Clustered Arrivals of Firearm-Injured Patients in an Urban Trauma System: A Silent Epidemic.

BACKGROUND: Recent attention has been paid to the role trauma centers play in responding to mass shootings. Although high-profile public events are the primary focus of media and policy makers, firearm-injured patients (FIPs) present in clusters to urban trauma centers every day. We examined the burden of FIP clusters from an urban trauma system perspective. STUDY DESIGN: In this descriptive epidemiologic study, we used data from the Philadelphia Police Department registry of shootings from 2005 to 2015. Variables included patient demographics, injury date and time, receiving hospital, and mortality. We defined clustered FIPs as those arriving within 15 minutes of another FIP. We used rolling temporal windows to calculate the number of FIP clusters for each hospital, assessed patient demographic characteristics and mortality, and used linear regression models to evaluate trends in FIP cluster rates. RESULTS: Of the 14,217 FIPs included, 22.1% were clustered. There were 54 events when 4 or more FIPs presented within 15 minutes and 92 events when 4 or more FIPs presented within 60 minutes. Clusters of FIP occurred most frequently during night shifts (7:00 pm to 7:00 am) (73.1%) at level I trauma centers (93.6%), with geographic clustering demonstrated at the hospital level. Compared with the overall FIP population, clustered FIPs were more likely to be female (p = 0.039), injured at night (p = 0.031), but less likely to die (p = 0.014). The rate of FIP clusters and mortality remained steady over the course of the study. CONCLUSIONS: In the trauma system studied, FIP clusters are common and are likely to occur at similar rates in other urban centers. Therefore, the immediate burden on health care resources caused by multiple FIPs presenting within a short period of time is not limited to traditionally defined mass shootings.

Acute right heart failure after hemorrhagic shock and trauma pneumonectomy-a management approach: A blinded randomized controlled animal trial using inhaled nitric oxide.

BACKGROUND: Hemorrhagic shock and pneumonectomy causes an acute increase in pulmonary vascular resistance (PVR). The increase in PVR and right ventricular (RV) afterload leads to acute RV failure, thus reducing left ventricular (LV) preload and output. Inhaled nitric oxide (iNO) lowers PVR by relaxing pulmonary arterial smooth muscle without remarkable systemic vascular effects. We hypothesized that with hemorrhagic shock and pneumonectomy, iNO can be used to decrease PVR and mitigate right heart failure. METHODS: A hemorrhagic shock and pneumonectomy model was developed using sheep. Sheep received lung protective ventilatory support and were instrumented to serially obtain measurements of hemodynamics, gas exchange, and blood chemistry. Heart function was assessed with echocardiography. After randomization to study gas of iNO 20 ppm (n = 9) or nitrogen as placebo (n = 9), baseline measurements were obtained. Hemorrhagic shock was initiated by exsanguination to a target of 50% of the baseline mean arterial pressure. The resuscitation phase was initiated, consisting of simultaneous left pulmonary hilum ligation, via median sternotomy, infusion of autologous blood and initiation of study gas. Animals were monitored for 4 hours. RESULTS: All animals had an initial increase in PVR. PVR remained elevated with placebo; with iNO, PVR decreased to baseline. Echo showed improved RV function in the iNO group while it remained impaired in the placebo group. After an initial increase in shunt and lactate and decrease in SvO2, all returned toward baseline in the iNO group but remained abnormal in the placebo group. CONCLUSION: These data indicate that by decreasing PVR, iNO decreased RV afterload, preserved RV and LV function, and tissue oxygenation in this hemorrhagic shock and pneumonectomy model. This suggests that iNO may be a useful clinical adjunct to mitigate right heart failure and improve survival when trauma pneumonectomy is required.

Noncardiac Surgical Procedures After Left Ventricular Assist Device Implantation.

