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

Acute arterial occlusion can be the result of acute thrombosis or systemic embolism. Paradoxical embolism of a venous thrombosis through a right-to-left shunt is an important cause of acute limb ischemia. We describe a young patient with acute limb ischemia who was found to have multiple deep venous thromboses causing arterial embolization through a patent foramen ovale. Essential thrombocytosis was found to be the risk factor for venous thromboses in this patient. The patient was managed with embolectomy and anticoagulation along with chemotherapeutic cytoreduction of platelet count. This case illustrates the importance of considering the systemic embolism as a cause of acute arterial occlusion. The presence of a hypercoagulable status such as chronic myeloproliferative disorder does not eliminate the possibility of systemic embolism in the event of acute arterial occlusion. Patients presenting with acute limb ischemia should be evaluated for embolic sources. The presence of deep venous thrombosis in such a patient should prompt the evaluation for a patent foramen ovale.
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PMID:Paradoxical arterial emboli causing acute limb ischemia in a patient with essential thrombocytosis. 1450 Dec 34

Vascular manifestations are the main clinical complication of essential thrombocythemia (ET). They include arterial thrombosis (30-40% of patients), venous thrombosis (5%), and ischemia due to microcirculatory disorders. Their incidence is highest at disease onset and diminishes gradually thereafter. The pathophysiology of ET involves dysmegakaryocytopoiesis, leading to platelet, leukocyte and vascular endothelial cell activation. The recent discovery of the V617F mutation of the JAK2 tyrosine kinase in 50-60% of patients with ET defined a new subgroup resembling polycythemia vera. This review examines biological findings and their correlation with the risk of thrombosis. Until now, stratification of the vascular risk has relied on a clinical case-control study showing that thrombotic and vascular complications are more frequent in patients over 60 and those with a history of thrombosis. These criteria, along with a rapid increase in thrombocytosis (>1500 G/L) leading to an increase in the bleeding risk, define a high-vascular-risk subgroup of patients warranting cytoreductive therapy. Although many biological markers of dysmegakaryocytopoiesis and cellular hyperactivation have been linked to an increase in the thrombotic risk, none is available for large-scale prediction of an intermediate vascular risk. The role of the JAK2 V617F mutation itself is controversial. Whatever the ET subgroup, antiplatelet therapy is largely used, based on the results of the ECLAP prospective controlled trial that showed a statistically significant reduction in thrombotic complications in patients receiving aspirin for polycythemia vera, a very similar myeloproliferative disorder.
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PMID:[Vascular complications of essential thrombocythemia]. 1807 51

Systemic sclerosis (SSc) patients typically experience Raynaud phenomena that is often complicated by digital ischemic lesions, gangrene, and digital loss. Other causes of peripheral ischemia, such as atherosclerosis, cryoglobulinemia, antiphospholipid syndrome, myeloproliferative disorders, paraneoplastic syndromes, and hyperadrenergic endocrine conditions, may be masked in SSc patients. We present a woman with limited SSc who developed toe necrosis and acute coronary events as a complication of a previously undiagnosed pheochromocytoma.
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PMID:Toe necrosis and acute myocardial infarction precipitated by a pheochromocytoma in a patient with systemic sclerosis. 1817 42

Portal vein thrombosis secondary to protein C deficiency is a rare finding. Diagnosing a portal vein thrombosis itself is difficult due to nonspecific symptoms such as nausea, vomiting, anorexia, and weight loss. Proving that a protein C deficiency is the cause of a portal vein thrombosis is even more difficult as an extensive and thorough workup is required to rule out malignancies, myeloproliferative disorders, and hypercoaguable states which can all lead to thromboses. Patients require anticoagulation to prevent two dangerous complications of portal vein thrombosis; portal hypertension leading to esophageal varices with massive hemetemesis and extension of thrombus from the portal vein into the mesenteric veins leading to intestinal ischemia and death. In this case report, we present a patient with the complaint of painless jaundice who was found to have an incidental finding of portal vein thrombosis secondary to protein C deficiency. The different etiologies of portal vein thrombosis, along with diagnosis and treatment options will be discussed and highlighted.
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PMID:A rare incidental finding in a case of painless jaundice. 3071 33

Inherited and acquired tendency to the formation of clots represents an important cause of morbidity and mortality for ischemic events in young people (aged between 40 and 50 years) that is more and more frequently identified. The haemostasis' disorders may happen on the venous or arterial side. Arterial thrombus is a 'white' thrombus, also called temporary thrombus. It consists of aggregate platelets only. On the contrary, venous thrombus is 'red' or permanent thrombus composed of platelets, red cells and fibrin. The first is the result of platelets' adhesion or aggregation. Instead, the permanent thrombus derives from the coagulant factors successively acting on 'white' thrombus. The different pathogenesis justifies both the distinction between 'hypercoagulability' and 'thrombophilia' and the different treatments employed. Antiphospholipid antibody syndrome, polycythemia vera, atrial fibrillation-acquired hyperhomocysteinemia, diabetes mellitus and myeloproliferative disease are the most frequent causes of acquired hypercoagulable state, prevalently responsible for deep venous thrombosis. Among the inherited forms, congenital hyperhomocysteinemia, factor V Leiden mutation, proteins C and S deficiency and antithrombin mutation are included. These may induce both venous and arterial acute events. Hyperhomocysteinemia can be congenital and acquired and is more correctly named as 'thrombophilia' rather than 'hypercoagulability'. That happens because it involves the platelets' aggregation rather than the coagulant cascade. The optimal treatment of thrombophilias consists of oral (warfarin) or injectable (heparins) anticoagulants. Direct thrombin inhibitors, platelet glycoprotein IIb/IIIa antagonists, and tissue factor inhibitors also appear to be some attractive approaches. For acquired forms, treatments of their aetiologies must also be carried out. For acquired hyperhomocysteinemia, both antiplatelets' therapy (aspirin + clopidogrel) and new direct thrombin inhibitors (as dabigatran) could be considered. Finally, as secondary prevention of an arterial acute event (stroke, IMA or peripheral ischemia) due to hyperhomocysteinemia, lifetime dual antiplatelets' therapy should be used.
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PMID:Some considerations about the hypercoagulable states and their treatments. 2134 57

