eMedicine Specialties > Pulmonology > Pulmonary Embolism

Pulmonary Embolism: Follow-up

Author: Nader Kamangar, MD, FACP, FCCP, FAASM,, Associate Professor of Clinical Medicine, Director of Hospitalist/Intensivist Program, Division of Pulmonary, Critical Care and Sleep Medicine, David Geffen School of Medicine at University of California Los Angeles; Associate Director, Combined Pulmonary and Critical Care Fellowship Program, Cedars-Sinai/Olive View-UCLA/West Los Angeles Veterans Affairs Medical Center
Coauthor(s): Mark S McDonnell, MD, MBA, Cardiology Fellow, University of Southern California; Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Contributor Information and Disclosures

Updated: Aug 25, 2009

Follow-up

Deterrence/Prevention

Heparin prophylaxis
The incidence of venous thrombosis, pulmonary embolism (PE), and death can be significantly reduced by embracing a prophylactic strategy in high-risk patients. Prevention of deep vein thrombosis (DVT) in the lower extremities inevitably reduces the frequency of pulmonary embolism; therefore, populations at risk must be identified, and safe and efficacious prophylactic modalities should be used. The risk groups identified in clinical practice and the prophylaxis recommended by the Sixth Consensus Conference on Antithrombotic Therapy are described in the Table.

