Sections

Pulmonary Embolism (PE)

Guidelines

Guidelines Summary

Guidelines for the diagnosis and management of pulmonary embolism (PE) have been issued by the following organizations:

American Academy of Family Physicians (AAFP)/American College of Physicians (ACP) ^[4]
American College of Physicians (ACP) ^[111]
American College of Emergency Physicians (ACEP) ^[112]
American College of Radiology (ACR) ^[69]
American College of Chest Physicians ^{[5, 113]}
American Heart Association (AHA) ^[106]
American College of Obstetricians and Gynecologists (ACOG) ^[114]
American Society of Hematology ^[115]

Clinical Scoring Guidelines

A 2007 clinical practice guideline from the American Academy of Family Physicians (AAFP) and the American College of Physicians (ACP) recommends that validated clinical prediction rules be used to estimate pretest probability of pulmonary embolism (PE) and to interpret test results.^[4]The guideline, Current Diagnosis of Venous Thromboembolism in Primary Care, advocates use of the Wells prediction rule for this purpose but notes that the Wells rule performs better in younger patients without comorbidities or a history of venous thromboembolism (VTE) than in other patients.

In 2015, the ACP released guidelines for the evaluation of patients with suspected acute PE, which included the following recommendations^[111]:

Plasma D-dimer tests are more appropriate for those at intermediate risk for a PE, and no testing may be necessary for some patients at low risk.
Use either the Wells or Geneva rules to choose tests based on a patient's risk for PE.
If the patient is at low risk, clinicians should use the eight Pulmonary Embolism Rule-Out Criteria (PERC); if a patient meets all eight criteria, the risks of testing are greater than the risk for embolism, and no testing is needed.
For patients at intermediate risk, or for those at low risk who do not meet all of the rule-out criteria, use a high-sensitivity plasma D-dimer test as the initial test.
In patients older than 50 years, use an age-adjusted threshold (age × 10 ng/mL, rather than a blanket 500 ng/mL), because normal D-dimer levels increase with age.
Patients with a D-dimer level below the age-adjusted cutoff should not receive any imaging studies.
Patients with elevated D-dimer levels should then receive imaging.
Patients at high risk should skip the D-dimer test and proceed to CT pulmonary angiography, because a negative D-dimer test does not eliminate the need for imaging in these patients.
Clinicians should only obtain ventilation-perfusion scans in patients with a contraindication to CT pulmonary angiography or if CT pulmonary angiography is unavailable.
Clinicians should use validated clinical prediction rules to estimate pretest probability in patients in whom acute PE is being considered.

In contrast, the 2011 guidelines of the American College of Emergency Physicians (ACEP) find that either objective criteria or gestalt clinical assessment can be used to risk-stratify patients with suspected PE. There is insufficient evidence to support the preferential use of one method over another (level B). For patients with a low pretest probability for suspected PE, PERC may be used to exclude the diagnosis based on historical and physical examination data alone (level B). Other key recommendations include the following^[112]:

Negative quantitative D-dimer assay results can be used to exclude PE in patients with a low pretest probability for PE (level A).
Negative quantitative D-dimer assay results may be used to exclude PE in patients with an intermediate pretest probability for PE (level C).
For patients with a low or PE unlikely (Wells score 4) pretest probability for PE who require additional diagnostic testing (eg, positive D-dimer result, or highly sensitive D-dimer test not available), a negative, multidetector CT pulmonary angiogram alone can be used to exclude PE (level B).
For patients with an intermediate or high pretest probability for PE and a negative CT pulmonary angiogram result in whom a clinical concern for PE still exists and CT venogram has not already been performed, consider additional diagnostic testing (eg, D-dimer, lower extremity imaging, VQ scanning, traditional pulmonary arteriography) prior to exclusion of VTE disease (level C).
Venous ultrasound may be considered as initial imaging in patients with obvious signs of deep venous thrombosis (DVT) for whom venous ultrasound is readily available, patients with relative contraindications for CT scan (eg, borderline renal insufficiency, CT contrast agent allergy), and pregnant patients. A positive finding in a patient with symptoms consistent with PE can be considered evidence for diagnosis of VTE disease and may preclude the need for additional diagnostic imaging in the emergency department (level B).

