Which of the following patients is at highest risk for pulmonary embolism?
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Anticoagulation is recommended as initial therapy in all patients with small to moderate PE without a contraindication. Show
For patients with low risk or intermediate-low risk PE, anticoagulation can be initiated right away with the direct oral anticoagulant (DOAC) rivaroxaban or apixaban; subcutaneous low–molecular-weight heparin (LMWH) or fondaparinux; or IV Unfractionated heparin (UFH). When oral anticoagulation is initiated, a DOAC is recommended over a vitamin K antagonist. 1.Oral rivaroxaban, a factor Xa inhibitor (15 mg bid for 3 wk, then 20 mg/d), has been studied as a treatment for DVT and PE, without prior parenteral therapy. For both DVT and PE, treatment with rivaroxaban alone was noninferior to treatment with LMWH followed by a vitamin K antagonist with regard to the endpoint of recurrent venous thromboembolism. Use of rivaroxaban should be avoided in patients with severe renal failure. 2.Apixaban, a factor Xa inhibitor (10 mg bid for a week, followed by 5 mg bid), is approved for the treatment of acute PE based on the data in the AMPLIFY and AMPLIFY-EXT trials, in which apixaban met its noninferiority mark in terms of efficacy and improved safety compared to warfarin. 3.Dabigatran, a direct thrombin inhibitor (150 mg bid following 5-10 days of parenteral anticoagulation), is approved for treatment of DVT and PE in patients with CrCl >30 mL/min based on data in the RE-COVER and RE-COVER II trials where it was non-inferior to warfarin. 4.Edoxaban, a factor Xa inhibitor (60 mg daily, or 30 mg daily if CrCl 15-50 ml/min or body weight ≤60 kg or if on certain P-glycoprotein inhibitors, following 5-10 days of parenteral anticoagulation) is approved for treatment of DVT and PE based on the Hokusai VTE trial where it was noninferior to warfarin. 5.UFH, subcutaneous LMWH, or subcutaneous fondaparinux can be used for initial treatment for at least 5 days when used with warfarin, dabigatran, or edoxaban. If IV unfractionated heparin is used, a bolus dose (80 U/kg) followed by a weight-based (18 U/kg/hr) continuous infusion to achieve therapeutic anti-factor Xa (or aPTT) levels should be used. LMWH and fondaparinux should be avoided in patients with severe renal failure. •For patients with intermediate-high risk or high risk PE, anticoagulation with LMWH or IV UFH (if LMWH is contraindicated due to renal failure or bleeding concerns) is recommended and can be transitioned to an oral agent prior to hospital discharge. •For patients with contraindications to anticoagulation, consider placement of atemporary inferior vena cava (IVC) filter and frequent reassessment of safety for initiation of anticoagulation as soon as possible. •For patients with intermediate-high risk PE (demonstrating RV strain by imaging and myocardial injury with positive biomarkers), attempts should be made to risk stratify individual patients as this cohort may have multiple therapeutic options including anticoagulation alone, catheter-directed therapies, or systemic thrombolysis at a reduced dose. In high volume centers, the distinction between treatment strategies in this group may occur via a multidisciplinary PERT team, often consisting of pulmonary and critical care, cardiology, hematology, and interventional radiology specialists. •For patients with massive or high risk PE without contraindications to thrombolytics (Box 1), thrombolytic agents (urokinase, tPA, streptokinase) provide rapid resolution of clots with some increased risk of major bleeding (up to 3% incidence of intracranial hemorrhage with systemic thrombolytic administration). The standard dosing for systemic thrombolytic is 100 mg of alteplase (synthetic tPA), administered over 2 hr. •In high risk patients with absolute contraindications to thrombolytics, catheter-directed thrombectomy or surgical embolectomy should be considered at centers with the appropriate level of expertise. Finally, in high risk PE patients in refractory shock or with cardiac arrest, additional mechanical support, such as extracorporeal membrane oxygenation (ECMO), may serve as a bridge to advanced therapies or recovery.Fig. 5 describes treatment of submassive pulmonary embolism.Fig. 6 illustrates the approach to high risk or massive pulmonary embolus. Long-term treatment for PE not associated with malignancy can be carried out with a DOAC, LMWH, or warfarin. •For PE associated with malignancy, DOACs or LMWH are recommended for long-term therapy. •If thrombolytics and anticoagulants are contraindicated (e.g., GI bleeding, recent CNS surgery, recent trauma) or if the patient continues to have recurrent PE despite anticoagulation therapy, an IVC filter is recommended. •In older adults, IVC filters are associated with higher 30-day and 1-yr mortality (11.6% and 20.5%, respectively, versus 9.3% and 13.4% in those who do not); however, these patients tended to be sicker. An IVC filter is not advised for patients with recurrent venous thromboembolism, unless risk for cardiopulmonary deterioration outweighs risk for IVC filter replacement.2 •For PE occurring in the setting of pregnancy, LMWH is the treatment of choice. Dosing is based on early pregnancy weight. Planneddelivery should be strongly considered to avoid complications with anticoagulation and spinal anesthesia. For a patient with a recent PE, LMWH should be switched to UFH approximately 36 hr prior to planned delivery and