 |
VOOZH | about |
|
VOOZH | about |
Pulmonary embolism (PE) is when a blood clot (thrombus) becomes lodged in an artery in the lung and blocks blood flow to the lung. Pulmonary embolism usually arises from a thrombus that originates in the deep venous system of the lower extremities; however, it rarely also originates in the pelvic, renal, upper extremity veins, or the right heart chambers (see the image below). After traveling to the lung, large thrombi can lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic compromise.
Pulmonary thromboembolism is not a disease in and of itself. Rather, it is a complication of underlying venous thrombosis. Under normal conditions, microthrombi (tiny aggregates of red cells, platelets, and fibrin) are formed and lysed continually within the venous circulatory system.
The classic presentation of PE is the abrupt onset of pleuritic chest pain, shortness of breath, and hypoxia. However, most patients with pulmonary embolism have no obvious symptoms at presentation. Rather, symptoms may vary from sudden catastrophic hemodynamic collapse to gradually progressive dyspnea. The diagnosis of pulmonary embolism should be suspected in patients with respiratory symptoms unexplained by an alternative diagnosis.
Patients with pulmonary embolism may present with atypical symptoms, such as the following:
See Clinical Presentation for more detail.
Evidence-based literature supports the practice of using clinical scoring systems to determine the clinical probability of pulmonary embolism before proceeding with testing. [3] Validated clinical prediction rules should be used to estimate pretest probability of pulmonary embolism. The use of a diagnostic algorithm based on a clinical decision rule, consisting of medical history and physical examination findings, combined with D-dimer testing is recommended in patients with clinically suspected PE to exclude the disease and thereby reduce the need for CT scans. [4]
Physical signs of pulmonary embolism include the following:
Testing
Perform diagnostic testing on symptomatic patients with suspected pulmonary embolism to confirm or exclude the diagnosis or until an alternative diagnosis is found. Routine laboratory findings are nonspecific and are not helpful in pulmonary embolism, although they may suggest another diagnosis.
A hypercoagulation workup should be performed if no obvious cause for embolic disease is apparent, including screening for conditions such as the following:
Potentially useful laboratory tests in patients with suspected pulmonary embolism include the following:
Imaging studies
Imaging studies that aid in the diagnosis of pulmonary embolism include the following:
See Workup for more detail.
PE severity is commonly classified three main categories based on easily obtainable clinical variables. High-risk PE is defined as presenting with hypotension, a systolic arterial pressure less than 90 mm Hg or drop of more than 40 mm Hg for at least 15 minutes and the need for vasopressor support. Intermediate-risk PE is defined by a patient being normotensive with evidence of RV dysfunction or myocardial ischemia. Low risk PE are patients that do not meet the criteria for intermediate-risk. The percentage of each classification are as follows [5] :
Anticoagulation and thrombolysis
Immediate full anticoagulation is mandatory for all patients suspected of having DVT or PE. [6] Diagnostic investigations should not delay empirical anticoagulant (blood thinner) therapy.
Thrombolytic therapy should be used in patients with acute pulmonary embolism who have hypotension (systolic blood pressure< 90 mm Hg) who do not have a high bleeding risk and in selected patients with acute pulmonary embolism not associated with hypotension who have a low bleeding risk and whose initial clinical presentation or clinical course suggests a high risk of developing hypotension. [6]
Long-term anticoagulation is critical to the prevention of recurrence of DVT or pulmonary embolism, because even in patients who are fully anticoagulated, DVT and pulmonary embolism can and often do recur.
Anticoagulation medications include the following:
Thrombolytic agents used in managing pulmonary embolism include the following:
Surgical options
Surgical management options include the following:
See Treatment and Medication for more detail.
Pulmonary embolism (PE) is a common and potentially lethal condition. Most patients who succumb to pulmonary embolism do so within the first few hours of the event. Despite diagnostic advances, delays in pulmonary embolism diagnosis are common and represent an important issue. [7] Pulmonary embolism is third most common cause of cardiovascular death after coronary artery disease and stroke, and the leading cause of death in patients with cancer after the cancer itself. It is also the leading cause of death in pregnant and post-partum women. [8]
In patients who survive a pulmonary embolism, recurrent embolism and death can be prevented with prompt diagnosis and therapy. Unfortunately, the diagnosis is often missed because patients with pulmonary embolism present with nonspecific signs and symptoms. If left untreated, approximately one third of patients who survive an initial pulmonary embolism die from a subsequent embolic episode. (See Prognosis.)
When a pulmonary embolism is identified, it is characterized as acute or chronic. In terms of pathologic diagnosis, an embolus is acute if it is situated centrally within the vascular lumen or if it occludes a vessel (vessel cutoff sign) (see the first image below). Acute pulmonary embolism commonly causes distention of the involved vessel. An embolus is chronic if it is eccentric and contiguous with the vessel wall (see the second image below), it reduces the arterial diameter by more than 50%, evidence of recanalization within the thrombus is present, and an arterial web is present.
A pulmonary embolism is also characterized as central or peripheral, depending on the location or the arterial branch involved. Central vascular zones include the main pulmonary artery, the left and right main pulmonary arteries, the anterior trunk, the right and left interlobar arteries, the left upper lobe trunk, the right middle lobe artery, and the right and left lower lobe arteries. A pulmonary embolus is characterized as high-risk when it involves both pulmonary arteries or when it results in hemodynamic compromise. Peripheral vascular zones include the segmental and subsegmental arteries of the right upper lobe, the right middle lobe, the right lower lobe, the left upper lobe, the lingula, and the left lower lobe. (See Physical Examination.)
The variability of presentation sets the patient and clinician up for potentially missing the diagnosis. The challenge is that the "classic" presentation with abrupt onset of pleuritic chest pain, shortness of breath, and hypoxia is rarely seen. Studies of patients who died unexpectedly of pulmonary embolism revealed that the patients had complained of nagging symptoms, often for weeks, before dying. Forty percent of these patients had been seen by a physician in the weeks prior to their death. [9] (See the images below.)
The most important conceptual advance regarding pulmonary embolism over the last several decades has been the realization that pulmonary embolism is not a disease; rather, pulmonary embolism is a complication of venous thromboembolism, most commonly deep venous thrombosis (DVT; shown in the image below). Virtually every physician who is involved in patient care encounters patients who are at risk for venous thromboembolism, and therefore at risk for pulmonary embolism. (See Etiology of Pulmonary Embolism.)
Clinical signs and symptoms for pulmonary embolism are nonspecific; therefore, patients suspected of having pulmonary embolism—because of unexplained dyspnea, tachypnea, or chest pain or the presence of risk factors for pulmonary embolism—must undergo diagnostic tests until the diagnosis is ascertained or eliminated or an alternative diagnosis is confirmed. Further, routine laboratory findings are nonspecific and are not helpful in pulmonary embolism, although they may suggest another diagnosis. Pulmonary angiography historically was the criterion standard for the diagnosis of pulmonary embolism, but with the improved sensitivity and specificity of CT angiography, it is now rarely performed. (See Workup.)