Imaging Guidelines

In its 2011 guidelines, the American College of Radiology (ACR) considers

multislice CT pulmonary angiography to be the standard of care for the detection of pulmonary embolism (PE). Additional recommendation include the following^[69]:

A chest radiograph cannot exclude or confirm PE, but it is important (as a complementary study) as it can guide further investigations and suggest alternative diagnoses.
Any test that can confirm either deep venous thrombosis (DVT) (ie, lower-extremity venous duplex) or PE is sufficient. Only certain studies, however, have sufficient accuracy to exclude PE.
Ventilation/perfusion (V/Q) scanning appears to have high overall accuracy.
In pregnancy, with radiation a particular concern, the choice between perfusion scanning and CT pulmonary angiography depends on local equipment and expertise, as well as patient factors (normal chest radiograph, ability to breathhold).

Antithrombotic and Thrombolytic Therapy Guidelines

In 2016, the American College of Chest Physicians (ACCP) updated recommendations on 12 topics that were in the 9th edition of their Antithrombotic Therapy for VTE Disease: Antithrombotic Therapy and Prevention of Thrombosis guidelines, and address three new topics.^[113]

Key new or revised recommendations include the following:

Dabigatran, rivaroxaban, apixaban, or edoxaban are preferred over vitamin K antagonist (VKA) therapy as long-term (first 3 months) anticoagulant therapy for noncancer patients (all grade 2B).
Low-molecular-weight heparin (LMWH) is recommended over VKA therapy, dabigatran, rivaroxaban, apixaban, or edoxaban as long-term (first 3 months) anticoagulant therapy for patients with cancer-associated thrombosis (all grade 2C).
Aspirin is recommended over no aspirin to prevent recurrent venous thromboembolism (VTE) in patients who are stopping anticoagulant therapy and do not have a contraindication to aspirin (grade 2B).
In most patients with acute pulmonary embolism (PE) not associated with hypotension, systemically administered thrombolytic therapy is recommended against (grade 1B).
In selected patients with acute PE who deteriorate after starting anticoagulant therapy but have yet to develop hypotension and who have a low bleeding risk, systemically administered thrombolytic therapy is preferred over no such therapy (grade 2C).

According to ACCP 9th edition guidelines, immediate therapeutic anticoagulation should be initiated for patients in whom deep venous thrombosis (DVT) or PE (grade 1B) is suspected.^[5]Anticoagulation therapy reduces mortality rates from 30% to less than 10%. Diagnostic investigations should not delay empirical anticoagulant therapy in patients with high or intermediate risk of PE (grade 2C).

For acute PE, the ACCP guidelines recommend starting LMWH or fondaparinux, preferred over unfractionated heparin (UFH) (grade 2C for LMWH; grade 2B for fondaparinux) or subcutaneous heparin (grade 2B for LMWH; grade 2C for fondaparinux).^[5]If patients are to be treated with LMWH, once-daily treatment is preferred to twice-daily treatment (grade 2C).

Patients who are considered to be low risk should be discharged early from hospital (grade 2B).

Patients should have an oral anticoagulant (warfarin) initiated at the time of diagnosis, and they should have UFH, LMWH, or fondaparinux discontinued only after the international normalized ratio (INR) is 2.0 for at least 24 hours but no sooner than 5 days after warfarin therapy has been started (grade 1B). The recommended duration of UFH, LMWH, and fondaparinux is based on evidence suggesting that the relatively long half-life of factor II, along with the short half-lives of protein C and protein S, may provoke a paradoxical hypercoagulable state if these agents are discontinued prematurely.

The ACCP guidelines for antithrombotic and thrombolytic therapy are summarized as follows^[5]:

Thrombolytic therapy should be used in patients with acute PE associated with hypotension (systolic BP < 90 mm Hg), who do not have a high bleeding risk (grade 2C).
Thrombolytic therapy is suggested in select patients with acute PE not associated with hypotension and with a low bleeding risk whose initial clinical presentation or clinical course after starting anticoagulation suggests a high risk of developing hypotension (grade 2C).
Assessment of PE severity, prognosis, and risk of bleeding dictates whether thrombolytic therapy should be started. Thrombolytic therapy is not recommended for most patients with acute PE not associated with hypotension (grade 1C).
All patients with unprovoked PE receive 3 months of treatment with anticoagulation rather than a shorter duration of treatment, and they have an assessment of the risk-to-benefit ratio of extended therapy at the end of 3 months (grade 1B).
Patients with a first episode of VTE and with a low or moderate risk of bleeding should have extended anticoagulant therapy (grade 2B). Patients with a first episode of VTE who have a high bleeding risk should have therapy limited to 3 months (grade 1B). In patients with a second unprovoked episode of VTE and low or moderate risk of bleeding, extended anticoagulant therapy is recommended (grades 1B and 2B, respectively). In patients with a second episode of VTE and a high risk of bleeding, 3 months of anticoagulation is preferred rather than extended anticoagulation (grade 2B).
Patients who have PE and preexisting irreversible risk factors, such as deficiency of antithrombin III, proteins S and C, factor V Leiden mutation, or the presence of antiphospholipid antibodies, should be placed on long-term anticoagulation.