Prophylaxis Against Venous Thromboembolism

Open table in new window

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Table
ConditionRisk (%)*Recommendations
General Surgery
Low risk3(1) Early ambulation
Moderate risk29(1) Unfractionated heparin: 5000 U SC given 2 h preoperatively and q12h postoperatively
(2) Dalteparin: 2500 U 1-2 hr before surgery, then once daily
Enoxaparin: 2000 U before surgery, then once daily
Nadroparin: 3100 U 2 hr before surgery, then once daily
Tinzaparin: 3500 U 2 hr before surgery, then once daily
High risk39(1) Unfractionated heparin: 5000 U SC given 2 h preoperatively and q8h postoperatively
(2) Dalteparin: 5000 U 10-12 before surgery, then once daily
Enoxaparin: 4000 U 10-12 hr before surgery, then once daily
Very high risk80(1) Unfractionated heparin: 5000 U SC given 2 h preoperatively and q8h postoperatively; dalteparin: 2500 U given 2 h preoperatively and qd; plus, intermittent pneumatic compression applied intraoperatively
(2) Dalteparin: 5000 U 10-12 before surgery, then once daily
Enoxaparin: 4000 U 10-12 hr before surgery, then once daily
(3) Perioperative warfarin: INR 2-3
Orthopedic Surgery/Neurological Surgery/Trauma
Total hip replacement51(1) Dalteparin: 5000 U 1-2 hr before surgery, then once daily
Enoxaparin: 3000 U 10-12 hr before surgery, then once daily
Nadroparin: 40 U/kg U 2 hr before surgery, then once daily
Tinzaparin: 50 U/kg 2 hr before surgery, then 75 U/kg once daily
(2) Warfarin: Preoperatively and adjusted to INR of 2-3 postoperatively, continue up to 4 wk after surgery
Total knee replacement61(1) Dalteparin: 5000 U 1-2 hr before surgery, then once daily
Enoxaparin: 3000 U 10-12 hr before surgery, then once daily
Nadroparin: 40 U/kg U 2 hr before surgery, then once daily
Tinzaparin: 50 U/kg 2 hr before surgery, then 75 U/kg once daily
(2) Warfarin: Preoperatively and adjusted to INR of 2-3 postoperatively, continue up to 4 wk after surgery
Hip fracture surgery48(1) Dalteparin: 5000 U 1-2 hr before surgery, then once daily
Enoxaparin: 3000 U 10-12 hr before surgery, then once daily
Nadroparin: 40 U/kg U 2 hr before surgery, then once daily
Tinzaparin: 50 U/kg 2 hr before surgery, then 75 U/kg once daily
(2) Warfarin: Preoperatively and adjusted to INR of 2-3 postoperatively, continue up to 4 wk after surgery
Neurosurgery24(1) Intermittent pneumatic compression
(2) Unfractionated heparin: 5000 U SC q12h and intermittent pneumatic compression for high-risk patients
Acute spinal cord injury with leg paralysis40(1) Unfractionated heparin: SC in doses adjusted to paralysis produce aPTT = 1.5 X control 6 h after dose
(2) Enoxaparin: 3000 U twice daily
(3) Warfarin: Adjusted to INR of 2-3 in rehabilitation phase
(4) Intermittent pneumatic compression plus unfractionated heparin: 5000 U SC q12h
Multiple trauma53(1) Intermittent pneumatic compression until further bleeding is unlikely; then, give
(2) Enoxaparin: 30 mg SC q12h or
(3) Warfarin: Adjusted to INR of 2-3
Medical Conditions
Acute myocardial infarction24Unfractionated heparin: 5000 U SC q12h unless therapeutic anticoagulation used
Ischemic stroke with paralysis42Unfractionated heparin: 5000 U SC q12h
Medical patients (cancer, bedrest, congestive heart failure, severe lung disease)20(1) Unfractionated heparin: 5000 U SC q12h
(2) Dalteparin: 2500 U once daily
Enoxaparin: 2000 U once daily
ConditionRisk (%)*Recommendations
General Surgery
Low risk3(1) Early ambulation
Moderate risk29(1) Unfractionated heparin: 5000 U SC given 2 h preoperatively and q12h postoperatively
(2) Dalteparin: 2500 U 1-2 hr before surgery, then once daily
Enoxaparin: 2000 U before surgery, then once daily
Nadroparin: 3100 U 2 hr before surgery, then once daily
Tinzaparin: 3500 U 2 hr before surgery, then once daily
High risk39(1) Unfractionated heparin: 5000 U SC given 2 h preoperatively and q8h postoperatively
(2) Dalteparin: 5000 U 10-12 before surgery, then once daily
Enoxaparin: 4000 U 10-12 hr before surgery, then once daily
Very high risk80(1) Unfractionated heparin: 5000 U SC given 2 h preoperatively and q8h postoperatively; dalteparin: 2500 U given 2 h preoperatively and qd; plus, intermittent pneumatic compression applied intraoperatively
(2) Dalteparin: 5000 U 10-12 before surgery, then once daily
Enoxaparin: 4000 U 10-12 hr before surgery, then once daily
(3) Perioperative warfarin: INR 2-3
Orthopedic Surgery/Neurological Surgery/Trauma
Total hip replacement51(1) Dalteparin: 5000 U 1-2 hr before surgery, then once daily
Enoxaparin: 3000 U 10-12 hr before surgery, then once daily
Nadroparin: 40 U/kg U 2 hr before surgery, then once daily
Tinzaparin: 50 U/kg 2 hr before surgery, then 75 U/kg once daily
(2) Warfarin: Preoperatively and adjusted to INR of 2-3 postoperatively, continue up to 4 wk after surgery
Total knee replacement61(1) Dalteparin: 5000 U 1-2 hr before surgery, then once daily
Enoxaparin: 3000 U 10-12 hr before surgery, then once daily
Nadroparin: 40 U/kg U 2 hr before surgery, then once daily
Tinzaparin: 50 U/kg 2 hr before surgery, then 75 U/kg once daily
(2) Warfarin: Preoperatively and adjusted to INR of 2-3 postoperatively, continue up to 4 wk after surgery
Hip fracture surgery48(1) Dalteparin: 5000 U 1-2 hr before surgery, then once daily
Enoxaparin: 3000 U 10-12 hr before surgery, then once daily
Nadroparin: 40 U/kg U 2 hr before surgery, then once daily
Tinzaparin: 50 U/kg 2 hr before surgery, then 75 U/kg once daily
(2) Warfarin: Preoperatively and adjusted to INR of 2-3 postoperatively, continue up to 4 wk after surgery
Neurosurgery24(1) Intermittent pneumatic compression
(2) Unfractionated heparin: 5000 U SC q12h and intermittent pneumatic compression for high-risk patients
Acute spinal cord injury with leg paralysis40(1) Unfractionated heparin: SC in doses adjusted to paralysis produce aPTT = 1.5 X control 6 h after dose
(2) Enoxaparin: 3000 U twice daily
(3) Warfarin: Adjusted to INR of 2-3 in rehabilitation phase
(4) Intermittent pneumatic compression plus unfractionated heparin: 5000 U SC q12h
Multiple trauma53(1) Intermittent pneumatic compression until further bleeding is unlikely; then, give
(2) Enoxaparin: 30 mg SC q12h or
(3) Warfarin: Adjusted to INR of 2-3
Medical Conditions
Acute myocardial infarction24Unfractionated heparin: 5000 U SC q12h unless therapeutic anticoagulation used
Ischemic stroke with paralysis42Unfractionated heparin: 5000 U SC q12h
Medical patients (cancer, bedrest, congestive heart failure, severe lung disease)20(1) Unfractionated heparin: 5000 U SC q12h
(2) Dalteparin: 2500 U once daily
Enoxaparin: 2000 U once daily

