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We designed a simple, low-cost workshop to teach surgical residents the basic skills of vascular anastomosis. We studied our ability to identify objective procedural and end-product metrics that could be used to measure improvement in vascular anastomotic skill before and after training.Ten postgraduate year 2 residents without previous vascular surgery experience and four attending surgeons (expert) performed end-to-side anastomosis using a synthetic graft. The residents were taught the basic skills of vascular anastomosis during three didactic workshops. The objective metrics included volume leakage after saline perfusion (leak) and the time needed to complete the anastomosis. Penalty points were assigned for broken sutures, air knots, locking sutures, and failure to maintain an outside-in to inside-out technique. The leak, time, and penalties before and after training were compared.The mean leak was 70.4 ± 13.7 mL and the mean completion time was 18.7 ± 3 min for the pretraining group versus 45.3 ± 10.6 mL (P0.01) and 8.5 ± 1 min (P0.001), respectively, for the attending group. After training, significant improvement was seen in resident leak (46.7 ± 6.8 mL; P0.001) and completion time (14.4 ± 3 min; P0.01). Leak was similar between the post-training and expert groups (46.7 ± 6.8 mL and 45.3 ± 10.6 mL, respectively; P = 0.77); however, a significant difference for the completion time remained (14.4 ± 3.0 min and 8.5 ± 1 min, respectively; P0.01). The mean number of technical errors improved from 2.7 in the pretraining group to zero for the post-training group after completing the workshop.We have reported an easy to implement workshop for teaching surgical residents the basic skills of performing vascular anastomosis.

Introduction Ventilator-associated pneumonia (VAP) occurs in up to 25% of mechanically ventilated patients, with an associated mortality up to 50%. Early diagnosis and appropriate empiric antibiotic coverage of VAP are crucial. Given the multitude of noninfectious clinical and radiographic anomalies within trauma patients, microbiology from bronchioalveolar lavage (BAL) is often needed. Empiric antibiotics are administered while awaiting BAL culture data. Little is known about the effects of these empiric antibiotics on patients with negative BAL microbiology if a subsequent VAP occurs during the same hospital course. Methods This is a retrospective chart review of intubated trauma patients undergoing BAL for suspected pneumonia over a 3-y period at a Level 1 trauma center. All patients with suspected VAP undergoing a BAL receive empiric antibiotics. If microbiology data are negative at 72 h, all antibiotics are stopped; however, if the BAL returns with ≥10 5 colony-forming units per milliliter, the diagnosis of VAP is confirmed. We divided patients into three groups. Group 1 consisted of patients in whom the initial BAL was positive for VAP. Group 2 consisted of patients with an initial negative BAL, who subsequently developed VAP at a later point in the hospital course. Group 3 consisted of patients with negative BAL who did not develop a subsequent VAP. Results We obtained 499 BAL specimens in 185 patients over the 3-y period. A total of 14 patients with 23 BAL specimens initially negative for VAP subsequently developed VAP later during the same hospital stay. These patients did not have an increase in the hospital length of stay, intensive care unit days, ventilator days, or mortality compared with those who had a positive culture on the first suspicion of VAP. There was a significant increase in the percentage of Enterobacter (21% versus 8%) and Morganella (8% versus 0%) as the causative organism in these 14 patients when the VAP occurred. Furthermore, the profile of the top two organisms in each group changed. Enterobacter (21%) and Pseudomonas (17%) were the principal organisms in the initial BAL-negative group, whereas the two predominant strains in the initial positive BAL group were methicillin-sensitive Staphylococcus aureus (21%) and Haemophilus influenza (11%). Interestingly, methicillin-resistant S. aureus remained the third most common organism in both groups. Empiric antibiotics also did not seem to induce the growth of multidrug-resistant organisms, and there was no increased rate of secondary infections such as Clostridium difficile . Conclusions Ventilator-associated pneumonia remains a significant cause of morbidity and mortality in mechanically ventilated trauma patients. The diagnosis and treatment of VAP continue to be challenging. Once clinically suspected, empiric coverage decreases morbidity and mortality. Our data demonstrate that patients who receive empiric coverage exhibit a significantly different microbiologic profile compared with those who had an initial positive BAL culture. Initial empiric antibiotics in BAL-negative patients were not associated with an increase in multidrug-resistant organisms, hospital, or intensive care unit length of stay, ventilator days, and mortality or secondary infections.

