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We encountered 16 cases of venous thromboembolism (VTE) in women during pregnancy and/or puerperium over the past 15 years at our perinatal center, representing 0.14% of all patients who delivered babies. The present study was undertaken to analyze the risk factors, clinical course and outcomes in these 16 cases. The ages of the patients varied from 29 to 39 years. Four women had pulmonary embolism (PE), 3 of which after caesarean section (C/S) at 35 to 40 weeks, and one case after ovarian cystectomy at 13 weeks of gestation. Twelve cases had deep venous thrombosis (DVT), 4 of which during pregnancy, and the remaining 8 cases after C/S. Four patients who had DVT during a normal course of pregnancy had severe thrombophilia: antiphospholipid antibody syndrome, a history of thrombosis and antithrombin (AT) deficiency. They were treated with heparin with or without AT and had healthy babies via successful vaginal deliveries. The common risk factors in 3 cases of PE with C/S was prolonged bed rest due to threatened premature delivery with total placenta previa, uterine myoma and Ehlers-Danlos syndrome. Other risk factors were massive bleeding, and positive lupus anticoagulant. However, the case of the ovarian cystectomy had only one risk factor, which was obesity. This patient died but the remaining patients recovered with treatment. Because of the low incidence of thrombosis in the Japanese population, prophylactic anticoagulant therapy has not routinely been given to patients undergoing obstetrical operations. However, proper management including prophylactic anticoagulant therapy might be considered for risk patients, depending on the risk factors.
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PMID:Clinical study of venous thromboembolism during pregnancy and puerperium. 1137 69

Many acquired risk factors may be identified to avoid the scholarly nature of these interminable lists, they may be reclassified with respect to their originality or their mechanism of action and those of current interest, whose data is still often hypothetical but recent, can be underlined. The following order may be proposed: risk factors which cannot be changed: age (which remains the principal factor) and gender (women being at higher risk than men); true acquired risk factors such as cancer, dysimmune conditions (more specifically, the antiphospholipid syndrome) and hormone replacement therapy (oestroprogestative contraception which has been updated by the debate about "third generation pills" and the risk related to progesterone-like substances themselves; hormone replacement therapy of the menopause which still has no clinical trials to assess "our" forms with natural hormones administered transdermally or transmucosally). Smoking has also been accused of being a risk factor for venous thrombosis in the latest clinical trials. Metabolic factors increase the risk of thrombosis: this is established for obesity, still suspected for hyperhomocystonaemia, the abnormalities being the result of complex gene-environment interactions. Other dysmetabolic conditions (diabetes, hypercholesterolaemia, hypertriglyceridaemia), responsible for arterial complications, are not clearly related to increased venous thromboembolic risk although a preventive effect of statins (yet another I) has just been reported. Similarly to these metabolic factors, the origin of which, genetic or environmental, is difficult to establish, interest has recently been shown in quantitative and functional changes in blood clotting factors. This has been established for arterial disease for fibrinogen but, in addition to this factor which slightly increases the risk of venous thrombosis, increases of factor VIII independent of inflammatory conditions, of blood group and Von Willebrand factor, which all influence the level of factor VIII, an increase by 150% of the normal increases the risk of venous thromboembolic disease by 3 or 4 times. As for factor VIII, increases in factor IX, factor XI, and resistance to activated C protein (independently of the Leiden mutation on the gene for factor V), are also associated in increased venous thromboembolic risk. Without knowing into which category to classify them, previous personal and family history of thromboembolic disease, in the absence of the already mentioned hereditary risk factors, must be noted. Finally, amongst the acquired risk factors, the authors also list conditions of blood stasis and vascular lesions with or without hypercoagulability (surgery, prolonged hospital stays, cardiac failure, paralysis, pregnancy...). Of these acquired conditions which increase the risk of thrombotic complications, particular attention has been given over the last few years to forced immobilisation in uncomfortable positions as in certain forms of transport. Although clinical reports have discordant results, it would seem that the risk is increased and the benefits of supportive elastic stockings have been confirmed. If the acquired risk is identified and quantified for a patient, it allows evaluation of global risk and the installation of appropriate therapeutic measures.
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PMID:[Venous thromboembolic pathology. New acquired risk factors or new data on acquired risk factors]. 1179 76

Large increases in mortality related to premature atherosclerosis with coronary artery disease and stroke have been reported in patients with systemic lupus erythematosus (SLE), antiphospholipid syndrome (APLS), or rheumatoid arthritis (RA). Studies found relative risks of 5 for myocardial infarction, 6 to 10 for stroke in SLE patients, and 3.6 for cardiovascular deaths in RA patients. The main risk factors for atherosclerosis included not only the classic factors identified in epidemiological studies such as the Framingham study (advanced age, high cholesterol levels, hypertension, diabetes mellitus, and obesity), but also prolonged glucocorticoid therapy, long duration of SLE, postmenopausal status, and heart failure. SLE per se is an independent risk factor. The current pathogenic hypothesis for atherosclerosis involves an inflammatory response (erythrocyte sedimentation rate, C-reactive protein, and fibrin), autoantibodies, immune complexes (containing antibodies to phospholipids, to oxidized LDLs, and to endothelial cells), cytokine-producing activated T cells, and bacterial or viral infections responsible for an immune response against heat shock proteins (endogenous HSP60 and its equivalent, bacterial HSP65). Early risk factor intervention and effective control of inflammation should be incorporated into the management of connective tissue disease with the goal of protecting patients against atherosclerosis.
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PMID:Atherosclerosis and connective tissue diseases. 1295 20

