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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A SERIOUS CONDITION: Critical ischemia results when severe chronic ischemia worsens, creating a threatening situation for tissue survival in the lower limbs. The degree of ischemia is related to the extent of impairment in microcirculation, adding further deleterious effects to stenoses and/or obstructions of the large vessels. MANAGEMENT DIFFICULTIES: Surgery is the mainstay therapy for critical ischemia of the lower limbs. Medical therapy is indicated as first intention treatment in only 10 to 15% of the patients and in a small proportion after partial or total surgical failure when immediate secondary amputation appears to be avoidable. TREATMENTS USED: Antithrombosis agents and drugs with a hemorrheologic effect are used in case of surgical failure or non-indication for surgery. Iloprost is one of the most extensively studied hemorrheology agents. Its use improves the chances of avoiding amputation within a mid-term delay. BUERGER DISEASE: Buerger disease is a specific condition different from the two other major causes (artherothrombosis and diabetes mellitus). The therapeutic management and functional prognosis are much different.
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PMID:[The role of drug therapy in the treatment of critical ischemia of the lower limbs]. 1022 68

Thromboangiitis obliterans (TAO) has been reported to become less common in general population but more common in women, and in elderly patients. The authors looked at the clinical characteristics of TAO in Poland where there was no significant decrease of smoking and the extent of aging of the general population is less profound. They retrospectively reviewed the records of 377 patients with the diagnosis of TAO hospitalized in their institution from 1970 to 1995. If young smoking males demonstrated distal-extremity ischemia with no bruits audible over major arteries, upper limbs involvement, or superficial thrombophlebitis, the diagnosis of TAO was considered certain. When at least one of those criteria was missed, and in men older than 35 years, but in all females, typical arteriographic findings were required for the diagnosis of TAO. Connective-tissue disease, hyperlipidemia, diabetes, and hypercoagulable state were excluded. Three hundred forty-two men (91%), and 35 (9%) women had a mean age of 29.5 years at the onset of the disease (the oldest patient was 50 years old). The prevalence of TAO in southwest Poland is 8.1/100,000 and the incidence of the disease steadily declines; there was no increase of TAO in women. Three hundred thirty-seven (89%) experienced rest pain, 321 (85%) had ischemic necrosis, and 233 (62%) thrombophlebitis at some (continued on next page) time in the course of the disease. Raynaud's phenomenon occurred in only 39 patients (10%). Those patients who had quit smoking had a 50% decrease of the disease recurrences compared to their smoking period. Because the cause of declining incidence of TAO is obscure, the authors critically evaluated previously used explanations of this phenomenon. They did not confirm the observation of a change in the TAO clinical spectrum: occurrence in women did not increase, the aging of the TAO population was not observed. In Poland TAO is still a disease affecting the peripheral circulation of young smoking males with recurrent episodes of superficial thrombophlebitis and common involvement of the upper extremities; Raynaud's phenomenon is rather infrequent. Smoking cessation ameliorates the course of the disease but does not invariably stop further exacerbations.
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PMID:Sustained classic clinical spectrum of thromboangiitis obliterans (Buerger's disease). 1070 22

Many factors, both intrinsic and extrinsic, may contribute to wound recalcitrance. For example, arterial circulation may be impaired by atherosclerosis, vasospastic disorders, microemboli, thromboangiitis obliterans, vasculitis, sickle cell anemia, and antiphospholipid syndrome, all of which may impair healing. Inflammatory disorders that may lead to recalcitrance include pyoderma gangrenosum and necrobiosis lipoidica. Chronic venous insufficiency, infection, diabetes mellitus, systemic malignancy, malnutrition, and exposure to pressure and shear prolong the healing process. Wounds secondary to primary skin carcinoma will not heal. Calciphylaxis, a life-threatening metabolic disorder, leads to multiple ulcerations that are especially difficult to heal. Knowledge of common factors that lead to wound recalcitrance is essential to the wound care clinician, as accurate diagnosis results in appropriate treatment. To arrive at the diagnosis, the wound care clinician must perform a thorough history and physical examination and order relevant investigative studies. Treatment is based on correction of the identified underlying condition. By utilizing a systematic approach in the management of each patient with a chronic wound, the wound care clinician increases the probability of achieving wound closure.
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PMID:Considerations for the global assessment and treatment of patients with recalcitrant wounds. 1073 37

