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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thrombolysis with tissue plasminogen activator (tPA) has been used to treat myocardial infarction and pulmonary embolism in humans. This plasminogen activator may also be useful in treating certain strokes. We infused tPA or saline in rabbits 15 minutes after selective internal carotid artery embolization with 18-hour aged autologous clot. By serial angiography, the tPA-treated group demonstrated rapid angiographic reperfusion of the occluded vascular territory in 7 of 8 animals, whereas none of 6 saline controls did. None of the animals in either group developed macroscopic cerebral hemorrhage. Both groups showed cerebral infarction, predominantly in the territory of the occluded vessel; the extent of infarction did not differ between tPA-treated animals and controls. Early tPA therapy can allow reperfusion of occluded cerebral arteries safely and effectively in a rabbit cerebral embolization model.
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PMID:The safety and angiographic efficacy of tissue plasminogen activator in a cerebral embolization model. 313 92

Pulmonary embolism remains a frequent and often fatal disorder. For the majority of patients, anticoagulation with heparin followed by warfarin represents the primary mode of treatment. Thrombolytic therapy is recommended for the patient with massive pulmonary embolism that has produced hypotension. Embolectomy is reserved for the patient with post embolic systemic hypotension who has an absolute contraindication to thrombolysis or who deteriorates despite thrombolytic therapy. Following successful embolectomy the surgeon must treat the complications of the surgery and prevent recurrence. Complications include cerebral infarction, pulmonary infarction and endobronchial hemorrhage, right ventricular failure, local or systemic bleeding and venous stasis. A case of successful pulmonary embolectomy with a complicated postoperative course is presented and the pathophysiology and treatment of the complications are discussed.
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PMID:Ongoing role of pulmonary embolectomy. 322 60

Aneurysm of the extracranial internal carotid artery is a rarely observed condition. Intra-aneurysmatic thrombosis, cerebral embolism with possible neurological consequences, and rupture are the most common complications. Operations were performed on 20 patients for aneurysm of the internal carotid artery. The cases included 14 "genuine" arteriosclerotic aneurysms and seven "false" aneurysms in the wake of shell splinter injuries, tonsillectomy, thrombo-arteriectomy, and blunt traumata. Pulsating tumour was the most important clinical symptom in all aneurysm cases. Arterial continuity was restored by resection of aneurysm in all cases. Sixteen patients were dehospitalised without any complaint. Two patients with preoperative cerebral infarction were left with residual paresis. One patient died of pulmonary embolism, and one patient operated on for rupture died in shock.
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PMID:[Aneurysm of the extracranial internal carotid artery]. 354 7

Among 53 patients with hereditary protein C deficiency belonging to 20 families three women were encountered who, aged 27, 34, and 38 respectively, had had cerebral haemorrhagic infarction, probably due to intracranial venous thrombosis. All three had also had venous thrombosis of the leg and pulmonary embolism either before or after their cerebral infarction. One patient sustained cerebral infarction while receiving an oral contraceptive, but infarction in the two others occurred "spontaneously." One patient also had an intraventricular and subarachnoid haemorrhage during the induction phase of coumarin treatment, which was assumed to have resulted from haemorrhagic infarction of the chorioid plexus, analogous to coumarin provoked haemorrhagic skin necrosis in protein C deficiency. Hereditary protein C deficiency should be considered in young patients with acute or subacute cerebral symptoms, especially if they have a family or personal history of venous thromboembolism.
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PMID:Cerebral haemorrhagic infarction in young patients with hereditary protein C deficiency: evidence for "spontaneous" cerebral venous thrombosis. 391 15

Pathologists' opinions of cause of death given at the end of post-mortem (PM) reports have often been used to validate clinicians' death certificates. Information about strokes, common coincident conditions and complications in 120 full PM reports was compared with the pathologists' opinions of cause of death given at the end of the reports. Intracranial haemorrhage and myocardial infarction were mentioned as frequently in the cause of death as in the full PM report. On the other hand, cerebral infarction, precerebral artery occlusion, severe cerebral atheroma, coronary artery occlusion, bronchopneumonia and pulmonary embolism were all under-cited in the causes of death. Whether a pathological condition mentioned in the full PM report also appeared in the cause of death varied with the decedent's age, the extent of the condition and type of stroke. Consideration should be given to using all the information in PM reports rather than just pathologists' opinions of cause of death given at the end of PM reports when studying the validity of clinicians' death certificates.
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PMID:Information about strokes lost between post-mortem and reported cause of death. 399 79

Clinicopathologic correlations were reviewed in 100 cases of recent cerebral infarctions in the internal carotid artery distribution. The most frequent cause of death was transtentorial herniation, followed in frequency by pneumonia, cardiac causes, and pulmonary embolism. Thirty-six percent of all patients and 47% of those with transtentorial herniation died within 48 hours of cerebral infarction. Of the treatable extracerebral causes of death determined at autopsy, only 34% were recorded premortem in the clinician's death summary.
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PMID:Mechanisms and timing of deaths from cerebral infarction. 731 70

A cohort of 8 patients with myxoma of the left atria and neurological manifestations is reported. Cerebral ischaemia, sometimes responsible for epileptic seizures, led to the discover of the myxoma (5 cases) or recurrence after exeresis (1 case) with imaging evidence of cerebral infarction in 5 cases. The first manifestation was a retinal embolism and temporary ischaemia in 1 case and pulmonary embolism with regressive cerebral ischaemia in another case with bilateral myxoma. Some clinical particularities should be underlined including exercise-induced neurological defect (3 cases), systemic embolism associated with cerebral infarction (3 cases), migraine headache as the initial manifestation (1 case) preceding by a pseudolupic syndrome suggesting the possibility of cerebral vasculitis or infectious endocarditis (1 case). The prognosis depends on the risk of recurrent atrial tumour formation (1 case). Metastases are rare. Multiple cerebral aneurysms (3 cases) did not lead to haemorrhagic complications.
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PMID:[Myxoma of the left atrium with neurologic manifestations: 8 cases]. 759 71