The death of a formed fetus is one of the most emotionally devastating events for parents and clinicians. With improved care for conditions such as RhD alloimmunization, diabetes, and preeclampsia, the rate of fetal death in the United States decreased substantially in the mid twentieth century. However, the past several decades have seen much greater reductions in neonatal death rates than in fetal death rates. As such, fetal death remains a significant and understudied problem that now accounts for almost 50% of all perinatal deaths. The availability of prostaglandins has greatly facilitated delivery options for patients with fetal death. Risk factors for fetal death include African American race, advanced maternal age, obesity, smoking, prior fetal death, maternal diseases, and fetal growth impairment. There are numerous causes of fetal death, including genetic conditions, infections, placental abnormalities, and fetal-maternal hemorrhage. Many cases of fetal death do not undergo adequate evaluation for possible causes. Perinatal autopsy and placental examination are perhaps the most valuable tests for the evaluation of fetal death. Antenatal surveillance and emotional support are the mainstays of subsequent pregnancy management. Outcomes may be improved in women with diabetes, hypertension, red cell alloimmunization, and antiphospholipid syndrome. However, there is considerable room for further reduction in the fetal death rate.
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PMID:Fetal death. 1719 1

The vasculature plays a crucial role in inflammation, angiogenesis, and atherosclerosis associated with the pathogenesis of inflammatory rheumatic diseases, hence the term 'vascular rheumatology'. The endothelium lining the blood vessels becomes activated during the inflammatory process, resulting in the production of several mediators, the expression of endothelial adhesion molecules, and increased vascular permeability (leakage). All of this enables the extravasation of inflammatory cells into the interstitial matrix. The endothelial adhesion and transendothelial migration of leukocytes is a well-regulated sequence of events that involves many adhesion molecules and chemokines. Primarily selectins, integrins, and members of the immunoglobulin family of adhesion receptors are involved in leukocyte 'tethering', 'rolling', activation, and transmigration. There is a perpetuation of angiogenesis, the formation of new capillaries from pre-existing vessels, as well as that of vasculogenesis, the generation of new blood vessels in arthritis and connective tissue diseases. Several soluble and cell-bound angiogenic mediators produced mainly by monocytes/macrophages and endothelial cells stimulate neovascularization. On the other hand, endogenous angiogenesis inhibitors and exogenously administered angiostatic compounds may downregulate the process of capillary formation. Rheumatoid arthritis as well as systemic lupus erythematosus, scleroderma, the antiphospholipid syndrome, and systemic vasculitides have been associated with accelerated atherosclerosis and high cardiovascular risk leading to increased mortality. Apart from traditional risk factors such as smoking, obesity, hypertension, dyslipidemia, and diabetes, inflammatory risk factors, including C-reactive protein, homocysteine, folate deficiency, lipoprotein (a), anti-phospholipid antibodies, antibodies to oxidized low-density lipoprotein, and heat shock proteins, are all involved in atherosclerosis underlying inflammatory rheumatic diseases. Targeting of adhesion molecules, chemokines, and angiogenesis by administering nonspecific immunosuppressive drugs as well as monoclonal antibodies or small molecular compounds inhibiting the action of a single mediator may control inflammation and prevent tissue destruction. Vasoprotective agents may help to prevent premature atherosclerosis and cardiovascular disease.
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PMID:Vascular involvement in rheumatic diseases: 'vascular rheumatology'. 1894 76

While uncommon, isolated avulsion fractures of the lesser trochanter occur in children and adolescents prior to the fusion of this apophysis as a result of athletic activities. In the elderly, isolated fractures of the lesser trochanter are rare but can occur as a result of trauma. They have been identified in patients with primary or secondary bone malignancies, which were previously considered pathognomonic for metastatic disease. In the absence of trauma, weakening of the bone due to systemic disorders such as osteoporosis or osteomalacia chronica renal failure may also be responsible. Diagnosis may be difficult with physical examination and radiographs alone. This case report details this rare fracture in 2 patients suffering from debilitating chronic disease. Patient 1 was a 30-year-old woman with an 18-year history of type 1 diabetes mellitus, a 6-year history of end-stage renal disease, hypertension, hypothyroidism, peripheral vascular disease, and a 3-year history of systemic lupus erythematosus with antiphospholipid syndrome treated with warfarin. Patient 2 was a 66-year-old woman with a history of type 2 diabetes mellitus, peripheral neuropathy, obesity, chronic obstructive pulmonary disease, gout, hypertension, and chronic neck and low back pain. Both were assessed with magnetic resonance imaging following physical examination, which revealed atraumatic avulsion of the distal iliopsoas tendon from the lesser trochanter. Following retraction of the iliopsoas tendon, the patients were treated with conservative therapy and anti-inflammatory medication. These 2 cases broaden the range of patients for whom spontaneous avulsion of the distal iliopsoas tendon should be considered in the differential diagnosis.
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PMID:Atraumatic avulsion of the distal iliopsoas tendon: an unusual cause of hip pain. 2070

