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.


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.

Interstitial Lung Disease

*** In Progress *** Brandon Fainstad, MD

1. Describe common radiographic features of various interstitial lung disease
2. Identify distinguishing characteristics of the most common and reversible etiologies of interstitial lung disease

65 year-old-man presents to the ED with progressive shortness of breath and dry cough over the past 5 years that has accelerated in recent weeks to the point that he can no longer ambulate.  He denies fevers, chills, chest pain, weight changes, joint pain or skin changes.  Past medical history is notable for atherosclerotic disease with coronary and carotid stents placed 15 years ago, obesity, hypertension and OSA. Only medications are aspirin and a statin.  He has a 90 year tobacco pack year, quit 15 years ago. He is afebrile, HR 110bpm, BP 140/80 with SpO2 74% on room air, improved to 93% after 5 minutes on 100% non-rebreather.

Exam notable for increased work of breathing and diffuse lung crackles.


Diffuse, bilateral ground glass opacities with central densities.  Also notable for small lung volumes, apical emphysema, and traction bronchiectasis.


Follow this three step approach to describing radiographic lung changes:

1. Distribution

Apical vs. Basilar predominance

Central vs. Peripheral

2. Extent

Focal vs. Diffuse vs. Isolated Diffuse

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

e.g. UIP / IPF

Case 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. Chronic infection (e.g. necrotizing pneumonia, chronic aspiration, TB, ABPA etc.)
2. Poor airway clearance (e.g. cystic fibrosis or ciliary dysfunction)
3. Obstruction from malignancy or foreign body

Signet Ring

Case courtesy of A.Prof Frank Gaillard, From the case rID: 2587

Tram Tracking

Case courtesy of Dr Ian Bickle, From the case rID: 40909

Traction Bronchiectasis 
occurs when parenchymal scaring causes loss of lung volumes and “pulls” the airways apart

Courtesy of Dr. Brandon Fainstad

An irregularly bordered opacity – either dense or patchy

e.g. Pulmonary infarct – dense pleural based consolidation with surrounding ground glass opacity

Courtesy 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 metastases

Courtesy 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. Sarcoidosis

Courtesy 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 – silicosis

Case 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 opacity

Courtesy 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. NSIP

Courtesy of Brandon Fainstad, MD


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

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.