Double Major for Slashing: Management of Blunt Popliteal Fossa Trauma in Ice Hockey in the Setting of Popliteal Artery Entrapment Syndrome.

ABSTRACT: Popliteal artery entrapment syndrome (PAES) is a rare condition that produces calf claudication in young patients. It is most commonly a result of aberrant anatomy of the popliteal fossa. If undiagnosed, PAES can lead to acute ischemia and a threatened limb as a result of complete arterial occlusion or embolism. Ice hockey is a contact sport, and slashing on the covered legs is well described as a strategy and contact point. We present a unique case that highlights a blunt popliteal artery injury in a young player with an underlying type 2 PAES. We discuss the initial diagnosis and endovascular/vascular surgical treatment, followed by the delayed management of the popliteal artery injury. We also provide considerations for popliteal fossa blunt trauma and need for future protection of the popliteal fossa for athletes.

Importance of diversity, equity, and inclusion in the community practice setting.

Vascular surgeons of all backgrounds play an important role in providing high quality vascular surgical care in their communities. In America, with our diverse population and communities, patients presenting with vascular disease are very common and could pattern the community demographic. Often faced with the challenges of community hospital politics and demand, the vascular surgical workforce has continued to be active members in their communities, focusing on their strengths to lead vascular surgery healthcare in an environment of high patient demand. Having a varied vascular surgery workforce provides all patients afflicted by vascular disease a comfortable opportunity for compassionate and empathic vascular care. This is a significant strength of vascular care when diversity, equity, and inclusion are supported by the leadership.

Ensuring equity, diversity, and inclusion in the Society for Vascular Surgery: A report of the Society for Vascular Surgery Task Force on Equity, Diversity, and Inclusion.

Diversity, equity, and inclusion represent interconnected goals meant to ensure that all individuals, regardless of their innate identity characteristics, feel welcomed and valued among their peers. Equity is achieved when all individuals have equal access to leadership and career advancement opportunities as well as fair compensation for their work. It is well-known that the unique backgrounds and perspectives contributed by a diverse workforce strengthen and improve medical organizations overall. The Society for Vascular Surgery (SVS) is committed to supporting the highest quality leadership, patient care, surgical education, and societal recommendations through promoting diversity, equity, and inclusion within the SVS. The overarching goal of this document is to provide specific context and guidance for enhancing diversity, equity, and inclusion within the SVS as well as setting the tone for conduct and processes beyond the SVS, within other national and regional vascular surgery organizations and practice settings.

Early application of an intermittent pneumatic compression device is safe and results in proximal arteriovenous fistula enlargement.

INTRODUCTION:: Delays in arteriovenous fistula maturation can cause care delays and increased costs. Increased distention pressure and intermittent wall shear stress may dilate veins based on prior research. Early use of non-invasive devices may help assist clinical arteriovenous fistula dilation. METHODS:: This was an Institutional Review Board approved study. After arteriovenous fistula creation, a novel, intermittent pneumatic compression device (Fist Assist®) was applied 15 cm proximal to arteriovenous fistula enabling 60 mmHg of cyclic compression for 6 h daily for 30 days. Among the patients who completed 1 month follow-up, 30 (n = 30) arteriovenous fistula patients were in the study arm to test vein dilation with Fist Assist. Controls (n = 16) used a sham device. Vein size was measured and recorded at baseline and after 30 days by duplex measurement. Clinical results (percentage increase) were recorded and tested for significance. RESULTS:: No patients experienced thrombosis or adverse effects. Patient compliance and satisfaction was high. After 1 month, the mean percentage increase in vein diameter in the Fist Assist treatment group was significantly larger (p = 0.026) than controls in the first 5 mm segment of the fistula after the anastomosis. All fistulas treated with Fist Assist are still functional with no reported thrombosis or extravasations. CONCLUSIONS:: Early application of an intermittent pneumatic compression device may assist in arteriovenous fistula dilation and are safe. Non-invasive devices like Fist Assist may have clinical utility to help fistulae development and decrease costs as they may eventually assist maturation.

Early application of an intermittent pneumatic compression device assists dilation of radiocephalic fistulas.