Guidelines on Advanced Therapies for Acute VTE

In 2011, guidelines to help emergency department and other physicians determine which patients with venous thromboembolism (VTE) should receive advanced therapies rather than simple anticoagulation were issued by the American Heart Association (AHA).^[106]Recommendations for management of acute pulmonary embolism (PE) are as follows:

Therapeutic anticoagulation with subcutaneous low-molecular-weight heparin (LMWH), intravenous or subcutaneous unfractionated heparin (UFH) with monitoring, unmonitored weight-based subcutaneous UFH, or subcutaneous fondaparinux should be given to patients with objectively confirmed PE and no contraindications to anticoagulation (class I).
Therapeutic anticoagulation during the diagnostic workup should be given to patients with intermediate or high clinical probability of PE and no contraindications to anticoagulation (class I).
Fibrinolysis is reasonable for patients with massive acute PE and acceptable risk of bleeding complications (class IIa).
Fibrinolysis may be considered for patients with submassive acute PE judged to have clinical evidence of adverse prognosis (new hemodynamic instability, worsening respiratory insufficiency, severe right ventricular dysfunction, or major myocardial necrosis) and low risk of bleeding complications (class IIb).
Fibrinolysis is not recommended for the following patients(class III): (1) Low-risk PE; (2) Submassive acute PE with minor right ventricular dysfunction, minor myocardial necrosis, and no clinical worsening; and (3) With undifferentiated cardiac arrest.

Recommendations for catheter-based interventions include the following:

For patients with massive PE and contraindications to fibrinolysis, catheter embolectomy and fragmentation or surgical embolectomy is reasonable, depending on the expertise available (class IIa).
For patients with massive PE who remain unstable after receiving fibrinolysis, catheter embolectomy and fragmentation or surgical embolectomy is reasonable (class IIa).
For patients with massive PE who cannot receive fibrinolysis or who remain unstable after fibrinolysis, consider transfer to an institution experienced in either catheter embolectomy or surgical embolectomy if these procedures are not available and safe transfer can be achieved (class IIa).
Either catheter embolectomy or surgical embolectomy may be considered for patients with submassive acute PE judged to have clinical evidence of adverse prognosis (new hemodynamic instability, worsening respiratory failure, severe right ventricular dysfunction, or major myocardial necrosis) (class IIb).
Catheter embolectomy and surgical thrombectomy are not recommended for patients with low-risk PE or submassive acute PE with minor right ventricular dysfunction, minor myocardial necrosis, and no clinical worsening (class III).

Recommendations for use of vena cava filters include the following:

Patients with confirmed acute PE (or proximal deep venous thrombosis [DVT]) with contraindications to anticoagulation or with active bleeding complications should receive an inferior vena cava (IVC) filter (class I).
Anticoagulation should be resumed in patients with an IVC filter once contraindications to anticoagulation or active bleeding complications have resolved (class I).
Patients who receive retrievable IVC filters should be evaluated periodically for filter retrieval within the specific filter’s retrieval window (class I).
Placement of an IVC filter is reasonable for patients with recurrent acute PE despite therapeutic anticoagulation (class IIa).
A permanent IVC filter device is reasonable for patients with a long-term contraindication to anticoagulation (class IIa).
A retrievable IVC filter device is reasonable for patients with a short-term contraindication to anticoagulation therapy (class IIa).
Placement of an IVC filter may be considered for patients with acute PE and very poor cardiopulmonary reserve, including those with massive PE (class IIb).
An IVC filter should not be used routinely as an adjuvant to anticoagulation and systemic fibrinolysis in the treatment of acute PE (class III).