Continued assessment and redesign of the curriculum is essential for optimal surgical education. For the last 3 y, we have asked the residents to reflect on the previous week and describe "the best thing" they learned. We hypothesize that this statement could be used to assess the weaknesses or strengths of our curriculum.Starting in 2007, residents filled out surveys approximately 4 times/y at the start of a mandatory conference. They were asked to describe the "best thing" they learned that week, where it was learned, and who taught it. Residents were not asked to classify the item learned by core competency (communication, knowledge, patient care, practice-based learning, professionalism, and systems-based practice). This categorization into core competencies was done as part of our study design. Attending, fellow, resident, or other were used as groups designating who taught each item. Where the item was learned was fit into either clinic, conference, operating room (OR), wards, or self. The impact of postgraduate year (PGY) level on learning was also assessed. χ(2) analysis was used to compare groups.During the study period, 304 surveys were completed and returned by 65 residents. The majority of responses came from PGY 1 residents (134, 43%). Patient care and knowledge were the most common core competencies learned. As PGY level increased, learning of professionalism (P = 0.035) increased. A majority of learning was experiential (wards and OR, P0.0125). Self-learning and learning in clinic was a minor component of learning (P0.0125). Learning on wards (P0.001) decreased as residents progressed and learning from the OR (P = 0.002) had the opposite trend.Patient care and knowledge are the most frequently cited competencies learned by the residents. Self-learning is not a significant source of learning, and the majority of the learning is experiential. It is not known if this was a sign that there was a lack of self-directed learning or that self-directed learning was not an efficient method of learning. In addition, each PGY level learns differently (teacher and location of learning), perhaps reflecting the different needs and/or structure of each PGY. We believe the reflective statement has been and will be a useful tool to assess our curriculum.

Background. Although it is known that pentoxifylline (PTX) produces various beneficial effects during sepsis, it remains unknown whether this agent has any salutary effects on the depressed vascular responsiveness to adrenomedullin (ADM), a novel potent vasodilatory peptide, under such conditions. Materials and methods. Adult male Sprague–Dawley rats were subjected to polymicrobial sepsis by cecal ligation and puncture (CLP). One hour after CLP, PTX (50 mg/kg body wt) or vehicle (normal saline) was infused intravenously over 90 min. Twenty hours after CLP (i.e., the late, hypodynamic stage of sepsis), the thoracic aorta and small intestine were isolated and preconstricted by norepinephrine. Rat ADM (10−7 M) was applied, and the percentage of ADM-induced relaxation in the aortic rings and resistance vessels in the small intestine was determined. In addition, plasma ADM was determined by radioimmunoassay and tumor necrosis factor α (TNF-α), interleukin (IL)-1β, and IL-6 levels were measured by enzyme-linked immunosorbent assay. Results. The percentage of ADM-induced vascular relaxation in the aortic rings and resistance vessels of the isolated gut was significantly reduced 20 h after CLP. Administration of PTX early after the onset of sepsis, however, prevented the decrease in vascular ADM responsiveness at the macro- and microcirculatory levels. Plasma ADM levels increased after CLP, irrespective of PTX infusion, indicating that the effect of PTX was not mediated by altering ADM release. The upregulated TNF-α, IL-1β, and IL-6 during late sepsis were, however, attenuated by PTX administration, suggesting that maintenance of ADM responsiveness by this agent appears to be due to downregulation of these cytokines. Conclusions. Since early administration of PTX maintains vascular ADM responsiveness even during the late stage of sepsis, this agent appears to be a useful adjunct in preventing the deterioration in hemodynamics and cardiovascular function during the progression of polymicrobial sepsis.

