Myocarditis and pericarditis with tamponade associated with disseminated tuberculosis

Tuberculous involvement of the myocardium is relatively rare. Tuberculous pericarditis with tamponade and myocarditis in a young woman with no evidence of immunosuppression and disseminated tuberculosis is described. Three distinct forms of myocardial involvement are recognized: nodular tubercles (tuberculomas) of the myocardium; miliary tubercles of the myocardium; and an uncommon diffuse infiltrative type. The myocardium is involved by a hematogenous route, by lymphatic spread or contiguously from the pericardium. The diagnosis can be made by endomyocardial biopsy if clinical suspicion is strong and echocardiographic findings are suggestive. Antituberculosis drugs may be curative. With an increasing prevalence of tuberculosis, the possibility of potentially lethal myocardial tuberculosis is important to consider.     

Aortic aneurysm with vena cava thrombosis occurring in Behcet's disease

We report a case of Behcet's disease complicated by aortic aneurysm and contiguous vena cava thrombosis due to compression. Arterial aneurysms are uncommon in the course of Behcet's disease and are associated with a poor prognosis owing to the risk of rupture. Vena cava thrombosis is found in 10% of cases; pulmonary embolism is infrequent. Venous and arterial lesions usually evolve independently. In most cases they are consecutive to vasculitis. The case reported herein is uncommon because of simultaneous and contiguous venous and arterial lesions. Eighteen months after aorto bi-iliac graft and inferior vena cava ligature, there is no recurrence of thrombosis nor aneurysm with a treatment including heparin, colchicine and azathioprine.     

Aneurysms of the popliteal vein. Description of 2 cases

Primitive vein popliteal aneurysms are an extremely rare pathology whose treatment is still matter of controversy. Its rare incidence, the diagnostic and clinical problems ensuing to the possible pulmonary embolism, explain the interest developed by these lesions. The authors report two cases of popliteal vein aneurysm observed in their Institute and diagnosed because seat of vein thrombosis and source of pulmonary embolism.     

Acute gastroduodenal lesions in patients with venous thromboembolism. Identification of patients at risk

The prime complication of heparin therapy is bleeding, and the gastrointestinal tract is the most common site of bleeding in patients treated with heparin. We recently reported that gastroduodenal lesions are common in patients admitted because of acute venous thromboembolism, and now we present our experience in a larger series of patients. The aims of the study were to try to validate our previous findings and to identify clinical factors that could increase the likelihood of having an acute, potential bleeding lesion in the gastroduodenal tract. Upper gastrointestinal endoscopy was performed on admission in 155 consecutive patients with acute venous thromboembolism (118 with deep vein thrombosis, 37 with pulmonary embolism). Acute lesions (both peptic ulcers and diffuse erosions) were found in 19 of 118 patients (16 percent) with venous thrombosis, and in 14 of 37 patients (38 percent) with pulmonary embolism (p = 0.005). When only patients with pulmonary embolism were considered, lesions were more commonly found in men, and in patients with severe hypoxemia on admission. When considered overall, only the timing of endoscopy was statistically significant; acute lesions were more commonly found when endoscopy was performed early after admission. No significant differences were found in terms of age, sex, smoking habits, alcohol intake, concomitant drug ingestion, comorbid diseases, or previous history of ulcer. The very high incidence of upper GI tract lesions in these patients will have long-term diagnostic/therapeutic implications which cannot be ignored. Who should receive prophylactic H2 blockers and for how long remains to be determined.     

Thrombosis of the superior vena cava disclosing Beh?et's disease

The authors report the case of a 29 year old North African patient with Beh?et's disease presenting with sudden thrombosis of the superior vena cava. Venous disorders are the fourth major sign of this disease. Although superficial thrombophlebitis is a common presenting sign, caval thrombosis is rare and usually occurs after several years' evolution. Superior vena caval thrombosis may be life threatening due to complications such as pulmonary embolism and haemoptysis. The anatomical substrate of this form of vascular disease is the same as that of the other visceral lesions of Beh?et's disease: predominantly venous vasculitis with perivascularitis and secondary thrombosis. The pathogenesis of this thrombotic diathesis is discussed.     