As left ventricular assist devices (LVADs) are increasingly used for patients with end-stage heart failure, the need for noncardiac surgical procedures (NCSs) in these patients will continue to rise. We examined the various types of NCS required and its outcomes in LVAD patients requiring NCS. The National Inpatient Sample Database was examined for all patients implanted with an LVAD from 2007 to 2010. Patients requiring NCS after LVAD implantation were compared to all other patients receiving an LVAD. There were 1,397 patients undergoing LVAD implantation. Of these, 298 (21.3%) required 459 NCS after LVAD implantation. There were 153 (33.3%) general surgery procedures, with abdominal/bowel procedures (n = 76, 16.6%) being most common. Thoracic (n = 141, 30.7%) and vascular (n = 140, 30.5%) procedures were also common. Patients requiring NCS developed more wound infections (9.1 vs. 4.6%, p = 0.004), greater bleeding complications (44.0 vs. 24.8%, p < 0.001) and were more likely to develop any complication (87.2 vs. 82.0%, p = 0.001). On multivariate analysis, the requirement of NCSs (odds ratio: 1.45, 95% confidence interval: 0.95-2.20, p = 0.08) was not associated with mortality. Noncardiac surgical procedures are commonly required after LVAD implantation, and the incidence of complications after NCS is high. This suggests that patients undergoing even low-risk NCS should be cared at centers with treating surgeons and LVAD specialists.

The evil of good is better: Making the case for basic life support transport for penetrating trauma victims in an urban environment.

BACKGROUND: Controversy remains over the ideal way to transport penetrating trauma victims in an urban environment. Both advance life support (ALS) and basic life support (BLS) transports are used in most urban centers. METHODS: A retrospective cohort study was conducted at an urban Level I trauma center. Victims of penetrating trauma transported by ALS, BLS, or police from January 1, 2008, to November 31, 2013, were identified. Patient survival by mode of transport and by level of care received was analyzed using logistic regression. RESULTS: During the study period, 1,490 penetrating trauma patients were transported by ALS (44.8%), BLS (15.6%), or police (39.6%) personnel. The majority of injuries were gunshot wounds (72.9% for ALS, 66.8% for BLS, 90% for police). Median transport minutes were significantly longer for ALS (16 minutes) than for BLS (14.5 minutes) transports (p = 0.012). After adjusting for transport time and Injury Severity Score (ISS), among victims with an ISS of 0 to 30, there was a 2.4-fold increased odds of death (95% confidence interval [CI], 1.3-4.4) if transported by ALS as compared with BLS. With an ISS of greater than 30, this relationship did not exist (odds ratio, 0.9; 95% CI, 0.3-2.7). When examined by type of care provided, patients with an ISS of 0 to 30 given ALS support were 3.7 times more likely to die than those who received BLS support (95% CI, 2.0-6.8). Among those with an ISS of greater than 30, no relationship was evident (odds ratio, 0.9; 95% CI, 0.3-2.7). CONCLUSION: Among penetrating trauma victims with an ISS of 30 or lower, an increased odds of death was identified for those treated and/or transported by ALS personnel. For those with an ISS of greater than 30, no survival advantage was identified with ALS transport or care. Results suggest that rapid transport may be more important than increased interventions. LEVEL OF EVIDENCE: Therapeutic study, level IV.

Examining Noncardiac Surgical Procedures in Patients on Extracorporeal Membrane Oxygenation.

As extracorporeal membrane oxygenation (ECMO) is increasingly used for patients with cardiac and/or pulmonary failure, the need for noncardiac surgical procedures (NCSPs) in these patients will continue to increase. This study examined the NCSP required in patients supported with ECMO and determined which variables affect outcomes. The National Inpatient Sample Database was examined for patients supported with ECMO from 2007 to 2010. There were 563 patients requiring ECMO during the study period. Of these, 269 (47.8%) required 380 NCSPs. There were 149 (39.2%) general surgical procedures, with abdominal exploration/bowel resection (18.2%) being most common. Vascular (29.5%) and thoracic procedures (23.4%) were also common. Patients requiring NCSP had longer median length of stay (15.5 vs. 9.2 days, p = 0.001), more wound infections (7.4% vs. 3.7%, p = 0.02), and more bleeding complications (27.9% vs. 17.3%, p = 0.01). The incidences of other complications and inpatient mortality (54.3% vs. 58.2%, p = 0.54) were similar. On logistic regression, the requirement of NCSPs was not associated with mortality (odds ratio [OR]: 0.91, 95% confidence interval [CI]: 0.68-1.23, p = 0.17). However, requirement of blood transfusion was associated with mortality (OR: 1.70, 95% CI: 1.06-2.74, p = 0.03). Although NCSPs in patients supported with ECMO does not increase mortality, it results in increased morbidity and longer hospital stay.

