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

Thrombotic occlusion of the arteries and veins are categorized as acute and chronic presentations. Acute arterial occlusion results in severe ischemia because of poor or no development of the collateral arteries. They should be treated promptly by thrombectomy or thrombolysis. On the other hand, chronic arterial occlusion is preferably treated by bypass surgeries. Although the vascular surgeries in the chronic arterial occlusion have undergone remarkable development in the recent years, the treatment of acute occlusion still lags behind poor with prognosis. The treatment of acute venous occlusion is aimed to prevent postphlebitic syndrome except for the ischemic type such as venous gangrene. The purpose of the treatment of chronic venous occlusion is to assist the pump function of the calf muscles to avoid venous stasis. Pulmonary embolism is the most severe complication and its treatment remains controversial.
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PMID:[Clinical characteristics of thrombotic diseases of arteries and veins]. 1042 43

Arteriosclerosis obliterans (ASO) and Buerger's disease are representative arterial occlusive disease which causes chronic lower limb ischemia. In ASO, ischemia is produced by atherosclerotic stenosis and/or occlusion of major arterial trees mainly from the abdominal aorta to the femoral arteries, and in Buerger's disease, smaller arteries distal to the calf and the elbow are generally affected by non-specific panarteritis. Thrombotic occlusion at the affected vessels and proximal and/or distal progression of the secondary thrombosis often deteriorate leg ischemia. In chronic limb ischemia, microcirculation distal to affected vessels is also deteriorated by activation of white blood cells and platelets which induce vasoconstriction, injury of intimal cells, platelet aggregation, increased permeability, etc. Fontaine's classification of chronic limb ischemia based on clinical signs and symptoms is useful for grading severity of ischemia and selecting an optimal treatment. Recently, the concept of chronic critical limb ischemia is advocated, which is a condition that the limb amputation will be inevitable without restoration of blood flow. Diagnostic modalities for chronic arterial occlusion and assessment for severity of ischemia are outlined.
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PMID:[Clinico-pathological aspects of the lower limb ischemia in chronic arterial occlusive disease]. 1042 67

Increased fibrinolytic activity and consumption coagulopathy are common consequences of liver transplantation and are a major cause of morbidity and death. In the present investigation the effects of hepatic ischemia on the coagulation mechanism were studied in the stump-tail monkey. The results suggest that, although fibrinolytic activity is induced by both major intraabdominal operations as well as one hour of hepatic ischemia, consumption coagulopathy, presumably due to intravascular clotting, is enhanced by the revascularization of the ischemic liver, possibly because of clotting within the liver itself. Release of a plasminogen activator from the liver due to hepatic ischemia alone is not demonstrated by these studies. It is believed that the first phase of intravascular coagulation after liver transplantation is due to release of tissue activators from vascular endothelium, which may be minimized by the action of ganglionic blocking agents. The severity of fibrinolysis in this stage is aggravated by the "liverless state," in which no clearance of plasminogen activators occurs. The degree of liver injury directly affects the ability of the liver to control hypercoagulability in the second phase. Thrombus formation which we believe occurs during this phase may be minimized by use of continuous controlled heparinization.
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PMID:Effects of hepatic ischemia on coagulation in primates. Application to liver transplantation. 1048 79