A case of pulmonary thromboembolism after interruption of treatment with unfractionated heparin

Pulmonary embolism is a quite frequent event (incidence 1/10000/year), and blood stasis, endothelial lesions and coagulation disorders are predisposable factors. Elective treatment is heparin, but the use of this medication is associated with a possible ipercoagulative rebound effect. The case presented is a patient with unstable angina treated with heparin infusion, who developed pulmonary embolism after discontinuation of heparin treatment; the patient didn't present a genetic coagulopathy. Others risk factors have been analyzed and it was observed that discontinuation of heparin infusion could have a predominant role in the development of thrombosis. A MedLine research on the rebound effect of heparin and how to reduce it has been carried out.     

Comparison of fibrinolytic treatment with interruption of the inferior caval vein in the prevention of pulmonary embolism

The procedure of interruption of the inferior caval vein is designed to prevent pulmonary embolism, but its effectiveness has yet to be compared with thrombolytic therapy. Sixty patients hospitalized for pulmonary embolism and proximal deep vein thrombosis were divided into two groups of 31 and 29 patients, respectively. The patients were selected because of persistent venous thrombosis in the inferior caval, iliac or femoral veins. The patients in the first group (mean age 53.2 years) were treated by interruption of the inferior caval vein. The second group of patients (mean age 57) received only fibrinolytic treatment. From those patients having caval venous interruption due to peri-operative myocardial infarction 1 died and 3 others presented pulmonary embolism (massive in two cases). No patients treated by fibrinolysis suffered from pulmonary embolism. Five patients died of cancer, 2 having had caval interruption, as opposed to only 2 having fibrinolysis. Eight patients undergoing surgery had a severe functional handicap. This study demonstrated a high recurrence of pulmonary embolism in patients with persistent venous thrombosis who were treated by interruption of the inferior caval vein. These patients also had a high morbidity. Fibrinolytic treatment (even in the presence of persistent venous thrombosis) appeared to be more effective in avoiding recurrence of pulmonary embolism.     

Thrombosis of an apparently normal thoracic aorta and arterial embolism

With the advent of new imaging techniques, the aorta has been increasingly identified as a source of arterial embolism. The majority of thrombi occur in aneurysms or are adherent to atherosclerotic lesions in the abdominal aorta. Thrombi in the thoracic aorta are much less common, particularly in apparently normal aortas. Consequently, the natural history and optimal treatment of these lesions are not well-defined. The aim of this article was to describe the clinical characteristics, treatment, and outcome in three patients with thoracic aorta thrombosis and arterial embolism. Currently available literature on this pathology is reviewed and the differential diagnosis of these lesions is discussed.     

A population-based study of the effectiveness of inferior vena cava filter use among patients with venous thromboembolism

BACKGROUND: There are few population-based data regarding the effectiveness of inferior vena cava filter use in the prevention of symptomatic pulmonary embolism. OBJECTIVE: To determine the 1-year cumulative incidence of rehospitalization for venous thrombosis or pulmonary embolism among patients with thromboembolism treated with a vena cava filter compared with the incidence in a control population with thromboembolism. PATIENTS AND METHODS: Population-based retrospective analysis of linked hospital discharge abstracts in California. From January 1, 1991, through December 30, 1995, 3632 patients were treated with a filter and 64,333 controls were admitted with a principal diagnosis of venous thromboembolism. RESULTS: Filter-treated patients had significantly greater comorbidity, with a higher frequency of previous pulmonary embolism, recent major bleeding, malignant neoplasm, and stroke. Patients who initially manifested pulmonary embolism were significantly more likely to be rehospitalized for pulmonary embolism than patients with an initial diagnosis of venous thrombosis alone, among filter-treated patients (relative risk, 6.72; 95% confidence interval, 3.61-12.49) and controls (relative risk, 5.30; 95% confidence interval, 4.61-6.10). Risk-adjusted proportional hazards modeling showed no significant difference between filter-treated patients and controls in the relative hazard of rehospitalization for pulmonary embolism. However, filter placement was associated with a significantly higher relative hazard of rehospitalization for venous thrombosis among patients who initially manifested pulmonary embolism (relative hazard, 2.62; 95% confidence interval, 2.09-3.29), but not among those who presented with venous thrombosis (relative hazard, 1.14; 95% confidence interval, 0.92-1.43). CONCLUSIONS: Insertion of a vena cava filter was not associated with a significant reduction in the 1-year incidence of rehospitalization for pulmonary embolism. Use of a filter was associated with a higher incidence of rehospitalization for venous thrombosis, but only among patients who initially manifested pulmonary embolism. A prospective clinical study is needed to determine the efficacy of filter use among patients with pulmonary embolism who do not meet strict guidelines for insertion of a vena cava filter.     