Envenomation by the Bothrops lanceolatus, a snake found only in Martinique, leads to swelling and pain, and occasionally to systemic signs and/or coagulopathy. Severe thromboses at some distance from the site of the bite may appear within 48 hr. Uncertainties as to the actual development of thrombotic complications in patients appearing to be suffering from moderate poisoning and as to the availability and the toxicity of a monospecific antivenom (AVS) initially led us to reserve antivenom for the most severe cases, and to use anticoagulants to prevent thromboses in all patients. This approach was modified after we observed serious thromboses in patients with moderate poisoning. Of 50 adult snake bite cases hospitalized between June 1991 and August 1994, 11 developed serious thrombotic complications at 36 /+- 27 hr (mean +/- SD) (range 12-96) following envenomation, despite early preventive anticoagulant therapy. Those included pulmonary embolism (two cases), cerebral infarction (six cases), myocardial infarction (one case), and cerebral and myocardial infarctions (two cases). Sixteen patients were not treated with AVS: 10 of these recovered without complications and six developed systemic thrombosis causing permanent disability in three cases. Thirty were treated with an intravenous infusion of 2-6 vials of AVS given 2-48 hr after the bite. Of these, three died of cerebral infarction that developed before the initiation of serotherapy. All others recovered. Among patients treated with AVS, three presented with mild anaphylactic reactions, while one developed serum sickness that responded to steroids. These data indicate that preventive anticoagulant therapy is of limited efficacy in Martinique.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevention of thromboses in human patients with Bothrops lanceolatus envenoming in Martinique: failure of anticoagulants and efficacy of a monospecific antivenom. Research Group on Snake Bites in Martinique. 777 8

A formal statistical overview of all truly randomised trials was undertaken to determine whether antithrombotic therapy is effective and safe in the early treatment of patients with acute stroke. There were 15 completed randomised controlled trials of the value of early antithrombotic treatment in patients with acute stroke. The regimes tested in acute presumed or confirmed ischaemic stroke were: heparin, 10 trials with 1047 patients: oral anticoagulants, one trial with 51 patients: antiplatelet therapy, three trials with 103 patients. Heparin was tested in one trial with 46 patients with acute haemorrhagic stroke. Outcome measures were deep venous thrombosis (confirmed by I125 scanning or venography), pulmonary embolism, death from all causes, haemorrhagic transformation of cerebral infarction, level of disability in survivors. In patients with acute ischaemic stroke, allocation to heparin was associated with a highly significant 81% (SD 8, 2p < 0.00001) reduction in deep venous thrombosis detected by I125 fibrinogen scanning or venogram. Only three trials systematically identified pulmonary emboli, which occurred in 6/106 (5.7%) allocated control vs 3/132 (2.3%) allocated heparin, a non-significant 58% reduction (SD 45.7, 2p > 0.1). There were relatively few deaths in the trials in patients with presumed ischaemic stroke: 94/485 (19.4%) among patients allocated to the control group vs 79/497 (15.9%) among patients who were allocated heparin. The observed 18% (SD 16) reduction in the odds of death was not statistically significant. The least biased estimated of the effect of treatment on haemorrhagic transformation of the cerebral infarct (HTI) comes from trials where all patients were scanned at the end of treatment, irrespective of clinical deterioration; using this analysis, haemorrhagic transformation occurred in 7/102 (6.9%) control vs 8/106 (7.5%) treated, a non-significant 12% increase (SD 56, 2p > 0.1). These data cannot exclude the possibility that heparin substantially increases the risks of HTI. No data on disability in survivors could be obtained. Early heparin treatment might be associated with substantial reductions in deep venous thrombosis (and probably also pulmonary embolism) and possibly a one fifth reduction in mortality (equivalent to the avoidance of 20-40 early deaths per thousand patients treated.) However, the data were wholly inadequate on safety, particularly on the risk of haemorrhagic transformation of the infarct and on the hazards of heparin therapy in patients with known intracerebral haemorrhage. The trials of oral anticoagulants (15 deaths among 57 patients) and antiplatelet therapy (two deaths among 103 patients) were too small to be informative. Much larger randomized trials-comparing aspirin, heparin and the combination of both drugs against control-in patients with acute ischaemic stroke are justified (and several are now planned or underway).
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PMID:Antithrombotic therapy in acute ischaemic stroke: an overview of the completed randomised trials. 812 24

We examined hemostatic molecular markers in various thrombotic disorders. The efficacy of treatment in relation to the disseminated intravascular coagulation (DIC) score when the treatment was begun showed that greater efficacy was achieved in Pre-DIC than in DIC patients. The outcome was poorer with increasing DIC score, suggesting that early treatment is important. The sensitivity in some of molecular markers was high for both DIC and Pre-DIC. Receiver operating characteristic analysis suggest that soluble fibrin monomer level could be the most useful marker for the diagnosis of DIC. In examination of these markers in deep vein thrombosis, pulmonary embolism, acute myocardial infarction, and cerebral infarction, plasminogen activator inhibitor-1 and activated protein C-protein C inhibitor complex were useful marker for the diagnosis. Increased plasma GMP-140 was suggested to be the activation of platelets. The patients with high levels of plasma thrombomodulin (TM) considered to be a marker of vascular endothelial injuries became poor outcome. We will term these patients with high TM as systemic vascular endothelium injuries syndrome, and treat those by protecting the vascular endothelium.
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PMID:[Study of hemostatic molecular marker]. 913 93


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