Immediate full anticoagulation is mandatory for all patients suspected to have DVT or pulmonary embolism. Diagnostic investigations should not delay empirical anticoagulant therapy. (See Treatment.)
Long-term anticoagulation is critical to the prevention of recurrence of DVT or pulmonary embolism. The general consensus is that a significant reduction in recurrence is associated with 3-6 months of anticoagulation. (See Medication.)
Knowledge of bronchovascular anatomy (seen in the image below) is the key to the accurate interpretation of CT scans obtained for the evaluation of pulmonary embolism. A systematic approach in identifying all vessels is important. The bronchovascular anatomy has been described on the basis of the segmental anatomy of lungs. The segmental arteries are seen near the accompanying branches of the bronchial tree and are situated either medially (in the upper lobes) or laterally (in the lower lobes, lingula, and right middle lobe).
Pulmonary thromboembolism is not a disease in and of itself. Rather, it is a complication of underlying venous thrombosis. Under normal conditions, microthrombi (tiny aggregates of red cells, platelets, and fibrin) are formed and lysed continually within the venous circulatory system. This dynamic equilibrium ensures local hemostasis in response to injury without permitting uncontrolled propagation of clot. (See Etiology of Pulmonary Embolism.)
There are both respiratory and hemodynamic consequences associated with pulmonary embolism.
Acute respiratory consequences of PE include the following:
Additional consequences that may occur include regional loss of surfactant and pulmonary infarction (see the image below). Arterial hypoxemia is a frequent, but not universal, finding in patients with acute embolism. The mechanisms of hypoxemia include ventilation-perfusion mismatch, intrapulmonary shunts, reduced cardiac output, and intracardiac shunt via a patent foramen ovale. Pulmonary infarction is an uncommon consequence because of the bronchial arterial collateral circulation.
Pulmonary embolism reduces the cross-sectional area of the pulmonary vascular bed, resulting in an increment in pulmonary vascular resistance, which, in turn, increases the right ventricular afterload. If the afterload is increased severely, right ventricular failure may ensue. In addition, the humoral and reflex mechanisms contribute to the pulmonary arterial constriction. Following the initiation of anticoagulant therapy, the resolution of emboli usually occurs rapidly during the first 2 weeks of therapy; however, it can persist on chest imaging studies for months to years. Chronic pulmonary hypertension may occur with failure of the initial embolus to undergo lyses or in the setting of recurrent thromboemboli.
Three primary influences predispose a patient to blood clot formation; these form the so-called Virchow triad, which consists of the following [10, 11, 12] :
Thrombosis usually originates as a platelet nidus on valves in the veins of the lower extremities. Further growth occurs by accretion of platelets and fibrin and progression to red fibrin thrombus, which may either break off and embolize or result in total occlusion of the vein. The endogenous thrombolytic system leads to partial dissolution; then, the thrombus becomes organized and is incorporated into the venous wall.
Pulmonary emboli usually arise from thrombi originating in the deep venous system of the lower extremities; however, they may rarely originate in the pelvic, renal, or upper extremity veins or the right heart chambers. After traveling to the lung, large thrombi can lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic compromise. Smaller thrombi typically travel more distally, occluding smaller vessels in the lung periphery. These are more likely to produce pleuritic chest pain by initiating an inflammatory response adjacent to the parietal pleura. Most pulmonary emboli are multiple, and the lower lobes are involved more commonly than the upper lobes.
The causes for pulmonary embolism are multifactorial and are not readily apparent in many cases. The causes described in the literature include the following:
A study by Malek et al confirmed the hypothesis that individuals with HIV infection are more likely to have clinically detected thromboembolic disease. [13] The risk of developing a pulmonary embolism or DVT is increased 40% in these individuals.
Venous stasis leads to accumulation of platelets and thrombin in veins. Increased viscosity may occur due to polycythemia and dehydration, immobility, raised venous pressure in cardiac failure, or compression of a vein by a tumor.
The complex and delicate balance between coagulation and anticoagulation is altered by many diseases, by obesity, or by trauma. It can also occur after surgery.
Concomitant hypercoagulability may be present in disease states where prolonged venous stasis or injury to veins occurs.
Hypercoagulable states may be acquired or congenital. Factor V Leiden mutation causing resistance to activated protein C is the most common risk factor. Factor V Leiden mutation is present in up to 5% of the normal population and is the most common cause of familial thromboembolism.
Primary or acquired deficiencies in protein C, protein S, and antithrombin III are other risk factors. Deficiency of these natural blood thinners is responsible for 10% of venous thrombosis in younger people.
Immobilization leads to local venous stasis by accumulation of clotting factors and fibrin, resulting in blood clot formation. The risk of pulmonary embolism increases with prolonged bed rest or immobilization of a limb in a cast.
In the Prospective Investigation of Pulmonary Embolism Diagnosis II (PIOPED II) study, immobilization (usually because of surgery) was the risk factor most commonly found in patients with pulmonary embolism.
A prospective study by Geerts and colleagues indicated that major trauma was associated with a 58% incidence of DVT in the lower extremities and an 18% incidence in proximal veins. [14]
Surgical and accidental traumas predispose patients to venous thromboembolism by activating clotting factors and causing immobility. Pulmonary embolism may account for 15% of all postoperative deaths. Leg amputations and hip, pelvic, and spinal surgery are associated with the highest risk.
Fractures of the femur and tibia are associated with the highest risk of fracture-related pulmonary embolism, followed by pelvic, spinal, and other fractures. Severe burns also carry a high risk of DVT or pulmonary embolism.
The incidence of thromboembolic disease in pregnancy has been reported to range from 1 case in 200 deliveries to 1 case in 1400 deliveries (see Epidemiology). Fatal events are rare, with 1-2 cases occurring per 100,000 pregnancies.
Estrogen-containing birth control pills have increased the occurrence of venous thromboembolism in healthy women. The risk is proportional to the estrogen content and is increased in postmenopausal women on hormonal replacement therapy. The relative risk is 3-fold, but the absolute risk is 20-30 cases per 100,000 persons per year.
Malignancy has been identified in 17% of patients with venous thromboembolism. Pulmonary emboli have been reported to occur in association with solid tumors, leukemias, and lymphomas. This is probably independent of the indwelling catheters often used in such patients. [15] The neoplasms most commonly associated with pulmonary embolism, in descending order of frequency, are pancreatic carcinoma; bronchogenic carcinoma; and carcinomas of the genitourinary tract, colon, stomach, and breast.
Hereditary factors associated with the development of pulmonary embolism include the following:
Acute medical illnesses associated with the development of pulmonary embolism include the following:
Risk factors for pulmonary embolism also include the following:
In the PIOPED II study, 94% of patients with pulmonary embolism had 1 or more of the following risk factors [17] :
In contrast to adults, most children (98%) diagnosed with pulmonary emboli have an identifiable risk factor or a serious underlying disorder (see Epidemiology).