the drip should be stopped 4 to 6 hr prior to delivery, with a normal partial thromboplastin time (PTT) at the time of spinal anesthesia initiation. LMWH should be restarted as soon as it is deemed safe by the obstetrician. Duration of anticoagulation should be at least 3 mo total with at least 6 wk of anticoagulation after delivery. Breastfeeding mothers can be prescribed either LMWH or warfarin. Thrombolytic therapy should only be used for life-threatening PE during pregnancy due to the high risk of peri-partum and post-partum bleeding. Pulmonary Embolism : Presentation, Natural History, and TreatmentAnton N. Sidawy MD, MPH, in Rutherford's Vascular Surgery and Endovascular Therapy, 2019 PrognosisThe prognosis of acute PE strongly varies, depending on the severity of pulmonary arterial obstruction and its impact on the RV function. RV failure is the most common cause of death in acute PE. As discussed earlier, RV strain is associated with an adverse in-hospital outcome, not only in hypotensive but in hemodynamically stable patients too. PE without RV dysfunction has a less than 2% death rate. RV dysfunction shifts mortality rates to 3% to 15% for normotensive and greater than 15%.50,51,120 Anticoagulation, contemporary supportive treatment, and thrombolytic therapies continuously decrease these rates.121,122 Among survivors, later mortality is unlikely to be related to PE, and it is most frequently attributed to other cardiovascular risk factors or underlying malignancies.123,124 However, PE recurrence or CTEPH should be anticipated. PE recurrence is not infrequent; for this reason, certain patient cohorts (e.g., cancer or unprovoked PE) are candidates for indefinite anticoagulant treatment after an initial episode. Recurrence while on anticoagulation is commonly the result of subtherapeutic anticoagulation. As a general rule, anticoagulants are discontinued when the perceived risk of anticoagulation-related bleeding and the inconvenience of remaining on treatment outweigh the risk of recurrent PE. Late recurrence has been reported to be 13% at 1 year, 23% at 5 years, and 30% at 10 years.125,126 Interestingly, a recent large prospective study showed similar recurrence rates in patients with symptomatic subsegmental versus more proximal PE; however, the topic remains controversial.127,128 CTEPH is usually the result of at least one or multiple recurrent PEs, even if many times they may go unnoticed. Residual accumulating thrombus in the pulmonary arterial tree is remodeled into connective and elastic tissue, leading to vessel narrowing and remodeling. This will subsequently progress to small-vessel arteriolar vasculopathy.44,129 Pulmonary hypertension results when the capacitance of the remaining healthy vascular beds cannot absorb the cardiac output. It is defined as mean pulmonary-artery pressure greater than 25 mm Hg that persists 6 months after the PE event, and, although it may be subclinical for a long period, it may eventually manifest as dyspnea, fatigue, and exercise intolerance. It is estimated to occur in 2% to 4% of patients after acute PE, usually within 2 years.130,131 There is some evidence that thrombolysis may potentially decrease the clinical occurrence of CTEPH because it seems to alter exercise tolerance and quality of life.56,58,59,132 It is recommended that patients 6 weeks after an acute PE should be screened with an echocardiogram for persistent pulmonary hypertension that may predict the development of CTEPH.44 Pulmonary EmbolismS.C. Berngard, J. Mandel, in Encyclopedia of Cardiovascular Research and Medicine, 2018 AbstractPulmonary embolism (PE) is a common and sometimes fatal disease that continues to persist despite advances in diagnosis and management. Patients who develop PE often have inherited as well as acquired risk factors. PE causes pulmonary and cardiovascular derangements well beyond the simple mechanical obstruction of the clot itself. Symptoms of PE are nonspecific and overlap with other disease states, so a high index of clinical suspicion is a key factor in subsequently establishing a diagnosis. Advances in diagnostic testing have improved the sensitivity and specificity for detecting PE. The mainstay of treatment is anticoagulation, but specific circumstances may require additional therapies. A minority of patients do not resolve their clot and go on to develop chronic thromboembolic disease. This review will discuss the epidemiology, pathophysiology, diagnosis, and treatment of PE. View chapterPurchase book Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780128096574997011 Pulmonary EmbolismDouglas P. Zipes MD, in Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 2019 State-of-the-Art Findings in Pulmonary EmbolismPulmonary embolism (PE) and deep vein thrombosis (DVT) together constitute one of the “big three” cardiovascular diseases, the other two being myocardial infarction (MI) and stroke.Venous thromboembolism (VTE) encompasses PE and DVT. Estimates of the global incidence of VTE range from 1.2 to 2.7 per 1000 per year.1 There is seasonality in hospitalizations for PE. The highest number of admissions is in the winter, and the lowest number is in the summer.2 In the United States, PE causes more than 100,000 deaths annually. Most deaths in hospitalized patients with PE result from right heart failure due to the initial PE or from recurrent PE despite anticoagulation. PE has an approximately 4% in-hospital case fatality rate in adults 65 years of age or older in the