A 30-year-old healthy woman was involved in a road traffic accident. She sustained a fracture dislocation of T11/12 with a complete Frankel A paraplegia below T11. She had no associated injuries. High Dose Methylprednisolone was administered according to the NASCIS III protocol (48 h) together with low molecular weight Heparin and gastroprotected medication. Complete transection of the spinal cord and an anterior haematoma from T11 to T12 were confirmed on X rays, CT's and MRI scans. Posterior surgical stabilisation was performed using Isola instrumentation, starting 8 h post injury. Her post surgical period was uneventful except for some episodes of low blood pressure (85/60 mmHg) from which she had no symptoms. On the 12th post operative day, while in the physiotherapy department, she complained of right scapular pain. This occurred every time she was sat up and was associated with paraesthesia of both upper limbs. Two days later she deteriorated neurologically and her level ascended initially to T8 and then to T3. MRI of the spine with and without gadolinium showed spinal cord oedema between C3 and T1. There was no evidence of haemorrhage or syringomyelia. The authors discussed this case making different hypotheses. They are mainly the following: (1) Gradually ascending ischaemia due to a vascular disorder; (2) Double spinal trauma; (3) Ischaemia related to repeated hypotensive episodes; (4) Low grade intramedullary tumour; and (5) Thrombus of the Radicularis Magna artery. The case has been recognised as being very rare and interesting. In the conclusions, the presenting author stresses the importance of adopting MRI-compatible instrumentation for the surgical stabilisation of the spine, and careful monitoring of blood pressure during the acute phase of spinal cord injury. Dr Aito agrees with Mr El Masry about the opportunity of forming a group of clinicians in order to discuss protocols to cope with this devastating complication.
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PMID:Ascending myelopathy in the early stage of spinal cord injury. 1049 Aug 52

Diabetic retinopathy (DR) still remains the leading cause of blindness in the working population of Japan and western world, though therapies such as retinal photocoagulation and vitrectomy can be remarkably effective when administered at an appropriate stage in the disease process. Consequently, there is a need for further investigation of the pathogenesis of DR to develop better therapy. DR is characterized by gradually progressive alterations in the retinal microvasculature, leading to three fundamental morbidities: 1. vascular hyperpermeability, 2. vascular occlusion, and 3. neovascularization. Recent studies have revealed that hyperglycemia causes several metabolic disorders which cause DR directly or indirectly through the abnormal expression of cytokines including vascular endothelial growth factor (VEGF). In this study, we performed precise tests of the correlation between intraocular VEGF and the three fundamental changes in the diabetic retina mentioned above. Ultrastructural study of the human retina revealed that two major pathways are responsible for hyperpermeability of diabetic retinal vessels, i.e., intercellular or paracellular transport (opening of the tight junctions) and intracellular or transcellular transport (caveolae, intracytoplasmic vesicles, and fenestration). All these pathways were induced by intravitreal injection of VEGF. The major trigger of VEGF overexpression is tissue ischemia caused by vascular occlusion. However, the retinas from the eyes with background DR revealed increased expression of VEGF without apparent incidence of vascular occlusion. We have identified accumulation of advanced glycation end products (AGEs) in these retinas, and found that AGEs are a major stimulus for VEGF overexpression in background DR. Retinal vascular occlusion was caused by thrombus formation primarily in the capillary vessels. Thrombi mainly consisted of fibrin, platelets, and leucocytes in the early stage of their formation, and glial cells and macrophages were also involved in the later stage. The blood coagulation process plays an important role in fibrin formation in thrombi. The expression of tissue factor (TF), an initiator of extrinsic blood coagulation, was upregulated by VEGF in retinal vascular endothelial cells (REC). In addition, AGEs were also thrombogenic through the induction of TF expression and suppression of the expression of prostacyclin stimulating factor (PSF), which stimulate prostacyclin synthesis in vascular endothelial cells. These findings suggest that AGEs, VEGF, and TF could interact in a vicious circle because AGEs and VEGF could induce retinal vascular occlusion which results in further increase in VEGF expression. Intravitreal injection of VEGF could induce retinal neovascularization. VEGF stimulates vascular endothelial cell proliferation by binding to a specific receptor named kinase insert domain-containing receptor/fetal liver kinase (KDR/FIk-1, KDR). AGEs and basic fibroblast growth factor (bFGF) induced expression of KDR in REC, and a transcription factor Sp 1 was involved in this process. Since the expression of KDR as well as VEGF was already upregulated in the retinas with background DR, VEGF appeared to start to induce the proliferative changes long before the actual onset of proliferative DR. These findings indicated that VEGF and its receptor system plays a pivotal role all through the disease process of DR. We considered that amelioration of the activated VEGF and its receptor system could lead to the development of new therapy for DR. We have developed two novel methods to prevent retinal neovascularization by inhibiting VEGF and its receptor system. 1. An insulin sensitizing agent (troglitazone) inhibited proliferation, migration, and in vitro tube formation by REC as well as oxygen-induced retinal neovascularization in a mouse model. Thus, glycemic control by troglitazone could reduce the incidence of neovascularization in diabetic eyes. 2. (ABSTRACT TRUNCATED)
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PMID:[Cell biology of intraocular vascular diseases]. 1064 94