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.

Still making the case against prehospital intubation: a rat hemorrhagic shock model.

BACKGROUND: Prehospital intubation does not appear to result in a survival advantage for patients experiencing penetrating trauma; yet, there is still resistance to the practice of "scoop and run" to speed access to advanced care. An animal model was used to determine whether intubation provides a survival advantage during potentially lethal hemorrhage. METHODS: The carotid arteries of Sprague-Dawley rats were cannulated, and mean arterial pressure (MAP) was measured. One group of animals (n = 10) was intubated and placed on a ventilator, whereas the other (n = 9) was administered with 100% oxygen via nose cone. Rats were exsanguinated to a MAP of 40 mm Hg and then bled periodically to maintain a MAP between 40 mm Hg and 45 mm Hg. The primary end-point was time until death. Secondary end-points included lactic acid and base excess levels measured in blood collected at 30-minute intervals after inducing shock. RESULTS: There was no significant difference in time until death between the intubated and nose cone groups (85.5 vs. 93.3 minutes, p = 0.60). Intubated animals had higher lactic acid levels at 90 minutes (6.1 vs. 3.5 mmol/L; p = 0.02) and 120 minutes (7.7 vs. 2.6 mmol/L, p = 0.03) after the initiation of shock. In addition, intubated animals had worse base excess at 90 minutes (-13.5 vs. -7.9 mmol/L, p = 0.04). CONCLUSION: Intubation does not result in a survival advantage in this rat model of hemorrhagic shock. Positive pressure ventilation may cause decreased venous return and accentuate end-organ hypoperfusion. Large animal studies are needed to further investigate these findings.

Cephalosporin-induced leukopenia following rechallenge with cefoxitin.

OBJECTIVE: To describe a case of cefazolin-induced leukopenia in a critically ill patient who developed this adverse reaction upon rechallenge with cefoxitin. CASE SUMMARY: A 22-year-old male was admitted after a motor vehicle crash. beta-Lactam therapy was initiated with vancomycin, cefepime, and metronidazole and, upon identification of methicillin-sensitive Staphylococcus aureus bacteremia 4 days later, therapy was narrowed to cefazolin 1 g every 12 hours. The dose was adjusted to 1 g every 12 hours during continuous venovenous hemodialysis. Imipenem was given for 2 days, resulting in a total of 18 days of beta-lactam treatment, at which time he developed significant leukopenia (white blood cell [WBC] count 0.9 x 10(3)/microL). Antimicrobial treatment was changed to tigecycline and continued for suspected pleural space infection. The patient's WBC count recovered within 4 days after the change in therapy. He was taken to surgery 8 days after cefazolin was discontinued and received perioperative prophylaxis with cefoxitin (total dose 3 g). Subsequently, the patient again became severely leukopenic (WBC count 2.4 x 10(3)/microL). Within a week after surgery, the patient developed septic shock secondary to multidrug-resistant Escherichia coli bacteremia and died. DISCUSSION: beta-Lactam-induced leukopenia is a rare but well-described adverse drug reaction. It is a cumulative dose-dependent phenomenon reported to occur most often after 2 weeks of therapy. The mechanism of leukopenia is thought to be secondary to either an immune-mediated response or direct bone marrow toxicity. Rechallenge with a different beta-lactam antibiotic has not been shown to consistently cause recurrent leukopenia. The case described here suggests an immune-related mechanism for the development of leukopenia. Use of the Naranjo probability scale determined the association between cephalosporin use and leukopenia to be probable. CONCLUSIONS: Cefazolin was a probable cause of this patient's leukopenia. It is important for clinicians to recognize beta-lactam-induced leukopenia and maybe recommend use of a drug from a different antibiotic class if continued treatment is indicated.