Pregnancy and Gynecological Surgery Guidelines

In 2011, the American College of Obstetricians and Gynecologists (ACOG) published a practice bulletin on the diagnosis, management, and prevention of thromboembolism during pregnancy. The key recommendations included the following^[114]:

Compression ultrasonography of the proximal veins is the recommended initial diagnostic test when signs or symptoms suggest new-onset deep veinous thrombosis (DVT) (level A).
Women with a history of thrombosis who have not been thoroughly evaluated for possible underlying causes should receive testing for antiphospholipid antibodies, as well as for inherited thrombophilias (level C).
Heparin compounds are preferred for anticoagulation (level B).
Anticoagulation is recommended for women with acute thromboembolism during the current pregnancy or those at high risk of venous thromboembolism (VTE), such as women with mechanical heart valves (level C).
In the last month of pregnancy, or sooner if delivery appears imminent, women receiving either therapeutic or prophylactic anticoagulation may be converted from low-molecular-weight heparin (LMWH) to unfractionated heparin (UFH), which has a shorter half-life (level C).
Neuraxial blockade should be withheld for 10-12 hours after the last prophylactic dose of LMWH or 24 hours after the last therapeutic dose of LMWH (level C).
For all women not already receiving thromboprophylaxis, placement of pneumatic compression devices before cesarean delivery is recommended. However, an emergency cesarean delivery should not be delayed for the placement of compression devices (level C).
To minimize postpartum bleeding complications, a reasonable strategy is to resume anticoagulation therapy no sooner than 4-6 hours after vaginal delivery or 6-12 hours after cesarean delivery (level B).
For women in whom restarting anticoagulation is planned after delivery, pneumatic compression devices should be left in place until the woman is ambulatory and anticoagulation therapy is resumed (level C).
Warfarin, LMWH, and UFH are compatible with breastfeeding because they do not accumulate in breast milk and do not lead to anticoagulation in the infant (level B).

Anticoagulation Therapy Guidelines for VTE

The guidelines on optimal management of anticoagulation therapy for venous thromboembolism (VTE) were released on November 7, 2018, by the American Society of Hematology (ASH).^[115]

Initial anticoagulant dose selection

In obese patients receiving low-molecular-weight heparin (LMWH) for treatment of acute VTE, it is suggested that initial LMWH dose selection be based on actual body weight rather than on a fixed maximum daily dose (ie, capped dose).

Drug-interaction management

For patients requiring administration of inhibitors or inducers of P-glycoprotein (P-gp) or strong inhibitors or inducers of cytochrome P450 (CYP) enzymes, it is suggested to use an alternative anticoagulant (eg, a vitamin K antagonist [VKA] or LMWH) rather than a direct oral anticoagulant (DOAC) to treat VTE.

Point-of-care INR testing

For patients receiving maintenance VKA therapy for VTE, home point-of-care international normalized ratio (INR) testing (patient self-testing [PST]) is suggested in preference to any other INR testing approach except patient self-management (PSM) in suitable patients (those who have demonstrated competency to perform PST and who can afford this option).

For patients receiving maintenance VKA therapy for VTE, point-of-care INR testing by the patient at home with self-adjustment of VKA dose (PSM) is suggested in preference to any other management approach, including PST in suitable patients (those who have demonstrated competency to perform PSM and who can afford this option).

Selecting the timing between INR measurements (INR recall interval)

For patients receiving VKA therapy for VTE, an INR recall interval of 4 weeks or less is suggested rather than an interval longer than 4 weeks after VKA dose adjustment due to an out-of-target-range INR.

For patients receiving maintenance VKA therapy for VTE, a longer (6-12 weeks) INR recall interval is suggested rather than a shorter (4 weeks) interval during periods of stable INR control.

Laboratory monitoring of anticoagulant response

For patients with renal dysfunction (creatinine clearance, < 30 mL/min) or obesity receiving LMWH therapy for VTE, it is suggested not to use anti–factor Xa concentration monitoring to guide LMWH dose adjustment.

For patients receiving DOAC therapy for VTE, it is suggested not to measure the DOAC anticoagulant effect during management of bleeding.

Transitions between anticoagulants

For patients transitioning from DOAC to VKA, overlapping DOAC and VKA therapy until the INR is within the therapeutic range is suggested in preference to LMWH or UFH “bridging therapy.”

Use of specialized AMS

For patients receiving anticoagulation therapy for VTE, specialized anticoagulation-management service (AMS) care is suggested in preference to care provided by the patient’s usual healthcare provider.