Diabetic retinopathy (DR) still remains the leading cause of blindness in the working population of Japan and western world, though therapies such as retinal photocoagulation and vitrectomy can be remarkably effective when administered at an appropriate stage in the disease process. Consequently, there is a need for further investigation of the pathogenesis of DR to develop better therapy. DR is characterized by gradually progressive alterations in the retinal microvasculature, leading to three fundamental morbidities: (1) vascular hyperpermeability, (2) vascular occlusion, and (3) neovascularization. Recent studies have revealed that hyperglycemia causes several metabolic disorders which cause DR directly or indirectly through the abnormal expression of cytokines including vascular endothelial growth factor (VEGF). In this study, we performed precise tests of the correlation between intraocular VEGF and the three fundamental changes in the diabetic retina mentioned above.Ultrastructural study of the human retina revealed that two major pathways are responsible for hyperpermeability of diabetic retinal vessels, ie intercellular or paracellular transport (opening of the tight junctions) and intracellular or transcellular transport (caveolae, intracytoplasmic vesicles, and fenestration). All these pathways were induced by intravitreal injection of VEGF. The major trigger of VEGF overexpression is tissue ischemia caused by vascular occlusion. However, the retinas from the eyes with background DR revealed increased expression of VEGF without apparent incidence of vascular occlusion. We have identified accumulation of advanced glycation end products (AGEs) in these retinas, and found that AGEs are a major stimulus for VEGF overexpression in background DR. Retinal vascular occlusion was caused by thrombus formation primarily in the capillary vessels. Thrombi mainly consisted of fibrin, platelets, and leucocytes in the early stage of their formation, and glial cells and macrophages were also involved in the later stage. The blood coagulation process plays an important role in fibrin formation in thrombi. The expression of tissue factor (TF), an initiator of extrinsic blood coagulation, was upregulated by VEGF in retinal vascular endothelial cells (REC). In addition, AGEs were also thrombogenic through the induction of TF expression and suppression of the expression of prostacyclin stimulating factor (PSF), which stimulate prostacyclin synthesis in vascular endothelial cells. These findings suggest that AGEs, VEGF, and TF could interact in a vicious circle because AGEs and VEGF could induce retinal vascular occlusion which results in further increase in VEGF expression.Intravitreal injection of VEGF could induce retinal neovascularization, VEGF stimulates vascular endothelial cell proliferation by binding to a specific receptor named kinase insert domain-containing receptor/fetal liver kinase (KDR/Flk-1, KDR). AGEs and basic fibroblast growth factor (bFGF) induced expression of KDR in REC, and a transcription factor Sp 1 was involved in this process. Since the expression of KDR as well as VEGF was already upregulated in the retinas with background DR, VEGF appeared to start to induce the proliferative changes long before the actual onset of proliferative DR. These findings indicated that VEGF and its receptor system plays a pivotal role all through the disease process of DR.We considered that amelioration of the activated VEGF and its receptor system could lead to the development of new therapy for DR. We have developed two novel methods to prevent retinal neovascularization by inhibiting VEGF and its receptor system. (1) An insulin sensitizing agent (troglitazone) inhibited proliferation, migration, and in vitro tube formation by REC as well as oxygen-induced retinal neovascularization in a mouse model. Thus, glycemic control by troglitazone could reduce the incidence of neovascularization in diabetic eyes. (ABSTRACT TRUNCATED)
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PMID:Cell biology of intraocular vascular diseases 1091 68

