F. William Blaisdell

The Pathophysiology of Skeletal Muscle Ischemia and the Reperfusion Syndrome: A Review:

There are two components to the reperfusion syndrome, which follows extremity ischemia. The local response, which follows reperfusion, consists of limb swelling with its potential for aggravating tissue injury and the systemic response, which results in multiple organ failure and death. It is apparent that skeletal muscle is the predominant tissue in the limb but also the tissue that is most vulnerable to ischemia. Physiological and anatomical studies show that irreversible muscle cell damage starts after 3 h of ischemia and is nearly complete at 6 h. These muscle changes are paralleled by progressive microvascular damage. Microvascular changes appear to follow rather than precede skeletal muscle damage as the tolerance of capillaries to ischemia vary with the tissue being reperfused. The more severe the cellular damage the greater the microvascular changes and with death of tissue microvascular flow ceases within a few hours-the no reflow phenomenon. At this point tissue swelling ceases. The inflammatory responses following reperfusion varies greatly. When muscle tissue death is uniform, as would follow tourniquet ischemia or limb replantation, little inflammatory response results. In most instances of reperfusion, which follows thrombotic or embolic occlusion, there will be a variable degree of ischemic damage in the zone where collateral blood flow is possible. The extent of this region will determine the magnitude of the inflammatory response, whether local or systemic. Only in this region will therapy be of any benefit, whether fasciotomy to prevent pressure occlusion of the microcirculation, or anticoagulation to prevent further microvascular thrombosis. Since many of the inflammatory mediators are generated by the act of clotting, anticoagulation will have additional benefit by decreasing the inflammatory response. In instances in which the process involves the bulk of the lower extremity, amputation rather than attempts at revascularization may be the most prudent course to prevent the toxic product in the ischemic limb from entering the systemic circulation.

Why small caliber vascular grafts fail: a review of clinical and experimental experience and the significance of the interaction of blood at the interface.

The results using polytetrafluoroethylene (PTFE) and tanned human umbilical cord vein (HUV) grafts are discussed. These two grafts perform well for reconstructions above the knee and the results are similar to the autogenous saphenous vein (ASV) grafts in several series; however, in more distal reconstructions the PTFE and HUV are far inferior to ASV grafts. The factors responsible for graft failure including the events which take place at the blood interface are reviewed. New material surfaces under investigation such as degradable grafts, heparin-bonded surfaces, and endothelial-seeded fabrics are also addressed.

Late results of axillary-femoral bypass grafting

Abstract An analysis of the results of axillary-femoral bypass demonstrates that a single axillary artery can restore satisfactory blood flow to both lower extremities, but the late patency of the reconstruction does not compare favorably with conventional intra-abdominal aortic reconstruction. Technical modifications, including the use of a 10 mm weaveknit prosthesis combined with a crossover femorofemoral bypass, have substantially improved late patency, so that a comparison of the cumulative patency rates with this prosthesis closely parallels the cumulative survival rate of the group of poor risk patients for whom the operation was intended. Current indications for the use of the operation include the restoration of blood flow to the leg after removal of an infected intra-abdominal prosthesis, and treatment of advanced ischemia in elderly poor risk patients in whom conventional intra-abdominal vascular reconstruction carries a high morbidity and mortality.

Ligation and extraanatomic arterial reconstruction for the treatment of aneurysms of the abdominal aorta

PURPOSE Since Blaisdell et al. first described axillobifemoral bypass and aortic exclusion to treat patients at high risk with abdominal aortic aneurysms in 1965, this approach has been controversial. To help define the appropriate application of this procedure, the recent experience of the authors was reviewed. METHODS Twenty-six patients underwent operation between March 1980 and August 1992. Mean age was 71 +/- 7 years. Average aneurysm diameter was 7.0 +/- 1.5 cm. Sixty-nine percent of the aneurysms were symptomatic; 21% were suprarenal. All patients had serious comorbid factors. All underwent axillobifemoral bypass with iliac artery ligation; the infrarenal aorta was also ligated in 62%. RESULTS There were two postoperative deaths (7.7%). One- and two-year survival rates were 59% and 38%, respectively. Three patients died of aneurysm rupture (11.5%); the aorta had not been ligated in two of these patients. The remaining late deaths were due to comorbid conditions. Extraanatomic bypass grafts thrombosed in five patients; no limbs were lost. CONCLUSIONS Axillobifemoral bypass without aortic ligation does not effectively reduce the risk of aneurysm rupture. However, axillobifemoral bypass with aortic ligation is an acceptable treatment for patients with severe medical problems and symptomatic, anatomically complicated, or large abdominal aortic aneurysms. Because the risk of aneurysm rupture is not completely eliminated, this procedure should be reserved for patients with high-risk aneurysms who would not tolerate direct aortic replacement.

