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

Cerebral haemorrhage is the main life-threatening complication of oral anticoagulant therapy. In order to identify a means of prevention, the authors undertook a retrospective study of 68 consecutive cases of anticoagulant-related intracerebral haemorrhage. The mortality was 38.5%. The respective frequency of intracerebral haemorrhage, subarachnoid haemorrhage, acute and chronic subdural haematomas was 63.2, 16.2, 10.3 and 10.3%, respectively. On admission, nearly half the patients (53%) had prothrombin ratios inferior to 25%. A predisposing factor was found in 58% of cases: hypertension (30.6%), head injury (14.5%), alcoholism or drug interaction (11.2%), and one case of intracerebral aneurysm. A history of a transient ischaemic attack or of a cerebrovascular accident was found in 10.2% of cases and 11.7% had a previous anticoagulant related extracranial haemorrhage. The initial indications for oral anticoagulation were ischaemic heart disease (32%), atrial fibrillation (20.5%), secondary prevention of venous thromboembolic disease (17.6%) and primary prevention of venous thrombosis (11.7%). The duration of treatment for isolated ischaemic heart disease was over 6 months in all cases: the average duration of treatment was 12.4 months in phlebitis and pulmonary embolism. A critical review of the indications of treatment in the light of recent recommendations showed that if inappropriate indications were rare, the sometimes unnecessary prolongation of treatment was more common. Nearly half of these cases were receiving anticoagulants when the potential benefits were questionable at the time of the haemorrhagic complication. Clinical and biological follow-up is necessary for patients on anticoagulants; minor bleeding complications may be the prelude to major haemorrhage. Biological follow-up is based on control of the international normalised ratio.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The causes of intracranial hemorrhagic complications induced by antivitamins K]. 778 12

Twenty patients having routine laboratory control of oral anticoagulation after total hip or knee arthroplasty were consecutively included in the study and were anticoagulated at an International Normalized Ratio (INR) between 2.5 and 3.5. Patients with mechanical heart valve prostheses (n = 20), deep venous thrombosis or pulmonary embolism (n = 20), at the same level of oral anticoagulation, served as control groups. Plasma concentrations of prothrombin fragment 1 + 2 and D-dimer were measured and compared. In the mechanical heart valve prosthesis and deep venous thrombosis groups the median prothrombin fragment 1 + 2 concentrations were significantly lower than in the orthopaedic patient group (0.15 and 0.17 nmol/l versus 0.29 nmol/l). The D-dimer concentrations displayed a similar picture (150 and 200 micrograms/l versus 840 micrograms/l). The D-dimer/prothrombin fragment 1 + 2 ratios in the patients after total hip or knee arthroplasty were significantly higher (12.4) than in the control groups (5.3 and 6.0). These data show that the fibrinolysis/coagulation balance is enhanced, mainly due to a disproportional rise in D-dimer. After assessing when the D-dimer concentration returns to normal in this anticoagulated group, this parameter may indicate the appropriate duration of oral anticoagulant treatment after surgery for total knee or hip replacement.
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PMID:Coagulation activation and reactive fibrinolysis in patients receiving oral anticoagulation after total hip or knee replacement. 784 18

Prothrombin fragments (F1+2) can be used to monitor oral anticoagulation; their generation is also suppressed by heparin. We studied the course of F1+2, aPTT, heparin doses administered and heparin concentrations, as well as prothrombin time, during the first 7 days of heparin therapy (target aPTT 70 s) and overlapping oral anticoagulation (target INR 2-3) in 26 patients routinely treated for deep venous thrombosis (deep venous thrombosis +/- pulmonary embolism, 23 patients) or pulmonary embolism with a history of recurring deep venous thrombosis (3 patients). Although we found significant suppression of F1+2 between all pre- and post-treatment values, a transient, significant increase was seen on days 2-4. The amount of heparin given was stable from day 1-5; the fact of a transient increase in F1+2 might thus indicate that heparin doses routinely used are too low for the treatment of hypercoagulability in deep venous thrombosis in patients. We also found a decrease in heparin concentration on day 2, which may be explicable by changed pharmacokinetics of heparin in individuals with deep venous thrombosis. In conclusion, F1+2 may be useful for monitoring heparin treatment and oral anticoagulation in deep venous thrombosis patients from a laboratory point of view. However, larger studies are necessary to confirm these results. It remains to be clarified whether monitoring of anticoagulation by molecular markers might improve therapy of deep venous thrombosis. Such studies are in progress.
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PMID:[Is the assessment of prothrombin fragment F1+2 for monitoring of heparin therapy in patients with deep vein thrombosis useful?]. 789 70

