Venous Thromboembolism (VTE)

Meagan Wong, MD
Brandon Fainstad, MD
David Garcia, MD – expert review (hematologist, University of Washington)

1. Determine IF a venous thromboembolus warrants anticoagulation versus further evaluation.
2. Determine WHERE anticoagulation should be initiated, inpatient or outpatient.
3. Select WHICH anticoagulation agent to use.
4. Develop a framework for determining HOW LONG to anticoagulate.


VTE Teacher’s Guide
VTE Learner’s Handout

Initial management of venous thromboemboli (VTE) depends on vascular location, an individual’s ongoing thrombosis risk and their risk of bleeding. We will work through four separate cases and in the process, answer four basic questions: 1. IF the thrombus should be treated with anti-coagulation, 2. WHERE the anti-coagulation should be initiated, 3. WHAT is the most appropriate long-term agent and 4. HOW LONG to anti-coagulate.

Board Set-up:

Stage 1 – IF (Should you start immediate anti-coagulation)?

Case A
A 45-year-old man involved in a motor vehicle accident suffers a right humerus fracture and multiple rib fractures along with a tension pneumothorax. He is admitted to the surgical ICU following surgery and chest tube placement. On hospital day five, the anticipated day of discharge, he is noted to have a slightly swollen ankle. A venous duplex study reveals an acute 2cm non-occlusive DVT in his posterior tibial vein without any proximal thrombi identified. He is ambulating independently and expected to spend the majority of the day out of bed over the subsequent weeks.

How would you classify this VTE? Do you want to initiate anticoagulation?

Case B

An 82-year-old man with COPD and recent diverticular bleed presents to the ED with increased shortness of breath and left-sided pleuritic chest pain. HR is 95bpm, BP 120/80 and SpO2 92%. His ECG reveals sinus tachycardia and CXR with slightly increased lung volumes but otherwise unremarkable. He is found to have multiple left-sided segmental PEs on a chest CTA. He denies any recent history of prolonged travel, surgery or immobility.

How would you define this VTE? Do you want to initiate anticoagulation?

Case C

A 38-year-old woman presents to the ED with three days of right-sided chest pain and shortness of breath. She is afebrile, HR 100bpm, BP 110/75, SpO2 94%. Her CXR, ECG, and troponins are unremarkable. A CT PE reveals two sub-segmental PEs in the right lower lung base. When asked, she admits to possibly having slight swelling in her right leg last week. She denies any recent history of prolonged travel, immobilization or surgery. She is pre-menopausal and not on hormonal birth control. Her mother had an unprovoked VTE at age 48, it is unknown if she has an inheritable hypercoagulation mutation.

How would you define this VTE? Do you want to initiate anticoagulation?

Case D

A 65-year-old man with prostate cancer metastatic to his spine presents to clinic with increased swelling and mild pain in his LEFT leg over the past week. The RIGHT leg is unchanged, and he is still able to walk on both feet. He denies shortness of breath, orthopnea/PND, significant weight gain, fevers or chills. He lives with his wife who is healthy and available to take care of him 24/7. A lower extremity duplex reveals an acute occlussive DVT in the left common femoral vein.

How would you define this VTE? Do you want to initiate anticoagulation?

Stage 2 – WHERE (to initiate treatment)?

Case A?

Case B?

Case C?

Case D?

Stage 3 – WHICH (anticoagulation agent)?

Stage 4 – HOW LONG (to treat)?

Case A?

Case B?

Case C?

Case D?

Final Board



Kearon, Clive, et al. “Antithrombotic Therapy for VTE Disease.” Chest, vol. 149, no. 2, 2016, pp. 315–352., doi:10.1016/j.chest.2015.11.026.

Aujesky, Drahomir, et al. “Derivation and Validation of a Prognostic Model for Pulmonary Embolism.” American Journal of Respiratory and Critical Care Medicine, vol. 172, no. 8, 2005, pp. 1041–1046., doi:10.1164/rccm.200506-862oc.

Stevens, Scott M., et al. “Guidance for the Evaluation and Treatment of Hereditary and Acquired Thrombophilia.” Journal of Thrombosis and Thrombolysis, vol. 41, no. 1, 2016, pp. 154–164., doi:10.1007/s11239-015-1316-1.

Raskob, G. E., et al. “Edoxaban for the Treatment of Cancer-Associated Venous Thromboembolism.” New England Journal of Medicine,378(7), 2018, pp. 615-624. doi:10.1056/nejmoa1711948

Young, Annie M., et al. “Comparison of an Oral Factor Xa Inhibitor With Low Molecular Weight Heparin in Patients With Cancer With Venous Thromboembolism: Results of a Randomized Trial (SELECT-D).” Journal of Clinical Oncology, vol. 36, no. 20, Oct. 2018, pp. 2017–2023., doi:10.1200/jco.2018.78.8034.

