Surgical management of chronic venous insufficiency.
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Publications and source records attributed to A B Lumsden.
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BACKGROUND: Acute aortic occlusion most commonly results from aortic saddle embolus or thrombosis of an atherosclerotic abdominal aorta. The purpose of this study was to review the experience at a university hospital to better define the diagnosis and management of this uncommon process. METHODS: A retrospective chart review was performed from patients admitted to Emory University Hospital with acute occlusion of the abdominal aorta from 1985 through 1997. RESULTS: Thirty-three patients were identified. In group EMB (n = 16), occlusion was due to saddle embolus. In group IST (n = 17), occlusion was attributed to in situ thrombosis of a severely diseased aorta. Operative procedures performed included transfemoral embolectomy (15), aorto-bifemoral bypass (9), axillobifemoral bypass (5), fasciotomy (3), and thrombolysis (1). The in-hospital mortality rate was 21% (31% EMB, 12% IST), and morbidity was significant and included mesenteric ischemia (6%), bleeding complications (9%), subsequent amputation (12%), renal failure (15%), recurrent embolization or thrombosis (21%), and cardiac complications (42%). CONCLUSIONS: Acute aortic occlusion has tremendous morbidity and mortality even with optimal surgical care.
BACKGROUND: The majority of patients with peripheral vascular disease have associated medical illnesses that contribute to a substantial incidence of perioperative complications. Some of the these complications may be related to the choice of anesthetic used. An ideal anesthetic would provide good analgesia, have few complications associated with its use, including minimizing hemodynamic instability, and provide an adequate surgical environment. MATERIALS AND METHODS: Ten patients with an occluded superficial femoral artery and claudication or rest pain were selected. Eligibility criteria were a non-obese thigh and an above knee popliteal segment of at least 10 cm. Lidocaine local anesthesia with systemic sedation was employed. Above knee femoropopliteal bypasses were performed in all patients. Intraoperative fluid volume, anesthetic dose and perioperative morbidity were recorded. RESULTS: All patients tolerated the procedure well. The operating environment was excellent. Intraoperative fluid requirements were less for patients receiving local anesthesia as compared with a similar group of patients undergoing above knee femoropopliteal bypass receiving regional anesthesia (mean 1750 ml versus 3386 ml). The mean dosage of lidocaine (0.5%) was 367 mg over a mean of 116 min operating time. All patients ambulated within 8 hours. There was no perioperative morbidity, mortality or graft occlusion. CONCLUSION: This technique is easy to perform and further reduces the systemic magnitude of anesthesia, while providing excellent perioperative analgesia and a satisfactory surgical environment. It may be ideal for the high risk patient, as intraoperative fluid volume requirements are reduced. In an era where endoluminal bypass grafting is being increasingly advocated, this technique retains the benefits of bypass grafting while possibly reducing the physiological insult.
To evaluate the direct effect of nitric oxide (NO) on vascular smooth muscle cell (SMC) proliferation in vivo, we used an expanded polytetrafluoroethylene (ePTFE)-based local infusion device to deliver an NO donor, proline/NO (PROLI/NO), to the luminal boundary layer of endarterectomized artery and the distal anastomosis of the graft in a canine model. Once delivered to the blood, PROLI/NO releases NO by a mechanism involving pH-dependent decomposition. Six dogs underwent bilateral femoral artery endarterectomies. ePTFE infusion devices, blindly primed with PROLI/NO to one artery or proline to the contralateral vessel, were anastomosed proximal to the injured segments so that each animal served as its own control. PROLI/NO or proline was continuously delivered for 7 days from an osmotic reservoir, through the wall of the graft infusion device. Euthanasia was carried out at 7 days, and the processed specimens were blindly analyzed for SMC proliferation at both graft anastomoses and endarterectomized segments by a bromodeoxyuridine index assay. All dogs survived with no clinical side effects. In comparing the treated and control vessels, NO released from PROLI/NO significantly reduced SMC proliferation by 43% (13.24 +/- 1.24% versus 23.24 +/- 1.01%, P = 0.004) at the distal anastomoses and by 68% (10.58 +/- 1.63% versus 25.17 +/- 3.39%, P = 0.007) at endarterectomized segments. However, there was no significant difference in blood flow measurements between treated and control arteries (56.25 +/- 6.50 ml/min versus 46.50 +/- 3.20 ml/min, P = 0.094). These data demonstrate that local boundary layer infusion of NO released from PROLI/NO significantly reduces SMC proliferation in injured arteries with no effect on regional blood flow. This study suggests a new strategy to inhibit early SMC proliferation in injured arteries and probably to control intimal hyperplastic lesion formation in the manipulated vessels.
