Life Beyond Medicine | Why I Write

I recently wrote a piece for our Life Beyond Medicine series explaining why running specifically, and physical activity more generally, is such a central part of my mental well-being as a resident. On writing it, however, I realised that something big was missing: Running is an important process for me, but I hadn’t spoken at all about writing, which is another essential part of how I make sense of the world and stay sane during my medical training.

When something scary, overwhelming, or exciting happens at work, the gears in my head start to turn, and I get the itch to sit in front of my computer and write. I may submit my story to a publication or publish it on my personal blog, This Liminal Space (, but just as often the story sits on my computer unread. I may open it once or twice, adding detail or editing, but more often the story remains unchanged on my hard drive after initial edits, a record of a difficult, joyous, sad, or angry time during my training.

The process of writing matters to me more than the content.  Here’s why:

  1. Writing helps me understand my own feelings.

After a public reading of a piece I had written, a friend paid me one of the highest compliments I had ever received. She said that I somehow knew how to put into words the feelings she didn’t know she had. I thanked her, but didn’t share something that was equally true: I often put into words feelings I don’t know I have. I find that process of writing that liberates my emotional experience. Sitting in front of a computer, picking and choosing words and phrases, lets me tap into an emotional experience I’m often not aware of. Understanding how I feel about something that has happened to me (or someone else) lets me deal with it productively, instead of letting it fester under the surface.


  1. Writing helps me understand the feelings of others.

If I’ve ever been in the thick of something emotional with you, you had better believe you’ve become a character in one of my stories. I may have been angry with you at the outset, but by the time I’ve finished writing, I’ve likely come to a better understanding of your actions. To write someone as a character means to try to find a way to understand his or her motivations and thought processes,. I like to write characters from the inside out, and that can involve some serious emotional work. Usually I come out with a better understanding of the players in my story, and consequently greater compassion and empathy than I had had before.


  1. Putting an experience down on paper takes the experience out of my head.

Have you ever heard the advice that you should write your worries on a piece of paper before you go to bed? It’s supposed to help you get to sleep. Something about writing out your worries takes away your need to think about them as you lay in bed. I don’t really understand how this works, but writing, more generally, seems to do the same for me. I may turn an experience over in my mind for hours, days, or weeks before I feel ready to write my thoughts down. Then, having written out the experience, I’ll stop thinking about it as intensely. That can be a huge relief! I’m not sure whether it’s because I’ve processed the experience, or because I’ve acknowledged my emotions, but there’s something magically stress-relieving about writing.

Not everyone is a natural writer (I’m not!), just like not everyone is a natural runner (again, I’m not!), but if you want to try writing, my best advice is to grab pen and paper (or your laptop), set a time limit (10 minutes is a nice place to start), and write about something you know (there are lots of writing prompts available online if you need a place to start). Like your cardiovascular system or your leg muscles, writing ability is something that is developed with practice. And don’t forget that editing is a magical thing – most writing doesn’t turn out great on the first try, even for experienced authors. So give it a shot! It’s cheaper than therapy and safer than drugs for dealing with the stressors of a life in medicine.

Reviewed by staff (Dr. Heather Murray)


Author information

Sarah Luckett-Gatopoulos
Sarah Luckett-Gatopoulos
Junior Resident Editor at BoringEM
Luckett is a resident at McMaster University. Newbie to the #FOAMed world. Interested in literacy, health advocacy, creative writing, and near-peer mentorship.

The post Life Beyond Medicine | Why I Write appeared first on BoringEM and was written by Sarah Luckett-Gatopoulos.

JellyBean 015 with David Anderson

David Anderson floats gracefully around the Twitterverse as @expensivecare

David Anderson is an eloquent and erudite individual that shares my interest with end of life care in the critical care world. He has a conspicuous interest in both Intensive Care and Palliative Care and the overlap. In fact this is possibly the person that I would most like to glide into my own ICU cubicle to tell me that I was about to die. (That’s a compliment.) We sat down and chatted with our respective comedy celtic accents while over in Middle Earth a while back. We are not promoting cigars. Really.

I love this guy. It’s not his sartorial elegance. It’s not his gorgeous accent. It’s not the fact that he has a very cool career; from Paramedic to Intensive Care. It’s his interest in the educational nirvana that is Lego.


(We’re not promoting penne alla arrabbiata either.)

