Antibiotics and open fractures of the lower extremity: less is more.

PURPOSE: Infectious complications in open lower extremity fractures contribute to significant morbidity. Historically, orthopedic guidelines have recommended Grade III fractures receive a first generation cephalosporin and an aminoglycoside. Despite these guidelines, few studies have evaluated the utility of adding an aminoglycoside in this patient population. At our trauma center, we have a unique trauma service where half of our surgeons treat Grade III open fractures with a cephalosporin alone and half use a cephalosporin + aminoglycoside. We hypothesized that our outcomes were the same between the two groups. METHODS: We identified all Grade III fractures of the lower extremity admitted to our urban Level I Trauma Center over the 5-year study period. Charts were retrospectively reviewed to identify demographic information, injury severity score (ISS), fracture location, grade of fracture, type of antibiotic administered, incidence of acute kidney injury (AKI), surgical site infection (SSI), hardware removal, hospital length of stay (HLOS), and disposition. Patients were classified into two groups: those treated with a cephalosporin alone (CEPH) or cephalosporin + an aminoglycoside (CEPH + AG). RESULTS: A total of 126 grade III fractures of the lower extremity were admitted our Trauma Center during the 5-year study period. There were 65 (52%) patients in the CEPH group and 61 (48%) in the CEPH + AG group. Demographics, ISS, fracture location, grade of fracture, rate of SSI, need for hardware removal, and disposition were not different between the two groups. In contrast, patients in the CEPH group had a 4% incidence of AKI, while the incidence was 10% of patients in the CEPH + AG group (p < 0.05). CONCLUSION: The addition of an AG to antibiotic prophylaxis in open lower extremity fractures was associated with a significant increase in AKI with no change in the incidence of wound infection or hardware removal. Cephalosporins alone may be sufficient for prophylaxis in Grade III open fractures of the lower extremity. A large-scale prospective randomized trial is needed to confirm these findings and inform clinical practice.

Impact of pelvic fractures on the early clinical outcomes of severely injured trauma patients.

BACKGROUND: Pelvic fractures contribute to morbidity and mortality following injury. We sought to study the impact of pelvic fractures on the clinical course and outcomes of trauma patients with a pelvic fracture in comparison to patients with similar injury severity without pelvic fracture to identify potential parameters to track patients' clinical course post-injury. METHODS: A cohort of 206 consecutive blunt trauma survivors, studied over a 5-year period in a level I trauma center of which 75 patients (36.4%) had a pelvic fracture, was included in the study. To perform a retrospective cohort study with matched controls, 60 patients of the pelvic fracture group [(PF), 41 males and 19 females; age: 40 ± 17; injury severity score (ISS): 26.6 ± 9.3] were compared to 60 patients without pelvic fracture (non-PF) trauma as controls (41 males and 19 females; age: 40 ± 13; ISS: 26.9 ± 7.7), both with matching age (±5 years), sex, and ISS (±5 points). RESULTS: Statistically significant differences were observed in Intensive Care Unit (ICU) length of stay (LOS), total LOS, and Marshall MOD score between PF and non-PF groups, respectively. Acid-base markers such as pH, lactate, LDH, and base deficit were all significantly altered in PF compared to non-PF cohort upon admission. Moreover, our analysis showed significant differences in inflammatory biomarkers (Prolactin, CRP, and IL-6), and clinical parameters (CPK, Hgb, Platelets count, and WBC) over the 7-day clinical course in patients with PF when compared to non-PF cohort. CONCLUSION: In this matched cohort, patients with pelvic fractures exhibited biochemical and physiological alterations upon admission. Furthermore, our results suggest that pelvic fracture affects the clinical outcomes in severely injured patients, independently of injury severity, mechanism of injury, age or gender.

Impact of haemorrhagic shock intensity on the dynamic of alarmins release in porcine poly-trauma animal model.

PURPOSE: Traumatic insults result in an altered inflammatory response, in which alarmins release has a central role. The impact of haemorrhagic shock intensity on the long-term kinetics of alarmins is not yet fully elucidated. We investigated these aspects in a combined trauma (chest, abdominal, and extremities injury) porcine model with different severities and durations of haemorrhagic shock. METHODS: After induction of combined trauma (tibia fracture, lung contusion, and liver laceration), haemorrhagic shock was induced at different intensities: moderate haemorrhage (MH; n = 15): mean arterial pressure (MAP) <30 ± 5 mmHg [maximum loss of total blood volume (TBVmax): 45 %] for 90 min, and severe haemorrhage (SH; n = 10): MAP <25 ± 5 mmHg (TBVmax 50 %) for 120 min. Resuscitation was performed using a standardized crystalloid infusion protocol. Animals were mechanically ventilated and underwent ICU-monitoring for 48 h (MH) and 48.5 h (SH). Blood samples were collected over the clinical time course, and systemic levels of serum alarmins [High-Mobility Group Protein B-1 (HMGB-1) and Heat Shock Protein 70 (HSP70)] were measured using an ELISA kit. RESULTS: Heart rate, systemic blood pressure, lactate, and base excess were significantly altered as a function of haemorrhagic shock in both trauma groups (MH and SH). Systemic HMGB-1 levels were significantly elevated in both trauma groups when compared to the sham group. Haemorrhagic shock severity and duration were positively correlated with HMGB-1 levels and compared to baseline values, concentrations remained significantly increased in SH when compared to MH. On the other hand, we observed a significant decrease in the systemic HSP70 levels of trauma groups (MH, and SH) when compared to the sham group, which was significantly decreased compared to baseline values in SH over the entire time course. CONCLUSION: Our data show that haemorrhagic shock duration and severity affect the systemic levels of HMGB-1 and HSP70. This early alarmins release after trauma can be used to guide the treatment strategies (e.g. surgical procedures) of polytrauma patients.

Characterization of blunt chest trauma in a long-term porcine model of severe multiple trauma.

Chest trauma has a significant relevance on outcome after severe trauma. Clinically, impaired lung function typically occurs within 72 hours after trauma. However, the underlying pathophysiological mechanisms are still not fully elucidated. Therefore, we aimed to establish an experimental long-term model to investigate physiological, morphologic and inflammatory changes, after severe trauma. Male pigs (sus scrofa) sustained severe trauma (including unilateral chest trauma, femur fracture, liver laceration and hemorrhagic shock). Additionally, non-injured animals served as sham controls. Chest trauma resulted in severe lung damage on both CT and histological analyses. Furthermore, severe inflammation with a systemic increase of IL-6 (p = 0.0305) and a local increase of IL-8 in BAL (p = 0.0009) was observed. The pO2/FiO2 ratio in trauma animals decreased over the observation period (p < 0.0001) but not in the sham group (p = 0.2967). Electrical Impedance Tomography (EIT) revealed differences between the traumatized and healthy lung (p < 0.0001). In conclusion, a clinically relevant, long-term model of blunt chest trauma with concomitant injuries has been developed. This reproducible model allows to examine local and systemic consequences of trauma and is valid for investigation of potential diagnostic or therapeutic options. In this context, EIT might represent a radiation-free method for bedside diagnostics.