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Query: UMLS:C0034065 (pulmonary embolism)
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A great variety of clinical and immunological features have been described in patients with the antiphospholipid syndrome (APS), but information on their prevalence and characteristics in Latin American mestizo patients with the primary APS is scarce. To analyze the prevalence and characteristics of the main clinical and immunological manifestations in a cohort of patients with primary APS of mestizo origin from Latin America and to compare them with the European white patients, clinical and serological characteristics of 100 patients with primary APS from Colombia, Mexico, and Ecuador were collected in a protocol form that was identical to that used to study the "Euro-Phospholipid" cohort. The cohort consisted of 92 female patients (92.0%) and eight (8.0%) male patients. They were all mestizos. The most common manifestations were deep vein thrombosis (DVT; 23.0%), livedo reticularis (18.0%), migraine (18.0%), and stroke (18.0%). The most common pregnancy morbidity was early pregnancy losses (54.1% of pregnancies). Several clinical manifestations were more prevalent in the Latin American mestizo than in the European patients (transient global amnesia, pulmonary microthrombosis, arthralgias, and early pregnancy losses) and vice-versa (DVT, stroke, pulmonary embolism, and thrombocytopenia). Latin American mestizo patients with primary APS have a wide variety of clinical and immunological manifestations with several differences in their prevalence in comparison with European white patients.
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PMID:Primary antiphospholipid syndrome in Latin American mestizo patients: clinical and immunologic characteristics and comparison with European patients. 1815 95

Management of thrombosis of the dural sinus and cerebral veins (CVT) includes treatment of the underlying condition, antithrombotic treatment, symptomatic treatment, and the prevention or treatment of complications. Intravenous heparin or subcutaneous low-molecular-weight heparin should be used in acute CVT to prevent thrombus propagation and pulmonary embolism and to increase the chances of recanalization. Anticoagulation is safe and can be used in patients with acute CVT who have intracranial hemorrhagic lesions. Endovascular thrombolysis (with or without mechanical thrombus disruption) is an experimental treatment to be used in experienced centers for severe cases or patients who fail to improve on anticoagulation. Local thrombolysis is not useful in patients with large infarcts and impending herniation. In patients with severe headache and papilledema, intracranial hypertension can be reduced and symptoms relieved through a therapeutic lumbar puncture. Hemicraniectomy may be lifesaving in patients with parenchymal lesions leading to herniation. In patients with acute seizures and supratentorial lesions, antiepileptic drugs should be prescribed. Prophylactic use of these drugs can also be considered for patients with one of these risk factors but should be avoided in patients with neither of them. To reduce the risk of recurrent deep venous thrombosis of the limbs, vitamin K antagonists are given for a variable period depending on the patient's inherent risk of thrombosis, aiming at an International Normalized Ratio of 2 to 3.5. If CVT is related to a transient risk factor (eg, pregnancy, infection), we recommend anticoagulants for 3 months. In patients with idiopathic CVT or CVT associated with "mild" thrombophilia, the period of anticoagulation must be extended to 6 to 12 months. In patients with "severe" thrombophilia (eg, two or more prothrombotic abnormalities or antiphospholipid syndrome), anticoagulants should be given for life. Patients with persistent symptoms of increased intracranial hypertension, visual loss, or both can be treated with repeated lumbar punctures or a lumboperitoneal shunt. For the prevention of remote seizures, antiepileptic drugs are recommended for patients with seizures in the acute phase and for those who experience a seizure after the acute phase. These drugs can also be considered for patients without seizures who have supratentorial hemorrhagic lesions or motor deficits.
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PMID:Acute treatment of cerebral venous and dural sinus thrombosis. 1833 35

