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PubMed2000

[Thromboembolism in plastic surgery: review of the literature and proposal of a prophylaxis algorithm].

There is still less incidence of venous thromboembolic accidents in plastic surgery (% of unknown deep vein thrombosis and pulmonary embolism unknown) than in general surgery (6 to 12% of deep vein thrombosis and 0.3 to 1.1% of pulmonary embolism). However, these accidents present a dangerous and dreaded complication. Based on the recommendations of the Assistance Publique--Hôpitaux de Paris and on a recently published medical study, an algorithm of preventive measures is proposed. The combination of the type of surgical procedure (liposuction, dermolipectomy and abdominoplasty) and the predisposing individual patient risk factors (age, obesity, varicose veins, estrogens, venous thromboembolism history, inherited disorders of coagulation) defines the level of thromboembolic risk which can be mild, moderate or high. Prevention is based on general guidelines (early mobilization, leg elevation, etc.); in addition, at every level of potential risk, the use of low molecular weight heparin (LMWH) and/or wearing anti-thrombosis stockings, as well as surveillance of detection of venous thromboembolism, notably the duplex venous scanning of lower limbs, will be adapted to each patient. This algorithm is a means to elaborate a rational, but unfixed strategy or protocol of prevention to reduce the risk of venous thromboembolic complications, and if they occur, to detect them at an early stage and to treat them in order to avoid evolution towards pulmonary embolism, notably mortal pulmonary embolism.

Algorithms↗
PubMed2005

Can thromboembolism be the result, rather than the inciting cause, of acute vascular events such as stroke, pulmonary embolism, mesenteric ischemia, and venous thrombosis?: a maladaptation of the prehistoric trauma response.

Thromboembolism is considered the inciting cause of many vascular disorders including acute coronary syndrome (ACS), ischemic stroke, pulmonary embolism (PE), deep vein thrombosis (DVT), and mesenteric ischemia. Adrenergia and inflammation are known to accompany these conditions, particularly among arterial thromboembolic disorders, but the teleologic basis of these associations remains poorly understood. We argue that thromboembolism may sometimes be the result, rather than the cause, of acute vascular events, and may be precipitated by underlying adrenergia. Thromboembolic events are most prone to occur during parts of the circadian, seasonal, lifespan, and reproductive cycles with sympathetic dominance, as well as during behavioral, exertional, physiologic, and iatrogenic activation of sympathetic stress. Molecular evidence suggests that adrenergia and inflammation can promote coagulation and lead to co-activation of the pathways. Acute vascular events that occur without angiographic evidence of occlusion suggest that some infarcts may be attributable to adrenergia alone. "Embolic" disorders may represent asynchronous systemic phenomena rather than clot migration. During acute thromboembolism, downstream tissue hypoxia can activate maladaptive self-propelling cycles of sympathetic bias, inflammation, and coagulation. The counterproductive co-activation of these pathways may reflect a maladaptive interlink forged during the primordial evolution of trauma physiology. Their rapid co-mobilization enables rapid control of hemorrhage, microbial defense, and perfusion maintenance during trauma, but the pathways may behave maladaptively in the setting of modern diseases where endothelial injury may be more often precipitated by smoking, diabetes, dyslipidemia, or hypertension. Sympathetic blockade is already employed in ACS, and beta-blockers are used as antihypertensives to prevent stroke. Our hypothesis suggests that the benefits of beta-blockers in stroke may be independent of antihypertensive effects, and that adrenergia may represent a target for managing all thromboembolic disorders, independent of anti-coagulative and thrombolytic therapies. Perhaps reducing adrenergia, rather than maintaining high cerebral perfusion pressure, may represent a counterintuitive strategy for treating stroke and for reducing reperfusion injury. Plausible mechanisms by which autonomic dysfunction may induce venous thrombosis are discussed, especially in those with baroreceptor dysfunction, immobilization, or dehydration. Unexplained hypercoagulability of cancer may also operate through tumor-induced adrenergia and inflammation.

Humans↗
PubMed1994

Venous thromboembolism in neurosurgery and neurology patients: a review.

Thromboembolism is a common problem in neurosurgery and neurology patients. Within this diverse population are subpopulations of patients with varying degrees of thromboembolic risk: low, moderate, and high. Patients at substantial risk for deep vein thrombosis and pulmonary embolism include those with spinal cord injury, brain tumor, subarachnoid hemorrhage, head trauma, stroke, and patients undergoing a neurosurgical operation. There are prophylactic strategies that can be applied to these various risk groups that will dramatically reduce the incidence of thromboembolism. The risk of pulmonary embolism or fatal pulmonary embolism typically exceeds the risk of severe or fatal bleeding from adequate prophylaxis, and these techniques should be applied on a routine basis. To adequately care for patients with deep venous thrombosis and pulmonary embolism, the physician requires a thorough understanding of the methods of diagnosis, the pharmacokinetics of heparin and warfarin, and a knowledge of their role in the treatment strategies that have proven efficacy and safety. In addition, an awareness of the low molecular weight heparins and heparinoids is becoming essential. These new agents have a potentially promising role in both the prophylaxis and treatment of patients with neurological disease. The principles concerning the prophylaxis, diagnosis, and clinical management of venous thromboembolic disease in neurosurgery and neurology patients are dealt with in this review.

Anticoagulants↗
PubMedDate not supplied

[Pulmonary embolism--complication of proximal deep venous thrombosis in colorectal cancer. Diagnosis and management].