In an effort to characterize intimal hyperplastic lesions, we have undertaken a time-course study in a canine endarterectomy model of intimal hyperplasia. Twenty dogs underwent surgical endarterectomies of the carotid arteries. A total of 23 of 27 (85%) injured arteries were patent, which consisted of 6, 8, 5, and 4 arteries found to be patent at 1, 2, 5, and 11 weeks, respectively. Measurable intimal thickening developed at 1 week (0.08 +/- 0.01 mm) and at 2 weeks (0.13 +/- 0.02 mm), maximized at 5 weeks (0.29 +/- 0.03 mm), and subsided at 11 weeks (0.21 +/- 0.01 mm) after injury. Endothelial cells covering intimal hyperplastic tissues were seen only at 11 weeks. The intimal cell proliferation rate reached a maximum of 24% at 1 week, decreased dramatically at 2 weeks, and remained at low levels but higher than baseline levels at 5 and 11 weeks. Extracellular matrix (ECM) content accounted for 29% of total intimal volume at 1 week after endarterectomy and increased to 37, 40, and 47% at 2, 5, and 11 weeks, respectively. These data demonstrate that maximum intimal cell proliferation occurs at 1 week and maximum intimal hyperplasia at 5 weeks after arterial injury. Intimal ECM content increased with time after injury throughout the duration of this study. The uniform and consistent intimal lesion that was established in this large animal model is clinically relevant and can be used to study cellular and molecular mechanisms of restenosis and to evaluate therapeutic interventions.
We examined the effects of human recombinant basic fibroblast growth factor (bFGF) on the proliferation and migration of cultured dog smooth muscle cells (SMCs) and endothelial cells (ECs) and the effect of continuous local boundary layer infusion of bFGF on intimal hyperplasia in endarterectomized dog artery. In vitro proliferation and migration of dog SMCs or ECs were performed using direct counting and Boyden's chamber, respectively. At a dose of 10 ng/mL, bFGF significantly promoted both SMC and EC proliferation (7- and 4-fold, respectively) and migration (2.3- and 1.9-fold, respectively). Six dogs underwent bilateral carotid endarterectomies. A newly designed local infusion device with an osmotic pump continuously delivered bFGF to one artery or vehicle solution to the contralateral artery for 14 days. The intimal thickness and area in the bFGF-treated vessels were increased by 72 and 81%, respectively, compared with control arteries (P < 0.05). As assessed by the bromodeoxyuridine index, the proliferative activity was increased by 73% in bFGF-treated arteries (P = 0.03). Furthermore, cell proliferation at the distal anastomoses of local infusion device was significantly increased in the bFGF-infused grafts compared with distal anastomoses in the control grafts (13.24 +/- 1.24% versus 5.24 +/- 1.01%, P < 0.01). These data demonstrate that human recombinant bFGF has a potent effect on dog SMC and EC proliferation and migration, and that local infusion of exogenous bFGF significantly enhances the intimal hyperplasia formation and cell proliferation to vascular injury. We conclude that the bFGF pathway may contribute to the development of intimal hyperplastic lesions.
Maintenance of dialysis access continues to plague care of the patient with ESRD. Because of the poor outcomes from surgical revision, there is increasing interest in balloon angioplasty as a technique for dilating stenoses in the functioning, but compromised graft. Forty patients treated with percutaneous transluminal angioplasty (PTA), without subsequent intervention, for graft dysfunction were retrospectively studied. Time to thrombosis of the graft was noted. Patency was determined using the Kaplan-Meier technique. Patency following PTA at 1, 6, and 12 months was 76, 27, and 10%. Patency following PTA of arteriovenous graft stenoses results in disappointing medium and long-term patency. Alternate strategies for improving patency of these conduits should be explored.
In this report we describe the outcome of a 6-week study of the valve-stent device in a goat model. Six female goats underwent endoscopic subcutaneous harvest of a valve-containing segment of external jugular vein. This segment was sutured inside a 10-mm Wallstent (Schneider Inc., USA), and the device was compressed and loaded into a 12 Fr. introducer sheath and deployed through a venotomy into the contralateral external jugular vein. The animals were anticoagulated for 1 week and euthanized at 6 weeks. Flow studies, manual strip test, and angioscopic evaluation were performed prior to sacrifice. All six valve-stents were patent at harvest by Doppler flow studies, and five of six were competent as demonstrated by the manual strip test. At angioscopic evaluation, the valves were open. Gross and histologic examination revealed intact valve leaflets in five specimens. This technique is a minimally invasive approach to valve harvest and transplantation with a valve-stent device. We have demonstrated that valve-stent can remain patent and competent for up to 6 weeks. This technique may have potential application in venous valvular incompetence.