In 1993, David et al reported that 21% of children with DVT and/or pulmonary emboli had an indwelling central venous catheter. [18] Additional series have reported the presence of central lines in as many as 36% of patients. [19] A clot may form as a fibrin sleeve that encases the catheter. When the catheter is removed, the fibrin sleeve is often dislodged, releasing a nidus for embolus formation. In another scenario, a thrombus may adhere to the vessel wall adjacent to the catheter.
David and colleagues also reported that 5-10% of children with venous thromboembolic disease have inherited disorders of coagulation, such as antithrombin III, protein C, or protein S deficiency. [18] In 1997, Nuss et al reported that 70% of children with a diagnosis of pulmonary embolism have antiphospholipid antibodies or coagulation-regulatory protein abnormalities. [20] However, this was a small study in a population with clinically recognized pulmonary emboli; hence, its applicability to the broader pediatric population is uncertain.
A study reported that major thrombosis or pulmonary embolism was present in more than 33% of children treated with long-term hyperalimentation and that pulmonary embolism was the major cause of death in 30% of these children. Fat embolization may exacerbate this clinical picture. [21]
Dehydration, especially hyperosmolar dehydration, is typically observed in younger infants with pulmonary emboli.
The incidence of pulmonary embolism in the United States is estimated to be 1 case per 1000 persons per year. [22] Studies from 2008 suggest that the increasing use of computed tomography (CT) scanning for assessing patients with possible pulmonary embolism has led to an increase in the reported incidence of pulmonary embolism. [23, 24]
From 1979-1998, the age-adjusted death rate for pulmonary embolism in the United States decreased from 191 deaths per million population to 94 deaths per million population. [22] Regional studies covering the years after 1998 found either a slight decrease in the incidence of mortality or no change in the frequency. [23, 24]
Pulmonary embolism is present in 60-80% of patients with DVT, even though more than half these patients are asymptomatic. Pulmonary embolism is the third most common cause of death in hospitalized patients, with at least 650,000 cases occurring annually. Autopsy studies have shown that approximately 60% of patients who have died in the hospital had pulmonary embolism, with the diagnosis having been missed in up to 70% of the cases. Prospective studies have demonstrated DVT in 10-13% of all medical patients placed on bed rest for 1 week, 29-33% of all patients in medical intensive care units, 20-26% of patients with pulmonary diseases who are given bed rest for 3 or more days, 27-33% of patients admitted to a critical care unit after a myocardial infarction, and 48% of patients who are asymptomatic after a coronary artery bypass graft.
Venous thromboembolism is a major health problem. The average annual incidence of venous thromboembolism in the United States is 1 person per 1000 population, [3, 25, 26] with about 250,000 incident cases occurring annually.
A challenge in understanding the real disease has been that autopsy studies have found an equal number of patients diagnosed with pulmonary embolism at autopsy was were initially diagnosed by clinicians. [25, 27] This has led to estimates of between 650,000 to 900,000 fatal and nonfatal venous thromboembolic events occurring in the US annually. The incidence of venous thromboembolism has not changed significantly over the last 25 years. [25] Capturing the true incidence going forward will be challenging because of the decreasing rate of autopsy. In a longitudinal, 25-year prospective study from 1966-1990, autopsy rates dropped from 55% to 30% over the study period. [25] Current trends would suggest a continued decline in autopsy rate.
The incidence of PE may differ substantially from country to country; observed variation is likely due to differences in the accuracy of diagnosis rather than in the actual incidence.
Canadian data derived from 15 tertiary care centers showed a frequency of 0.86 events per 10,000 pediatric hospital admissions for patients aged 1 month to 1 year. [28] Frequency of pulmonary embolism in developed countries has been increasing when compared with historical data. This increase in frequency is linked with the increased use of central venous lines in the pediatric population. [29] The overall frequency in children is still considerably less than that in adults.
Data are conflicting as to whether male sex is a risk factor for pulmonary embolism; however, an analysis of national mortality data found that death rates from pulmonary embolism were 20-30% higher among men than among women. [22] The incidence of venous thromboembolic events in the older population is greater among men than women. In patients younger than 55 years, the incidence of pulmonary is higher in females. The overall age- and sex-adjusted annual incidence of venous thromboembolism is reported to be 117 cases per 100,000 people (DVT, 48 cases per 100,000; pulmonary embolism, 69 cases per 100,000). [25]
A prospective cohort study of female nurses found an association between idiopathic pulmonary embolism and hours spent sitting each week. Women who reported in both 1988 and 1990 that they sat more than 40 hours per week had more than twice the risk of pulmonary embolism compared with women who reported both years that they sat less than 10hours per week. [30]
The incidence of pulmonary embolism appears to be significantly higher in blacks than in whites. [31] Mortality rates from pulmonary embolism for blacks have been 50% higher than those for whites, and those for whites have been 50% higher than those for people of other races (eg, Asians, Native Americans). [22] Asian/Pacific Islanders/American Indian patients have a markedly lower risk of thromboembolism. [22, 32]
Pulmonary embolism is increasingly prevalent among elderly patients, yet the diagnosis is missed more often in these patients than in younger ones because respiratory symptoms often are dismissed as being chronic. Even when the diagnosis is made, appropriate therapy frequently is inappropriately withheld because of bleeding concerns. An appropriate diagnostic workup and therapeutic anticoagulation with a careful risk-to-benefit assessment is recommended in this patient population.
DVT and pulmonary embolism are rare in pediatric practice. In 1993, David et al identified 308 children reported in the medical literature from 1975-1993 with DVT of an extremity and/or pulmonary embolism. [18] In 1986, Bernstein reported 78 episodes of pulmonary embolism per 100,000 hospitalized adolescents. [33] Unselected autopsy studies in children estimate the incidence of pulmonary embolism from 0.05-3.7%.
However, among pediatric patients in whom DVT or pulmonary emboli do occur, these conditions are associated with significant morbidity and mortality. Various authors suggest that pulmonary embolism contributes to the death of affected children in approximately 30% of cases. [34] (Others, however, have reported pulmonary embolism as a cause of death in fewer than 5% of affected children. [35] )
A population-based study covering the years 1966-1995 collated the cases of DVT or pulmonary embolism in women during pregnancy or postpartum. The relative risk was 4.29, and the overall incidence of venous thromboembolism (absolute risk) was 199.7 incidents per 100,000 woman-years. Among postpartum women, the annual incidence was 5 times higher than in pregnant women (511.2 vs 95.8 incidents per 100,000 women, respectively).