Outpatient treatment of patients with deep-vein thrombosis or pulmonary embolism

There have been a large number of randomized trials comparing standard unfractionated intravenous heparin with low-molecular-weight heparin for the treatment of deep-vein thrombosis, but only two of these have looked at outpatient therapy. There have been only two randomized trials including patients with symptomatic pulmonary embolism, and neither of these provided outpatient therapy. Postmortem and clinical studies have shown a strong association between pulmonary embolism and the presence of venous thrombosis in the lower limbs. Based on similar rates of venous thromboembolic recurrence and death, these studies suggest that initial treatment should be the same for deep-vein thrombosis and pulmonary embolism. The feasibility of providing outpatient care to many patients seeking treatment for deep-vein thrombosis or acute pulmonary embolism at certain tertiary care hospitals has become evident, but the data suggest that the proportion of eligible patients is institution dependent and may vary from 18% to 91%. In the author's institution, approximately 50% of patients with pulmonary embolism could be treated as outpatients, but there have been no other reports on outpatient therapy for patients with pulmonary embolism. If patients with pulmonary embolism meet criteria demonstrated to result in a higher risk of death, it is, of course, reasonable to not treat such patients on an outpatient basis. Low-molecular-weight heparin followed by oral anticoagulant therapy provides adequate therapy in most patients with deep-vein thrombosis or pulmonary embolism, and many patients can be treated as outpatients.     

Venous thromboembolism in patients hospitalized with nephrotic syndrome

Purpose

Whether pulmonary embolism in patients with the nephrotic syndrome is caused by deep venous thrombosis or renal vein thrombosis is controversial. To determine which is the likely cause of pulmonary embolism in patients with the nephrotic syndrome, we investigated data from the National Hospital Discharge Survey.

Methods

The number of patients discharged from nonfederal short-stay hospitals in the United States with a diagnostic code of nephrotic syndrome, deep venous thrombosis, renal vein thrombosis, and pulmonary embolism was obtained using ICD-9-M (International Classification of Diseases, Ninth Revision, Clinical Modification) codes.

Results

From 1979 to 2005, 925,000 patients were discharged from hospitals with the nephrotic syndrome and 898,253,000 patients did not have the nephrotic syndrome. With the nephrotic syndrome, 5000 (0.5%) had pulmonary embolism, 14,000 (1.5%) had deep venous thrombosis, and fewer than 5000 had renal vein thrombosis. The relative risk of pulmonary embolism comparing patients with the nephrotic syndrome to those who did not have it was 1.39, and the relative risk of deep venous thrombosis was 1.72. Among patients aged 18-39 years, the relative risk of deep venous thrombosis was 6.81. From 1991-2005, after venous ultrasound was generally available, the relative risk of deep venous thrombosis (all ages) was 1.77.

Conclusion

The nephrotic syndrome is a risk factor for venous thromboembolism. This is strikingly apparent in young adults. Renal vein thrombosis was uncommon. Therefore, pulmonary embolism, if it occurs, is likely to be due to deep venous thrombosis and not renal vein thrombosis.     

Unexpected high prevalence of silent pulmonary embolism in patients with deep venous thrombosis

In patients presenting with clinically suspected deep vein thrombosis, symptomatic pulmonary embolism is rarely apparent. To assess the prevalence of silent pulmonary embolism in outpatients with proven deep vein thrombosis but without symptoms of pulmonary embolism, perfusion ventilation lung scans were performed in 101 consecutive patients at presentation. Fifty-one percent of these patients had a high probability lung scan at the initiation of treatment. In comparison, in patients referred with suspected venous thrombosis, but who on subsequent objective testing did not have venous thrombosis (n = 44), the prevalence of a high probability-scan for pulmonary embolus was only 5 percent. At repeat lung scanning, performed after one week of anticoagulant treatment, complete to partial improvement was observed in 68 percent of the patients with initially abnormal scans. Lung-scan detected asymptomatic pulmonary embolism occurs frequently in patients presenting with symptomatic deep venous thrombosis, and the majority of these emboli showed significant to complete resolution within one week of anticoagulant treatment.     