A prospective, randomized, controlled clinical trial was performed comparing the antithrombotic efficacy of the low molecular weight heparin LMWH 21-23, (Braun) with an unfractionated heparin in elective general surgical patients over an observation period of 7 postoperative days. A total of 230 patients were admitted: 103 (group I) received low molecular weight heparin and 100 (group II) low-dose unfractionated heparin treatment given subcutaneously. In group I 41 patients (46%) were operated on for malignant disease and in group II 54 patients (54%). Due to the large amount of great abdominal procedures the intra- and perioperative application of hydroxyethyl starch was allowed for volume substitution. None of the patients died due to fatal pulmonary embolism. In group I four patients revealed positive 125I-labeled fibrinogen uptake (3.9%); two patients belonged to the hydroxyethyl starch subgroup. In group II five patients displayed a positive fibrinogen uptake (5%); two belonged to the hydroxyethyl starch subgroup. The results of the hemostaseological investigations (e.g., prothrombin time, activated partial thromboplastin time, thrombin clotting time, fibrinogen, antithrombin III, protein C, plasminogen, alpha 2-antiplasmin, tissue-type plasminogen activator, plasminogen activator inhibitor) revealed no statistically significant differences between groups I and II or their subgroups, although a tendency to prolonged clotting times was observed. The antifactor Xa activity values, however, displayed a statistically significant difference between the two groups (P < 0.05). The antifactor Xa activity measured up to 0.16 U/ml for the low molecular weight heparin (group I) and 0.05 U/ml for the unfractionated heparin (group II) in the postoperative period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prospective randomized clinical study in general surgery comparing a new low molecular weight heparin with unfractionated heparin in the prevention of thrombosis. 789 22

Patients receiving chemotherapy for metastatic breast cancer are at high risk of thromboembolic disease. Long-term oral anticoagulant therapy is needed but increases the risk of haemorrhagic complications. We have assessed the safety and efficacy of warfarin in very low doses as prophylaxis. Women receiving chemotherapy for metastatic breast cancer were randomly assigned either very-low-dose warfarin (152 patients) or placebo (159). The warfarin dose was 1 mg daily for 6 weeks and was then adjusted to maintain the prothrombin time at an international normalised ratio (INR) of 1.3 to 1.9. Study treatment continued until 1 week after the end of chemotherapy. The average daily dose from initiation of titration was 2.6 (SD 1.2) mg for the warfarin group and the mean INR was 1.52. The mean time at risk of thrombosis was 199 (126) days for warfarin-treated patients and 188 (137) days for placebo recipients (p = 0.45). There were 7 thromboembolic events (6 deep-vein thrombosis, 1 pulmonary embolism) in the placebo group and 1 (pulmonary embolism) in the warfarin group, a relative risk reduction of about 85% (p = 0.031). Major bleeding occurred in 2 placebo recipients and 1 warfarin-treated patient. There was no detectable difference in survival between the treatment groups. Very-low-dose warfarin is a safe and effective method for prevention of thromboembolism in patients with metastatic breast cancer who are receiving chemotherapy.
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PMID:Double-blind randomised trial of a very-low-dose warfarin for prevention of thromboembolism in stage IV breast cancer. 791 87