The incidence of DVT was 3 times higher than that of pulmonary embolism (151.8 vs 47.9 incidents, respectively, per 100,000 women). Pulmonary embolism was relatively less common during pregnancy than in the postpartum period (10.6 vs 159.7 incidents, respectively, per 100,000 women, respectively). [26] A national review of severe obstetric complications from 1998-2005 found a significant increase in the rate of pulmonary embolism associated with the increasing rate of cesarean delivery. [36]
Pulmonary embolism may account for 15% of all postoperative deaths. Leg amputations and hip, pelvic, and spinal surgery are associated with the highest risk.
The prognosis of patients with PE depends on two factors: the underlying disease state and appropriate diagnosis and treatment. According to the CDC, sudden death will occur in 25% of individuals with a PE. [8] Mortality for acute pulmonary embolism can be broken down into three categories: high-risk pulmonary embolism and low- or moderate-risk pulmonary embolism.
Anticoagulant treatment decreases mortality to less than 5%. At 5 days of anticoagulant therapy, 36% of lung scan defects are resolved; at 2 weeks, 52% are resolved; and at 3 months, 73% are resolved. Most patients treated with anticoagulants do not develop long-term sequelae upon follow-up evaluation. The mortality in patients with undiagnosed pulmonary embolism is 30%.
In the PIOPED study, the 1-year mortality rate was 24%. [37] The deaths occurred due to cardiac disease, recurrent pulmonary embolism, infection, and cancer.
The risk of recurrent pulmonary embolism is due to the recurrence of proximal venous thrombosis; approximately 17% of patients with recurrent pulmonary embolism were found to have proximal DVT. In a small proportion of patients, pulmonary embolism does not resolve; hence, chronic thromboembolic pulmonary arterial hypertension results.
Elevated plasma levels of natriuretic peptides (brain natriuretic peptide and N -terminal pro-brain natriuretic peptide) have been associated with higher mortality in patients with pulmonary embolism. [38] In one study, levels of N -terminal pro-brain natriuretic peptide greater than 500 ng/L were independently associated with central pulmonary embolism and were a possible predictor of death from pulmonary embolism. [39]
In a study of 270 adult patients with symptomatic pulmonary embolism that was objectively confirmed, researchers found that elevated plasma lactate levels (≥2 mmol/L) were associated with an increased risk of mortality and other adverse outcomes, independent of shock, hypotension, right-sided ventricular dysfunction, or injury markers. [40]
The 30-day mortality rates for high-, intermediate- and low-risk PE are approximately 65%, 5% to 25% and 1% respectively. [4, 5]
The importance of adherence to the treatment regimen should be repeatedly stressed. The patient should be instructed regarding what to do in the event of any bleeding complications. Because most patients are administered warfarin or low molecular weight heparin upon discharge from the hospital, they must be advised regarding potential interactions between these agents and other medications.
For patient education resources, see the patient education articles Pulmonary Embolism and Blood Clot in the Legs.
Amesquita M, Cocchi MN, Donnino MW. Pulmonary Embolism Presenting as Flank Pain: A Case Series. J Emerg Med. 2009 Mar 26. [QxMD MEDLINE Link].
Carrascosa MF, Batán AM, Novo MF. Delirium and pulmonary embolism in the elderly. Mayo Clin Proc. 2009. 84(1):91-2. [QxMD MEDLINE Link]. [Full Text].
Tapson VF. Acute pulmonary embolism. N Engl J Med. 2008 Mar 6. 358(10):1037-52. [QxMD MEDLINE Link].
[Guideline] Konstantinides SV, Meyer G, Becattini C, et al, The Task Force for the diagnosis and management of acute pulmonary embolism of the European Society of Cardiology (ESC). 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS): The Task Force for the diagnosis and management of acute pulmonary embolism of the European Society of Cardiology (ESC). Eur Respir J. 2019 Sep. 54 (3):[QxMD MEDLINE Link]. [Full Text].
Russell C, Keshavamurthy S, Saha S. Classification and Stratification of Pulmonary Embolisms. Int J Angiol. 2022 Sep. 31 (3):162-165. [QxMD MEDLINE Link]. [Full Text].
[Guideline] Guyatt GH, Akl EA, Crowther M, Gutterman DD, Schuünemann HJ, American College of Chest Physicians Antithrombotic Therapy and Prevention of Thrombosis Panel. Executive summary: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012 Feb. 141 (2 Suppl):7S-47S. [QxMD MEDLINE Link].
Ozsu S, Oztuna F, Bulbul Y, et al. The role of risk factors in delayed diagnosis of pulmonary embolism. Am J Emerg Med. 2011 Jan. 29(1):26-32. [QxMD MEDLINE Link].
Centers for Disease Control and Prevention. Venous Thromboembolism: Impact of Blood Clots on the United States. Available at https://www.cdc.gov/blood-clots/toolkit/impact-of-blood-clots.html. MAY 15, 2024; Accessed: June 30, 2024.
Kline JA, Runyon MS. Pulmonary embolism and deep venous thrombosis. In: Marx JA, Hockenberger RS, Walls RM, eds. Rosen's Emergency Medicine Concepts and Clinical Practice. 6th ed. 1368-1382. Vol 2.:
Boyden EA. Segmental Anatomy of the Lungs: Study of the Patterns of the Segmental Bronchi and Related Pulmonary Vessels. New York, NY: McGraw-Hill; 1955:. 23-32.
Mitchell RN, Kumar V. Hemodynamic disorders, thrombosis, and shock. In: Kumar V, Cotran RS, Robbins SL, eds. Basic Pathology. 6th ed. Philadelphia, Pa: WB Saunders; 1997:. 60-80.
Wharton LR, Pierson JW. JAMA. Minor forms of pulmonary embolism after abdominal operations.
Malek J, Rogers R, Kufera J, Hirshon JM. Venous thromboembolic disease in the HIV-infected patient. Am J Emerg Med. 2011 Mar. 29(3):278-82. [QxMD MEDLINE Link].
Geerts WH, Code KI, Jay RM, Chen E, Szalai JP. A prospective study of venous thromboembolism after major trauma. N Engl J Med. 1994 Dec 15. 331(24):1601-6. [QxMD MEDLINE Link].
van den Heuvel-Eibrink MM, Lankhorst B, Egeler RM, Corel LJ, Kollen WJ. Sudden death due to pulmonary embolism as presenting symptom of renal tumors. Pediatr Blood Cancer. 2008 May. 50(5):1062-4. [QxMD MEDLINE Link].
Arzt M, Luigart R, Schum C, Lüthje L, Stein A, Koper I, et al. Sleep-disordered breathing in deep vein thrombosis and acute pulmonary embolism. Eur Respir J. 2012 Oct. 40(4):919-24. [QxMD MEDLINE Link].
Stein PD, Beemath A, Matta F, Weg JG, Yusen RD, Hales CA, et al. Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II. Am J Med. 2007 Oct. 120(10):871-9. [QxMD MEDLINE Link]. [Full Text].
David M, Andrew M. Venous thromboembolic complications in children. J Pediatr. 1993 Sep. 123(3):337-46. [QxMD MEDLINE Link].