Myocardial infarction beginning with cerebral symptoms in 30 cases of cardio-cerebral apoplexy

A clinicopathological analysis of myocardial infarction with an onset of stroke-like symptoms was carried out on 30 autopsy cases at the Tokyo Metropolitan Geriatric Hospital. The cases were classified into four groups according to the types of brain lesions, I: embolism (n = 17), II: thrombosis (n = 9), III: bleeding (n = 2), and IV: no remarkable focal lesion (n = 2). Classification was made based on clinical findings, and pathological features. The characteristic clinical findings were conciousness disturbance, no elevation of blood pressure at the onset of stroke, hemiplegia and shock. However, the typical anginal chest pain was found in only 17% of cases. The underlying diseases and complications were hypertension, atrial fibrillation (Af), disseminated intravascular coagulation (DIC), renal failure, malignant neoplasma, and diabetes mellitus. The incidences of Af, DIC, mural thrombus, non-bacterial thrombotic endocarditis (NBTE) were significantly higher in the group with cerebral embolism than in the group with cerebral thrombosis. The coronary stenotic index was also smaller in the group with cerebral embolism. Therefore, the major etiology of cardio-cerebral apoplexy was a simultaneous embolism to the brain and heart due to Af, NBTE or, DIC.     

Disseminated arterial occlusions revealing bilateral venous thrombosis with paradoxical embolisms

Paradoxical embolism is a diagnosis of exclusion. Clinical triad associates deep venous thrombosis with or without pulmonary embolism, arterial embolism, and intracardiac communication with right-to-left shunt. The intracardiac communication is generally related to a patent foramen ovale (PFO). We report a 75-year-old patient, who presented with bilateral deep venous thrombosis of the legs, complicated by massive pulmonary embolism and paradoxical embolisms through a PFO. This resulted in cerebral, mesenteric, splenic and bilateral kidney infarctions. A promptly initiated anticoagulant treatment allowed a favourable outcome.     

Management of venous thromboembolism: a clinical practice guideline from the American College of Physicians and the American Academy of Family Physicians

Venous thromboembolism is a common condition affecting 7.1 persons per 10,000 person-years among community residents. Incidence rates for venous thromboembolism are higher in men and African Americans and increase substantially with age. It is critical to treat deep venous thrombosis at an early stage to avoid development of further complications, such as pulmonary embolism or recurrent deep venous thrombosis. The target audience for this guideline is all clinicians caring for patients who have been given a diagnosis of deep venous thrombosis or pulmonary embolism. The target patient population is patients receiving a diagnosis of pulmonary embolism or lower-extremity deep venous thrombosis.     

Tuberculous aortitis with an aortoduodenal fistula presenting as recurrent gastrointestinal bleeding.

Tuberculous aortitis with a tuberculous mycotic aneurysm and an aortoduodenal fistula was diagnosed in a 38-year-old man with tuberculous cervical lymphadentitis and a 3-month history of recurrent gastrointestinal bleeding, in whom extensive investigation of the digestive tract had not revealed a bleeding lesion. Either by septic embolism or by direct extension from a neighboring focus, tuberculous infection can cause a mycotic aortic aneurysm with subsequent fistulation to the duodenum.     

Silent Pulmonary Embolism in Patients with Deep Venous Thrombosis: A Systematic Review

Purpose

To determine, by systematic review of the literature, the prevalence of silent pulmonary embolism in patients with deep venous thrombosis.

Methods

Twenty-eight included published investigations were identified through PubMed. Studies were selected if methods of diagnosis of pulmonary embolism were described; if pulmonary embolism was stated to be asymptomatic; and if raw data were presented. Studies were stratified according to whether silent pulmonary embolism was diagnosed by a high-probability ventilation-perfusion lung scan using criteria from the Prospective Investigation of Pulmonary Embolism Diagnosis, computed tomography pulmonary angiography, or conventional pulmonary angiography (Tier 1), or by lung scans based on non-Prospective Investigation of Pulmonary Embolism Diagnosis criteria (Tier 2).

