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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systemic causes of leg edema include idiopathic cyclic edema, heart failure, cirrhosis, nephrosis and other hypoproteinemic states. Lymphedema may be primary, or secondary to neoplasm, lymphangitis, retroperitoneal fibrosis and, rarely (in the U.S.), filariasis. Thrombophlebitis and chronic venous insufficiency are not uncommon causes. Finally, infection, ischemia, lipedema, vascular anomalies, tumors and trauma can be responsible for the swollen leg.
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PMID:The swollen leg. 18 30

Peculiarities of collateral circulation following isolated and combined ligations of the femoral vessels were studied in experiments on 62 dogs through physiologic and anatomic investigation methods. It has been shown that the ligation of the vein prevents the exsanguination of the limb, arising from an injury to the main artery, favours an accelerated anatomic reconstruction of the arterial collaterals, but increases microcirculatory disturbances, aggravates tissue ischemia and disorder of the acid-base balance, which as a whole evidences a detrimental effect of concomitant venous insufficiency upon the process of the restoration of the circulation in the limb.
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PMID:[Anatomical and physiological assessment of the collateral circulation in experimental femoral artery ligation in venous insufficiency]. 52 87

The division of the venous circulation in to two sectors, one constituted by the superficial and deep venous trunks (macrocirculation) and the other by the capillaries and precapillary venules (microcirculation), is surely schematical but aids the comprehension of many hemodynamic effects connected to hampered venous return and to the incompetence of the valvular devices. In fact many of the effects of stasis and venous hypertension (oedema, red cell diapedesis, skin dystrophies) cannot be explained merely by hydraulic mechanisms but require a primary alteration of the microvascular wall associated with structural changes of the perivascular connective tissue. The alterations that occur in microcirculation are of the utmost importance in the formation of the venules ulcerations. The passage of fibrinogen through large pores in the venules of the patients affected by venous hypertension derived from venous insufficiency creates a pericapillary fibrin deposition that cannot be removed because of inadequate blood and tissue fibrinolysis. This accumulation acts as a barrier to the diffusion of oxygen and other nutrients, determining a stasis dermatitis that may lead to tissue necrosis and ulceration. The more precise knowledge of the phenomena connected with the venous stasis at the level of microcirculation (pericapillary fibrin deposition, endothelial ischemia, blocked lymphatic drainage) will not only allow a deeper comprehension of the clinical signs but hopefully will lead to a more effective treatment of the postphlebitic syndrome.
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PMID:[Physiopathology of venous stasis at the microcirculation level]. 129 20

The degree of cutaneous microangiopathy at the medial ankle correlates with the severity of chronic venous insufficiency, most probably it is the trigger factor for development of trophic skin lesions. Using intravital fluorescence videomicroscopy, microlymphography, transcutaneous oxygen tension measurement and laser Doppler flowmetry, the microangiopathy is characterized by morphological alterations of blood and lymph capillaries and by dynamic changes (decreased transcutaneous oxygen tension reflecting microvascular ischemia, increased skin perfusion). Microangiopathy in patients with chronic venous insufficiency is recognized by the presence of dilated, elongated and tortuous (glomerulus-like) capillaries and by an increase in diameter of the pericapillary space (halo) filled by Na-fluorescein. In severe CVI a reduction of the capillary number can be observed, probably as a result of previous capillary thrombosis. Lymphatic drainage is disturbed and lymph capillaries are obliterated in part. Laser Doppler flowmetry, which detects flux in deeper, non-nutrient skin vessels, shows increased blood flow. However, the postural vasoconstrictive response remains intact and there is little alteration in the spontaneous rhythmic flux waves. In contrast to deeper skin flux transcutaneous oxygen tension is reduced, in keeping with the microangiopathy observed in the superficial nutrient capillaries. These pronounced morphological and dynamic changes explain the development of trophic skin lesions.
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PMID:[Microangiopathies in chronic venous insufficiency (CVI)]. 178 Aug 1

Plugging of skin capillaries by activated white blood cells is one of the proposed mechanisms by which skin damage may be initiated in chronic venous insufficiency. The aim of this study was to determine whether a microcirculatory deficit was induced in the skin by raising the venous pressure proximally for thirty minutes. Seventeen subjects with no evidence of venous or arterial disease had laser Doppler velocimetry performed in the goiter region of the leg; 8 different subjects had the measurement done on the dorsum of the hand. Peak hyperemic response following three minutes of ischemia was measured before and after a thirty-minute period of sustained venous hypertension applied by a proximal tourniquet inflated to 80 mm Hg. A decrease in the peak flow: baseline flow ratio (median ratio 2.25 before, 1.70 after, p less than 0.02) and an increase in the time taken to reach maximal hyperemia (median time ten seconds before, twenty seconds after, p less than 0.01) were observed after the period of venous hypertension in the lower limb. The second parameter, but not the first, was significantly affected in the upper limb. The authors conclude that a microvascular deficit in the skin is demonstrable after a short period of venous hypertension. This is consistent with the white-cell-trapping theory, but other possible explanations are discussed.
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PMID:The effect on skin blood flow of short-term venous hypertension in normal subjects. 182 74