*Approximate risk without prophylaxis for all and/or proximal DVT or symptomatic PE.

Sequential compression devices

Compression stockings provide a compression of 30-40 mm Hg gradient and are a safe and effective therapy to prevent venous thromboembolism in patients who are at high risk when heparin therapy is not desirable or is contraindicated. These devices provide a gradient of compression that is highest at the toes and gradually decreases to the level of the thigh. This mechanism reduces the capacitative venous volume by approximately 70% and increases the measured velocity of blood flow by a factor of 5 or more in lower extremity veins.

A meta-analysis calculated a DVT risk ratio of 0.28 for gradient compression stockings (compared with no prophylaxis) in patients undergoing abdominal surgery, gynecologic surgery, or neurosurgery. Other studies have reported that gradient compression stockings and low molecular weight heparin (LMWH) were the most effective modalities in reducing the incidence of DVT after hip surgery.

The universal white stockings, known as antiembolic stockings or Ted stockings, produce a maximum compression of only 18 mm Hg. Ted stockings rarely are fitted in such a way as to provide adequate gradient compression to the deep venous system. Therefore, Ted stockings have no proven efficacy in the prevention of DVT and pulmonary embolism.

Gradient compression pantyhose (30-40 mmHg) are available in pregnant sizes. They are recommended by many specialists for all women who are pregnant because they prevent DVT and reduce or prevent the development of varicose veins.

Although strict bed rest was recommended in the past for acute DVT to reduce the risk of pulmonary embolism, a study has shown no benefit from prescribing bed rest. Therefore, strict bed rest for 5 days is not justified if adequate therapy with LMWH and adequate compression is assured.

Complications

  • Sudden cardiac death
  • Obstructive shock
  • Pulseless electrical activity
  • Atrial or ventricular arrhythmias
  • Secondary pulmonary arterial hypertension
  • Cor pulmonale
  • Severe hypoxemia
  • Right-to-left intracardiac shunt
  • Lung infarction
  • Pleural effusion
  • Paradoxical embolism

Prognosis

  • The prognosis of patients with pulmonary embolism depends on 2 factors: (1) the underlying disease state and (2) appropriate diagnosis and treatment.
  • Most patients treated with anticoagulants do not develop long-term sequelae upon follow-up evaluation.
  • At 5 days of anticoagulant therapy, 36% of lung scan defects are resolved; at 2 weeks, 52% are resolved; at 3 months, 73% are resolved.
  • The mortality rate in patients with undiagnosed pulmonary embolism is 30%.
  • 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.39 In one study, levels of N -terminal pro-brain natriuretic peptide greater than 500 ng/L was independently associated with central pulmonary embolism and was a possible predictor of death from pulmonary embolism.40  
  • In the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) (PIOPED) study, the 1-year mortality rate was 24%.7 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.

