Use of plasma-first resuscitation in the helicopter system creates a field ready, mobile blood bank, allowing early resuscitation of the patient demonstrating need for massive transfusion. There was early treatment of trauma-induced coagulopathy. Although there was not a survival benefit demonstrated, there was resultant damage control resuscitation extending to 24 hours in the plasma-first cohort.

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There is concern that the global burden of coronavirus disease of 2019 (COVID-19) due to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection might yield an increased occurrence of Guillain-Barré syndrome (GBS). It is currently unknown whether concomitant SARS-CoV-2 infection and GBS are pathophysiologically related, what biomarkers are useful for diagnosis, and what is the optimal treatment given the medical comorbidities, complications, and simultaneous infection. We report a patient who developed severe GBS following SARS-CoV-2 infection at the peak of the initial COVID-19 surge (April 2020) in New York City and discuss diagnostic and management issues and complications that may warrant special consideration in similar patients.

Background Surgical stabilization of rib fracture (SSRF) is increasingly used for treatment of rib fractures. There are few data on the incidence, risk factors, outcomes, and optimal management strategy for hardware infection in these patients. We aimed to develop and propose a management algorithm to help others treat this potentially morbid complication. Methods We retrospectively searched a prospectively collected rib fracture database for the records of all patients who underwent SSRF from August 2009 through March 2014 at our institution. We then analyzed for the subsequent development of hardware infection among these patients. Standard descriptive analyses were performed. Results Among 122 patients who underwent SSRF, most (73%) were men; the mean (SD) age was 59.5 (16.4) years, and median (interquartile range [IQR]) Injury Severity Score was 17 (13–22). The median number of rib fractures was 7 (5–9), and 48% of patients had flail chest. Mortality at 30 days was 0.8%. Five patients (4.1%) had a hardware infection on mean postoperative day 12.0 (6.6). Median Injury Severity Score (17 [13–42]) and hospital length of stay (9 [6–37] days) in these patients were similar to the values for those without infection (17 [13–22] and 9 [6–12] days, respectively). Patients with infection underwent a median (IQR) of 2 (2–3) additional operations, which included wound débridement (n=5), negative-pressure wound therapy (n=3), and antibiotic beads (n=4). Hardware was removed in 3 patients at 140, 190, and 192 days after index operation. Cultures grew only gram-positive organisms. No patients required reintervention after hardware removal, and all achieved bony union and were taking no narcotics or antibiotics at the latest follow-up. Conclusions Although uncommon, hardware infection after SSRF carries considerable morbidity. With the use of an aggressive multimodal management strategy, however, bony union and favorable long-term outcomes can be achieved. Level of Evidence Therapeutic study, level V.

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Lipid mediators regulate bone regeneration during fracture healing. Prostaglandins and leukotrienes are well-known lipid mediators that regulate inflammation and are synthesized from the O-6 fatty acid, arachidonic acid. Cyclooxygenase (COX-1 or COX-2) and 5-lipoxygenase (5-LO) catalyze the initial enzymatic steps in the synthesis of prostaglandins and leukotrienes, respectively. Inhibition or genetic ablation of COX-2 activity impairs fracture healing in animal models. Genetic ablation of COX-1 does not affect the fracture callus strength in mice, suggesting that COX-2 activity is primarily responsible for regulating fracture healing. Inhibition of cyclooxygenase activity with nonsteroidal anti-inflammatory drugs (NSAIDs) is performed clinically to reduce heterotopic ossification, although clinical evidence that NSAID treatment impairs fracture healing remains controversial. In contrast, inhibition or genetic ablation of 5-LO activity accelerates fracture healing in animal models. Even though prostaglandins and leukotrienes regulate inflammation, loss of COX-2 or 5-LO activity appears to primarily affect chondrogenesis during fracture healing. Prostaglandin or prostaglandin analog treatment, prostaglandin-specific synthase inhibition and prostaglandin or leukotriene receptor antagonism also affect callus chondrogenesis. Unlike the O-6-derived lipid mediators, lipid mediators derived from O-3 fatty acids, such as resolvin E 1 (RvE1), have anti-inflammatory activity. In vivo, RvE1 can inhibit osteoclastogenesis and limit bone resorption. Although O-6 and O-3 lipid mediators have clear-cut effects on inflammation, the role of these lipid mediators in bone regeneration is more complex, with apparent effects on callus chondrogenesis and bone remodeling.

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BACKGROUND Surgical stabilization of rib fractures (SSRF) is increasingly used for severe rib fractures/flail chest. There are no reports discussing mechanisms of failure of implanted hardware, its clinical presentation, or consequences. The purpose of this study was to evaluate the incidence, presenting signs, and clinical sequela of hardware failure after SSRF. METHODS A multicenter, retrospective study was performed by a group of surgeons with a large SSRF case volume. All cases with known hardware failure from January 1, 2010, to December 31, 2017, were included. The surgeon's experience at the time of hardware implantation, specific implant used, number of failures the surgeon had experienced with the same system, and time from implantation to hardware failure were recorded. Additionally, patient demographics, including age, comorbid conditions, and number and location of rib fractures were recorded. Symptomatology associated with hardware failure and need for explant and/or reimplantation of hardware was also recorded. Nonparametric statistical tests were used to compare cohorts. RESULTS Of 1,224 patients who underwent SSRF, 38 patients with 233 rib fractures and 279 fracture segments experienced hardware failure and were enrolled in the study. Twelve patients presented more than 3 months following injury. Median age was 54 years old and 34% were active smokers. One hundred forty-four plates were implanted with a median of four plates per patient. Median number of SSRF cases by each surgeon was 100 (range, 1–280). Fractures and hardware failure were most frequent in the anterolateral/lateral region. Hardware failure was mostly due to screw migration and plate fracture. Hardware failure was asymptomatic in 40% and presented as pain in 42% of cases. Fifty-five percent of the cases required explantation of hardware, and only 10% required SSRF again. There was no difference between the acute and chronic fracture cohorts. CONCLUSION Hardware failure after SSRF is rare and often asymptomatic. When present, it rarely requires redo SSRF. LEVEL OF EVIDENCE Therapeutic, level V.