clamping. Fluid resuscitation and epinephrine were titrated by protocol to maintain mean arterial pressure ≥40 mm Hg for 6 h. Sequential laboratory results were obtained and serum levels of FLU and 2-hydroxy-flutamide (FLUOH) were measured by mass spectrometry. RESULTS: Mean requirements for injured control swine were 14.6 (± 1.21 standard error of the mean [SEM]) L crystalloid saline and 0.59 (± 0.29 SEM) g epinephrine, compared with 16.30 (± 1.33 SEM) L and 0.54 (± 0.16 SEM) g, respectively, in the FLU-CYD group (both P > 0.05). There were no significant differences in central hemodynamics between control and experimental groups. No significant differences for pH, bicarbonate, fibrinogen, or international normalized ratio were evident. FLU-CYD resuscitation was associated with a significant increase in lactate levels compared with controls (10.1 versus 5.7 mmol/L, P < 0.05). Histologic injury was significantly increased in the livers of FLU-CYD compared with sham (P = 0.022). High serum levels of FLU and the active metabolite FLUOH were measurable throughout the resuscitation period. CONCLUSIONS: Flutamide failed to show any benefit to resuscitation in a model of severe injury and was associated with increased acidosis, hemodilution, and liver injury compared with standard crystalloid resuscitation.