This study attempts to prevent neointimal hyperplasia by coating the graft luminal surface with a derivative of phosphorylcholine (PC), thereby providing a biocompatible surface with the assumption of limiting pannus tissue ingrowth from the graft anastomoses. Bilateral carotid artery bypass grafts were placed in six dogs using expanded polytetrafluoroethylene (ePTFE). In each animal, one carotid arterial-arterial conduit was constructed using a graft having a PC coating over the entire luminal surface of the graft. On the contralateral side, uncoated graft served as a control. The processed specimens were analyzed for graft neointimal area and neointimal thickness. Cell proliferation was assessed by staining for bromodeoxyuridine (BrdU) incorporation. All grafts were patent except one control graft that was occluded at 4 weeks. There was a significant reduction in the anastomotic graft neointimal area between the treated and control groups (0.27 +/- 0.17 mm2 versus 0.53 +/- 0.13 mm2, respectively; p = 0.008). Furthermore, the BrdU labeling index in the graft neointimal tissues was significantly smaller (p < 0.001) in the treated group (2.64 +/- 0.77%) as compared with the control group (5.07 +/- 0.83%). These data demonstrate that PC coating of ePTFE significantly reduces graft neointimal hyperplasia and cell proliferation in a canine carotid artery bypass model. The application of PC within the ePTFE graft effectively blocks tissue ingrowth from the adjacent native vessel, thereby preserving the anastomosis luminal diameter.
PURPOSE: Maintenance of hemodialysis access grafts represents an enormous social and clinical problem. Current grafts and graft salvage techniques are inadequate. Consequently, there has been increasing interest in the use of minimally invasive catheter techniques to prophylactically treat stenoses in functioning arteriovenous grafts. Prophylactic balloon angioplasty has been widely suggested as prolonging assisted primary patency. We have performed a prospective randomized trial to compare patients who underwent percutaneous transluminal angioplasty (PTA) for graft stenoses > 50% with a control group that received no intervention. Our hypothesis was that to be efficacious a minimal benefit of 20% prolongation in patency would be necessary. METHODS: Color flow duplex scanning was used to detect > 50% stenoses in functioning expanded polytetrafluoroethylene grafts. Patients were then subjected to confirmatory angiographic evaluation. Those who had angiographic stenoses > 50% were randomized to balloon angioplasty or observation. Patients were followed-up with duplex scanning every 2 months. Statistical analysis was performed using the Kaplan-Meier technique. Although demographically the patient groups were well matched, there were more prior interventions and concurrent central stenoses in the treatment group. Outcomes were graft thrombosis, graft dysfunction that precluded dialysis, and six or more PTA procedures within 18 months. RESULTS: In the treatment and observation groups, the 6-month patency rates were 69% +/- 7% and 70% +/- 7%, respectively. The 12-month patency rates for the treatment and observation groups were 51% +/- 6% and 47% +/- 4%, respectively. There was no significant difference between these two groups (p = 0.97), with an 80% confidence limit for detection of a difference greater than 20%. CONCLUSIONS: This study demonstrates that a generic approach of PTA to treat all polytetrafluoroethylene grafts with stenoses > 50% does not prolong patency and cannot be supported.
PURPOSE: Recently, very late antigen-4 (VLA-4) has been shown to mediate initial monocyte adhesion and migration to the injured artery. We hypothesized that blocking monocyte adhesion using a specific monoclonal antibody against VLA-4 may reduce intimal hyperplasia. METHODS: Bilateral carotid endarterectomies were performed in eight adult baboons. Among them, five animals received an intravenous bolus injection of anti-VLA-4 antibody (3 mg/kg) during surgery and again after 2 weeks. Three animals underwent bilateral carotid endarterectomies and served as untreated control subjects. Specimens were harvested at 4 weeks and subjected to morphometric analysis, cell proliferation assay, and immunostaining for macrophages. RESULTS: All of the endarterectomized arteries were patent except for one in the treated group. The number of macrophages in the intimal tissues was significantly reduced in the treated arteries compared with that in the control vessels (15.78 +/- 3.05 cells/section versus 33.50 +/- 6.13 cells/section; p < 0.001). The cell proliferation rate was significantly lower (p < 0.001) in the treated vessels (2.88% +/- 1.07%) compared with the control vessels (4.89% +/- 0.77%). The intimal area at the endarterectomized sites of carotid arteries was significantly less (p < 0.05) in the group treated with the anti-VLA-4 antibody (1.10 +/- 0.68 mm2) than in the control group (2.00 +/- 0.52 mm2). CONCLUSION: These data show that blocking monocyte adhesion by use of an anti-VLA-4 antibody significantly reduces the number of intimal macrophages, intimal cell proliferation, and intimal hyperplasia in injured carotid arteries in baboons. This study supports a central role for macrophages in the development of intimal hyperplasia and may suggest a new therapeutic strategy to prevent clinical restenosis.