Biss TT, Brandão LR, Kahr WH, Chan AK, Williams S. Clinical features and outcome of pulmonary embolism in children. Br J Haematol. 2008 Sep. 142(5):808-18. [QxMD MEDLINE Link].
Nuss R, Hays T, Chudgar U, Manco-Johnson M. Antiphospholipid antibodies and coagulation regulatory protein abnormalities in children with pulmonary emboli. J Pediatr Hematol Oncol. 1997 May-Jun. 19(3):202-7. [QxMD MEDLINE Link].
Dollery CM. Pulmonary embolism in parenteral nutrition. Arch Dis Child. 1996 Feb. 74(2):95-8. [QxMD MEDLINE Link]. [Full Text].
Horlander KT, Mannino DM, Leeper KV. Pulmonary embolism mortality in the United States, 1979-1998: an analysis using multiple-cause mortality data. Arch Intern Med. 2003 Jul 28. 163(14):1711-7. [QxMD MEDLINE Link].
Burge AJ, Freeman KD, Klapper PJ, Haramati LB. Increased diagnosis of pulmonary embolism without a corresponding decline in mortality during the CT era. Clin Radiol. 2008 Apr. 63(4):381-6. [QxMD MEDLINE Link].
DeMonaco NA, Dang Q, Kapoor WN, Ragni MV. Pulmonary embolism incidence is increasing with use of spiral computed tomography. Am J Med. 2008 Jul. 121(7):611-7. [QxMD MEDLINE Link]. [Full Text].
Silverstein MD, Heit JA, Mohr DN, Petterson TM, O'Fallon WM, Melton LJ 3rd. Trends in the incidence of deep vein thrombosis and pulmonary embolism: a 25-year population-based study. Arch Intern Med. 1998 Mar 23. 158(6):585-93. [QxMD MEDLINE Link].
Heit JA. The epidemiology of venous thromboembolism in the community. Arterioscler Thromb Vasc Biol. 2008 Mar. 28(3):370-2. [QxMD MEDLINE Link]. [Full Text].
Sandler DA, Martin JF. Autopsy proven pulmonary embolism in hospital patients: are we detecting enough deep vein thrombosis?. J R Soc Med. 1989 Apr. 82(4):203-5. [QxMD MEDLINE Link]. [Full Text].
Kotsakis A, Cook D, Griffith L, Anton N, Massicotte P, MacFarland K, et al. Clinically important venous thromboembolism in pediatric critical care: a Canadian survey. J Crit Care. 2005 Dec. 20(4):373-80. [QxMD MEDLINE Link].
Van Ommen CH, Peters M. Acute pulmonary embolism in childhood. Thromb Res. 2006. 118(1):13-25. [QxMD MEDLINE Link].
Kabrhel C, Varraso R, Goldhaber SZ, Rimm E, Camargo CA Jr. Physical inactivity and idiopathic pulmonary embolism in women: prospective study. BMJ. 2011 Jul 4. 343:d3867. [QxMD MEDLINE Link].
Schneider D, Lilienfeld DE, Im W. The epidemiology of pulmonary embolism: racial contrasts in incidence and in-hospital case fatality. J Natl Med Assoc. 2006 Dec. 98(12):1967-72. [QxMD MEDLINE Link]. [Full Text].
Meyer G, Planquette B, Sanchez O. Long-term outcome of pulmonary embolism. Curr Opin Hematol. 2008 Sep. 15(5):499-503. [QxMD MEDLINE Link].
Bernstein D, Coupey S, Schonberg SK. Pulmonary embolism in adolescents. Am J Dis Child. 1986 Jul. 140(7):667-71. [QxMD MEDLINE Link].
Evans DA, Wilmott RW. Pulmonary embolism in children. Pediatr Clin North Am. 1994 Jun. 41(3):569-84. [QxMD MEDLINE Link].
Rajpurkar M, Warrier I, Chitlur M, Sabo C, Frey MJ, Hollon W, et al. Pulmonary embolism-experience at a single children's hospital. Thromb Res. 2007. 119(6):699-703. [QxMD MEDLINE Link].
Kuklina EV, Meikle SF, Jamieson DJ, Whiteman MK, Barfield WD, Hillis SD, et al. Severe obstetric morbidity in the United States: 1998-2005. Obstet Gynecol. 2009 Feb. 113(2 Pt 1):293-9. [QxMD MEDLINE Link]. [Full Text].
Worsley DF, Alavi A. Comprehensive analysis of the results of the PIOPED Study. Prospective Investigation of Pulmonary Embolism Diagnosis Study. J Nucl Med. 1995 Dec. 36(12):2380-7. [QxMD MEDLINE Link].
Cavallazzi R, Nair A, Vasu T, Marik PE. Natriuretic peptides in acute pulmonary embolism: a systematic review. Intensive Care Med. 2008 Dec. 34(12):2147-56. [QxMD MEDLINE Link].
Alonso-Martínez JL, Urbieta-Echezarreta M, Anniccherico-Sánchez FJ, Abínzano-Guillén ML, Garcia-Sanchotena JL. N-terminal pro-B-type natriuretic peptide predicts the burden of pulmonary embolism. Am J Med Sci. 2009 Feb. 337(2):88-92. [QxMD MEDLINE Link].
Vanni S, Viviani G, Baioni M, Pepe G, Nazerian P, Socci F, et al. Prognostic value of plasma lactate levels among patients with acute pulmonary embolism: the thrombo-embolism lactate outcome study. Ann Emerg Med. 2013 Mar. 61(3):330-8. [QxMD MEDLINE Link].
Vedovati MC, Becattini C, Agnelli G, Kamphuisen PW, Masotti L, Pruszczyk P, et al. MULTIDETECTOR COMPUTED TOMOGRAPHY FOR ACUTE PULMONARY EMBOLISM: EMBOLIC BURDEN AND CLINICAL OUTCOME. Chest. 2012 May 24. [QxMD MEDLINE Link].
Restrepo CS, Artunduaga M, Carrillo JA, Rivera AL, Ojeda P, Martinez-Jimenez S, et al. Silicone pulmonary embolism: report of 10 cases and review of the literature. J Comput Assist Tomogr. 2009 Mar-Apr. 33(2):233-7. [QxMD MEDLINE Link].
Vichinsky EP, Neumayr LD, Earles AN, Williams R, Lennette ET, Dean D, et al. Causes and outcomes of the acute chest syndrome in sickle cell disease. National Acute Chest Syndrome Study Group. N Engl J Med. 2000 Jun 22. 342(25):1855-65. [QxMD MEDLINE Link].
Douma RA, Mos IC, Erkens PM, Nizet TA, Durian MF, Hovens MM, et al. Performance of 4 clinical decision rules in the diagnostic management of acute pulmonary embolism: a prospective cohort study. Ann Intern Med. 2011 Jun 7. 154(11):709-18. [QxMD MEDLINE Link].
