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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recurrent retinal branch artery occlusions, carotid thromboembolism, cerebral venous thrombosis, transient brainstem ischemia, and massive brainstem and cerebral infarction complicated the course of inflammatory bowel disease in 5 patients. Three patients had ulcerative colitis and 2 had regional enteritis. The usual risk factors for stroke were absent. Neuropathological examination in 1 patient showed in situ thrombosis of small cerebral and brainstem arteries and veins. Coagulation studies showed thrombocytosis, short partial thromboplastin times, and elevation of fibrinogen and Factor VIII levels. Platelet counts and coagulation factors returned toward normal after control of intestinal inflammation in each of the 4 surviving patients. Inflammatory bowel disease can be accompanied by a hypercoagulable state that predisposes to stroke.
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PMID:Cerebral and retinal vascular complications of inflammatory bowel disease. 44 68

Ischemic optic neuropathy and retinal arterial occlusion are 2 forms of arterial occlusive disease affecting the eye. Reports in the literature suggest platelet hyperactivity in acute arterial occlusive diseases affecting other organ systems. Therefore, 14 patients with ischemic optic neuropathy and 17 patients with central or branch retinal artery occlusion were studied to determine whether platelets have a role in the pathogenesis of these vascular occlusive disorders. The results of the following investigations were no different in these patients compared with those in 18 control patients with non-vascular eye diseases: prothrombin times, partial thromboplastin times, plasma fibrinogen, factor V, factor VIII, platelet counts and threshold concentrations of ADP, epinephrine and collagen resulting in secondary platelet aggregation and serotonin release. In contrast, platelet coagulant activities concerned with the early stages of intrinsic coagulation were significantly increased in patients with retinal artery occlusion without hypertension or type IV hyperlipoproteinemia, but generally normal in patients with ischemic optic neuropathy and in patients with retinal artery occlusion associated with hypertension, type IV hyperlipoproteinemia, diabetes mellitus and generalized atherosclerosis. These results are consistent with a platelet contribution to retinal arterial occlusive disease in patients without other known contributing factors such as hypertension, serum lipid abnormalities, diabetes mellitus and generalized atherosclerosis and may have implications regarding prophylaxis.
Stroke
PMID:Platelet coagulant activities in arterial occlusive disease of the eye. 50 1

Fifteen Marine recruits with acute heat stroke were examined for (1) predisposing factors, (2) blood coagulation disturbances, (3) renal function abnormalities, and (4) blood composition alterations. Epidemiologic data identified the following risk factors; previous residence in a temperate climate, first phase of training, fatigue, and strenuous exercise in hot, humid conditions. Results of blood coagulation studies disclosed an increase in prothrombin and partial thromboplastin times, with a decrease in platelet count, probably indicating a transient, low-grade consumptive process. Blood urea nitrogen and creatinine levels and creatinine clearance were normal. Only mild elevations of SGOT, SGPT, and lactic dehydrogenase levels were noted, and in combination with clinical observations, they argued against significant muscle damage. No deaths or instances of renal failure occurred.
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PMID:Acute heat stroke. Epidemiologic, biochemical, renal, and coagulation studies. 124 74

Antibodies directed against phospholipids are highly associated with episodes of venous and arterial thrombosis, which are often recurrent. There seems to be a skewed frequency of cerebral thrombosis when the arterial circulation is affected. Clinical clues that should lead to evaluation for aPL include stroke in a young adult, recurrent thrombosis or miscarriage, and thrombocytopenia. Associated laboratory abnormalities include a biologically false-positive test for syphilis, abnormal antinuclear antibody titers, and a high erythrocyte sedimentation rate. If the activated partial thromboplastin time is prolonged on routine screening and does not correct with mixing studies, a lupus anticoagulant should be suspected. However, more sensitive and specific tests are usually necessary to detect aPL. Many in vitro and more recently in vivo systems strongly suggest that aPL may be directly implicated in the pathogenesis of thrombosis. Optimal management of patients with aPL-associated thrombosis is unknown. The use of aggressive therapeutic management schemes with such agents as warfarin or corticosteroids is sometimes required.
Heart Dis Stroke
PMID:Antiphospholipid antibodies and ischemic stroke. 134 35

To assess the incidence, risk factors, and clinical importance of deep vein thrombosis in acute stroke, we studied 70 consecutive patients who underwent hemostasis screening at the time of entry into the study and followed up these patients with serial venous Doppler examinations and the iodine 125-labeled fibrinogen uptake test. Mortality was significantly higher among the 20 patients who developed a deep vein thrombosis, and eight of them had necropsy evidence of pulmonary embolism. Severity of leg paresis and a shortened activated partial thromboplastin time were significantly associated with subsequent deep vein thrombosis with multivariate analysis. Significantly higher levels of fibrinopeptide A were found in patients with postmortem evidence of pulmonary embolism. Deep vein thrombosis is a frequent complication of acute stroke and may influence the prognosis by inducing pulmonary embolism. Our findings allow rapid identification of high-risk patients who may benefit maximally from prophylactic treatment of venous thromboembolism.
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PMID:Venous thromboembolism in acute stroke. Prognostic importance of hypercoagulability. 153 31

Several coagulation assays identify lupus anticoagulants, but there is no uniform opinion regarding minimum criteria for the diagnosis or the most sensitive procedure to be used to screen for lupus anticoagulants. Based on test availability and the cumulative literature, a sensitive activated partial thromboplastin time appears to be the most appropriate screening test. The dilute Russell's viper venom time may be used as both a screening and a confirmatory procedure. The platelet neutralization procedure is the most sensitive and specific of the confirmatory procedures that use an increased amount of phospholipid to either "bypass" or "neutralize" the lupus anticoagulant.
Stroke 1992 Feb
PMID:Coagulation assays for the lupus anticoagulant: review and critique of current methodology. 156 67