The authors are reporting their experience about the treatment of the acute finger ischemia concerning 14 patients. Twelve men and two women were concerned. The average age was 39 years old (18 to 65 years old). The acute finger ischemia was caused by emboli released by an ulnar aneurysm in nine cases and consecutive to an atrial fibrillation in five cases. The angiography was realized each time systemically in the emergency context. The medical or surgical etiological treatment was associated each time an emboli was found on the digital arteries. A microsurgical dissection of the digital collateral arteries permitted to perform a thrombectomy. The transversal arteriotomies were closed after collateral arteries were washed. The most proximal emboli were accessible to an extraction with a Fogarty's probe up to the superficial palmar arcade. An anticoagulant treatment was conducted in the early postoperative period. Considering this aggressive treatment, no secondary amputation was necessary up to today. The average follow-up was five years. This method has no indication for the chronic digital ischemias (diabetes, Buerger's disease) and for infectious or auto-immune arteriopathy.
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PMID:[Acute digital ischemia: a microsurgical emergency]. 1134 Sep 40

This study analyses some demographic characteristics of the amputees in Croatia, reason and level of amputation, care the amputees receive, the first prosthetic supply and functional level after rehabilitation. Anonymised data on all amputees in the Clinical Institute for Rehabilitation and Orthopaedic Aids in Zagreb (a national centre) were collected during the year 2000. Follow-up was undertaken for one year. As a result, the authors analysed 221 patients, classified into 3 groups according to the level of amputations: trans-tibial, except foot (TT), trans-femoral (TF) and bilateral amputations (bilateral). Among the population there were: 76% men and 24% women with average age of about 62 years (the average age of women was 8 years more than men). The most common diseases that resulted in amputation were: diabetes mellitus (DM) 48.9%; obstructive vascular diseases (OD): occlusive peripheral arterial disease, Buerger's disease and atherosclerosis 27.1%; trauma 11.3%; both OD and DM 7.2%; osteomyelitis (OM) 3.2% and tumours (TM) 2.3%. Average period from the amputation to admission for prosthetic supply was over 190 days but the average period from admission to discharge from the Institute was about 40 days. Prosthetic supply was accompanied by certain complications: flexion contractures of neighbouring joints, knee 37.9% and hip 35.2%; local complications of soft tissues: necrosis, wound dehiscence, soft tissue surplus, ischaemic tissue damage (the most frequent in TT amputation 35.9%) and phantom pain (55.7% of patients). Hours of daily use of the prosthesis at discharge was about 5 hours. Greater independence in fitting and removing the prosthesis was observed in patients with TT amputation (86.4%). In conclusion, it can be said that the time between the amputation and the beginning of the prosthetic supply, mobility at the time of admission, frequency of general and local complications and number of days in prosthetic supply, are very important for the result of rehabilitation.
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PMID:Experience in prosthetic supply of patients with lower limb amputations in Croatia. 1222 55

The wide variation in the way coronary artery disease (CAD) affects different ethnic groups and the associated risk factor profiles of these groups have been extensively studied, but ethnic differences in the clinical manifestations of peripheral vascular disease (PVD) have been relatively neglected. The aim of the present review is to provide an overview of PVD in different ethnic groups and to explore possible pathophysiological factors accounting for these differences. Atherosclerotic PVD is generally less prevalent in Indo-Asians and Afro-Caribbeans than in caucasians, despite the 'classical' risk factors being as prevalent, if not more so, suggesting the possibility of as yet unidentified risk factors in these groups. Angiographic and microscopic evidence suggests that patients of African or Afro-Caribbean origin suffer from a different pattern of PVD, which primarily affects the distal arteries. In contrast, Indo-Asians tend to suffer from thromboangiitis obliterans (Buerger's disease) far more frequently than other ethnic groups; thus, their arterial disease appears to present much earlier and with greater severity. However, if this sub-category of patient is excluded, they seem to suffer much less from 'simple' atherosclerotic disease than their caucasian counterparts. Despite a higher prevalence of diabetes among Indo-Asians, the prevalence of intermittent claudication is considerably less in this ethnic group.
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PMID:Ethnic differences in peripheral vascular disease. 1242 70

Thromboangiitis obliterans (TAO) is a nonatherosclerotic, nonnecrotizing, nonspecific, segmental inflammatory obliterative vasculitis, characterized by decreased flow to the distal extremities and increased risk of amputation. While smoking cessation is viewed as critical to successful treatment, various therapeutic options have been employed. While many treatment regimens seek to diminish platelet function, there are relatively few studies of platelet function in this disease entity and even fewer that have offered evidence of increased platelet activity. The authors report here 2 cases of TAO in which evaluations for hypercoagulable states and of platelet function were performed. Platelet contractile force (PCF) was found to be 82% higher than a normal control in 1 TAO patient and 340% higher than normal in the second patient. This was true despite the fact that platelet aggregations confirmed suppression of aggregation by antiplatelet medications. Elevated PCF has been seen in a variety of conditions, such as coronary artery disease and diabetes mellitus, in which endothelial function is abnormal. Whether high PCF values play a role in the pathogenesis of these diseases or simply serve as markers of enhanced platelet function and/or endothelial dysfunction awaits additional evaluations.
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PMID:Enhanced platelet force development despite drug-induced inhibition of platelet aggregation in patients with thromboangiitis obliterans--two case reports. 1247 39