Thrombosis of the celiac artery trunk is a rare cause of acute abdominal pain. Thrombosis of the celiac artery carries a high mortality and morbidity when the diagnoses and treatment are delayed. It is frequently associated with other cardiovascular events. The most common etiology is atherosclerosis. 20-30% of cases may have symptoms of chronic mesenteric ischemia. Main goal of the treatment is to reestablish the diminished or stopped mesenteric blood flow and to avoid end-organ ischemia. Essential thrombocythemia is a chronic myeloproliferative disorder characterized by marked increase in thrombocyte number and clinical presentation may be with thrombotic episodes, hemorrhage, or both. To our knowledge this is the first report of celiac artery thrombosis and superior mesenteric artery stenoses in a patient with essential thrombocythemia. The patient was managed successfully with surgical treatment.
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PMID:Celiac artery thrombosis and superior mesenteric artery stenoses with essential thrombocythemia: a case report. 2330 60

Mesenteric vein thrombosis is increasingly recognized as a cause of mesenteric ischemia. Acute thrombosis commonly presents with abdominal pain and chronic type with features of portal hypertension. Contrast enhanced CT scan of abdomen is quite accurate for diagnosing and differentiating two types of mesenteric venous thrombosis. Prothrombotic state, hematological malignancy, and local abdominal inflammatory conditions are common predisposing conditions. Over the last decade, JAK-2 (janus kinase 2) mutation has emerged as an accurate biomarker for diagnosis of myeloproliferative neoplasm, an important cause for mesenteric venous thrombosis. Anticoagulation is the treatment of choice for acute mesenteric venous thrombosis. Thrombolysis using systemic or transcatheter route is another option. Patients with peritoneal signs or refractory to initial measures require surgical exploration. Increasing recognition of mesenteric venous thrombosis and use of anticoagulation for treatment has resulted in reduction in the need for surgery with improvement in survival.
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PMID:Mesenteric venous thrombosis. 2575 68

Essential thrombocytosis (ET) is a myeloproliferative disorder characterized by an anomalous increase in platelet production. Many patients with ET are asymptomatic. Few studies have reported ET-associated thromboembolism in large vessels such as the aorta. We report a patient with ET who presented with peripheral embolism from an abdominal aortic thrombus and developed acute limb ischemia. The patient underwent aortic replacement successfully. The patient's platelet count was controlled with hydroxyurea, and no recurrence was noted over 2 years of follow-up.
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PMID:Essential Thrombocytosis-Associated Thromboembolism in the Abdominal Aorta. 2773 3

Portal vein thrombosis is an uncommon finding that typically arises in the context of cirrhosis. In the acute setting, it may present with abdominal pain, portal hypertension, ascites, gastrointestinal bleeding, or mesenteric ischemia. Local risk factors that predispose its formation include: cirrhosis, hepatocellular carcinoma, pancreatitis, and intraabdominal infection. Systemic factors, including hypercoagulable states and sepsis, also pose an increased risk. JAK2 V617F positive myeloproliferative disorders are associated with systemic prothrombotic states and are a less frequently identified cause of portal vein thrombosis. We present a case of acute unprovoked portal vein thrombosis diagnosed in a 59-year-old male without local disease factors. Computed tomography, magnetic resonance cholangiopancreatography, and ultrasound demonstrated the presence of portal vein thrombosis with neighboring periportal and pancreatic head edema. Peripheral blood testing detected the presence of JAK2 V617F mutation. The patient was discharged on 6-month anticoagulation therapy and outpatient follow-up.
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PMID:Acute portal vein thrombosis in a 59-year-old male with JAK2 V617F mutation. 3025 17

Essential thrombocythemia is a myeloproliferative neoplasm characterized by platelet aggregation and thrombosis. Clinically, essential thrombocythemia increases the risk of both thrombosis and bleeding. Essential thrombocythemia is more involved in micro- and small-sized arteries than in large arteries. Many essential thrombocythemia patients exhibit various symptoms, including microvascular thrombosis with acute coronary disease, digital ischemia, and transient ischemic attack. This study reports a rare case of recurrent thrombosis in relatively large vessels including splanchnic, lower extremity arteries, and aorta in essential thrombocythemia. A 70-year-old woman was admitted to the emergency room with abdominal pain and fever for a day. The patient underwent three operations due to recurrent arterial thrombosis of superior mesenteric, splenic, aorta, and lower extremities. She had recurrent diarrhea and acute kidney injury because of short bowel syndrome after extensive bowel resection. In conclusion, essential thrombocythemia patients aged >60 years and who have risk factors such as history of major ischemic events or severe leukocytosis must be careful of thrombosis of the medium- and large-sized arteries, including splanchnic and lower extremity arteries.
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PMID:Recurrent thrombosis of splanchnic and lower extremity arteries with essential thrombocythemia. 3163 77


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