Structured patient education

For patients receiving oral anticoagulation therapy for VTE, supplementary patient education is suggested in addition to basic education.

Efforts to improve adherence to anticoagulant regimen

For patients receiving anticoagulation therapy for VTE, it is suggested not to use a daily lottery, electronic reminders, or a combination of the two to improve medication adherence. It is also suggested not to use visual medication schedules (provided to patients at each visit, along with brief counseling) to improve medication adherence.

Invasive procedure management

For patients at low-to-moderate risk for recurrent VTE who require interruption of VKA therapy for invasive procedures, VKA interruption alone is recommended in preference to periprocedural bridging with LMWH or UHF.

For patients interrupting DOAC therapy for scheduled invasive procedures, it is suggested not to perform laboratory testing for DOAC effect before procedures.

Excessive anticoagulation and bleeding management

For patients receiving VKA therapy for VTE with INR higher than 4.5 but lower than 10 and without clinically relevant bleeding, temporary cessation of VKA alone is suggested, without the addition of vitamin K.

For patients with life-threatening bleeding during VKA therapy for VTE and an elevated INR, use of four-factor prothrombin complex concentrates (PCCs) is suggested in preference to fresh frozen plasma (FFP) as an addition to cessation of VKA and IV vitamin K.

For patients with life-threatening bleeding during oral direct Xa inhibitor therapy for VTE, it is suggested to use either four-factor PCC administration as an addition to cessation of oral direct Xa inhibitor or cessation of oral direct Xa inhibitor alone.

For patients with life-threatening bleeding during oral direct Xa inhibitor therapy for VTE, it is suggested to use coagulation factor Xa (recombinant), inactivated-zhzo in addition to cessation of oral direct Xa inhibitor rather than no coagulation factor Xa (recombinant), inactivated-zhzo.

For patients with life-threatening bleeding during dabigatran therapy for VTE, it is suggested to use idarucizumab in addition to cessation of dabigatran rather than no idarucizumab.

For patients with life-threatening bleeding during LMWH or unfractionated heparin (UFH) therapy for VTE, it is suggested to use protamine in addition to LMWH/UFH cessation rather than no protamine.

Anticoagulant resumption following bleeding

For patients receiving anticoagulation therapy for VTE who survive an episode of major bleeding, resumption of oral anticoagulation therapy within 90 days is suggested in preference to discontinuance of oral anticoagulation therapy.