The clinical and histopathologic findings in 13 patients with lipomembranous changes in the subcutaneous adipose tissue as part of the inflammatory reaction are presented. Nine patients had clinical evidence of vascular disease and four had clinical evidence of connective tissue disease. Histopathologic evidence of endarteritis obliterans, venous stasis, and hemorrhage was present in more than half the patients, and the clinical lesion of liposclerosis was frequently present. These findings suggest that the histologic changes of lipomembranous panniculitis may be the result of an inflammatory reaction in patients who have the liposclerosis of venous insufficiency with connective tissue disease or previous leg ischemia or both.
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PMID:Lipomembranous changes in chronic panniculitis. 304 17

Gangrene of the hand associated with acute upper extremity venous insufficiency has been seen in four limbs in three patients treated at Vanderbilt University Medical Center. All three patients had life-threatening illnesses associated with diminished tissue perfusion, hypercoagulability, and venous injury. One patient progressed to above-elbow amputation, but venous thrombectomy in one limb and thrombolytic therapy in two others were successful in preventing major tissue loss. All three patients eventually died from their underlying illness. Thirteen previously reported patients with "venous gangrene" of the upper extremity have been analyzed. An underlying life-threatening illness was present in the majority of these patients (7/13, 54%) and, like the Vanderbilt series, amputations were frequent (7/13, 54%) and mortality (5/13, 38%) was high. This unusual form of ischemia appears to be produced by permutations of global circulatory stasis, subclavian or axillary vein occlusion, and peripheral venous thrombosis. Early, aggressive restoration of adequate cardiac output and thrombectomy and/or thrombolytic therapy may provide the best chance for tissue salvage and survival in this group of patients.
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PMID:Venous gangrene of the upper extremity. 397 53

The diagnosis of venous insufficiency and hypertension was established in 53 patients using standard diagnostic methods including ascending and descending venography, venous pressure measurements, and photoplethysmography. Autogenous vein valve transplant, which is gaining acceptance as a treatment for this condition, was employed in this group of patients to relieve venous valvular insufficiency. Biopsy specimens of the gastrocnemius muscle were obtained before surgery in all 53 patients and studied pathologically. Three types of morphologic injury were encountered, suggesting that disuse, denervation, and ischemia may each be partially responsible for damage in skeletal muscle subjected to venous insufficiency and hypertension. Skeletal muscle injury probably explains the preoperative elevations of serum creatine kinase levels in many of our patients and may account for the failure of venous pressures to return to normal levels following surgery.
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PMID:Muscle changes in venous insufficiency. 674 10

While controversy continues over the exact pathophysiology of and optimal therapy for phlegmasia cerulea dolens, increasing evidence favors the role of elevated interstitial pressure in the generation of extremity ischemia. We report the use of intramuscular pressure measurements in the assessment of a patient suffering massive venous occlusion of one leg. Significant elevations in pressure were found in association with symptomatic ischemia. Successful thrombectomy restored blood flow, relieved symptoms, and produced an immediate decrease in intramuscular pressure. In this disorder, measurement of compartment pressures can be useful in assessing the severity of venous insufficiency and in monitoring the response to therapy.
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PMID:Measurement of intramuscular pressure in the management of massive venous occlusion. 746 32

In an overview the microvascular involvement in chronic venous insufficiency (CVI) is described. Microangiopathy in the lower leg areas is characterized by the presence of typical enlarged and ramified blood capillaries, reduced capillary number, microvascular thrombosis and obliterations, and/or increased permeability of microlymphatics. Transcutaneous oxygen tension (tcPO2) is decreased and directly correlated to the number of perfused capillaries, whereas laser Doppler flux is enhanced. This apparent paradox may be explained by hyperperfusion in the deeper skin layers (mainly shunt vessels) and hypoperfusion in the superficial nutritive vessels. Microvascular changes are of patchy distribution. Trophic changes up to overt venous ulceration are mainly caused by microvascular ischemia and edema formation due to increased capillary permeability and deficient lymphatic drainage.
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PMID:Microvascular changes in venous disease: an update. 899 40


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