Prevention of deep vein thrombosis and pulmonary embolism following surgery.
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The echocardiographic detection of a right thromboembolus, although rare, should be considered as a cardiological emergency that could lead to death for massive pulmonary embolism. The case of a 70 year-old man admitted to our Institution with the suspicion of pulmonary embolism is described. The echocardiogram performed showed a large mobile thrombus in the right atrium prolapsing through the tricuspid valve during diastole. After thrombolytic therapy with r-TPA, the patient faced a progressive hemodynamic deterioration and died of electromechanical dissociation.
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Critically ill patients have multiple risk factors for deep vein thrombosis and pulmonary embolism. The majority of patients with pulmonary embolism have a lower extremity deep vein thrombosis as a source of origin. Pulmonary embolism causes a high mortality rate in the hemodynamically compromised individual. Awareness of risk factors relative to the development of deep vein thrombosis and pulmonary embolism is important for the critical care nurse. Understanding the pathophysiology can help guide prophylaxis and treatment plans. The therapies, from invasive to mechanical, all carry risks and benefits, and are weighed for each patient. The advanced practice nurse, whether in the direct or indirect role, has an opportunity to impact the care of the high risk patient. Options range from teaching the nurse who is new to critical care, to teaching patients and families. Development of multidisciplinary protocols and clinical pathways are ways to impact the standard of care. Improved delivery of care methods can optimize the care rendered in an ever changing field of critical care.
BACKGROUND: Long-term anticoagulation prevents recurrent thrombosis in patients with idiopathic deep venous thrombosis or pulmonary embolism, but with a risk of clinically important so-called major bleeding. Physician- and patient-based decisions on the optimal duration of therapy are sensitive to the bleeding risk. The Outpatient Bleeding Risk Index potentially provides a means of calculating the potential risk of bleeding using easily elicited clinical findings, but, to our knowledge, the authors of the index have provided the only published validation of it. We sought to determine the accuracy of the index in our population of patients. METHODS: We prospectively applied the Outpatient Bleeding Risk Index to consecutive patients in our clinic who had been objectively diagnosed as having pulmonary embolism or deep venous thrombosis and who were about to undergo standard therapy. Standard therapy consisted of a minimum of 5 days of low-molecular-weight heparin therapy overlapped with warfarin sodium therapy, and continuation of warfarin therapy for at least 3 months, with a target international normalized ratio of 2.5. Patients were placed in 3 risk groups (low, moderate, or high), as defined by the index. The survival curves of the groups, using major hemorrhages as the events, were then compared by the log-rank test. RESULTS: Bleeding rates were lower than expected, but the index did discriminate between low- and moderate-risk groups (P =.03, log-rank test). The rate of major hemorrhage per 100 person-years was 0% (95% confidence interval, 0%-2.8%) in the low-risk group and 4.3% (95% confidence interval, 1.1%-11.1%) in the moderate-risk group. The rate in the high-risk group could not be defined because only 2 patients were at high risk. CONCLUSION: The Outpatient Bleeding Risk Index discriminates between low- and moderate-risk patients, and could be used to guide decisions on the optimal duration of anticoagulant therapy.
Venous thromboembolic disease, including deep venous thrombosis (DVT) and pulmonary embolism (PE), is an under-diagnosed and under-appreciated medical problem that results in significant patient morbidity and mortality. Inadequate venous thromboprophylaxis in surgical as well as medically ill patients results in DVT and PE that negatively impact patient outcomes and increase health-care costs. A high index of clinical suspicion combined with an evidence-based use of diagnostic tests helps identify patients with acute thrombosis. Failure to accurately and promptly diagnose and treat DVT and PE can result in excess morbidity and mortality due to postthrombotic syndrome, pulmonary hypertension, and recurrent thrombosis. Conversely, unnecessary anticoagulation provides risk in the absence of any tangible benefit. The immediate commencement of parenteral anticoagulant therapy with intravenous unfractionated heparin or a subcutaneous low molecular weight heparin (LMWH) upon presentation with DVT or PE (often even before objective diagnosis confirmation) is necessary to minimize propagation, embolization, and recurrence rates. We favor weight-based LMWH therapy in most of our patients with DVT because of the ability to treat exclusively or primarily in the outpatient setting. We still admit patients with PE for a minimum duration of 2 days for close observation. Subsequent conversion to oral anticoagulation with warfarin (target INR of 2.0 to 3.0 in most patients) should include an overlap with parenteral therapy of at least 4 to 5 days and until a stable target INR has been achieved. A minimum of 3 to 6 months of anticoagulation is recommended following a first episode of idiopathic DVT and any PE. A shorter course of therapy may be sufficient following a situational (eg, after surgery and postpartum) or calf DVT. Long-term, and at times lifelong, therapy should be considered in patients with thrombosis in the setting of a persistent acquired or inherited hypercoagulable state. Thrombolytic therapy probably should be reserved for young patients with iliofemoral DVT, any patient with a threatened limb due to impending venous limb gangrene, and those with PE who have objective evidence of cardiopulmonary compromise. Unfavorable risk-to-benefit and cost-to-benefit ratios make more extensive use of thrombolytics undesirable. The prevention of the postthrombotic syndrome with fitted, graduated compression garments and age- and gender-appropriate cancer screening are indicated in all patients with DVT in an attempt to minimize morbidity and mortality. Hypercoagulable state testing is indicated when the results of individual tests will significantly impact the choice of anticoagulant, intensity of therapy, therapeutic monitoring, family screening, family planning, prognosis determination, and most of all, duration of therapy.