Although hepatocellular dysfunction occurs following trauma and hemorrhagic shock, whether severe hypotension even in the absence of blood loss depresses hepatocellular function remains unknown. The aim of this study, therefore, was to determine whether chemically induced severe hypotension causes hepatocellular dysfunction and, if so, whether IL-6 and PGE 2 are associated with this dysfunction. To study this, hypotension was induced in adult male rats by intravenous infusion of a high dosage of ATP–MgCl 2 solution (3.2 ± 0.45 μmol/min/kg body wt) for 60 min. Blood pressure decreased from 108 ± 6 mm Hg to an average of 43 mm Hg during the infusion period and returned to normal levels immediately after the completion of ATP–MgCl 2 infusion. At 0 and 4 h after hypotension, hepatocellular function [i.e., maximum velocity of indocyanine green clearance ( V max ) and its efficiency ( K m )] was measured using a fiberoptic catheter and in vivo hemoreflectometer. Cardiac output was determined by dye dilution. Microvascular blood flow was assessed by laser Doppler flowmetry. Plasma levels of PGE 2 and IL-6 were measured by radioimmunoassay and bioassay, respectively. The results indicate that severe hypotension in the absence of any blood loss depresses hepatocellular function (i.e., decreased V max and K m ) despite stable cardiac output and hepatic perfusion at 0 and 4 h after the completion of hypotension. Moreover, severe hypotension resulted in significantly increased plasma levels of PGE 2 (only at 0 h) and IL-6. Thus, chemically induced severe hypotension in the absence of any blood loss, which does not significantly reduce cardiac output and hepatic perfusion, depresses hepatocellular function and upregulates IL-6 and PGE 2 production.

Background. Although studies suggest that the gut may be the “motor” responsible for producing sepsis and multiple organ failure after injury, it is not known whether enterectomy prior to the onset of hemorrhage alters proinflammatory cytokines TNF and IL-6 and, if so, whether hepatocellular dysfunction and damage are prevented or attenuated under such conditions. Materials and methods. Under methoxyflurane anesthesia, an enterectomy in the rat was performed by excision of the duodenum, jejunum, and ileum. The rats were then bled to and maintained at a mean arterial pressure of 40 mm Hg until 40% of the maximal shed volume was returned in the form of Ringer's lactate. The animals were then resuscitated with four times the volume of shed blood with Ringer's lactate over 1 h. At 1.5 h after the completion of resuscitation, hepatocellular function [i.e., the maximal velocity ( V max ) and transport efficiency ( K m ) of indocyanine green (ICG) clearance] was assessed by an in vivo ICG clearance technique. Blood samples were taken for the measurement of TNF, IL-6, and liver enzymes (i.e., SGPT and SGOT). Cardiac output and microvascular blood flow were determined by ICG dilution and laser Doppler flowmetry, respectively. Results. The increase in circulating levels of TNF but not IL-6 was prevented by enterectomy prior to hemorrhage. The reduced V max and K m and elevated SGPT and SGOT following hemorrhage and resuscitation, however, were not significantly affected by prior enterectomy. Moreover, enterectomy before hemorrhage further reduced hepatic perfusion. Conclusion. Since enterectomy prior to the onset of hemorrhage does not prevent or attenuate the reduced ICG clearance and elevated liver enzymes despite downregulation of TNF production, it appears that the small intestine does not play a significant role in producing hepatocellular dysfunction and injury following trauma and hemorrhagic shock.