INTRODUCTION:: Radiocephalic fistulas are the preferred type of arteriovenous fistula due to their advantageous location. However, radiocephalic fistula maturation has historically been inferior to brachiocephalic fistulas. Research indicates that intermittent compression may aid in forearm vein dilation. Early use of a compression device may assist radiocephalic fistula maturation. OBJECTIVES:: This prospective, randomized, placebo controlled study evaluates device safety and the effect of intermittent compression on vein size of radiocephalic fistulas and brachiocephalic fistulas. METHODS:: This was an institutional review board-approved study. After fistula creation, a novel, intermittent pneumatic compression device (Fist Assist®) was worn 15 cm proximal to fistulas 6 h daily for 30 days. Those in the treatment group (n = 43) wore Fist Assist® (24 with brachiocephalic fistulas and 19 with radiocephalic fistulas). Clinical controls (n = 16) wore a sham device. Vein diameter was measured at 0 and 30 days by duplex measurement. Percentage increase was recorded and tested for significance. RESULTS:: After 30 days, the mean percentage increase in vein diameter in the radiocephalic fistula treatment group was significantly larger than brachiocephalic fistulas in the treatment group at all proximal locations from the anastomosis. Increases in percentage vein dilation for those in the radiocephalic fistula treatment group were significantly larger than those in the control group. All fistulas treated with Fist Assist® are still functional with no reported complications. CONCLUSION:: Early application of the Fist Assist® device may be more effective at helping radiocephalic fistula mature as compared to brachiocephalic fistulas. Successful radiocephalic fistula maturation may decrease vascular access costs, reduce complications, and preserve upper arm veins for future use in vascular access.

Training vascular access surgeons: technicians or specialists?

Internationally, vascular access (VA) surgery is delivered in a varied and diverse fashion and subsequently, training in vascular access is poorly defined. Experience of VA during surgical training has implications on future practice. The scope of VA procedures is increasing, yet the focus in vascular training remains largely in the technical aspects of surgery rather than the more comprehensive aspects of surgery applied to dialysis and renal care. To achieve special skills in vascular access surgery may require a change to traditional training with an additional focus on developing an extended portfolio of knowledge and skills. A small number of specialized courses and training facilities are developing to address these issues.

Ultrastructure of endothelial cells under flow alteration.

Endothelial cells are stable and quiet in normal animals. They arrange regularly and have a smooth lumen surface and thin endothelial wall. According to Thoma's principle (1893) and Kamiya and Togawa's principle (1980) on the relationship of the vascular diameter to flow alteration, blood flow is in equilibrium to the diameter and in a physiological state. That is to say, there is no fast flow or slow flow. To understand the nature of the endothelial cells, we should investigate endothelial cells under flow alteration to break the equilibrium state. Endothelial cells under increased flow were studied in arteries with an arteriovenous fistula or in the capillaries of myocardium with volume-overloaded hearts or of the skeletal muscle by electrical stimulation. Those under decreased flow were studied by the closure of the fistula or by ceasing the stimulation. Endothelial cells in the coarctation of the arteries were also observed. Endothelial cells were activated by increased flow in the arteries and capillaries, while they were inactivated by decreased flow. Endothelial activation is characterized as lumen protrusions, increase of cytoplasmic organelles, abluminal protrusions, basement membrane degradation, internal elastic lamina degradation in the arteries, and sproutings in the capillaries. These are ultrastructurally comparable to angiogenesis. Endothelial inactivation is characterized by the decrease of endothelial cell number with apoptosis, which is ultrastructurally comparable to angioregression. We assume that endothelial cells respond to increased flow by angiogenesis and to decreased flow by angioregression.

Acute aortoiliac and femoral artery thrombosis complicating diabetic ketoacidosis.

Acute abdominal aortic occlusion is a devastating event with high associated rates of morbidity and mortality even with surgical intervention. This report describes a case of acute aortoiliac and femoral artery occlusion likely resulting from a hypercoagulable state caused by diabetic ketoacidosis (DKA). Vascular thrombosis is a little-known but potentially devastating complication of DKA that should be considered in every patient treated for DKA and should be added to the differential diagnoses when attempting to determine the etiology of a thrombosed vessel.

Endovascular repair of traumatic aortic pseudoaneurysm with associated celiacomesenteric trunk.

PURPOSE: To report stent-graft repair of a traumatic aortic pseudoaneurysm in proximity to a celiacomesenteric trunk. CASE REPORT: An 18-year-old woman suffered a large gunshot wound to the right flank. At laparotomy, only a large, nonexpanding right retroperitoneal hematoma was found, which was thought to represent significant penetrating trauma to the kidney mass. The patient was monitored in the intensive care unit. One week later, computed tomography revealed a partially infarcted right kidney and a 2.3-cm supraceliac aortic pseudoaneurysm, with adjacent bullet fragments. An angiogram confirmed the pseudoaneurysm and showed it to be 7 mm from the celiacomesenteric trunk. Endovascular repair was undertaken with a 16 x 55-mm AneuRx stent-graft, which was successfully placed across the aortic pseudoaneurysm without covering the celiacomesenteric trunk. Imaging at 12 months revealed no endoleak and full pseudoaneurysm exclusion. CONCLUSIONS: This operative approach is appropriate for the individual patient who has suitable anatomy and a clinical course that requires immediate repair of an aortic injury to prevent further complications and delays in ancillary treatments.

