Trauma bypass performed by vascular surgeons demonstrate excellent long-term outcomes and limb preservation.

OBJECTIVE: Long-term outcomes in civilian trauma patients requiring upper or lower extremity revascularization is poorly studied secondary to limitations of certain large databases and the nature of the patients in this specific vascular subset. This study reports on the experience and outcomes of a Level 1 trauma center that serves both an urban and a large rural population over a 20-year period to identify bypass outcomes and surveillance protocols. METHODS: Database of a single vascular group at an academic center was queried for trauma patients requiring upper or lower extremity revascularization between January 1, 2002, and June 30, 2022. Patient demographics, indications, operative details, operative mortality, 30-day nonoperative morbidity, revisions, subsequent major amputations, and follow-up data were analyzed. RESULTS: A total of 223 revascularizations were performed, 161 (72%) lower and 62 (28%) upper extremities. One hundred sixty-seven patients (74.9%) were male, with a mean age of 39 years (range, 3-89 years). Comorbidities included hypertension (n = 34; 15.3%), diabetes (n = 6; 2.7%), and tobacco use (n = 40; 17.9%). Mean follow-up time was 23 months (range, 1-234 months), with 90 patients (40.4%) lost to follow-up. Mechanisms included blunt trauma (n = 106; 47.5%), penetrating trauma (n = 83; 37.2%), and operative trauma (n = 34; 15.3%). Bypass conduit was reversed vein (n= 171; 76.7%), prosthetic (n = 34; 15.2%), and orthograde vein (n = 11; 4.9%). Bypass inflow artery was superficial femoral (n = 66; 41.0%), above-knee popliteal (n = 28; 17.4%), and common femoral (n = 20; 12.4%) in the lower extremity, and brachial (n = 41; 66.1%), axillary (n = 10; 16.1%), and radial (n = 6; 9.7%) in the upper extremity. Lower extremity outflow artery was posterior tibial (n = 47; 29.2%), below-knee popliteal (n = 41; 25.5%), superficial femoral (n = 16; 9.9%), dorsalis pedis (n = 10; 6.2%), common femoral (n = 9; 5.6%), and above-knee popliteal (n = 10; 6.2%). Upper extremity outflow artery was brachial (n = 34; 54.8%), radial (n = 13; 21.0%), and ulnar (n = 13; 21.0%). Total operative mortality was nine patients (4.0%), all involving lower extremity revascularization. Thirty-day non-fatal complications included immediate bypass occlusion (n = 11; 4.9%), wound infection (n = 8; 3.6%), graft infection (n = 4; 1.8%), and lymphocele/seroma (n = 7; 3.1%). All major amputations (n = 13; 5.8%) were early and in the lower extremity bypass group. Late revisions in the lower and upper extremity groups were 14 (8.7%) and four (6.4%), respectively. CONCLUSIONS: Revascularization for extremity trauma can be performed with excellent limb salvage rates and has demonstrated long-term durability with low limb loss and bypass revision rates. The poor compliance with long-term surveillance is concerning and may require adjustment in patient retention protocols; however, emergent returns for bypass failure are extremely low in our experience.

Polyarteritis Nodosa Following Vaccination Against Hepatitis B Virus with Lower-Extremity Manifestations: A Case Report.

Polyarteritis nodosa is a progressive, often life-threatening, vasculitis affecting multiple organs, including the skin and peripheral nerves. We report a patient presenting with systemic features of the disease and with characteristic lesions in the feet 3 weeks after vaccination against hepatitis B virus infection.

Carotid interventions (CEA and CAS) in acute stroke patients: which procedure on which patient.

Treatment of carotid bifurcation disease in patients presenting with acute stroke has been a controversial issue over the past four decades. Classically, patients were asked to wait four to six weeks before intervention was entertained in order for the brain to stabilize and the risks of intervention to be minimized. Unfortunately, up to 20% of patients will have a secondary event after their index event and the window of opportunity to save potentially salvageable ischemic tissue will be missed. Early reports had demonstrated poor results with intervention. However, more recently, institutions such as ours have demonstrated excellent results with early intervention in patients who present with stable mild to moderate stroke with an NIH stroke scale less than 15 and preferably less than 10, present with stroke and ipsilateral carotid artery lesion of 50% or greater. Also more recently, we have been aggressively treating patients with larger ulcerative plaques even if the stenosis approaches 50%. In our and others experiences, patients who are treated at institutions that have comprehensive stroke centers (CSCs) where they have a multidisciplinary system that consists of vascular surgeons, neuro interventionalists, stroke neurologists, specifically trained stroke nursing staff and a neuro intensive ICU have had optimal results. Early assessment, diagnosis of stroke with recognition of cause of embolization is mandatory but patient selection is extremely important; finding those patients who will benefit the most from urgent intervention. Most studies have demonstrated the benefit of carotid endarterectomy in these patients. More recent studies have demonstrated acceptable results with carotid stenting, especially in smaller lesions, those less than 1.2 centimeters. Early intervention should be avoided in most patients who are obtunded or with an NIH stroke scale greater than 15 or who do not have any "brain at risk" to salvage. These patients may be better served by being treated medically and the small group of patients that do have some improvement may benefit from interval intervention.

TNF-alpha disruption of lung endothelial integrity: reduced integrin mediated adhesion to fibronectin.

Tumor necrosis factor-alpha (TNF-alpha) causes an increase in transendothelial protein permeability of confluent monolayers of calf pulmonary artery endothelial (CPAE) cells, and the addition of plasma fibronectin (pFn) to the culture medium can attenuate this increase in permeability. We determined if reduced integrin function had a role in decreased endothelial cell adhesion to immobilized Fn after exposure of the endothelial monolayers to TNF-alpha. TNF-alpha also causes a reorganization of the subendothelial Fn rich matrix and a significant loss in RGD-dependent adhesion of TNF-alpha treated CPAE cells to pFn coated surfaces. However, flow cytometry revealed no decrease in alpha(5)beta(1) or total beta(1) integrin expression on the surface of the CPAE cells after TNF-alpha. Reduced CPAE adhesion to immobilized Fn was, in part, due to a loss of beta(1)-integrin function since the beta(1)-integrin blocking antibody mAb 13 significantly (P < 0.05) prevented the adhesion of normal control CPAE cells but did not further reduce the adhesion of TNF-alpha-treated cells. In addition, antibodies which activate beta(1) integrins restored (P < 0.05) adhesion of TNF-alpha-treated cells to immobilized pFn but did not alter the adhesion of control cells. Despite reduced ability to adhere to immobilized Fn, TNF-alpha-treated CPAE monolayers demonstrated increased binding and incorporation of fluid-phase pFn into the subendothelial extracellular matrix (ECM) as measured by the analysis of the deoxycholate (DOC) detergent insoluble pool of (125)I-Fn in the cell layer. In contrast to the RGD-mediated adhesion of CPAE cells to matrix Fn, the increased binding of soluble pFn after TNF-alpha was not inhibited by RGD peptides or mAb 13. Thus reduced integrin-dependent adhesion of the CPAE cells to matrix Fn as well as disruption of the Fn matrix may contribute to the increased protein permeability of previously confluent endothelial monolayer after TNF-alpha. In addition, increased ability for the monolayer to incorporate fluid-phase Fn into the ECM after TNF-alpha via a non-beta(1)- integrin dependent mechanism may be a compensatory response to stabilize the Fn matrix and the endothelial barrier.