We studied 84 consecutive patients referred with the suspicion of pulmonary embolism (PE) to investigate the influence of clinical and hematological profiles on the diagnosis and severity of this disease and recovery. Diagnosis of PE was confirmed in 48 out of 84 patients by perfusion scintigraphy and/or pulmonary arteriography. Severity of PE and entity of recovery were investigated by measuring standard PaO2 on blood gas analysis and the number of unperfused lung segments ULS on perfusion scintigraphy. Most common clinical predisposing conditions were more frequent, though not significantly so, in embolic patients and a very low prevalence of PE was appreciable in patients without clear predisposing conditions. Among coagulation factors, only thrombin-antithrombin (TAT) complexes were twice as high in embolic as in nonembolic patients (14.0 +/- 13.6 vs. 7.0 +/- 4.2 ng/ml; p < 0.02), while there was no statistically significant difference between embolic and nonembolic patients for activated partial thromboplastin time, prothrombin time, antithrombin III, protein C, fibrinogen, plasminogen, alpha 2-plasmin inhibitor, and plasminogen activator inhibitor-1. Sensitivity and specificity of TAT complexes in diagnosis of PE were 95.8% and 30.5%, respectively. Therefore, normal values of TAT complexes may help exclude the diagnosis of PE, while abnormal values allow to reinforce the clinical suspicion of PE. No relation was found between coagulation parameters and the severity of PE. The follow-up of 48 patients with confirmed PE was favorable on the average; however, neither the presence of predisposing conditions nor abnormal coagulation parameters allow to predict the degree of functional and scintigraphic improvement during follow-up.
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PMID:Clinical, anamnestic and coagulation data in patients with suspected or confirmed pulmonary embolism. 800 95

Primary hepatocellular carcinoma can be revealed by recurrent pulmonary embolism as observed in this case of a 63-year-old woman initially hospitalized for abdominal pain and shortness of breath. The clinical diagnosis was confirmed by laboratory findings, a ventilation perfusion scan and pulmonary angiography which demonstrated peripheral basal artery cut-off and slow filling with delayed washout. The patient was treated with heparin then with nicoumarol and responded well. One month after discharge the patient again complained of shortness of breath and was readmitted. Anticoagulation was adequate as evidenced by a prothrombin time of 1.39 INR and the physical examination and laboratory tests again suggested pulmonary emboli, confirmed by a ventilation perfusion scan. Computed tomography of the chest and abdomen revealed multiple hypodense masses filling half of the liver volume and needle biopsy led to the diagnosis of hepatocellular carcinoma. Hypercoagulability in malignancy is well-known although cases of migratory thrombophlebitis are extremely rare. Pulmonary embolism has not been described as a presenting feature of hepatocellular carcinoma. In this case, there was no evidence of hepatic dysfunction and the pulmonary embolism occurred despite adequate anticoagulation. Clinicians should include occult carcinoma among the possible causes of recurrent pulmonary embolism and when searching for malignancy can include hepatocellular carcinoma among the causes of hypercoagulation.
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PMID:Pulmonary embolism as the presenting feature of hepatocellular carcinoma. 802 23

