A prospective randomized study of the efficacy of "Turning Point," an inpatient violence intervention program.

BACKGROUND: From 2002 to 2011, there were more than 17,000 shootings in Philadelphia. "Turning Point," Temple University Hospital's inpatient violence intervention program, takes advantage of the teachable moment that occurs after violent injury. In addition to receiving traditional social work services, Turning Point patients watch their trauma bay resuscitation video and a movie about violence, meet with a gunshot wound survivor and an outpatient case manager, and also undergo psychiatric assessment. The purpose of this study was to determine the efficacy of Turning Point in changing attitudes toward guns and violence among victims of penetrating trauma. METHODS: This prospective randomized study was conducted from January 2012 to January 2014. Patients who sustained a gunshot or stab wound were randomized to standard of care, which involved traditional social work services only, or Turning Point. The Attitudes Toward Guns and Violence Questionnaire was administered to assess attitude change. Analysis was performed with repeated-measures analysis of variance. A p < 0.05 was significant. RESULTS: A total of 80 of a potential 829 patients completed the study (40 standard of care, 40 Turning Point). The most common reason for exclusion was anticipated length of stay being less than 48 hours. The two groups were similar with respect to most demographics. Unlike the standard-of-care group, the Turning Point group demonstrated a 50% reduction in aggressive response to shame, a 29% reduction in comfort with aggression, and a 19% reduction in overall proclivity toward violence. CONCLUSIONS: Turning Point is effective in changing attitudes toward guns and violence among victims of penetrating trauma. Longer follow-up is necessary to determine if this program can truly be a turning point in patients' lives. LEVEL OF EVIDENCE: Therapeutic/care management study, level II.

Antiplatelet and anticoagulation medications and the surgical patient.

BACKGROUND: Acute coronary syndrome affects more than 750,000 Americans per year, and antiplatelet agents are the cornerstones of treatment. Atrial fibrillation affects 2.4 million patients in the United States, and venous thromboembolism occurs in 1 to 2 per 1,000 adults per year. Anticoagulants are commonly prescribed to affected patients. Surgeons are commonly called upon to care for patients taking medications that affect normal coagulation. It is important that the surgical community has a fundamental understanding of these agents' pharmacology, which may impact patients' clinical course. METHODS: A review of recent literature on pharmacologic agents that affect coagulation was performed. RESULTS: A number of medications that alter normal coagulation were reviewed in this article including their pharmacologic properties and reversal strategies. CONCLUSIONS: There are a variety of medications that affect a patient's coagulation ability, including many newer agents on the market. This review provides surgeons with the knowledge needed to assist in caring for individuals receiving these drugs.

Noncardiac surgery in patients on mechanical circulatory support.

This study examined outcomes in patients with left ventricular assist device (LVAD) and extracorporeal membrane oxygenation (ECMO) requiring noncardiac surgical procedures and identified factors that influence outcomes. All patients with mechanical circulatory support (MCS) devices at our institution from 2002 to 2013 undergoing noncardiac surgical procedures were reviewed. There were 148 patients requiring MCS during the study period, with 40 (27.0%) requiring 62 noncardiac surgical procedures. Of these, 29 (72.5%) had implantable LVAD and 11 (27.5%) were supported with ECMO. The two groups were evenly matched with regard to age (53.6 vs. 54.5 years, p = 0.87), male sex (71.4 vs. 45.5%, p = 0.16), and baseline creatinine (1.55 vs. 1.43 mg/dl, p = 0.76). Patients on ECMO had greater demand for postoperative blood products (0.8 vs. 2.8 units of packed red blood cells, p = 0.002) and greater postoperative increase in creatinine (0.07 vs. 0.44 mg/dl, p = 0.047). Median survival was markedly worse in ECMO patients. Factors associated with mortality included ECMO support, history of biventricular assist device, and postoperative blood transfusion. Preoperative aspirin was associated with survival. These findings demonstrate the importance of careful surgical hemostasis and minimizing perioperative blood transfusions in patients on MCS undergoing noncardiac surgical procedures. In addition, low-dose antiplatelet therapy should be continued perioperatively.

"Permissive hypoventilation" in a swine model of hemorrhagic shock.