Stein PD, Hull RD, Patel KC, Olson RE, Ghali WA, Brant R, et al. D-dimer for the exclusion of acute venous thrombosis and pulmonary embolism: a systematic review. Ann Intern Med. 2004 Apr 20. 140(8):589-602. [QxMD MEDLINE Link].
Kearon C, Ginsberg JS, Douketis J, Turpie AG, Bates SM, Lee AY, et al. An evaluation of D-dimer in the diagnosis of pulmonary embolism: a randomized trial. Ann Intern Med. 2006 Jun 6. 144(11):812-21. [QxMD MEDLINE Link].
Geersing GJ, Erkens PM, Lucassen WA, Büller HR, Cate HT, Hoes AW, et al. Safe exclusion of pulmonary embolism using the Wells rule and qualitative D-dimer testing in primary care: prospective cohort study. BMJ. 2012 Oct 4. 345:e6564. [QxMD MEDLINE Link]. [Full Text].
Konstantinides S. Clinical practice. Acute pulmonary embolism. N Engl J Med. 2008 Dec 25. 359(26):2804-13. [QxMD MEDLINE Link].
Kline JA, Hogg MM, Courtney DM, Miller CD, Jones AE, Smithline HA, et al. D-dimer and exhaled CO2/O2 to detect segmental pulmonary embolism in moderate-risk patients. Am J Respir Crit Care Med. 2010 Sep 1. 182(5):669-75. [QxMD MEDLINE Link]. [Full Text].
Turedi S, Gunduz A, Mentese A, Topbas M, Karahan SC, Yeniocak S, et al. The value of ischemia-modified albumin compared with d-dimer in the diagnosis of pulmonary embolism. Respir Res. 2008 May 30. 9:49. [QxMD MEDLINE Link]. [Full Text].
Tick LW, Nijkeuter M, Kramer MH, Hovens MM, Büller HR, Leebeek FW, et al. High D-dimer levels increase the likelihood of pulmonary embolism. J Intern Med. 2008 Aug. 264(2):195-200. [QxMD MEDLINE Link].
Meyer T, Binder L, Hruska N, Luthe H, Buchwald AB. Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction. J Am Coll Cardiol. 2000 Nov 1. 36(5):1632-6. [QxMD MEDLINE Link].
Jiménez D, Uresandi F, Otero R, Lobo JL, Monreal M, Martí D, et al. Troponin-based risk stratification of patients with acute nonmassive pulmonary embolism: systematic review and metaanalysis. Chest. 2009 Oct. 136(4):974-82. [QxMD MEDLINE Link].
Becattini C, Vedovati MC, Agnelli G. Diagnosis and prognosis of acute pulmonary embolism: focus on serum troponins. Expert Rev Mol Diagn. 2008 May. 8(3):339-49. [QxMD MEDLINE Link].
Kline JA, Zeitouni R, Marchick MR, Hernandez-Nino J, Rose GA. Comparison of 8 biomarkers for prediction of right ventricular hypokinesis 6 months after submassive pulmonary embolism. Am Heart J. 2008 Aug. 156(2):308-14. [QxMD MEDLINE Link].
Aksay E, Yanturali S, Kiyan S. Can elevated troponin I levels predict complicated clinical course and inhospital mortality in patients with acute pulmonary embolism?. Am J Emerg Med. 2007 Feb. 25(2):138-43. [QxMD MEDLINE Link].
Dellas C, Lankeit M, Reiner C, Schäfer K, Hasenfuß G, Konstantinides S. BMI-independent inverse relationship of plasma leptin levels with outcome in patients with acute pulmonary embolism. Int J Obes (Lond). 2012 Mar 20. [QxMD MEDLINE Link].
Söhne M, Ten Wolde M, Boomsma F, Reitsma JB, Douketis JD, Büller HR. Brain natriuretic peptide in hemodynamically stable acute pulmonary embolism. J Thromb Haemost. 2006 Mar. 4(3):552-6. [QxMD MEDLINE Link].
Kucher N, Printzen G, Goldhaber SZ. Prognostic role of brain natriuretic peptide in acute pulmonary embolism. Circulation. 2003 May 27. 107(20):2545-7. [QxMD MEDLINE Link].
Klok FA, Mos IC, Huisman MV. Brain-type natriuretic peptide levels in the prediction of adverse outcome in patients with pulmonary embolism: a systematic review and meta-analysis. Am J Respir Crit Care Med. 2008 Aug 15. 178(4):425-30. [QxMD MEDLINE Link].
Scherz N, Labarère J, Méan M, Ibrahim SA, Fine MJ, Aujesky D. Prognostic importance of hyponatremia in patients with acute pulmonary embolism. Am J Respir Crit Care Med. 2010 Nov 1. 182(9):1178-83. [QxMD MEDLINE Link]. [Full Text].
Ready T. Pulmonary Emboli Overdiagnosed by CT Angiography. Medscape [serial online]. Available at https://www.medscape.com/viewarticle/807439. July 05, 2013; Accessed: June 25, 2024.
Wiener RS, Schwartz LM, Woloshin S. When a test is too good: how CT pulmonary angiograms find pulmonary emboli that do not need to be found. BMJ. 2013 Jul 2. 347:f3368. [QxMD MEDLINE Link].
[Guideline] Remy-Jardin M, Pistolesi M, Goodman LR, Gefter WB, Gottschalk A, Mayo JR, et al. Management of suspected acute pulmonary embolism in the era of CT angiography: a statement from the Fleischner Society. Radiology. 2007 Nov. 245(2):315-29. [QxMD MEDLINE Link].
Patel S, Kazerooni EA. Helical CT for the evaluation of acute pulmonary embolism. AJR Am J Roentgenol. 2005 Jul. 185(1):135-49. [QxMD MEDLINE Link].
Stein PD, Woodard PK, Weg JG, Wakefield TW, Tapson VF, Sostman HD, et al. Diagnostic pathways in acute pulmonary embolism: recommendations of the PIOPED II Investigators. Radiology. 2007 Jan. 242(1):15-21. [QxMD MEDLINE Link].
[Guideline] Expert Panel on Cardiac Imaging, Kirsch J, Wu CC, Bolen MA, Henry TS, Rajiah PS, et al. ACR Appropriateness Criteria® Suspected Pulmonary Embolism: 2022 Update. J Am Coll Radiol. 2022 Nov. 19 (11S):S488-S501. [QxMD MEDLINE Link]. [Full Text].
Ward MJ, Sodickson A, Diercks DB, Raja AS. Cost-effectiveness of lower extremity compression ultrasound in emergency department patients with a high risk of hemodynamically stable pulmonary embolism. Acad Emerg Med. 2011 Jan. 18(1):22-31. [QxMD MEDLINE Link].
Drescher FS, Chandrika S, Weir ID, et al. Effectiveness and acceptability of a computerized decision support system using modified Wells criteria for evaluation of suspected pulmonary embolism. Ann Emerg Med. 2011 Jun. 57(6):613-21. [QxMD MEDLINE Link].