Venous thromboembolism is the leading cause of maternal death in the United States. Pregnancy is a risk factor for deep venous thrombosis, and risk is further increased with a personal or family history of thrombosis or thrombophilia. Screening for thrombophilia is not recommended for the general population; however, testing for inherited or acquired thrombophilic conditions is recommended when personal or family history suggests increased risk. Factor V Leiden and prothrombin G20210A mutation are the most common inherited thrombophilias, and antiphospholipid antibody syndrome is the most important acquired defect. Clinical symptoms of deep venous thrombosis may be subtle and difficult to distinguish from gestational edema. Venous compression (Doppler) ultrasonography is the diagnostic test of choice. Pulmonary embolism typically presents postpartum with dyspnea and tachypnea. Multidetector-row (spiral) computed tomography is the test of choice for pulmonary embolism. Warfarin is contraindicated during pregnancy, but is safe to use postpartum and is compatible with breastfeeding. Low-molecular-weight heparin has largely replaced unfractionated heparin for prophylaxis and treatment in pregnancy.
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PMID:Venous thromboembolism during pregnancy. 1861 81

Pulmonary embolism is the main pulmonary manifestation of primary antiphospholipid syndrome. Other pulmonary manifestations including intra-alveolar haemorrhage are less common. We report a 36-year-old man with a primary antiphospholipid syndrome who presented with an acute respiratory failure due to the association of pulmonary embolism and intra-alveolar haemorrhage. This diagnosis should be systematically considered as it is life threatening and requires a specific therapy.
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PMID:[Intra-alveolar pulmonary haemorrhage, an unusual manifestation of the primary antiphospholipid syndrome]. 1861 15

Nonbacterial thrombotic (noninfectious, pseudoinfectious--PIE) endocarditis is characterized by precipitation of thrombus, not containing bacteria, on the valve cusps. Mitral and aortal valves are affected most frequently. Vegetations, as a rule, do not exceed 6-7 mm and have a high inclination to embolism. Hypercoagulation plays a leading role in PIE pathogenesis. The most frequent acquired causes of sterile vegetation forming are malignant tumors and rheumatic diseases (especially systemic lupus erythematosus--SLE and antiphospholipid syndrome--APS). Valve pathology is most frequent lesion of heart in APS patients. It is supposed, that antibodies to phospholipids (aPL) have a special importance in valve lesion pathogenesis at APS, besides, changes in valve apparatus at SLE are associated exactly with aPL. Main problems of PIE patients are recurrent thromboembolism, development of valve dysfunction with clinical signs of heart failure (4-6% cases), difficulties in differential diagnostics: PIE is hard to diagnose if basic disease is accompanied by fever (diffuse diseases of connective tissue etc.). Transesophageal echocardiography is a leading method in PIE diagnostics. The main therapeutic option in PIE treatment is anticoagulant therapy: nonfractional or subcutaneous heparin in presence of systemic or pulmonary embolism, in patients with disseminated malignant tumors--complete doses of nonfractional heparin.
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PMID:[Pseudoinfectious endocarditis]. 1872 Jul 5

Antiphospholipid syndrome is a well-defined entity that is characterized by spontaneous abortion, thrombocytopenia, and recurrent arterial and venous thromboses. A partially calcified right atrial thrombus mimicking myxoma with recurrent pulmonary embolism has not been previously reported in a patient who also had systemic lupus erythematosus and secondary antiphospholipid syndrome. Herein, we describe the case of a 37-year-old woman with systemic lupus erythematosus and secondary antiphospholipid syndrome who was admitted to the hospital with progressive exertional dyspnea. Ventilation-perfusion scanning showed multiple parenchymal defects in the lungs that portended pulmonary embolism. In addition, the scanning revealed normal regional ventilation. Transthoracic and transesophageal echocardiography showed a right atrial mass that was highly suggestive of myxoma, and the patient subsequently underwent surgery. A histologic examination showed an organized, partially calcified thrombus. Intracardiac thrombus has been rarely reported as a complication of antiphospholipid syndrome. In our patient, the preoperative investigations could not differentiate the partially calcified right atrial thrombus from a myxoma, and the diagnosis was made postoperatively.
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PMID:Right atrial thrombus mimicking myxoma with pulmonary embolism in a patient with systemic lupus erythematosus and secondary antiphospholipid syndrome. 1915 41