Although intestinal mucosal immune dysfunction occurs after trauma and hemorrhage and appears to contribute to infectious complications, the mechanism is not known. In this regard, the inappropriate induction of immune cell apoptosis may contribute to the immune dysfunction following trauma and hemorrhage. To study this, we examined Peyer's patch cells for evidence of apoptosis and changes in Fas protein expression, as well as alterations in the relative lymphocyte subpopulations after trauma and hemorrhagic shock. Male C3H/HeN mice underwent sham operation, trauma (i.e., laparotomy), hemorrhagic shock (mean arterial blood pressure of 35 +/- 5 mmHg for 90 min, followed by adequate crystalloid resuscitation), or trauma plus hemorrhage. Peyer's patch cells were isolated at 24 and 72 hr after the procedure. The percentage of apoptotic cells, Fas protein expression, and cell percentage of phenotype were determined by flow cytometry. The results indicate that trauma alone induced no significant change in the measured parameters. However, (i) there were a significant decrease in total viable cell yield and an increased apoptosis in Peyer's patch cells at 24 and 72 hr following hemorrhage or trauma plus hemorrhage; (ii) the increased apoptosis in Peyer's patch was predominantly in cells of the B-cell lineage; (iii) the increased apoptosis was associated with an elevated Fas expression. In conclusion, hemorrhage alone or trauma plus hemorrhage can induce increased apoptosis in Peyer's patch cells, which is associated with the increased Fas expression. Thus, apoptotic involution may play an important role in the depression of intestinal mucosal immune function after trauma and hemorrhagic shock.

Although the thymus is an important organ in the ontogeny of T lymphocytes, little is known about the effects of hemorrhage and/or trauma on this organ. The objective of this study was to determine whether trauma–hemorrhage induces increased thymic apoptosis and, if so, which mediators may be involved. Male C3H/HeN mice underwent either sham operation, hemorrhagic shock (mean artery blood pressure of 35 ± 5 mmHg for 90 min, followed by blood and fluid resuscitation), fracture of the right tibia, or fracture plus hemorrhage, respectively. At 3 days after the procedure, total viable thymocyte yield, thymocyte apoptosis (flow cytometry), thymus-derived IL-3 (bioassay), and GM-CSF (ELISA) were determined. The results demonstrate that fracture alone induces no significant change in the parameters measured. However, (i) there was a significant decrease in total viable thymocyte yield and an increase in thymocyte apoptosis following hemorrhage or fracture plus hemorrhage; (ii) thymocyte IL-3 release was significantly reduced after hemorrhage as well as fracture plus hemorrhage; (iii) thymus-derived GM-CSF was significantly increased after fracture plus hemorrhage, but not with hemorrhage alone. In conclusion, severe hemorrhage alone or coupled with fracture can induce thymus atrophy via apoptosis. In addition, the decreased IL-3 release suggests that apoptotic thymic involution may be due to the lack of growth factor support. Such dyshomeostasis may contribute to inappropriate/inadequate T cell maturation leading to host immune suppression following trauma–hemorrhage. Increased thymus-derived GM-CSF might be in part responsible for the systemic inflammatory response following trauma–hemorrhage.

Bronchopulmonary injury secondary to smoke inhalation is a significant comorbid factor following major thermal trauma. The present study evaluates the effects of pentoxifylline (PTX) on pulmonary function in an ovine model of inhalation injury. Following smoke exposure to produce a moderate inhalation injury, 16 animals were divided into two groups. Group 1 animals (n = 8) were untreated; Group 2 animals (n = 8) were treated continuously with pentoxifylline following smoke exposure. The animals were observed in the unintubated, awake state for 48 hr. Cardiopulmonary variables and blood gases were measured serially. Ventilation perfusion distribution (VA/Q), analyzed using the multiple inert gas elimination technique, and bronchoalveolar lavage (BAL) were performed at 48 hr. The wet to dry lung weight ratio was measured following necropsy. In Group 2, the progressive hypoxemia observed following smoke inhalation was attenuated with less VA/Q mismatching than in Group 1 (P0.05). Pulmonary hypertension secondary to increased vascular resistance was also attenuated in Group 2 (P0.05). In BAL fluid, polymorphonuclear leukocytes, total protein content, and conjugated dienes were less in Group 2 than in Group 1 (P0.05). Plasma-conjugated diene levels were also lower in Group 2 at 48 hr. Extravascular lung water and decrease in lung compliance were greater in Group 1. There was less morphologic evidence of airway injury in Group 2 compared to Group 1. The improvement of pulmonary function following treatment with PTX suggests that this agent may be useful in the management of smoke inhalation injury.