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Deep venous thrombosis and its complication, pulmonary embolism, are common clinical problems in the elderly and are responsible for significant morbidity and mortality. Diagnosis on clinical grounds alone is notoriously unreliable, and objective tests are necessary to avoid overtreatment or undertreatment. Etiology, clinical evaluation and testing, diagnostic strategies, and prophylaxis are reviewed to present a current perspective on this serious problem.
BACKGROUND: Several small studies have indicated an association between deep venous thrombosis or pulmonary embolism and a subsequent diagnosis of cancer, but the subject is controversial. METHODS: We conducted a nationwide study of a cohort of patients with deep venous thrombosis or pulmonary embolism that was drawn from the Danish National Registry of Patients for the years 1977 through 1992. The occurrence of cancer in the cohort was determined by linkage to the Danish Cancer Registry. The expected number of cancer cases was estimated on the basis of national age-, sex-, and site-specific incidence rates. RESULTS: A total of 15,348 patients with deep venous thrombosis and 11,305 patients with pulmonary embolism were identified. We observed 1737 cases of cancer in the cohort with deep venous thrombosis, as compared with 1372 expected cases (standardized incidence ratio, 1.3; 95 percent confidence interval, 1.21 to 1.33). Among the patients with pulmonary embolism, the standardized incidence ratio was 1.3, with a 95 percent confidence interval of 1.22 to 1.41. The risk was substantially elevated only during the first six months of follow-up and declined rapidly thereafter to a constant level slightly above 1.0 one year after the thrombotic event. Forty percent of the patients given a diagnosis of cancer within one year after hospitalization for thromboembolism had distant metastases at the time of the diagnosis of cancer. There were strong associations with several cancers, most pronounced for those of the pancreas, ovary, liver (primary hepatic cancer), and brain. CONCLUSIONS: An aggressive search for a hidden cancer in a patient with a primary deep venous thrombosis or pulmonary embolism is not warranted.
The pathophysiology of deep-vein thrombosis (DVT) and pulmonary embolism (PE) is briefly discussed, and the efficacy, dosage and administration, laboratory monitoring, and adverse effects of thrombolytic agents, heparin, and warfarin are reviewed. Acute therapy of DVT and PE is usually initiated with intravenous heparin; however, thrombolytic agents such as streptokinase and urokinase may be preferred in patients with massive PE or severe DVT when clot lysis rather than clot stabilization is deemed necessary. For DVT or PE, an intravenous loading dose of streptokinase or urokinase is given, followed by a continuous infusion of the drug. Therapy with streptokinase is continued for 24 hours in patients with PE and for 72 hours in those with DVT; urokinase is continued for 12 hours in patients with PE. Monitoring of blood coagulation tests during thrombolytic therapy is recommended primarily for ensuring that a lytic state is achieved. Intravenous heparin is preferred for acute treatment of DVT or PE; controversy exists regarding whether administration by continuous infusion or intermittent bolus injection is superior. Heparin dosage is usually adjusted to maintain the activated partial-thromboplastin time (APTT) ratio between 1.5 and 2.5; however, the ideal therapeutic range has never been firmly established. After acute treatment with heparin, most patients should continue to receive either warfarin or subcutaneous heparin for several months to prevent recurrent thromboembolism. Bleeding is the major adverse effect of thrombolytic agents and anticoagulants. The risk of bleeding with heparin and warfarin therapy increases with excessive prolongation of the APTT and prothrombin time (PT), respectively. Future clinical trials should further define the role of thrombolytic agents in the treatment of DVT and PE and the efficacy of less-intense warfarin therapy for pulmonary embolism or arterial thromboembolic events.
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In a prospective nonrandomized study, a protocol was examined for prophylaxis of deep venous thrombosis and pulmonary embolism in patients with operative treatment of acetabular and pelvic fractures. There were 197 patients in the study with 203 fractures, including 148 acetabular and 55 pelvic fractures. There were 2 cases of bilateral acetabular fractures and 4 cases with both acetabular and pelvic fractures. The protocol involved preoperative noninvasive screening of the lower extremities, intraoperative and postoperative use of mechanical antithrombotic devices, and chemical prophylaxis with warfarin for 3 weeks following removal of surgical drains. There were 11 cases (6%) of preoperative deep venous thrombosis detected. There were 6 cases of postoperative deep venous thrombosis and 2 cases of pulmonary embolism. The incidence of postoperative venous thrombosis and pulmonary embolism was 3% and 1%, respectively. The protocol was found to be effective for preoperative detection of venous thrombosis and prevention of deep venous thrombosis and pulmonary embolism in trauma patients with minimal bleeding complications and no morbidity from embolic disease.