A 60-year-old man was admitted to the hospital with aortic dissection. An operative excision and replacement with a Y-graft was performed. Postoperatively he developed multiple organ dysfunction and required intermittent haemofiltration (anticoagulation with heparin). An ischemia of the left leg occurred at the third postoperative day. The initial platelet count was 99,000/microliter. Continuous haemofiltration (CVVH) was started three days later. Thrombotic obstructions of haemodialysis filters and catheters occurred frequently and heparin-induced thrombocytopenia (HIT II) was suspected. Antibodies against heparin were found in the HIPA test. Despite heparin free citrate dialysis and anticoagulation with danaparoid thrombotic obstructions of filters and catheters continued. Therefore the anticoagulation therapy during CVVH was changed to recombinant hirudin (lepirudin). Starting dose was a bolus of 0.01 mg/kg bw followed by the same amount as maintenance dose per hour. Anticoagulation was adjusted to an increase of aPTT (activated partial thromboplastin time) to 1.5-2 times its normal value. A dose of 0.005 mg/kg bw/h lepirudin was sufficient to maintain adequate anticoagulation. After changing to lepirudin no further catheter obstructions were observed and the platelets recovered slowly. Renal function improved and five weeks after admission endogenous creatinine clearance showed a value of 25 ml/min. We conclude that lepirudin is an effective anticoagulant during CVVH in patients with HIT II. In partly permeable polysulfon filters a dose of 0.005 mg/kg bw/h lepirudin is sufficient to maintain adequate anticoagulation. Monitoring anticoagulation by measuring the increase of aPTT (factor 1.5-2.0) seems to be safe. However, optimally the r-hirudin concentration should be measured directly using the Ecarin clotting time.
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PMID:Continuous haemofiltration with r-hirudin (lepirudin) as anticoagulant in a patient with heparin induced thrombocytopenia (HIT II). 1095 74

Thrombus formation on a disrupted atherosclerotic plaque is a threatening event that leads to vessel occlusion and acute ischemia. In this current perspective, we present evidence for apoptosis as a major determinant of the thrombogenicity of the plaque lipid core and a potential contributor to plaque erosion and associated thrombosis. Moreover, apoptosis may directly affect blood thrombogenicity through the release of apoptotic cells and microparticles into the bloodstream.
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PMID:Current perspective on the role of apoptosis in atherothrombotic disease. 1137 68

Thrombotic complications, particularly microthrombi involving intraabdominal veins leading to intestinal ischemia, have remained a major cause of morbidity in patients with paroxysmal nocturnal hemoglobinuria (PNH). While intestinal ischemia has been postulated to be the cause of recurrent bouts of abdominal pain in this population, direct antemortem evidence for this complication is scarcely documented in the literature. We describe a case of PNH in a patient who presented with abdominal distress three years after the initial diagnosis was established. Clinical features and a combination of diagnostic modalities, including radiography, endoscopy, and histology were used to make the prompt diagnosis of intestinal ischemia. This is the first case in which the electronic microscopy of the gastrointestinal lesion is described. Our patient was successfully treated with conservative measures and anticoagulation.
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PMID:Gastrointestinal involvement in paroxysmal nocturnal hemoglobinuria: first report of electron microscopic findings. 1183 33

Valvular calcification is a common consequence of systemic calcium deposition resulting from chronic renal failure. Thrombi can form on such vascular calcifications and embolize to the cerebral, myocardial, and mesenteric vasculature with devastating consequences. We report the unique case of a patient with myocardial and cerebrovascular ischemia resulting from emboli arising from a massive mitral annular calcification.
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PMID:Massive left atrial calcification and devastating systemic emboli in a patient with chronic renal failure. 1214 18


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