Remy-Jardin M, Remy J, Deschildre F, Artaud D, Beregi JP, Hossein-Foucher C, et al. Diagnosis of pulmonary embolism with spiral CT: comparison with pulmonary angiography and scintigraphy. Radiology. 1996 Sep. 200(3):699-706. [QxMD MEDLINE Link].
Becattini C, Agnelli G, Vedovati MC, et al. Multidetector computed tomography for acute pulmonary embolism: diagnosis and risk stratification in a single test. Eur Heart J. 2011 Jul. 32(13):1657-63. [QxMD MEDLINE Link].
Henzler T, Roeger S, Meyer M, Schoepf UJ, Nance JW Jr, Haghi D, et al. Pulmonary embolism: CT signs and cardiac biomarkers for predicting right ventricular dysfunction. Eur Respir J. 2012 Apr. 39(4):919-26. [QxMD MEDLINE Link].
Gottschalk A, Stein PD, Sostman HD, Matta F, Beemath A. Very low probability interpretation of V/Q lung scans in combination with low probability objective clinical assessment reliably excludes pulmonary embolism: data from PIOPED II. J Nucl Med. 2007 Sep. 48(9):1411-5. [QxMD MEDLINE Link].
Gupta A, Frazer CK, Ferguson JM, Kumar AB, Davis SJ, Fallon MJ, et al. Acute pulmonary embolism: diagnosis with MR angiography. Radiology. 1999 Feb. 210(2):353-9. [QxMD MEDLINE Link].
Meaney JF, Weg JG, Chenevert TL, Stafford-Johnson D, Hamilton BH, Prince MR. Diagnosis of pulmonary embolism with magnetic resonance angiography. N Engl J Med. 1997 May 15. 336(20):1422-7. [QxMD MEDLINE Link].
Vanni S, Polidori G, Vergara R, Pepe G, Nazerian P, Moroni F, et al. Prognostic value of ECG among patients with acute pulmonary embolism and normal blood pressure. Am J Med. 2009 Mar. 122(3):257-64. [QxMD MEDLINE Link].
Dresden S, Mitchell P, Rahimi L, Leo M, Rubin-Smith J, Bibi S, et al. Right Ventricular Dilatation on Bedside Echocardiography Performed by Emergency Physicians Aids in the Diagnosis of Pulmonary Embolism. Ann Emerg Med. 2013 Sep 23. [QxMD MEDLINE Link].
[Guideline] Stevens SM, Woller SC, Kreuziger LB, Bounameaux H, Doerschug K, Geersing GJ, et al. Antithrombotic Therapy for VTE Disease: Second Update of the CHEST Guideline and Expert Panel Report. Chest. 2021 Dec. 160 (6):e545-e608. [QxMD MEDLINE Link]. [Full Text].
Stein PD, Matta F. Thrombolytic therapy in unstable patients with acute pulmonary embolism: saves lives but underused. Am J Med. 2012 May. 125(5):465-70. [QxMD MEDLINE Link].
Stein PD, Matta F, Keyes DC, Willyerd GL. Impact of Vena Cava Filters on In-hospital Case Fatality Rate from Pulmonary Embolism. Am J Med. 2012 May. 125(5):478-84. [QxMD MEDLINE Link].
Chatterjee S, Chakraborty A, Weinberg I, Kadakia M, Wilensky RL, Sardar P, et al. Thrombolysis for pulmonary embolism and risk of all-cause mortality, major bleeding, and intracranial hemorrhage: a meta-analysis. JAMA. 2014 Jun 18. 311(23):2414-21. [QxMD MEDLINE Link].
Meyer G, Vicaut E, Danays T, Agnelli G, Becattini C, Beyer-Westendorf J, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism. N Engl J Med. 2014 Apr 10. 370(15):1402-11. [QxMD MEDLINE Link].
Elliott CG. Fibrinolysis of pulmonary emboli--steer closer to Scylla. N Engl J Med. 2014 Apr 10. 370(15):1457-8. [QxMD MEDLINE Link].
Barclay L. Fibrinolysis for Pulmonary Embolism Effective but Risky. Medscape [serial online]. Available at https://www.medscape.com/viewarticle/823427. April 10, 2014; Accessed: June 25, 2024.
Büller HR, Prins MH, Lensin AW, Decousus H, Jacobson BF, Minar E, et al. Oral rivaroxaban for the treatment of symptomatic pulmonary embolism. N Engl J Med. 2012 Apr 5. 366(14):1287-97. [QxMD MEDLINE Link].
Bauersachs R, Berkowitz SD, Brenner B, Buller HR, Decousus H, Gallus AS, et al. Oral rivaroxaban for symptomatic venous thromboembolism. N Engl J Med. 2010 Dec 23. 363(26):2499-510. [QxMD MEDLINE Link]. [Full Text].
Cohen AT, Dobromirski M. The use of rivaroxaban for short- and long-term treatment of venous thromboembolism. Thromb Haemost. 2012 Jun. 107(6):1035-43. [QxMD MEDLINE Link].
Romualdi E, Donadini MP, Ageno W. Oral rivaroxaban after symptomatic venous thromboembolism: the continued treatment study (EINSTEIN-extension study). Expert Rev Cardiovasc Ther. 2011 Jul. 9(7):841-4. [QxMD MEDLINE Link].
Hughes S. Rivaroxaban Stands up to standard anticoagulation for VTE treatment. Medscape Medical News. December 13, 2012. [Full Text].
Buller HR, on behalf of the EINSTEIN Investigators. Oral rivaroxaban for the treatment of symptomatic venous thromboembolism: a pooled analysis of the EINSTEIN DVT and EINSTEIN PE studies [abstract 20]. Presented at: 54th Annual Meeting and Exposition of the American Society of Hematology; December 8, 2012; Atlanta, Ga. [Full Text].
Cohen AT, Spiro TE, Büller HR, Haskell L, Hu D, Hull R, et al. Rivaroxaban for thromboprophylaxis in acutely ill medical patients. N Engl J Med. 2013 Feb 7. 368 (6):513-23. [QxMD MEDLINE Link]. [Full Text].
Spyropoulos AC, Ageno W, Albers GW, Elliott CG, Halperin JL, Hiatt WR, et al. Rivaroxaban for Thromboprophylaxis after Hospitalization for Medical Illness. N Engl J Med. 2018 Sep 20. 379 (12):1118-1127. [QxMD MEDLINE Link]. [Full Text].
Agnelli G, Buller HR, Cohen A, Curto M, Gallus AS, Johnson M, et al. Oral apixaban for the treatment of acute venous thromboembolism. N Engl J Med. 2013 Aug 29. 369(9):799-808. [QxMD MEDLINE Link]. [Full Text].
Agnelli G, Buller HR, Cohen A, Curto M, Gallus AS, Johnson M, et al. Apixaban for extended treatment of venous thromboembolism. N Engl J Med. 2013 Feb 21. 368(8):699-708. [QxMD MEDLINE Link]. [Full Text].