Between May 1990 and April 2000, 61 patients with severe occlusive arterial disease (44 with thromboangiitis obliterans, 13 with atherosclerosis, and four with diabetes mellitus), who had not responded to previous nonsurgical and surgical treatment and had chronic critical ischemia in the lower limbs, had corticotomy near major neurovascular bundles and periosteal elevation along the whole length of the bone. This corticotomy consisted of elevation of a longitudinal window in the lateral cortex of the tibia to induce formation of neovascularity. The neovascularity is a part of the inflammatory response to fracture and periosteal elevation. The longest followup was 10 years and the shortest was 6 months. In 50 of 61 patients there was complete relief from pain at rest and indefinite postponement of amputation. Digital subtraction angiography studies before and after surgery showed the presence of a new vascular collateral network across the affected arteries, a process that improved the circulatory status of the ischemic limbs. The induced neovascularity acted as endogenous biologic bypass conduits and seemed to provide relief for patients with small and diffuse artery disease, when vascular reconstruction otherwise was impossible.
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PMID:Induced angiogenesis for limb ischemia. 1283 75

Prothrombin activation requires the direct interplay of activated platelets and plasma clotting factors. Once formed, thrombin causes profound, irreversible activation of platelets and reinforces the platelet plug via fibrin formation. Delayed or deficient thrombin production increases bleeding risk. Commonly employed coagulation assays, the prothrombin and partial thromboplastin times, use clot formation as a surrogate marker of thrombin generation. These assays routinely utilize platelet-poor plasma and completely miss the effects of platelets. Other markers of thrombin generation, prothrombin fragment 1 + 2 (F1 + 2) and thrombin-antithrombin complex, are typically measured after the fact. We report a simple assay, which employs the onset of platelet contractile force (PCF) as a surrogate marker of thrombin generation. PCF generation occurs concomitant with the burst of F1 + 2 release. The time between assay start and PCF onset is termed the thrombin generation time (TGT). TGT is prolonged in clotting factor deficiencies and in the presence of direct and indirect thrombin inhibitors. TGT shortens to normal with clotting factor replacement and shortens with administration of recombinant factor VIIa. TGT is short in thrombophilic states such as coronary artery disease, diabetes and thromboangiitis obliterans and prolongs toward normal with oral and intravenous anticoagulants.
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PMID:Onset of force development as a marker of thrombin generation in whole blood: the thrombin generation time (TGT). 1294 Oct 40

Buerger's disease (thromboangiitis obliterans or TAO) is a clinical syndrome characterized by the development of segmental thrombotic occlusions of the medium and small arteries of the extremities. It is clinically and pathologically distinguishable from arteriosclerosis and necrotizing arteritis. Afflicted patients are mostly young, male, inveterate tobacco smokers who present with distal extremity ischemia, ischemic ulcers, or frank gangrene of the toes or fingers. Large arteries are typically spared, as are the coronary, cerebral, and visceral circulations. While mortality is not increased, patients with Buerger's disease often suffer from severe ischemic pain and tissue loss culminating in minor and major limb amputation. Clinical diagnostic criteria generally include the following: (1) history of smoking or tobacco abuse; (2) age of onset less than 45 to 50 years; (3) infrapopliteal, segmental arterial occlusions with sparing of the proximal vasculature; (4) frequent distal upper extremity arterial involvement (Raynaud's syndrome or digital ulceration); (5) superficial phlebitis; and (6) exclusion of arteriosclerosis, diabetes, true arteritis, proximal embolic source, and hypercoagulable states. Typical arteriographic patterns have been described that are suggestive, but not pathognomonic. While the cause of Buerger's disease remains unknown, the disease onset and clinical course are inextricably linked to tobacco abuse. Acute Buerger's disease is characterized histopathologically by intensely cellular vessel wall inflammation, giant cell foci, and hypercellular thrombi, but with preservation of the elastic lamina and the overall vascular wall architecture. Most investigators feel that Buerger's disease is an immune-mediated endarteritis; recent immunocytochemical studies have identified the linear deposition of immunoglobulins and complement factors along the elastic lamina. The inciting antigen has not been discovered. Tobacco abstinence generally results in disease quiescence and remains the mainstay of treatment.
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PMID:Buerger's disease in the 21st century: diagnosis, clinical features, and therapy. 1297 57


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