An increasing body of evidence suggests the likelihood of a link between venous and arterial thrombosis. The two vascular complications share several risk factors, such as age, obesity, diabetes mellitus, blood hypertension, hypertriglyceridemia, and metabolic syndrome. Moreover, there are many examples of conditions accounting for both venous and arterial thrombosis, such as the antiphospholipid antibody syndrome, hyperhomocysteinemia, malignancies, infections, and the use of hormonal treatment. Finally, several recent studies have consistently shown that patients with venous thromboembolism are at a higher risk of arterial thrombotic complications than matched control individuals. We, therefore, speculate the two vascular complications are simultaneously triggered by biological stimuli responsible for activating coagulation and inflammatory pathways in both the arterial and the venous system. Future studies are needed to clarify the nature of this association, to assess its extent, and to evaluate its implications for clinical practice.
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PMID:Venous and arterial thrombosis: Two aspects of the same disease? 2086 79

Recent studies have demonstrated a much higher incidence of venous thromboembolism (VTE) among Asian patients compared with previous studies. This study aims to determine dietary and behavioral factors that may have contributed to this increase. A case-control study was conducted. Cases were objectively confirmed VTE between 2006 and 2009 at King Chulalongkorn Memorial Hospital. Patients with underlying cancer, antiphospholipid syndrome and arterial thrombosis were excluded. Controls were age and sex-matched healthy volunteers. Food consumption was assessed using a food frequency questionnaire modified from the Thailand National Health Examination Survey III previously validated in the Thai population. There were 97 cases and 195 controls. The mean age was 54.6 years and 70% were women. VTE patients consumed significantly less vegetable, fish and spicy food compared with normal individuals with an odds ratio (OR) for venous thrombosis of 3.74 [95% confidence interval (CI) 2.24-6.26, P < 0.001], 2.05 (95% CI 1.24-3.41, P = 0.005) and 2.30 (95% CI 1.29-4.11, P = 0.01), respectively. Additionally, thrombosis was associated with overweight (OR 2.1, 95% CI 1.21-3.62, P = 0.002), obesity (OR 3.1, 95% CI 1.46-6.74, P = 0.001) and estrogen uses (OR 3.7, 95% CI 1.05-13.2, P = 0.02), but not with smoking or lack of exercise. A multivariate analysis showed that low vegetable consumption (OR 3.74, 95% CI 1.85-7.55, P < 0.001), female hormones (OR 5.80, 95% CI 1.51-22.22, P = 0.011) and body mass index (BMI, P = 0.048) were independently associated with VTE. Low vegetable intake, hormonal use and high BMI are the risk factors for noncancer-related VTE in Thai population.
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PMID:Low vegetable intake is strongly associated with venous thromboembolism in Thai population. 2088 94

Hypercoagulable states can be inherited or acquired. Inherited hypercoagulable states can be caused by a loss of function of natural anticoagulant pathways or a gain of function in procoagulant pathways. Acquired hypercoagulable risk factors include a prior history of thrombosis, obesity, pregnancy, cancer and its treatment, antiphospholipid antibody syndrome, heparin-induced thrombocytopenia, and myeloproliferative disorders. Inherited hypercoagulable states combine with acquired risk factors to establish the intrinsic risk of venous thromboembolism for each individual. Venous thromboembolism occurs when the risk exceeds a critical threshold. Often a triggering factor, such as surgery, pregnancy, or estrogen therapy, is required to increase the risk above this critical threshold.
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PMID:Hypercoagulable states. 2104 74

A retrospective cohort study of 2,218 patients with deep vein thrombosis or pulmonary embolism during a 25-year period from 1966-1990 in Minnesota showed an annual incidence of venous thromboembolism of 117 per 100,000 (deep vein thrombosis, 48 per 100,000; pulmonary embolism, 69 per 100,000). Higher rates were found in males than females (130 vs 110 per 100,000, respectively) after adjusting for age. Early diagnosis and appropriate treatment of DVT and PE have been shown to significantly reduce mortality and morbidity. Risk factors for venous thromboembolism include alterations in blood flow (surgery, injury or long-distance air travel, pregnancy, obesity), hypercoagulability (factor V Leiden mutation, prothrombin mutation, protein C deficiency, protein S deficiency, antithrombin deficiency, hyperhomocysteinemia, antiphospholipid syndrome, nephrotic syndrome, paroxysmal nocturnal hemoglobinuria) and vessel wall abnormalities. Eighty percent of deep venous thrombosis resolves spontaneously and less than 15% embolize to pulmonary arteries.
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PMID:Saddle pulmonary thromboembolism with zero Wells' score. 2147 78


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