We present the case of a 57 years old male, without cardiovascular history, with colorectal cancer and proximal deep venous thrombosis, who develops a massive pulmonary embolism. The surgical treatment consists in embolectomy of right ventricle, pulmonary trunk, left and right pulmonary artery. The specifics of the case is discussed: etiology and prevention of pulmonary embolism (caval filter) and treatment: the contraindications of thrombolytic therapy and the indications and perspectives of surgical treatment.

Colorectal Neoplasms↗
PubMed1998

Prevalence of deep vein thrombosis in suspected and proven pulmonary embolism: a meta-analysis.

The purpose of this study was to determine the prevalence of lower extremity deep venous thrombosis (DVT) in patients with suspected and proven pulmonary embolism (PE). A meta-analysis was performed, based on literature from January 1983 to June 1997. Papers obtained from a computer-aided literature search were divided into studies with pulmonary angiography or ventilation-perfusion (V/Q) scintigraphy as the reference study. Our own observational data of the prevalence of DVT in 149 patients suspected of PE were also reported. The estimated prevalence of DVT in patients with proven and suspected PE was calculated. In the 149 patients studied, the prevalence of DVT was 12% with suspected PE and 32% (95% confidence interval 20-46%) in patients with proven PE. The individual studies showed a considerable heterogeneity, the prevalence of DVT in proven PE ranged from 10 to 93%. The pooled estimate of the prevalence of DVT in patients suspected of PE, over all studies, was 18% (95% confidence interval 15-20%). The DVT prevalence in proven PE was 36% (95% confidence interval 22-52%) in the angiography-based studies, and 45% (95% confidence interval 33-58%) in the V/Q scintigraphy-based studies. In conclusion, the current meta-analysis shows that the prevalence of DVT in suspected PE is approximately 18%, and in proven PE 36-45%.

Adult↗
PubMed1978

A phlebographic study of the incidence and significance of venous thrombosis in the foot.

A total of 188 foot phelbograms in 100 patients with suspected venous thrombosis or pulmonary embolism were studied. Thrombus was demonstrated in 59 (31%) of the foot phlebograms. It is concluded that foot vein thrombosis is common, that it may be a source of pulmonary embolism, and that venous thrombus may start in the foot veins and spread into the calf. Foot phlebography should become part of the routine examination of patients with suspected deep venous thrombosis or pulmonary embolism.

Foot↗
PubMed2004

Thromboembolic complications after splenectomy for hematologic diseases.

Thromboembolic complications following splenectomy for hematologic diseases occur in up to 10% of patients and may range from portal vein thrombosis (PVT) to pulmonary embolism (PE) and deep vein thrombosis (DVT). Up to now there exist no recommendations for the duration and intensity of prophylactic anticoagulation, which usually follows local institutional protocols. We report on three consecutive patients with severe portal vein thrombosis and/or pulmonary embolism--one with fatal outcome--7 to 35 days after splenectomy for autoimmune hemolytic anemia, immunothrombocytopenia, and indolent lymphoma, respectively. Incidence and pathophysiology of thromboembolic events (TE) in this patient group as well as prophylactic anticoagulation will be discussed, including a review of the current literature on this topic.

Adult↗
PubMed1996

Diagnosis of pulmonary embolism.

The methods and strategy of the diagnosis of pulmonary embolism (PE) are reviewed. Pulmonary thromboembolic disease includes every condition in which the obstruction of pulmonary arteries by thrombi is observed. These emboli are usually the result of deep venous thrombosis of the lower extremities. Despite the progress made in the diagnostic methods of PE, in many cases diagnosis is delayed or missed. Thus, deep venous thrombosis and pulmonary embolism remain a frequent cause of morbidity and mortality. In order to avoid invasive methods in diagnosis of PE (i.e. pulmonary angiography), because of its high morbidity and mortality, many noninvasive methods have been developed. The technological and medical advances in diagnosis of deep venous thrombosis and pulmonary embolism by noninvasive methods deserve emphasis. Among the innovations are Doppler examination of venous blood flow, impedance plethysmography, phleborheography, radioisotope tagging of thrombi and real-time B-mode ultrasonography of the veins. In addition, progress has been made in the identification of pulmonary emboli with ventilation-perfusion scanning, computed tomography (CT) and magnetic resonance imaging (MRI). Finally, a plan of strategy for the identification of pulmonary emboli is proposed.

Humans↗
PubMed2006

Heparin-induced thrombocytopenia type II: a rare but significant complication of plasma exchange.

Type II heparin-induced thrombocytopenia (HIT) is a rare but well-recognised and potentially life-threatening complication of unfractionated heparin therapy, and has been reported in association with heparin locks for central venous lines. We report a case of type II HIT complicated by iliofemoral deep venous thrombosis and pulmonary embolism in a 43-year-old woman in the course of plasma exchange for myasthenia gravis. A Gamcath central venous line had been inserted femorally due to poor peripheral venous access, and this was locked with heparin 5000 U/ml between procedures. Twelve days after initial heparin exposure, she presented with new-onset thrombocytopenia, a painfully swollen right leg, and pleuritic pain. Deep venous thrombosis and pulmonary embolism were confirmed radiologically, and serology for heparin/PF4 antibodies was unequivocally positive. The line was removed, and she was successfully managed with intravenous lepirudin, switching to warfarin on platelet recovery. This case demonstrates that Type II HIT can occur in association with heparin line locks in the course of plasmapheresis, despite previous reports of successful use of plasma exchange to treat Type II HIT.

Adult↗
PubMed1994

Acute pulmonary embolism.

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)

Acute Disease↗