The purpose of this study was to evaluate a technique that accelerates intimal hyperplasia by reduction of blood flow. Bilateral endarterectomies were performed in both femoral and carotid arteries in six dogs. One week later, all animals underwent banding of an artery distal to the injured region to reduce the blood flow by 50%. The contralateral injured arteries served as controls. At 11 weeks, the specimens were harvested and analyzed. Five of 12 (42%) of the flow-restricted arteries and nine of 12 (75%) of the non-flow-restricted arteries were patent at 11 weeks (P<0.05). Marked stenotic intimal hyperplastic lesions developed in the flow-restricted arteries (69% stenosis) as compared with the non-flow-restricted arteries (37% stenosis). Mean(s.d.) intimal thickness, intimal areas, and intimal/medial area ratio were 0.52(0.19) mm, 3.17(1.11) mm2, and 1.12(0.33)%, respectively, in the flow-restricted arteries. Their counterparts in the non-flow-restricted arteries were 0.21(0.09) mm, 1.70(1.09) mm2, and 0.58(0.14)%, respectively (P<0.05). Extracellular matrix comprised 48% of total intimal volumes in the flow-restricted arteries. Cell proliferation and occluded arteries were also characterized. These data demonstrate that reduction of blood flow significantly accelerated intimal hyperplasia and occlusion rates in endarterectomized arteries. Advanced intimal hyperplastic lesions (>50% stenosis) possess a high extracellular matrix content. This new animal model is a reliable generator of advanced stenotic lesions in a relatively short time period and can be used to study biologic mechanisms of stenosis and evaluate therapeutic interventions.
Arteriovenous dialysis grafts are the most commonly implanted prosthetic grafts. Thrombectomy with selective graft revision is traditional therapy for occlusions, but patency is minimally prolonged. Stenoses are determined by tactile feedback from an embolectomy catheter and lack of prograde and retrograde bleeding. An objective method for studying the graft and inflow and outflow tracts that permits appropriate endoluminal or surgical correction is described. This approach is appealing because: (i) the current approach is inadequate; (ii) it offers an objective, quantitative method to determine frequency and severity of critical stenoses within the failed access graft; (iii) remote and perigraft stenoses can be treated at the same setting; and (iv) it promotes the development of endovascular skills by surgeons in a high-volume, low-risk setting.
Central venous stenosis occurs as a complication of central venous catheterization and significantly complicates delivery of dialysis through arteriovenous grafts in the ipsilateral upper limb. This report includes two separate studies. Functioning expanded polytetrafluorethylene grafts have been prospectively evaluated using duplex scanning and angiography performed in all patients with stenoses > 50%. From this, it has been prospectively established that the incidence of unsuspected central venous stenoses in patients with functioning grafts is 29%. In the second part of the report, the authors' experience in the treatment of 25 central venous stenoses with percutaneous angioplasty and stent placement has been retrospectively reviewed. Initial technical success rate was 88%. Primary patency was 84% at 1 month, 42% at 6 months, and 17% at 1 year. Mean primary patency was 5.7 months. Stents were placed in five patients. Prevention of central venous stenosis by avoiding subclavian catheterization is optimal. Balloon angioplasty provides short-term patency, but it is the only option in most cases. The role for endovascular stent placement remains to be defined but early results are not optimistic.