Schulman S, Kearon C, Kakkar AK, Mismetti P, Schellong S, Eriksson H, et al. Dabigatran versus warfarin in the treatment of acute venous thromboembolism. N Engl J Med. 2009 Dec 10. 361(24):2342-52. [QxMD MEDLINE Link]. [Full Text].
Schulman S, Kakkar AK, Goldhaber SZ, Schellong S, Eriksson H, Mismetti P, et al. Treatment of acute venous thromboembolism with dabigatran or warfarin and pooled analysis. Circulation. 2014 Feb 18. 129(7):764-72. [QxMD MEDLINE Link].
Büller HR, Décousus H, Grosso MA, Mercuri M, Middeldorp S, Prins MH, et al. Edoxaban versus warfarin for the treatment of symptomatic venous thromboembolism. N Engl J Med. 2013 Oct 10. 369(15):1406-15. [QxMD MEDLINE Link]. [Full Text].
Cohen AT, Harrington RA, Goldhaber SZ, Hull RD, Wiens BL, Gold A, et al. Extended Thromboprophylaxis with Betrixaban in Acutely Ill Medical Patients. N Engl J Med. 2016 Aug 11. 375 (6):534-44. [QxMD MEDLINE Link]. [Full Text].
Gibson CM, Chi G, Halaby R, Korjian S, Daaboul Y, Jain P, et al. Extended-Duration Betrixaban Reduces the Risk of Stroke Versus Standard-Dose Enoxaparin Among Hospitalized Medically Ill Patients: An APEX Trial Substudy (Acute Medically Ill Venous Thromboembolism Prevention With Extended Duration Betrixaban). Circulation. 2017 Feb 14. 135 (7):648-655. [QxMD MEDLINE Link].
Garcia D, Ageno W, Libby E. Update on the diagnosis and management of pulmonary embolism. Br J Haematol. 2005 Nov. 131(3):301-12. [QxMD MEDLINE Link].
Campbell IA, Bentley DP, Prescott RJ, Routledge PA, Shetty HG, Williamson IJ. Anticoagulation for three versus six months in patients with deep vein thrombosis or pulmonary embolism, or both: randomised trial. BMJ. 2007 Mar 31. 334(7595):674. [QxMD MEDLINE Link]. [Full Text].
Pinede L, Ninet J, Duhaut P, Chabaud S, Demolombe-Rague S, Durieu I, et al. Comparison of 3 and 6 months of oral anticoagulant therapy after a first episode of proximal deep vein thrombosis or pulmonary embolism and comparison of 6 and 12 weeks of therapy after isolated calf deep vein thrombosis. Circulation. 2001 May 22. 103(20):2453-60. [QxMD MEDLINE Link].
[Guideline] Ortel TL, Neumann I, Ageno W, Beyth R, Clark NP, Cuker A, et al. American Society of Hematology 2020 guidelines for management of venous thromboembolism: treatment of deep vein thrombosis and pulmonary embolism. Blood Adv. 2020 Oct 13. 4 (19):4693-4738. [QxMD MEDLINE Link]. [Full Text].
Aujesky D, Roy PM, Verschuren F, et al. Outpatient versus inpatient treatment for patients with acute pulmonary embolism: an international, open-label, randomised, non-inferiority trial. Lancet. 2011 Jul 2. 378(9785):41-8. [QxMD MEDLINE Link].
Götzinger F, Lauder L, Sharp ASP, Lang IM, Rosenkranz S, Konstantinides S, et al. Interventional therapies for pulmonary embolism. Nat Rev Cardiol. 2023 Oct. 20 (10):670-684. [QxMD MEDLINE Link]. [Full Text].
Jaff MR, McMurtry MS, Archer SL, Cushman M, Goldenberg N, Goldhaber SZ, et al. Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension: A Scientific Statement From the American Heart Association. Circulation. 2011 Apr 26. 123(16):1788-1830. [QxMD MEDLINE Link]. [Full Text].
Goldberg JB, Giri J, Kobayashi T, Ruel M, Mittnacht AJC, Rivera-Lebron B, et al. Surgical Management and Mechanical Circulatory Support in High-Risk Pulmonary Embolisms: Historical Context, Current Status, and Future Directions: A Scientific Statement From the American Heart Association. Circulation. 2023 Feb 28. 147 (9):e628-e647. [QxMD MEDLINE Link]. [Full Text].
Ballew KA, Philbrick JT, Becker DM. Vena cava filter devices. Clin Chest Med. 1995 Jun. 16(2):295-305. [QxMD MEDLINE Link].
Dempfle CE, Elmas E, Link A, et al. Endogenous plasma activated protein C levels and the effect of enoxaparin and drotrecogin alfa (activated) on markers of coagulation activation and fibrinolysis in pulmonary embolism. Crit Care. 2011 Jan 17. 15(1):R23. [QxMD MEDLINE Link].
Boutitie F, Pinede L, Schulman S, Agnelli G, Raskob G, Julian J, et al. Influence of preceding length of anticoagulant treatment and initial presentation of venous thromboembolism on risk of recurrence after stopping treatment: analysis of individual participants' data from seven trials. BMJ. 2011 May 24. 342:d3036. [QxMD MEDLINE Link]. [Full Text].
Hippisley-Cox J, Coupland C. Development and validation of risk prediction algorithm (QThrombosis) to estimate future risk of venous thromboembolism: prospective cohort study. BMJ. 2011 Aug 16. 343:d4656. [QxMD MEDLINE Link]. [Full Text].
[Guideline] American College of Emergency Physicians Clinical Policies Subcommittee (Writing Committee) on Thromboembolic Disease:, Wolf SJ, Hahn SA, Nentwich LM, Raja AS, Silvers SM, et al. Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Suspected Acute Venous Thromboembolic Disease. Ann Emerg Med. 2018 May. 71 (5):e59-e109. [QxMD MEDLINE Link]. [Full Text].
[Guideline] Kearon C, Akl EA, Ornelas J, Blaivas A, Jimenez D, Bounameaux H, et al. Antithrombotic Therapy for VTE Disease: CHEST Guideline and Expert Panel Report. Chest. 2016 Feb. 149 (2):315-52. [QxMD MEDLINE Link].
[Guideline] ACOG Practice Bulletin No. 196 Summary: Thromboembolism in Pregnancy. Obstet Gynecol. 2018 Jul. 132 (1):243-248. [QxMD MEDLINE Link].
[Guideline] Qaseem A, Snow V, Barry P, Hornbake ER, Rodnick JE, Tobolic T, et al. Current diagnosis of venous thromboembolism in primary care: a clinical practice guideline from the American Academy of Family Physicians and the American College of Physicians. Ann Fam Med. 2007 Jan-Feb. 5 (1):57-62. [QxMD MEDLINE Link]. [Full Text].