The antiphospholipid syndrome was diagnosed in 19 of 1078 patients treated between 1987 and 1991. All patients with antiphospholipid syndrome had either anticardiolipin antibody (16/19) or lupus anticoagulant (10/19); three patients had thrombocytopenia, eight patients had a prolonged partial thromboplastin time, and 10 patients had an elevated erythrocyte sedimentation rate. The most common site of involvement was the cerebral circulation (nine patients), manifested by transient ischemic attacks or stroke. Eight patients had upper extremity disease, characterized by symptoms of Raynaud's phenomenon, with angiographic lesions involving the brachial, radial, ulnar, and/or digital arteries. Lower extremity disease occurred in seven patients, with clinical presentations similar to those of atherosclerosis and varying angiographic patterns. In comparison with the population having atherosclerosis, patients with arterial manifestations of antiphospholipid syndrome were more likely to be women (13 of 19 versus 411 of 1078, p less than 0.02), were significantly younger (46.2 years versus 63.6 years, p less than 0.0001), did not smoke (1 of 19 patients versus 700 of 1078, p less than 0.0001), had a higher percentage of upper extremity involvement (8 of 18 versus 13 of 1078, p less than 0.0001), and had a higher incidence of early graft failure (9 of 12 grafts versus 13 of 371 grafts, p less than 0.0001). The syndrome is associated with the repetitive failure of vascular reconstructions and occlusion of native vessels. Antiphospholipid syndrome should therefore be suspected in young, female, nonsmokers with vascular disease, especially those with involvement of the upper extremity, cerebrovascular disease with normal findings on extracranial carotid angiography, and premature graft failure.
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PMID:Vascular disease in the antiphospholipid syndrome: a comparison with the patient population with atherosclerosis. 172 74

Venous thromboembolism is complex with a multifactorial etiology. The Virchow triad (changes in blood flow, changes in vessel wall, and changes in the properties of blood) gives the main factors involved in venous thromboembolism. Venous stasis during immobilization in general anesthesia, stroke with hemiparesis, and heart failure plays a central role. The thromboembolic process can be initiated by a disturbance in the normal "hemostatic balance," with an increased thrombogenic potential, due to release of thromboplastin and collagen exposure during vessel wall injury by stasis and hypoxia, decreased fibrinolysis during surgery, malignancy, among others. Many substances modify these processes, including heparan sulfate, AT III, protein C, t-PA inhibitor, and alpha 2-antiplasmin.
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PMID:Pathophysiology of venous thromboembolism. 175 82

We studied 2 groups of ischemic stroke patients who received therapeutic heparinization during the acute phase in order to prevent thromboembolic reinfarction. 530 patients were studied retrospectively (Group B) and 127 prospectively (Group A). Doses of 24,000-38,000 IE/24 h of heparin were given i.v., resulting in a partial thromboplastin time 2-3 times that of normal controls. Three patients from Group A suffered a massive intracranial hemorrhage. All of them had a large infarction (greater than 5 cm in diameter). They had been given anticoagulants within the first 12 h. Two of them presented with uncontrollable hypertension (systolic BP up to 240 mm Hg). Ischemic reinfarction during the first two weeks occurred in 2.3% and 2.4% of subgroups, respectively. This was less than would have been expected from the literature (approx. 14-15%). Features of these patients were 1.) insufficient heparin dosage, 2.) progression of hemodynamically relevant internal carotid artery lesions leading to critical low-flow or 3.) embolization of a floating thrombus from the internal carotid artery in the middle cerebral artery. It appears that therapeutic heparinization reduces the rate of reinfarction within the acute phase of ischemic strokes. This type of treatment should, however, be confined to patients with an embolic stroke mechanism. Careful surveillance of blood pressure and PTT are prerequisites. Anticoagulation should be avoided in patients with massive infarctions (greater than 5 cm in diameter) or uncontrollable hypertension.
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PMID:[Anticoagulation in acute cerebral infarct. Benefits, risks, therapeutic failures]. 194 10

A 55-year-old woman was transferred to our institution from another hospital. The history of her present illness began 17 days earlier with a right-sided cerebral vascular accident (CVA). Three days later she had a superior mesenteric artery (SMA) embolus with infarcted bowel. Her small bowel was resected leaving about 20-25 centimeters of small bowel. A cardiac echo on hospital day 6 documented the presence of a left ventricular embolus, which was considered to be the cause of her CVA and SMA embolus. The cardiologists recommended lifelong anticoagulation, preferably with warfarin when technically feasible. After one month of warfarin therapy, with doses as high as 25 mg/d, the patient's prothrombin times (PTs) were not changed from baseline; however, this was probably due to concomitant therapy with vitamin K. Heparin was incorporated into her total parenteral nutrition (TPN) in preparation for her discharge. Because the TPN was cycled, she required subcutaneous heparin twice daily while off TPN. This patient's clinical course while she was maintained on heparin therapy was complicated by bleeding episodes and extensive thigh and abdominal hematomas, which led to erratic heparin absorption and widely fluctuating partial thromboplastin times. Ten months after the initiation of anticoagulation the patient was again tried on an oral warfarin regimen. She was successfully titrated to achieve the desired PT ratio. This case led to a review of the literature of patients with short-bowel syndrome requiring anticoagulation.
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PMID:Oral anticoagulation in patients with short-bowel syndrome. 211 45


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