High flow drives vascular endothelial cell proliferation during flow-induced arterial remodeling associated with the expression of vascular endothelial growth factor.

Endothelial cell activation and proliferation are the essential steps in flow-induced arterial remodeling. We investigated endothelial cell turnover in the early stages of high-flow in the rabbit common carotid arteries using an arteriovenous fistula (AVF) model by kinetic investigation of cell proliferation and cell molecular analysis. BrdU was administrated to label endothelial cells (ECs) in DNA synthetic phase (S-phase) of the cell mitotic cycle. Pulse labeling revealed that ECs entered S-phase at 1.5 days of AVF (0.93 +/- 0.19%). Endothelial cell labeling index (EC-LI) peaked at 2 days of AVF (8.90 +/- 0.87%) with a high index of endothelial cell mitosis (EC-MI, 1.67 +/- 0.47%). Endothelial cell density increased remarkably at 3 days of AVF with a significant decrease in EC-LI (54%) and EC-MI (60%). Study of kinetics of EC proliferation revealed that endothelial cells took 16-24 h to finish one cycle of cell mitosis. Tracking investigation of pulse BrdU-labeled endothelial cells at 1.5 days showed that more than 66% of endothelial cells were BrdU-labeled 1.5 days after labeling. VEGF, integrin alphanubeta3, PECAM-1, and VE-cadherin were upregulated significantly preceding endothelial cell proliferation and kept at high levels during endothelial cell proliferation. These data suggest that endothelial cell proliferation is the initial step in flow-induced arterial remodeling. Hemodynamic forces may drive endothelial cell downstream migration. Expression of VEGF and cell junction molecules contribute to flow-induced arterial remodeling.

Arterial enlargement in response to high flow requires early expression of matrix metalloproteinases to degrade extracellular matrix.

This study investigated the effects of high flow and shear stress on the expression of matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinase-2 (TIMP-2) during flow-induced arterial enlargement using a model of arteriovenous fistula (AVF) creation on the carotid artery with the corresponding jugular vein in Japanese white male rabbits. Flow increased 8-fold 7 days after AVF. Endothelial cells (EC) and smooth muscle cells (SMC) proliferated with internal elastic lamina (IEL) degradation in response to high flow and shear stress. Expression of MMP-2 mRNA peaked at 2 days (1700-fold) and maintained high level expression. MMP-9 mRNA gave a 10.8-fold increase within 2 days and decreased later. Their proteins were detected in EC and SMC. Membrane type-1-MMP (MT1-MMP) mRNA increased 121-fold at 3 days and maintained high expression. TGF-beta1 was increased after AVF. Two-peak up-regulation of Egr-1 mRNA was recognized at 1 and 5 days of AVF. These results suggest that high flow and shear stress can mediate EC and SMC to express MMP-2 and MMP-9, which degrade cell basement membranes and IEL to induce arterial enlargement. The disproportional increase in MT1-MMP and TIMP-2 might contribute to MMP-2 activation. Egr-1 and TGF-beta1 might play important roles in this process.

Subnormal shear stress-induced intimal thickening requires medial smooth muscle cell proliferation and migration.

Arterial intimal thickening is consisted of predominately smooth muscle cells (SMC). The source of these SMCs and mechanisms response for their changes have not been well cleared. Using a model of rabbit common carotid artery (CCA) shear induced intimal thickening, we sought to identify and describe the source of SMCs in intima. The enlarged CCA 28 days after arteriovenous fistula (AVF) creation was subjected to subnormal wall shear stress (WSS) for 1, 3, and 7 days by closure of the AVF. To determine SMC proliferation, BrdU pulse labeling of SMCs was performed. BrdU-labeled SMCs were tracked over time to further confirm SMC migration. In response to subnormal WSS intimal thickening developed progressively. BrdU-labeled SMCs localized in the subendothelial area. When the BrdU-labeled medial SMCs were tracked 1 day after AVF closure, progenies of these BrdU-incorporated SMCs increased by 4.8-fold with 75% of them in the intima. They were 12-fold increased with 83% in the intima 7 days after. En face examination showed an accumulation of SMCs in internal elastic lamina gap after AVF closure, which later migrated into subendothelial area. In situ hybridization revealed increased TGF-beta1 mRNA expression in intimal SMCs. This study demonstrates that the medial SMCs are the predominant cells in subnormal WSS-induced intimal thickening. Early expression of TGF-beta1 may play an important role in the process of intimal thickening.