Extraanatomic Bypass Grafts

Extraanatomic arterial bypass grafting is used when risk of standard operations is high because of associated disease or technical problems, in patients with ischemic lower extremities as a result of severe pulmonary or cardiac disease. Results have been good with femoro-femoral or axillo-femoral bypass.

The Society for Vascular Surgery: As I remember – An interview with Dr. Michael E. DeBakey

Abstract As part of the activities to celebrate the first fifty years of the Society, the Celebration Committee decided to conduct a videotape interview of the two surviving founding members: Drs. Michael E. DeBakey and Harris B. Shumacker, Jr. Part of these two interviews will be shown at the 50th Annual Meeting in Chicago. The following transcript is from the interview with Dr. DeBakey conducted by Dr. F. William Blaisdell, Calvin B. Ernst, and James S. T. Yao.

Civil War Vascular Injuries

As the result of the insistence of the Surgeon General during the United States Civil War, there was extensive documentation of injuries to major blood vessels and their resulting complications. The specific treatment of vascular injuries during the Civil War was ligation of the injured vessel or amputation. This was before there was any knowledge of the cause and prevention of infection. Overall, the results were dismal, with a mortality rate of nearly 60% for the more than 1000 soldiers treated by arterial ligation. The most important contribution of these medical reports was to define how the injuries should be diagnosed and managed. Many of the principles that developed as the result of this post-war review are as valid today as they were then. Unfortunately, it seems that many of these lessons have had to be relearned by the surgeons who have participated in each of our subsequent military conflicts.

Changes in county hospitals during Sheldon’s tenure

Dramatic changes took place in county hospitals during Dr. Sheldons tenure, 1964 to 1985. The primary impact came from Medicaid and Medicare legislation in 1965. The secondary impact came as the result of the drug culture entering American cities.

Progress in prevention and treatment of venous thromboembolism : a worldwide problem : introduction

One hundred years ago, Virchow postulated that clinical thrombotic episodes resulted from endothelial damage, stasis, and hypercoagulability. Yet, despite major advances in the last decade due to a better understanding of the causes, prevention, and treatment of venous thromboembolism, there has been relatively little progress made in alleviating the problem. It has been pointed out by Dr. Kakkar that, despite advances in the management of pulmonary embolism, the overall mortality due to this condition in England and Wales is increasing as evidenced by the Registrar Generals mortality statistics. He has noted that between 50 and 200,000 deaths occur each year in the United Kingdom from pulmonary embolism and, although many of these deaths occur in the elderly and seriously ill, pulmonary embolism also affects a large number of patients undergoing elective surgery. Unfortunately, two-thirds of the deaths from pulmonary embolism occur within the first 30 minutes of the embolic event, too late to be benefited by any type of specific therapy. More than 80% of these emboli occur without premonitory signs of peripheral venous thrombosis. Consequently, prophylaxis or treatment of the latter has often not been given. During most of the past 100 years, the implication has been that clotting tendencies are acquired. In the past decade, congenital clotting conditions have not only been identified, but it is now evident that the incidence of these disorders exceeds that of the hereditary bleeding disorders. This symposium is an effort to bring together an international group of distinguished physicians and surgeons with a special interest in the prevention and treatment of peripheral venous thrombosis and its complications. The immediate problem of venous thrombosis and its relationship to the postoperative patient has already been alluded to. Moreover, as pointed out in this series of articles, peripheral venous thrombosis, which involves the lower extremities, not only results in the risk of pulmonary embolism, but also results in late morbidity from chronic deep venous insufficiency. This symposium will review the nature of the acquired and congenital clotting syndromes, update the status of prophylaxis of venous thrombosis in the surgical patient, and devote attention to the recognition of deep venous thrombosis, hopefully prior to any systemic event. It will also address the use of fibrinolytic agents in the treatment of venous thrombosis, and assess the status of surgical treatment related to preventing pulmonary embolism and reducing the morbidity of massive deep venous thrombosis. Finally, it will discuss the evolution of the postthrombotic syndrome.