Approach to Interstitial Lung Diseases

Interstitial Lung Disease

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Brandon Fainstad, MD – author
Diana Zhong, MD – edits
Cameron Baston, MD – expert review (pulmonologist, University of Pennsylvania)

1. Describe the typical radiographic features (distribution, extent, and characteristics) in common interstitial lung diseases.
2. Utilize a four-step approach to differentiate the common interstitial lung diseases.

** This talk takes ~60 minutes.  Consider breaking it up into two sections: 1. Case stem + terminology and 2. Differentiation of ILDs + case resolution. **

This talk was designed to provide learners with a framework for describing and interpreting imaging findings of ILD within a basic clinical context.  It is by no means a comprehensive approach to ILD, but should be a good place to start.  It  is intended to be delivered directly from the computer monitor or projector.  Due to the reliance on clinical images it is difficult to reproduce on a whiteboard.  Have a learner read the case and describe the chest imaging.  A formal interpretation is given below the images.  Next, review the proposed three-step process for describing lung findings and go through the images and explanations of the key characteristics detailed below.  After the learners are familiar with the terminology outline the four-step approach to narrowing the differential for ILD.  This approach focuses on what is most common, testable and treatable before attempting to tackle the idiopathic interstitial diseases and more rare ILDs. 

A 77 yo M presents with two months of nonproductive cough and exertional dyspnea. He denies any chest pain, orthopnea or lower extremity edema. He denies URI symptoms, fevers/chills or recent sick contacts. At baseline, he is able to walk several miles without difficulty and now is limited to < 1 city block. His PMH is notable for paroxysmal atrial fibrillation for which he has been on warfarin and amiodarone for several years. He also has an AICD for his history of non-ischemic cardiomyopathy (most recent EF of 40%).

There is diffuse basilar predominant fibrosis and ground glass opacities without honeycombing along with traction bronchectasis seen best on the coronal image in the left base. 

TERMINOLOGY - Follow this three-step approach to describing lung disease

1. Distribution

Apical vs. Basilar predominance
Central vs. Peripheral

2. Extent

Focal vs. Diffuse vs. Isolated
Dense vs. Patchy

3. Characteristics

Gray and hazy area with intact airway and vessel structures 
Non-specific finding that could represent:
1. Atalectasis, including normal exhalation
2. Alveolar filling
3. Interstitial thickening

e.g. Amioderone toxicity
   Case courtesy of A.Prof Frank Gaillard, From the case rID: 6539

Clustering or stacking of well defined cysts, usually at the bases and periphery
Usually represents irreversible interstitial scaring/fibrosis

e.g. UIP / IPFCase courtesy of Dr Ahmed Abdrabou, From the case rID: 25270

Abnormal dilation of the airways.
Defined as an airway being larger than it’s accompanying vessel (signet ring) and will have linear and parallel airways (tram tracking) rather than taper towards the periphery.Usually a result of chronic airway inflammation from:
1. Recurrent infection (e.g. necrotizing pneumonia, chronic aspiration, TB, ABPA, immune deficiency, etc.)
2. Poor airway clearance (e.g. cystic fibrosis or ciliary dysfunction)
3. Obstruction from malignancy or foreign body

e.g. “Signet Ring”Case courtesy of A.Prof Frank Gaillard, From the case rID: 2587

e.g. “Tram Tracking”Case courtesy of Dr Ian Bickle, From the case rID: 40909


e.g. traction bronchiectasis 
Occurs when parenchymal scaring causes loss of lung volumes and “pulls” the airways apartCourtesy of Dr. Brandon Fainstad

An irregularly bordered opacity – either dense or patchy

e.g. Pulmonary infarct – dense pleural-based consolidation with surrounding ground glass opacityCourtesy of Lauren Brown, MD

Well-circumscribed density (opposed to consolidation, ill-defined) that is less than 3cm (opposed to a mass, >3cm).

e.g. Pulmonary metastasesCourtesy of Lauren Brown, MD

Hilar Lymphadenopathy
Hilar “fullness” is often due to enlarged pulmonary arteries or lymphadenopathy.  This case is distinctly lymphadenopathy based on the bulbous appearance that does not taper peripherally as a vessel would.

e.g. SarcoidosisCourtesy of Lauren Brown, MD

Lymphatic and hematogenous spread of disease.  Small opacities located in the subpleura, fissues, intralobular Septa and often coalesce into a faint gray that can be mistaken as ground glass opacities.

e.g. lymphagitis carcinomatosis

Case courtesy of A.Prof Frank Gaillard, From the case rID: 8530

Small opacities along airways that spare the periphery

e.g. pneumoconioses – silicosisCase courtesy of A.Prof Frank Gaillard, From the case rID: 12515

Extending from the pleura inward
Either a direct extension of the pleura (e.g. mesothelioma) or a hematogenous process that terminated with greatest effect in the periphery (e.g. pulmonary infarct).