United States. However, the 30-day readmission rate is 15%, and the 6-month mortality rate jumps to 20% in this population.3 Patients residing in zip (postal) codes with lower socioeconomic status have increased in-hospital mortality rates and less frequently receive thrombolysis compared with patients residing in zip codes with higher socioeconomic status.4 Major long-term complications of VTE include recurrent VTE, chronic thromboembolic pulmonary hypertension (CTEPH),5 and postthrombotic syndrome (also called chronic venous insufficiency) of the legs.6 Postthrombotic syndrome patients report worse long-term physical health, mental health, and quality of life than controls.7 Newly diagnosed VTE patients cost the U.S. health care system $7 to $10 billion annually.8 The estimated cost of VTE for the European Union ranges from 1.5 billion to 13.2 billion Euros annually.9 In a European Registry of PE, the 30-day case fatality rate was 5%.10 Over a 13-year period in Europe, thrombolytic therapy use increased from 0.7% to 1.0%, and surgical embolectomy procedures doubled from 0.3% to 0.6%. The United States and Europe share common trends over the past decade: (1) an increase in the incidence of PE, (2) a decrease in the hospital length of stay, and (3) a decrease in the case fatality rate.11 Increased age12 and concomitant DVT13 are associated with a higher 30-day mortality rate. Cancer patients have a fourfold increased risk of VTE compared with the general population.14 When unprovoked VTE occurs, there is an increased likelihood that occult cancer will subsequently be detected, especially during the first 6 months after the diagnosis of VTE.15 Age, prior provoked VTE, and cigarette smoking may help predict the presence of occult cancer in patients with a first unprovoked episode of VTE.16 Nevertheless, it remains controversial whether to order abdominopelvic CT scans to try to diagnose occult cancer in patients with a first unprovoked episode of VTE.17 VTE is also a women's health disease. PE is the leading cause of maternal death in the United States. Overall, pregnancy increases the risk of VTE fivefold,18 and this risk persists for at least 12 weeks into the postpartum period.19 Pulmonary EmbolismMichael P. Gruber, Todd M. Bull, in Clinical Respiratory Medicine (Third Edition), 2008 EpidemiologyPE is a common clinical problem. In the United States, hospital-based studies estimate the incidence of PE at 1 case per 1000 persons per year, equating to 200,000–300,000 hospital admissions per year. Estimates suggest that as many as 30,000–50,000 people die from PE annually in the United States, with an estimated 3-month disease-specific mortality rate of 10%. In nearly 20% of cases, the initial clinical manifestation is sudden death. Figures for Europe and other parts of the world are broadly similar. Significant differences in mortality caused by pulmonary embolism by age, gender, and race have been observed. Age-adjusted PE mortality rates are as much as 50% higher among African-Americans than Caucasians. Among racial strata, PE mortality rates are 20–30% higher in men than women. African-American men have the highest reported mortality from PE, with an incidence rate of 6.0 deaths per 100,000 persons followed by African-American women at 4.8 deaths per 100,000 persons. The PE mortality for Caucasian males is 2.4 deaths per 100,000 persons and is the lowest for Caucasian females at 2.3 deaths per 100,000 persons. The incidence of PE is also age dependent, with increasing incidence of death occurring with advancing age. From 1979 to 1998, accounting for both gender and race, age-specific mortality rates doubled for each 10-year age group over 15–24 years. Over the past 25 years, the overall mortality rate from PE has decreased. From 1979 to 1998, the annual mortality decreased by approximately 30%. The decline in PE mortality has been observed across gender and ethnic groups. The decreasing mortality rates from PE have been attributed to improved VTE risk factor modification, including improved prophylaxis of DVT, better detection and treatment of DVT, and/or enhanced PE diagnostic techniques, which has led to a decrease in disease misclassification. Who is most at risk for pulmonary embolism?People at risk of developing a PE include those who:. Have a history of heart failure or stroke.. Have overweight (a Body Mass Index or BMI greater than 25)/obesity (a BMI greater than 30).. Are pregnant or have given birth in the previous six weeks.. Received a central venous catheter through their arm or leg.. What is the most likely cause of a pulmonary embolism?Pulmonary embolism is caused by a blocked artery in the lungs. The most common cause of such a blockage is a blood clot that forms in a deep vein in the leg and travels to the lungs, where it gets lodged in a smaller lung artery.
Which patient has the highest risk for development of a blood clot?The risk of blood clots is highest in HIV patients who have infections, are taking certain medicines, have been hospitalized, or are older than 45. Dehydration, a condition in which your body doesn't have enough fluids.
What are the client's risk factors for developing a pulmonary embolism?Anyone can get a pulmonary embolism (PE), but certain things can raise your risk of PE:. Having surgery, especially joint replacement surgery.. Certain medical conditions, including.. Hormone-based medicines, such as birth control pills or hormone replacement therapy.. Pregnancy and childbirth.. |