Results

Silent pulmonary embolism was diagnosed in 1665 of 5233 patients (32%) with deep venous thrombosis. This is a conservative estimate because many of the investigations used stringent criteria for the diagnosis of pulmonary embolism. The incidence of silent pulmonary embolism was higher with proximal deep venous thrombosis than with distal deep venous thrombosis. Silent pulmonary embolism seemed to increase the risk of recurrent pulmonary embolism: 25 of 488 (5.1%) with silent pulmonary embolism versus 7 of 1093 (0.6%) without silent pulmonary embolism.

Conclusion

Silent pulmonary embolism sometimes involved central pulmonary arteries. Because approximately one third of patients with deep venous thrombosis have silent pulmonary embolism, routine screening for pulmonary embolism may be advantageous.     

Myocardial fibrosis in mice with overexpression of human blood coagulation factor IX

Elevated circulatory levels of many blood coagulation factors are known to be a risk factor for deep vein thrombosis in humans. Here we report the first direct demonstration of a close association between elevated circulatory factor IX levels in mice with thrombosis as well as myocardial fibrosis. Transgenic mice overexpressing human factor IX at persistently high levels died at much younger ages than their cohorts expressing lower levels, or nontransgenic control animals. The median survival age of animals was inversely related to the circulatory levels of human factor IX. Prematurely dying animals had focal fibrotic lesions predominantly present in the left ventricular myocardium, and vasculatures in these lesions showed fibrin deposition. Thromboemboli were also present in other organs, including lung and brain. These observations support the hypothesis that persistently high circulatory levels of factor IX are a risk factor not only for thrombosis and/or thromboembolism, but also for myocardial fibrosis mimicking human myocardial infarction.     

Factors V leiden and II 20210A in patients with symptomatic pulmonary embolism and deep vein thrombosis

PURPOSE: Factor V Leiden and factor II 20210A are inherited disorders of the clotting system that occur frequently in patients with deep vein thrombosis. We conducted this study to determine whether these factors are also common in patients with pulmonary embolism. SUBJECTS AND METHODS: We determined the prevalence of factor V Leiden and factor II 20210A in 773 consecutive patients with objectively documented symptomatic deep vein thrombosis or symptomatic pulmonary embolism, or with a combination of these disorders. RESULTS: Isolated symptomatic deep vein thrombosis occurred in 345 patients; isolated symptomatic pulmonary embolism occurred in 236; and both anomalies occurred in 192. Factor V Leiden was present in 21 (9%) of the patients with isolated symptomatic pulmonary embolism, in 30 (16%) with both manifestations, and in 63 (18%) with isolated symptomatic deep vein thrombosis (P = 0.007). Factor V Leiden was more common among patients with deep vein thrombosis (odds ratio [OR] = 2.1; 95% confidence interval [CI]: 1.2 to 3.7; P = 0.006) or both pulmonary embolism and deep vein thrombosis (OR = 1.8; 95% CI: 1.0 to 3.3; P = 0.07) than among patients with isolated pulmonary embolism. Factor V Leiden was less common in massive pulmonary embolism (5% [7 of 127]) than in submassive pulmonary embolism (13% [21 of 155], P = 0.03). We found no significant difference in the prevalence of factor II 20210A among the three groups. CONCLUSION: Factors V Leiden and II 20210A vary in prevalence among patients with pulmonary embolism and deep vein thrombosis, suggesting that the risk of pulmonary embolization may vary among patients who have different causes of venous thromboses.     

肺癌患者并发静脉血栓与肺栓塞的危险因素分析简

目的 探讨肺癌患者并发静脉血栓或肺栓塞的高危因素.方法 分析我院收治的35例肺癌合并静脉血栓栓塞患者资料,选择同期未发生静脉血栓的病例资料做对照,探求肺癌并发静脉血栓或肺栓塞的危险因素.结果 （1）静脉血栓发生时间构成以确诊后3个月内比重最高,占31.4%;静脉血栓发生部位以左下肢深静脉血栓为主,占40.0%.（2）腺癌、高病理分级、D-二聚体升高是肺癌合并静脉血栓或肺栓塞的独立危险因素,各因素的OR值分别为7.207、3.480、2.863.结论 肺癌诊断3个月内是并发静脉血栓栓塞的高发时段;肿瘤分级高、腺癌、D-二聚体水平升高的肺癌患者易发生静脉血栓栓塞,临床应对上述因素高度警惕,及早进行预见性治疗.