e.g. Pulmonary infarct – dense pleural based consolidation with surrounding ground glass opacityCourtesy of Lauren Brown, MD

Margin of unaffected lung along the pleura

In direct contrast to pleural-based opacities, sub-pleural sparing describes an thin area of unaffected parenchyma along the periphery of the involved lobe.  This is a relatively specific, but not sensitive, finding for Non-Specific Interstitial Pneumonia (NSIP) and can help differentiate it from IPF.  

e.g. NSIPCourtesy of Brandon Fainstad, MD


Start by ruling out the most common, easily testable and easily treatable conditions.  After that, you are left with idiopathic interstitial pneumonias (IPP) and the very rare conditions.  

1. Is it sarcoidosis?

2. Obtain a good exposure history.

3. Rule out collagen vascular related disease with serologies.

4. If none of the above, it is likely an IPP.  Obtain a biopsy.  If it is acute, consider urgent immunosuppression. 

Approach to Interstitial Lung Diseases

The history of sub-acute and progressive respiratory symptoms in the setting of ongoing amiodarone use and basilar predominant fibrosis without honeycombing is most consistent with amiodarone-associated NSIP.  This was confirmed by biopsy which lacked histology typical of UIP.  The patient stopped taking amiodarone and was treated with a prolonged taper of steroids.  He recovered to his prior baseline with minimal to no residual disease on imaging:


Weissleder R, Wittenberg J, Harisinghani MG et-al. Primer of diagnostic imaging. Mosby Inc. (2007) ISBN:0323040683.

Schwaiblmair, Martin. “Drug Induced Interstitial Lung Disease.” The Open Respiratory Medicine Journal, vol. 6, no. 1, 2012, pp. 63–74., 

Crystal, RG. Interstitial lung disease. In: Wyngaarden, JB, Smith, LH, Jr, Bennett, JC, (Eds), Cecil Textbook of Medicine, 19th ed, WB Saunders Co, Philadelphia, 1992

Wide Complex Tachycardia

Nathan Cade, MD
Brandon Fainstad, MD
Andrew Prouse, MD

1. Identify the basic electrophysiology of the four causes of wide complex tachycardia.
2. Develop a simple framework for acute management of wide complex tachycardia.
3. Practice three cases with ECGs to differentiate ventricular tachycardia from other causes and determine the correct initial management.


Wide complex tachycardias are uniquely challenging due to the difficulty in interpreting the ECG and the need for immediate management.  Fortunately, there are only a handful of potential rhythms and a few options for management.   If you remember nothing else, remember this:

  1. Unstable -> SHOCK (synchronized cardioversion)
  2. Stable ->
    1. Place defibrillation pads
    2. If regular and monomorphic, attempt vagal maneuvers or adenosine
    3. If it is irregular and suspicious for atrial fibrillation with aberrancy, attempt rate control
    4. If it doesn’t work, consciously sedate and cardiovert.
    5. If conscious sedation is not a safe option, try procainamide.

CHALK TALK – 15 min
Board Set-up:

Stage 1 – Electrophysiology

Stage 2 – Management

Final Board

PRACTICE CASES – 10-15 min

Case 1
A 65-year-old man with a recent MI presents to the ED complaining of palpitations. He is cognitively intact without lightheadedness and has palpable pulses.

Courtesy of Andrew Prouse, MD

What is the rhythm?
How do you want to manage it?

Case 2
26-year-old male with chest pain and SOB and no history of structural heart disease. Hemodynamically stable.

Adapted with permission of Dr. Smith’s ECG blog,

What is the rhythm?
How do you want to manage it?

Case 3
A 60-year-old woman presents to the ED with fever, cough, and shortness of breath found to have the following ECG. She is tachycardic but has a normal blood pressure and cognitively intact. There is no prior ECG available for comparison.

Adapted with permission from Dr. Smiths ECG Blog (

What is the rhythm?
How do you want to manage it?



Ortiz M et al. Randomized Comparison of Intravenous Procainamide vs. Intravenous Amiodarone for the Acute Treatment of Tolerated Wide QRS Tachycardia: the PROCAMIO Study. Eur Heart J 2016.

Smith, Stephen W. “An Irregularly Irregular Wide Complex Tachycardia.” Dr. Smith’s ECG Blog, Aug. 2017,

Lazoff, Marjorie, et al. “VT versus SVT with Aberrancy.” LITFL • Life in the Fast Lane Medical Blog, 3 Sept. 2018,

Garner, John B, and John M Miller. “Wide Complex Tachycardia – Ventricular Tachycardia or Not Ventricular Tachycardia, That Remains the Question.” Arrhythmia & Electrophysiology Review, vol. 2, no. 1, 2013, p. 23., doi:10.15420/aer.2013.2.1.23.