Medication

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Media Gallery

A large pulmonary artery thrombus in a hospitalized patient who died suddenly.
Pulmonary embolism was identified as the cause of death in a patient who developed shortness of breath while hospitalized for hip joint surgery. This is a close-up view.
Lung infarction secondary to pulmonary embolism occurs rarely.
Posteroanterior and lateral chest radiograph findings are normal, which is the usual finding in patients with pulmonary embolism.
High-probability perfusion lung scan shows segmental perfusion defects in the right upper lobe and subsegmental perfusion defects in right lower lobe, left upper lobe, and left lower lobe.
A normal ventilation scan will make the noted defects in the previous image a mismatch and, hence, a high-probability ventilation-perfusion scan.
Anterior views of perfusion and ventilation scans are shown here. A perfusion defect is present in the left lower lobe, but perfusion to this lobe is intact, making this a high-probability scan.
A segmental ventilation perfusion mismatch is evident in a left anterior oblique projection.
A pulmonary angiogram shows the abrupt termination of the ascending branch of the right upper-lobe artery, confirming the diagnosis of pulmonary embolism.
A chest radiograph with normal findings in a 64-year-old woman who presented with worsening breathlessness.
This perfusion scan shows bilateral perfusion defects. The ventilation scan findings were normal; therefore, these are mismatches, and this is a high-probability scan.
This ultrasonogram shows a thrombus in the distal superficial saphenous vein, which is under the artery.
A posteroanterior chest radiograph showing a peripheral wedge-shaped infiltrate caused by pulmonary infarction secondary to pulmonary embolism. Hampton hump is a rare and nonspecific finding. Courtesy of Justin Wong, MD.
Computed tomography angiogram in a 53-year-old man with acute pulmonary embolism. This image shows an intraluminal filling defect that occludes the anterior basal segmental artery of the right lower lobe. Also present is an infarction of the corresponding lung, which is indicated by a triangular, pleura-based consolidation (Hampton hump).
Computed tomography angiography in a young man who experienced acute chest pain and shortness of breath after a transcontinental flight. This image demonstrates a clot in the anterior segmental artery in the left upper lung (LA2) and a clot in the anterior segmental artery in the right upper lung (RA2).
Computed tomography angiogram in a 55-year-old man with possible pulmonary embolism. This image was obtained at the level of the lower lobes and shows perivascular segmental enlarged lymph nodes as well as prominent extraluminal soft tissue interposed between the artery and the bronchus.
Computed tomography venograms in a 65-year-old man with possible pulmonary embolism. This image shows acute deep venous thrombosis with intraluminal filling defects in the bilateral superficial femoral veins.
The pathophysiology of pulmonary embolism. Although pulmonary embolism can arise from anywhere in the body, most commonly it arises from the calf veins. The venous thrombi predominately originate in venous valve pockets (inset) and at other sites of presumed venous stasis. To reach the lungs, thromboemboli travel through the right side of the heart. RA, right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle.
A spiral CT scan shows thrombus in bilateral main pulmonary arteries.
CT scan of the same chest depicted in Image 18. Courtesy of Justin Wong, MD.
Longitudinal ultrasound image of partially recanalized thrombus in the femoral vein at mid thigh.
Sequential images demonstrate treatment of iliofemoral deep venous thrombosis due to May-Thurner (Cockett) syndrome. Far left, view of the entire pelvis demonstrates iliac occlusion. Middle left, after 12 hours of catheter-directed thrombolysis, an obstruction at the left common iliac vein is evident. Middle right, after 24 hours of thrombolysis, a bandlike obstruction is seen; this is the impression made by the overlying right common iliac artery. Far left, after stent placement, image shows wide patency and rapid flow through the previously obstructed region. Note that the patient is in the prone position in all views. (Right and left are reversed.)
Lower-extremity venogram shows outlining of an acute deep venous thrombosis in the popliteal vein with contrast enhancement.
Lower-extremity venogram shows a nonocclusive chronic thrombus. The superficial femoral vein (lateral vein) has the appearance of 2 parallel veins, when in fact, it is 1 lumen containing a chronic linear thrombus. Although the chronic clot is not obstructive after it recanalizes, it effectively causes the venous valves to adhere in an open position, predisposing the patient to reflux in the involved segment.
Pulmonary embolus.

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Author

Daniel R Ouellette, MD, FCCP Associate Professor of Medicine, Wayne State University School of Medicine; Medical Director, Pulmonary Medicine General Practice Unit (F2), Senior Staff and Attending Physician, Division of Pulmonary and Critical Care Medicine, Henry Ford Hospital

Daniel R Ouellette, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society, Society of Critical Care Medicine

Disclosure: Received research grant from: Sanofi Pharmaceutical.

Coauthor(s)

Annie Harrington, MD Fellow in Pulmonary and Critical Care Medicine, Cedars-Sinai Medical Center

Annie Harrington, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians

Disclosure: Nothing to disclose.

Nader Kamangar, MD, FACP, FCCP, FCCM Professor of Clinical Medicine, University of California, Los Angeles, David Geffen School of Medicine; Chief, Division of Pulmonary and Critical Care Medicine, Vice-Chair, Department of Medicine, Olive View-UCLA Medical Center

Nader Kamangar, MD, FACP, FCCP, FCCM is a member of the following medical societies: Academy of Persian Physicians, American Academy of Sleep Medicine, American Association for Bronchology and Interventional Pulmonology, American College of Chest Physicians, American College of Critical Care Medicine, American College of Physicians, American Lung Association, American Medical Association, American Thoracic Society, Association of Pulmonary and Critical Care Medicine Program Directors, Association of Specialty Professors, California Sleep Society, California Thoracic Society, Clerkship Directors in Internal Medicine, Society of Critical Care Medicine, Trudeau Society of Los Angeles, World Association for Bronchology and Interventional Pulmonology

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women's Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society

Disclosure: Nothing to disclose.

Acknowledgements

Judith K Amorosa, MD, FACR Clinical Professor and Program Director, Department of Radiology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School; Consulting Staff, Department of Radiology, Robert Wood Johnson University Hospital

Judith K Amorosa, MD, FACR is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, Association of University Radiologists, Radiological Society of North America, and Society of Thoracic Radiology