Management of the patient with end stage renal disease and peripheral vascular disease represents a major challenge to the vascular surgeon. In this review, we developed guidelines for intervention based on our own institutional experience as well as literature review. There have been more than 290 patients reported to have 369 ischemic legs with threatened limb loss. There was an overall graft patency rate of 71% (range, 64% to 77%) and 60% (range, 48% to 90%) for 1 and 2 years, respectively. The mean limb salvage rate was 72% (range, 52% to 94%) at 2 years in these groups of patients. In the presence of rest pain and/or tissue loss, with favorable inflow and outflow (at least one vessel with direct flow into the foot), we strongly advised surgical bypass. In those patients who presented with rest pain and/or tissue loss, infragenicular surgical reconstruction led to a higher quality of life in comparison to patients with primary amputations. An indication for a primary amputation would be gangrene extending proximal to the mid foot. We have therefore outlined our findings and thoughts in the following article.
There is a clear association between the dorsal lithotomy position and the development of a postoperative compartment syndrome. Compartment syndrome occurs when elevated pressure in an osteofascial compartment compromises local perfusion and often results in neurovascular damage and permanent disability. Surgeons must recognize this association and provide appropriate preventative measures, have a high index of suspicion in all patients, and be prepared to make an early diagnosis when it is encountered. We will report four cases we encountered, discuss the etiology, analyze the literature, and propose a modification on patient positioning that has minimized the incidence of compartment syndrome at our institution. A variety of intraoperative events, including hypotension, hypoxemia, leg elevation, hip and knee flexion, direct pressure, and compressive bandages may all contribute to compartmental ischemia. Ischemia is followed by reperfusion, capillary leakage from the ischemic tissue, and a further increase in tissue edema. Increased edema causes further embarrassment of perfusion and perpetuation of the cycle, ultimately resulting in neuromuscular compromise secondary to ischemia. To prevent this destructive cycle, emphasis must be placed on maintaining a high index of suspicion in all patients, minimizing leg elevation, and on the importance of early diagnosis and intervention.
BACKGROUND: The plant cytotoxin saporin (SAP) is a potent ribosome-inactivating protein. When conjugated to basic fibroblast growth factor (FGF2), it selectively kills proliferating cells that have upregulated FGF receptors. In this study, we evaluated the effect of the recombinant chimeric mitotoxin rFGF2-SAP on venous anastomotic intimal hyperplasia, a major cause of failure of arteriovenous (AV) grafts. METHODS AND RESULTS: Recently designed expanded polytet-rafluoroethylene-based local infusion devices were implanted bilaterally as femoral AV conduits in six dogs. The venous anastomoses were the sites of continuous delivery of rFGF2-SAP (2.7 micrograms.kg-1.d-1) to one side and vehicle (4.6 microL.kg-1.d-1) as control to the contralateral side for 14 days. All animals survived, and all grafts were patent. Liver enzyme levels and histological analyses of liver, kidneys, and brain were normal, indicating the absence of systemic toxicity. Morphometric measurements and measurements of cell proliferation by bromodeoxyuridine index analysis were performed at both arterial and venous anastomoses. There were no significant differences between the treated grafts and the control grafts in intimal hyperplasia and intimal cell proliferation at the arterial anastomoses. In contrast, rFGF2-SAP reduced intimal thickness by 32%, intimal area by 40%, and cell proliferation index by 33% at the treated venous anastomoses compared with the control venous anastomoses (P < .05). CONCLUSIONS: These data demonstrate that local infusion of rFGF2-SAP significantly reduces venous anastomotic intimal hyperplasia and cell proliferation without systemic toxicity. This study suggests a new strategy for reducing intimal hyperplasia by the selective killing of proliferating smooth muscle cells with a potent chimeric mitotoxin through a novel local infusion device.
Renal ischemic and reperfusion injury is a significant complication of major aortic and renovascular surgery. The delivery of a preservative agent just prior to reperfusion of an ischemic kidney may decrease the reperfusion injury. The purpose of this study was to evaluate the effects of renal artery perfusates delivered at the termination of an ischemic period. Five groups of rats were evaluated. All rats underwent left nephrectomy. The right kidney was made ischemic for 45 min by occlusion of the renal artery and vein. Ischemic control animals had no renal artery perfusion. Nonischemic control animals had no renal vessel occlusion or perfusion. The other three groups were perfused during the final 4 min of ischemia with one of the following: normal saline (NS), phosphate-buffered saline (PBS), or anti-ICAM-1-antibody (mAb). The blood urea nitrogen (BUN), serum creatinine (Cr), and renal histopathologic injury of each group were compared. The ischemic control group had significantly better renal function than the group perfused with NS or mAb at 72 hr. There was no significant difference between the ischemic control and PBS groups in renal function or morphologic injury. It is concluded that none of the perfusates in the study had protected the kidney from ischemic and reperfusion injury. NS delivered in this manner was injurious to the kidney.