Anti Phospholipid Syndrome (APS) is a relatively new conception of syndrome complex first noticed in 1983. It may be primary or secondary to other diseases like SLE, RA, Systemic sclerosis, behchet's syndrome, temporal arteritis, sjogren's syndrome psoriatic arthropathy etc. Clinical manifestations are consequences of vascular thrombosis and embolism like DVT, pulmonary embolism, stroke, TIA, complication of pregnancy with pregnancy loss. We report a 34 years married female housewife who presented with sudden onset of nausea, vomiting, vertigo, dysphagia, dysarthria and ataxia. She had a chronic leg ulcer. Neurological findings were consistent with lateral medullary syndrome due to stroke though she was normotensive, nondiabetic with normal lipid profile. She had history of two abortions in last three years. Investigations were done accordingly and she fulfilled the diagnostic criteria of APS. No secondary cause was detected after thorough clinical examination and laboratory investigations. She was treated symptomatically along with oral anticoagulation. She improved slowly but steadily.
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PMID:Anti phospholipid syndrome. 1918 54

The antiphospholipid syndrome is a relatively common acquired cause of venous thrombosis. Up to 20% of cases of deep vein thrombosis, with and without pulmonary embolism, may be associated with antiphospholipid antibodies. These antibodies are typically detected in lupus anticoagulant assays and tests for anticardiolipin antibodies. Most antiphospholipid antibodies are directed against several phospholipid-binding plasma proteins. The most common antigens are beta2-glycoprotein I and prothrombin. Immunoassays using these purified antigens are now available. In addition to being markers for thrombotic risk, antiphospholipid antibodies have been shown to directly contribute to hypercoagulability in animal models and in various in vitro studies. Prevention of recurrent venous thrombosis in patients with the antiphospholipid syndrome requires long-term anticoagulation. The optimal intensity of warfarin therapy is an ongoing issue, but most clinicians currently favor a target INR in the 2.0 to 3.0 range. In certain patients, antiphospholipid antibodies may interfere with determination of the INR, requiring other approaches to monitor and adjust the warfarin dose. Low-dose aspirin is typically recommended for primary prevention of thrombosis in asymptomatic patients with moderate to high levels of antiphospholipid antibodies, although strong supporting data are lacking.
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PMID:Venous thrombosis in the antiphospholipid syndrome. 1922 5

Venous thromboembolism (VTE) has been a subject of great interest of late. Since Rudolph Virchow described the famous Virchow's triad in 1856, there have been rapid strides in the understanding of the pathogenesis and factors responsible for it. Discovery of various thrombophilic factors, both primary and acquired, in the last 40 years has revolutionized prognostication and management of this potentially life-threatening condition due to its associated complication of pulmonary thromboembolism. Detailed genetic mapping and linkage analyses have been underlining the fact that VTE is a multifactorial disorder and a complex one. There are many gene-gene and gene-environment interactions that alter and magnify the clinical picture in this disorder. Point in case is pregnancy, where the risk of VTE is 100-150 times increased in the presence of Factor V Leiden, prothrombin mutation (Prothrombin 20210A) and antithrombin deficiency. Risk of VTE associated with long-haul air flight has now been well recognized. Thrombotic events associated with antiphospholipid syndrome (APS) are 70% venous and 30% arterial. Deep venous thrombosis and pulmonary embolism are the most common venous events, though unusual cases of catastrophes due to central vein thrombosis like renal vein thrombosis and Budd-Chiari syndrome (catastrophic APS) may occur.
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PMID:Venous thromboembolism: the intricacies. 1924 82

Antiphospholipid syndrome (APS) is characterised by recurrent venous or arterial thrombosis and/or fetal losses. In APS, the homeostatic regulation of blood coagulation is altered, however, the mechanism of thrombosis is not yet defined and it has varied manifestations. Deep vein thrombosis with or without pulmonary embolism is the most common manifestation followed by arterial occlusion of cerebral, coronary and other arteries including subclavian, retinal, renal and pedal arteries. We report a case of a 42 years old female, with severe primary APS, who presented with symmetrical peripheral gangrene, an uncommon presentation and was treated successfully.
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PMID:Severe primary antiphospholipid syndrome. 1926 8


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