BACKGROUND: Many penetrating trauma patients in severe hemorrhagic shock receive positive pressure ventilation (PPV) upon transport to definitive care, either by intubation (INT) or bag-valve mask (BVM). Using a swine hemorrhagic shock model that simulates penetrating trauma, we proposed that severely injured patients may have better outcomes with "permissive hypoventilation," where manual breaths are not given and oxygen is administrated passively via face mask (FM). We hypothesized that PPV has harmful physiologic effects in severe low-flow states and that permissive hypoventilation would result in better outcomes. METHODS: The carotid arteries of Yorkshire pigs were cannulated with a 14-gauge catheter. One group of animals (n = 6) was intubated and manually ventilated, a second received PPV via BVM (n = 7), and a third group received 100% oxygen via FM (n = 6). After placement of a Swan-Ganz catheter, the carotid catheters were opened, and the animals were exsanguinated. The primary end point was time until death. Secondary end points included central venous pressure, cardiac output, lactate levels, serum creatinine, CO2 levels, and pH measured in 10-minute intervals. RESULTS: Average survival time in the FM group (50.0 minutes) was not different from the INT (51.1 minutes) and BVM groups (48.5 minutes) (p = 0.84). Central venous pressure was higher in the FM group as compared with the INT 10 minutes into the shock phase (8.3 mm Hg vs. 5.2 mm Hg, p = 0.04). Drop in cardiac output (p < 0.001) and increase in lactate (p < 0.05) was worse in both PPV groups throughout the shock phase. Creatinine levels were higher in both PPV groups (p = 0.04). The FM group was more hypercarbic and acidotic than the two PPV groups during the shock phase (p < 0.001). CONCLUSION: Although permissive hypoventilation leads to respiratory acidosis, it results in less hemodynamic suppression and better perfusion of vital organs. In severely injured penetrating trauma patients, consideration should be given to immediate transportation without PPV.

Examining prehospital intubation for penetrating trauma in a swine hemorrhagic shock model.

BACKGROUND: Prehospital intubation does not result in a survival advantage in patients experiencing penetrating trauma, yet resistance to immediate transportation to facilitate access to definitive care remains. An animal model was developed to determine whether intubation provides a survival advantage during severe hemorrhagic shock. We hypothesized that intubation would not provide a survival advantage in potentially lethal hemorrhage. METHODS: After starting a propofol drip, Yorkshire pigs were intubated (n = 6) or given bag-valve mask ventilation (n = 7) using 100% oxygen. The carotid artery was cannulated with a 14-gauge catheter, and a Swan-Ganz catheter was placed under fluoroscopy using a central venous introducer. After obtaining baseline hemodynamic and laboratory data, the animals were exsanguinated through the carotid line until death. The primary end point was time until death, while secondary end points included volume of blood shed, temperature, cardiac index, mean arterial pressure, lactic acid, base excess, and creatinine levels measured in 10-minute intervals. RESULTS: There was no difference in time until death between the two groups (51.1 [2.5] minutes vs. 48.5 [2.4] minutes, p = 0.52). Intubated animals had greater volume of blood shed at 30 minutes (33.6 [4.4] mL/kg vs. 28.5 [4.3] mL/kg, p = 0.03), 40 minutes (41.7 [4.7] mL/kg vs. 34.9 [3.8] mL/kg, p = 0.04), and 50 minutes (49.2 [8.6] mL/kg vs. 40.2 [1.0] mL/kg, p = 0.001). In addition, the intubated animals were more hypothermic at 40 minutes (35.5°C [0.4°C] vs. 36.7°C [0.2°C], p = 0.01) and had higher lactate levels (2.4 [0.1] mmol/L vs. 1.8 [0.4] mmol/L, p = 0.04) at 10 minutes. Cardiac index (p = 0.66), mean arterial pressure (p = 0.69), base excess (p = 0.14), and creatinine levels (p = 0.37) were not different throughout the shock phase. CONCLUSION: Intubation does not convey a survival advantage in this model of severe hemorrhagic shock. Furthermore, intubation in the setting of severe hemorrhagic shock may result in a more profuse hemorrhage, worse hypothermia, and higher lactate when compared with bag-valve mask ventilation.

Beta 2 microglobulin knockout mice are resistant to lethal intraabdominal sepsis.

beta 2 microglobulin knockout (beta2M-/-) mice lack CD8+ T and natural killer T cells. We hypothesized that beta 2M-/- mice are resistant to lethal intraabdominal sepsis. To test this hypothesis, mortality, cytokine production, and physiologic function were assessed in beta 2M-/- mice during sepsis caused by cecal ligation and puncture (CLP). beta 2M-/- mice survived significantly longer than wild-type mice after CLP but ultimately exhibited 100% mortality. Treatment of beta 2M-/- mice with anti-asialoGM1 to deplete natural killer cells conferred greater than 70% long-term survival. Compared with wild-type mice, beta 2M-/- mice treated with anti-asialoGM1 produced decreased amounts of proinflammatory cytokines and did not exhibit hypothermia or metabolic acidosis after CLP. Adoptive transfer of CD8+ T and natural killer cells into beta 2M-/- mice treated with anti-asialoGM1 re-established CLP-induced mortality. CD8 knockout mice treated with anti-asialoGM1, which are specifically deficient in CD8+ T and natural killer cells, exhibited 40% long-term survival after CLP. Furthermore, treatment of wild-type mice with antibodies to CD8 and asialoGM1 conferred a significant survival benefit compared with wild-type mice treated with nonspecific IgG. These findings demonstrate that beta 2M-/- mice treated with anti-asialoGM1 are resistant to CLP-induced mortality and that depletion of CD8+ T and natural killer cells largely accounts for the survival benefit observed in these mice.