The frequency and the localisation pattern of venous thrombosis and subsequent pulmonary embolism detected postmortem was studied by reviewing 5039 autopsy records from 1975 through 1980 and from 1987/88 of two university hospitals. The autopsy procedure was identical in both study periods. Thrombosis was documented overall in 34.2% with a slight increase from the first to the second series. Taking in account the cases of pulmonary embolism without detected source, the thrombosis rate was 42.6%. The rate of cases with thrombi in the vena cava superior system almost doubled (1975: 9.2%, 1987/88: 17.0%; p less than 0.05). Regarding the list of thrombus localisations the right internal jugular vein (16.9%) was second only to the left femoral vein (17.8%) in 1987/88. Pulmonary emboli were seen in 1500 of 5039 autopsies (29.8%); in 59.4% the source was found in the lower venous tree, in 12.6% in the upper venous tree. In 28.0% no source could be detected. In these cases we supposed a complete detachment of thrombi from the lower venous tree to be the most likely reason. In 628 of the 1500 cases (42.5%) pulmonary embolism was classified as fatal. Both rates, for total pulmonary embolism and for fatal thrombembolism showed a small, but significant decrease during the study period. In 8.3% (52/628) the source of fatal pulmonary emboli was situated in the upper venous tree including the right heart. This means that 10.2% (52/512) of all cases with isolated thrombosis in the vena cava superior system were associated with fatal pulmonary embolism. Venous thrombosis and pulmonary embolism are still frequent findings at autopsy.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVE: We sought to determine risk factors for deep vein thrombosis and pulmonary embolism during pregnancy or post partum. STUDY DESIGN: We performed a population-based case-control study. All Olmsted County, Minnesota, residents with a first lifetime deep vein thrombosis or pulmonary embolism during pregnancy or post partum from 1966 to 1990 were identified (N = 90). Where possible, a resident without deep vein thrombosis or pulmonary embolism was matched to each patient by date of the first live birth after the patient's child. The medical records of all remaining patients and all control subjects were reviewed for >25 baseline characteristics, which were tested as risk factors for deep vein thrombosis or pulmonary embolism. RESULTS: In multivariate analysis smoking (odds ratio, 2.4) and prior superficial vein thrombosis (odds ratio, 9.4) were independent risk factors for deep vein thrombosis or pulmonary thrombosis during pregnancy or post partum. CONCLUSION: Venous thromboembolism prophylaxis may be warranted for pregnant women with prior superficial vein thrombosis. Smoking cessation should be recommended, especially during pregnancy and the postpartum period.
The frequency of pulmonary embolism in patients with deep vein thrombosis can be assessed by pathological-anatomical and by nuclear medical studies. The frequency of deep vein thrombosis in autopsies ranges from 23.7% to 62%, by inclusion of microscopic thrombi the frequency increases to 72%. In most cases the localisation of the venous thrombosis is bilateral. In cases of venous thrombosis the frequency of pulmonary embolism is 52 to 79.4%, if microscopic thrombi are included, the number is 87.8%. 7.8% to 78.9% of all pulmonary emboli are considered as cause of death or severely contributing to death. The fatal embolisms originate preferentially from iliofemoral thrombosis. About 1/10 of all emboli originate from V. cava sup. and the right heart. In a small number of pulmonary emboli the origin could not be detected. The rate of correct intra vitam diagnosis is low, not more than 11 to 25% of all pathological-anatomical proven emboli had a correct diagnosis during life. In fatal pulmonary embolism the correct clinical diagnosis was made in 1/3. In nuclear medicine studies pulmonary embolisms are searched for from the clinical suspicion or the diagnosis of deep vein thrombosis with the perfusion-/ventilation- or inhalation scintigraphy. Patients with deep vein thromboses showed in 38 to 57.9% pulmonary embolism. In 80% of all pulmonary embolism multiple perfusion defects (2 to 9 perfusion defects) were detected, the lesions were evenly distributed in both lungs. The frequency of pulmonary embolism in calf vein thrombosis was 46%, in leg vein thrombosis 67% and reached 77% if the pelvic veins were involved. It is remarkable that the majority of all pulmonary emboli (46.3% to 100%) showed no clinical symptoms. The knowledge about the high frequency of pulmonary embolism in patients with deep vein thrombosis can improve the diagnosis of pulmonary embolism. For the diagnostic process of pulmonary embolism the presence of acute deep vein thrombosis increases the pre-test probability (prevalence of more than 50%). Every positive test for pulmonary embolism will gain a very high post-test probability according to Bayes' theorem.