Quantitative Evaluation of Embolic Load in Femoral and Tibial Shaft Fractures Treated With Reamed Intramedullary Fixation.

OBJECTIVES: To compare the volume of embolic load during intramedullary fixation of femoral and tibial shaft fractures. Our hypothesis was that tibial intramedullary nails (IMNs) would be associated with less volume of intravasation of marrow than IM nailing of femur fractures. DESIGN: Prospective observational study. SETTING: Urban Level I trauma center. PATIENTS/PARTICIPANTS: Twenty-three patients consented for the study: 14 with femoral shaft fractures and 9 with tibial shaft fractures. INTERVENTION: All patients underwent continuous transesophageal echocardiography, and volume of embolic load was evaluated during 5 distinct stages: postinduction, initial guide wire, reaming (REAM), nail insertion, and postoperative. MAIN OUTCOME MEASUREMENTS: Volume of embolic load was measured based on previously described luminosity scores. The embolic load based on fracture location and procedure stage was evaluated using a mixed effects model. RESULTS: The IMN procedure increased the embolic load by 215% (-12% to 442%, P = 0.07) in femur patients relative to tibia patients after adjusting for baseline levels. Of the 5 steps measured, REAM was associated with the greatest increase in embolic load relative to the guide wire placement and controlling for fracture location (421%, 95% confidence interval: 169%-673%, P < 0.01). CONCLUSIONS: Femoral shaft IMN fixation was associated with a 215% increase in embolic load in comparison with tibial shaft IMN fixation, with the greatest quantitative load during the REAM stage; however, both procedures produce embolic load. LEVEL OF EVIDENCE: Prognostic Level II. See Instructions for Authors for a complete description of levels of evidence.

Total face, double jaw, and tongue transplant research procurement: an educational model.

BACKGROUND: Transplantation of a facial vascularized composite allograft is a highly complex procedure that requires meticulous planning and affords little room for error. Although cadaveric dissections are an essential preparatory exercise, they cannot simulate the true clinical experience of facial vascularized composite allograft recovery. METHODS: After obtaining institutional review board approval to perform a facial vascularized composite allograft research procurement, a 66-year-old, brain-dead donor was identified. The family graciously consented to donation of a total face, double jaw, and tongue allograft and multiple solid organs. RESULTS: A craniofacial computed tomographic angiogram was obtained preoperatively to define the vascular anatomy and facilitate virtual computerized surgical planning. The allograft was procured in 10 hours, with an additional 2 hours required for an open tracheostomy and silicone facial impression. The donor was coagulopathic throughout the recovery, resulting in an estimated blood loss of 1500 ml. Fluorescence angiography confirmed adequate perfusion of the entire allograft based on lingual and facial arterial and external jugular and thyrolinguofacial venous pedicles. The solid organ transplant team initiated abdominal organ isolation while the facial allograft procurement was in progress. After completion of allograft recovery, the kidneys and liver were recovered without complication. CONCLUSIONS: Before conducting a clinical face transplant, adequate preparation is critical to maximize vascularized composite allotransplantation outcomes and preserve solid organ allograft function. As more centers begin to perform facial transplantation, research procurement of a facial vascularized composite allograft offers a unique educational opportunity for the surgical and anesthesia teams, the organ procurement organization, and the institution.

Thromboembolic complications associated with factor VIIa administration.

BACKGROUND: Factor VIIa (FVIIa) is given to promote hemostasis in coagulopathic trauma patients at high risk for death. FVIIa is associated with thromboembolic complications, but the incidence is not known, nor is which patients are at risk. We examined our experience with FVIIa to better understand this issue. METHODS: Medical records of patients who received FVIIa from 2001 to 2006 were reviewed for evidence of thromboembolic events, including ischemic cardiovascular accident, myocardial ischemia or infarct, mesenteric infarct, peripheral arterial thromboembolism, deep venous thrombosis, or pulmonary embolus. Indication for FVIIa dosing, timing of complication, and clinical outcome were recorded. Each event was assessed by a panel of experienced clinicians to determine the contribution of FVIIa to the event and to patient outcome. RESULTS: Two hundred eighty-five medical records were reviewed. Twenty-seven patients (9.4%) had thromboembolic complications after administration of FVIIa. Nine events were thought to be highly related to FVIIa, and 10 of 14 deaths were, in part, caused by the thrombotic complication. Eighteen of the events, including all cardiovascular accidents and most cases of mesenteric ischemia, were attributed to a combination of FVIIa and a definable, high-energy vascular injury. CONCLUSION: FVIIa is a potent procoagulant, with the potential for adverse thromboembolic events in susceptible patients. Our experience suggests that caution should be exercised in administration of FVIIa to patients with arterial injuries. Injured mesenteric and cerebral vessels may be especially susceptible to thrombosis.

Factor VIIa for correction of traumatic coagulopathy.

INTRODUCTION: Activated factor VIIa (FVIIa) was developed to treat hemophiliacs with high-titer antibodies to factor VIII. FVIIa initiates thrombin formation by binding with exposed tissue factor. Anecdotal reports have described the utility of FVIIa in correcting coagulopathy from trauma, but no large series exists. We present our experience with 81 coagulopathic trauma patients treated using FVIIa in years 2001-2003, compared with "control" patients matched from the trauma registry from the same time period. METHODS: Use of FVIIa was restricted to active hemorrhage with clinical coagulopathy. We recorded the cause of coagulopathy, dose of FVIIa administered, effect on clinical coagulation, pertinent laboratory values, length of stay, number and type of blood products administered, and patient outcome. For the same time period we also examined outcomes in coagulopathic patients who did not receive FVIIa. RESULTS: Causes of coagulopathy were diverse, and included acute traumatic hemorrhage (46 patients), traumatic brain injury (20), warfarin use (9), congenital Factor VII deficiency (2), and other acquired hematologic defects (4). Coagulopathy was reversed in 61/81 cases (75%), with an associated reduction in PT from 19.6 to 10.8 (p=0.000018). 34 patients (42%) survived to hospital discharge (20/46 traumatic hemorrhage, 5/20 TBI, 4/9 on warfarin, 2/2 factor deficient, 3/4 other). Patients died from irreversible shock, multiple organ system failure, or traumatic brain injury. FVIIa patients had a higher mortality than coagulopathic controls matched by specific anatomic injuries, admission lactate value, and predicted probability of survival. Only a group identified by all three characteristics had a similar mortality to the FVIIa cohort, but the number of patients that could be matched this way was too small to be meaningful. CONCLUSION: FVIIa therapy lead to an immediate reduction in coagulopathic hemorrhage in most cases, accompanied by a significant improvement in laboratory measures. Application of FVIIa as a therapy of last resort makes the identification of equivalent control patients difficult. Use of FVIIa should be considered for any patient with coagulopathic hemorrhage in which surgically-accessible bleeding has been controlled. Prospective trials of FVIIa in patients with traumatic coagulopathy are strongly indicated, and should focus on appropriate patient selection and the dose and timing of therapy.