Patient Education

For excellent patient education resources, visit eMedicine's Lung and Airway Center and Circulatory Problems Center. Also, see eMedicine's patient education articles Pulmonary Embolism and Blood Clot in the Legs.

Miscellaneous

Medicolegal Pitfalls

Pulmonary embolism (PE) is an extremely common disorder. It presents with nonspecific clinical features and requires specialized investigations for confirmation of diagnosis. Therefore, many patients die from unrecognized pulmonary embolism. The other common pitfalls are as follows:  

  • Disregarding patient's complaints of unexplained dyspnea as anxiety or hyperventilation
  • Blaming complaints of unexplained chest pain on musculoskeletal pain
  • Failing to recognize, diagnose, and treat deep vein thrombosis (DVT)
  • Failing to initiate an appropriate diagnostic workup in patients with symptoms consistent with pulmonary embolism
  • Failing to initiate therapeutic anticoagulant therapy with heparin in patients suspected to have pulmonary embolism, before the V/Q scan or other investigations

The role of thrombolytic therapy in patients who are hemodynamically stable remains uncertain. No particular diagnostic strategy appears to be superior to another at present. More clinical studies are needed to evaluate the utility of new diagnostic approaches for pulmonary embolism. The availability of the diagnostic tests, the expertise of the radiologists, cost-effective analysis, and local traditions appear to be the considerations in the workup of a patient suspected to have pulmonary embolism.

Special Concerns

  • Pregnancy
    • The risk of venous thromboembolism is increased during pregnancy and the postpartum period. Pregnant women who are in a hypercoagulable state or have had previous venous thromboembolism should receive prophylactic anticoagulation during pregnancy.
    • Pulmonary embolism is the leading cause of death in pregnancy. Guidelines by the professional societies make this difficult diagnosis easier and reduce the risks of radiation to the fetus. If the patient has a low pretest probability for pulmonary embolism and a normal D-dimer test result, clinical exclusion from further investigations is recommended. When the suspicion is high, the patients should have bilateral leg Doppler assessment. If the results are positive, the patient should be treated for pulmonary embolism. If the results are negative, CT pulmonary angiography is the next step. To rule out contrast-induced hypothyroidism, all neonates exposed to the iodinated contrast in utero should have their serum thyrotropin  level checked in the first week of life.
    • Pregnant patients diagnosed with DVT or pulmonary embolism are treated with unfractionated heparin or LMWH throughout their pregnancy. Warfarin is contraindicated because it crosses the placental barrier and can cause fetal malformations. Therefore, either subcutaneous unfractionated heparin or LMWH at full anticoagulation doses should be continued until delivery. Women experiencing a thromboembolic event during pregnancy should receive therapeutic treatment with unfractionated heparin or LMWH during pregnancy, with anticoagulation continuing for 4-6 weeks postpartum, and for a total of at least 6 months.
  • Heparin-induced thrombocytopenia
    • Heparin-induced thrombocytopenia (HIT) is a transient prothrombotic disorder initiated by heparin.
    • Main features are (1) thrombocytopenia resulting from immunoglobulin G–mediated platelet activation and (2) in vivo thrombin generation and increased risk of venous and arterial thrombosis.
    • The highest frequency of HIT, 5%, has been reported in post-orthopedic surgery patients receiving up to 2 weeks of unfractionated heparin. HIT occurred in approximately 0.5% of post-orthopedic surgery patients receiving LMWH for up to 2 weeks.
    • HIT may manifest clinically as extension of the thrombus or formation of new arterial thrombosis. HIT should be suspected whenever the patient's platelet count falls to less than 100,000/µL or less than 50% of the baseline value, generally after 5-15 days of heparin therapy. The definitive diagnosis is made by performing a platelet activation factor assay.
    • The treatment of patients who develop HIT is to stop all heparin products, including catheter flushes and heparin-coated catheters, and to initiate an alternative nonheparin anticoagulant, even when thrombosis is not clinically apparent. Preferred agents include direct thrombin inhibitors such as lepirudin or argatroban. Start warfarin while the patient receives an alternative nonheparin anticoagulant and only when the platelet count has recovered to at least 100,000/µL, preferably 150,000/µL.
  • Resistance to heparin
    • Few patients with venous thromboembolism require large doses of heparin for achieving an optimal activated partial thromboplastin time (aPTT). These patients have increased plasma concentrations of factor VIII and heparin-binding proteins. Increased factor VIII concentration causes a dissociation between aPTT and plasma heparin values. The aPTT is suboptimal, but patients have adequate heparin levels upon protamine titration. This commonly occurs in patients with a concomitant inflammatory disease.
    • Monitoring the antifactor Xa assay results in this situation is safe and effective and results in less escalation of the heparin dose when compared with monitoring with aPTT. Whenever a therapeutic level of aPTT cannot be achieved with large doses of unfractionated heparin administration, either determination of plasma heparin concentration or therapy with LMWH should be instituted.
  • Elderly individuals
    • Pulmonary embolism is increasingly prevalent among elderly patients, yet the diagnosis is missed more often in this population 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.
  • Future research
    • The advances over the past several decades have significantly improved diagnostic abilities and have refined the treatment of patients with pulmonary embolism. However, several areas need further research and properly conducted therapeutic trials. The role of LMWH and the optimal duration of anticoagulant therapy in different subgroups of patients with venous thromboembolism require further study.
    • Future studies should determine whether less intense warfarin therapy (international normalized ratio [INR] <2), which will result in less bleeding, is effective in preventing recurrences.
    • Whether drugs that inhibit the action of thrombin (eg, hirudin) are useful in treating patients with venous thromboembolic disease needs to be determined by future trials.
 