Prevention of deep venous thrombosis is fundamental in the prevention of pulmonary embolism. Deep venous thrombosis is common after all surgical procedures, but the frequency differs, as does the effectiveness of various methods of prevention. Low-dose heparin, low molecular weight heparin, graduated compression elastic stockings, intermittent pneumatic compression, and oral anticoagulants have a role in the prevention of deep venous thrombosis, depending on the risks of deep venous thrombosis and their demonstrated effectiveness (or lack of effectiveness) in the particular circumstance. The optimal method of prophylaxis is specific to the predisposing condition. Heparin continues to be a mainstay of anticoagulant therapy. Major bleeding is rare in patients treated with low doses of heparin to prevent deep venous thrombosis. With therapeutic doses, however, major bleeding occurs in about 5% of patients. The optimal dose of warfarin and the method of evaluating the anticoagulant effect of warfarin have undergone modifications in recent years. It is now recognized that the prothrombin time ratio depends on the activity of the thromboplastin used for measuring the prothrombin time. An International Normalized Ratio, which relates to a standardized thromboplastin, has been developed, thus avoiding differences of the prothrombin time ratio that occur from batch to batch of thromboplastin reagent from the same manufacturer and that occur with different thromboplastin reagents from different animal sources and different manufacturers. The bedside diagnosis of pulmonary embolism is useful in helping a physician determine the extent to which diagnostic tests should be pursued. A sound bedside impression also contributes strongly to the formulation of a noninvasive diagnosis of pulmonary embolism. The clinical manifestations of pulmonary embolism form a recognizable constellation of findings that often lead to a correct diagnosis or exclusion of pulmonary embolism. Important clues to the diagnosis of pulmonary embolism relate to the initial syndrome. The presentation of pulmonary embolism is most often in the form of the pulmonary hemorrhage-pulmonary infarction syndrome. The next most common presentation is unexplained dyspnea, unaccompanied by pulmonary hemorrhage or infarction. Least common, but most severe, is the syndrome of circulatory collapse. Immobilization, usually caused by surgery, is the most frequent predisposing factor. Most patients with clinically recognizable pulmonary embolism have dyspnea or tachypnea. Dyspnea or tachypnea or pleuritic pain occurs in nearly all patients who have clinically apparent pulmonary embolism (97%). Ordinary tests such as the electrocardiogram and chest radiograph are helpful if the physician is attentive to nonspecific abnormalities.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute pulmonary embolism. 807

This study reports the efficacy in the prevention of thromboembolic complications of adapted low-dose oral anticoagulants following total hip replacement. 750 patients undergoing total hip replacement received oral anticoagulants as exclusive drug prophylaxis for thromboembolic complications. These patients were considered preoperatively not to present any particular risk for the development of postoperative thrombosis. Anticoagulant therapy was commenced on the evening of the operation. Eleven pulmonary embolisms (1.5 per cent) were observed, but none of them were fatal. The risk of thrombosis was evaluated in 100 of these 750 patients by means of bilateral venography of the lower limbs: 21 patients developed distal thrombosis (sural veins) and 2 patients developed proximal femoral thrombosis. Only one haemorrhagic complication occurred in the 750 patients of this series. The prothrombin profile determined in the patients developing thrombosis or pulmonary embolism was not significantly different from that of the patients free of any thromboembolic complications. Although oral anticoagulants appear to be particularly effective for the prevention of fatal pulmonary embolism, it is not clear that their efficacy is directly related to the prothrombin time.
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PMID:[Prevention of thromboembolic complications with adapted low-dose of antivitamins K after total hip prosthesis]. 808 39

Fibrin D-Dimer (D-Di), prothrombin activation fragment (F 1+2) and thrombin-antithrombin III complexes (TAT) were measured using ELISA procedures in the plasma of patients with an acute deep venous thrombosis (DVT), at presentation and on days 2, 6 and 10 after initiation of heparin treatment. Patients were randomly allocated into two treatment groups: 44 patients received adapted doses of continuous intravenous unfractionated heparin (UH) whereas 47 received 1 mg/kg every twelve hours of a low molecular weight heparin (enoxaparin) subcutaneously. A phlebography and a perfusion lung scan were performed before inclusion and on day 10. Failure of therapy (n = 9) was defined by venogram worsening or confirmed pulmonary embolism. Improvement (n = 44) or stationary state (n = 38) were defined by venogram evolution in the absence of new leg scan defects. At presentation, D-Di, F 1+2 and TAT were above cut-off values in 97, 66 and 89% of patients respectively. D-Di levels correlated with the extent of venous thrombosis whereas TAT and F 1+2 did not. Mean levels of D-Di decreased sharply during the first days of treatment but were still abnormal on day 10. A secondary increase of D-Di on days 6 or 10 by more than 3 micrograms/ml occurred in 4 of the 9 patients who developed a thromboembolic recurrence but in none of the 72 patients who had a more favorable outcome. F 1+2 and TAT time-courses were not related to clinical evolution. In the Enoxaparin group, there was no relationship between antifactor Xa activities and any biological markers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Markers of hemostatic system activation in acute deep venous thrombosis-evolution during the first days of heparin treatment. The DVTENOX Study Group. 816 10


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