More on Pulmonary Embolism

Overview: Pulmonary Embolism
Differential Diagnoses & Workup: Pulmonary Embolism
Treatment & Medication: Pulmonary Embolism
Follow-up: Pulmonary Embolism
Multimedia: Pulmonary Embolism
References
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Further Reading

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Keywords

pulmonary embolism, pulmonary emboli, venous thromboembolism, PE, obstructive shock, deep vein thrombosis, deep venous thrombosis, DVT, hemodynamic collapse, acute pulmonary infarction, pulmonary hypertension, cor pulmonale

pleuritic chest pain, hemoptysis, venous stasis, polycythemia, immobility, hypercoagulability, factor V Leiden mutation, pancreatic carcinoma, bronchogenic carcinoma, carcinoma of the genitourinary tract, colon cancer, breast cancer, congestive heart failure, stroke, obesity, varicose veins, inflammatory bowel disease

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Contributor Information and Disclosures

Author

Nader Kamangar, MD, FACP, FCCP, FAASM,, Associate Professor of Clinical Medicine, Director of Hospitalist/Intensivist Program, Division of Pulmonary, Critical Care and Sleep Medicine, David Geffen School of Medicine at University of California Los Angeles; Associate Director, Combined Pulmonary and Critical Care Fellowship Program, Cedars-Sinai/Olive View-UCLA/West Los Angeles Veterans Affairs Medical Center
Nader Kamangar, MD, FACP, FCCP, FAASM, is a member of the following medical societies: American Academy of Sleep Medicine, American Association of Bronchology, American College of Chest Physicians, American College of Physicians, American Lung Association, American Medical Association, American Thoracic Society, California Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Mark S McDonnell, MD, MBA, Cardiology Fellow, University of Southern California
Mark S McDonnell, MD, MBA is a member of the following medical societies: American College of Physicians, American Heart Association, and American Medical Association
Disclosure: Nothing to disclose.

Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Gregory Tino, MD, Director of Pulmonary Outpatient Practices, Associate Professor, Department of Medicine, Division of Pulmonary, Allergy, and Critical Care, University of Pennsylvania Medical Center and Hospital
Gregory Tino, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Gregg T Anders, DO, Medical Director, Great Plains Regional Medical Command , Brook Army Medical Center; Clinical Associate Professor, Department of Internal Medicine, Division of Pulmonary Disease, University of Texas Health Science Center at San Antonio
Gregg T Anders, DO is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.

 
 
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