JellyBean Large

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Management of Patients on Novel Oral Anticoagulants with Bleeding

Management of Patients on Novel Oral Anticoagulants with Bleeding

By Christie Sun MD
(EM Resident Physician, Georgetown University School of Medicine/Medstar Washington Hospital Center),

Maryann Mazer-Amirshahi PharmD MD/MPH
(Assistant Professor of Emergency Medicine, Georgetown University School of Medicine/Medstar Washginton Hospital Center)

Edited by Alex Koyfman MD (@EMHighAK) and Stephen Alerhand MD (@SAlerhand)


In recent years, novel oral anticoagulants (NOAC’s) have been introduced as therapeutic alternatives to warfarin, the gold standard for anticoagulation. These agents offer significant advantages over warfarin, including less drug and dietary interactions as well as no need for frequent therapeutic monitoring.1-4 There is also evidence that NOAC’s are as effective or even superior to warfarin in reducing the number of strokes and systemic embolic events in patients with atrial fibrillation.2-4 The major drawback to NOAC’s is that their anticoagulant effects are not easily reversed, which complicates the management of patients who present with bleeding, overdose, or with the need for urgent procedures.

Pharmacology and Physiology

NOAC’s currently approved in the U.S. fall into two categories: direct thrombin inhibitors (DTIs) and Factor Xa inhibitors. Dabigatran (Pradaxa®) is a DTI that is FDA-approved for the treatment of venous thromboembolism (VTE) and stroke prevention in the setting of non-valvular atrial fibrillation.5,6 It is a univalent DTI that binds to the active site of thrombin, preventing the conversion of fibrinogen to fibrin.5 Factor Xa inhibitors including rivaroxaban (Xarelto®) and apixaban (Eliquis®) are also approved for the prevention and treatment of VTE as well as stroke prevention. In January 2015, the FDA approved a third agent, edoxaban (Savaysa®). Factor Xa is made up of a prothrombinase complex and these agents bind to the active site of free Factor Xa as well as complex-bound forms to prevent the generation of thrombin.7

Clinical Presentation

The most significant adverse effect of these agents is the development of bleeding complications. Bleeding may present in a variety of clinical contexts, and may range from minor ecchymosis to life-threatening hemorrhage. The more common scenario is the patient who presents with spontaneous bleeding often in the setting of renal insufficiency, although intentional and unintentional overdoses do occur. Reported bleeding events include intracranial bleeding, epistaxis, hemoptysis, gastrointestinal bleeding, and hematuria.8

Diagnostic Testing

Diagnostic testing for patients presenting with bleeding who are currently taking a NOAC include a basic metabolic panel to determine renal function, baseline and serial complete blood counts, coagulation studies (PT/INR, aPTT), and a type and cross. Interpretation of routine coagulation studies can be difficult in these patients. DTI’s cause an increase in aPTT, but this relationship is not linear and there is a plateau effect at higher drug concentrations. PT can also be elevated in patients taking dabigatran, but measurements do not correlate with toxicity. More sensitive tests for DTI’s include the ecarin clotting time (ECT) and the dilute thrombin time (dTT); however, these tests are not routinely available in most institutions.9 Like DTI’s, factor Xa inhibitors can prolong PT and aPTT, but this does not correlate with clinical toxicity. Anti-factor Xa concentrations will be elevated in these patients. Specific modified anti-factor Xa concentrations correlate well with anticoagulation, but this assay is not routinely available.10 (Table)

Additional diagnostic testing is based on the clinical presentation. For patients with head trauma or altered mental status, a non-contrast head CT should be obtained. The patient should also be assessed for gastrointestinal bleeding and hematuria and other sources of bleeding as guided by history and physical examination. In the setting of an intentional overdose, diagnostic testing should also include evaluation for co-ingestions as indicated.

Interpretation of Laboratory Tests in Setting of NOAC Administration

NOAC chart


Patients taking NOAC’s that present with bleeding should be rapidly assessed and stabilized based on the degree of hemorrhage. For patients who present with significant blood loss and hemodynamic instability, packed red blood cell transfusion is indicated. Fresh frozen plasma (FFP) can be used as part of a balanced transfusion strategy but will not reverse coagulopathy. There are limited data evaluating the optimal reversal strategies for NOAC’s. Early consultation with specific subspecialties (gastroenterology, neurosurgery) may be indicated based on patient presentation. Although these medications are bound by activated charcoal, it is of little utility in overdose once bleeding has manifested and may impede endoscopy when indicated.9,11

There are limited options for the reversal of clinically significant bleeding in patients taking dabigatran. Prothrombin complex concentrates (PCC’s), which contain high doses of vitamin K dependent clotting factors as well as Protein C and S, may be effective for dabigatran reversal.11 Hemodialysis has also been shown to be effective in removal of dabigatran in patients with end-stage renal disease, but the benefit of dialysis in patients with normal renal function is controversial.12 There are also logistical concerns surrounding the risks of placing a large bore catheter in patients who are coagulopathic as well as the fact that patients with significant bleeding are often hypotensive and cannot tolerate hemodialysis. Recombinant activated factor VII (rVIIa), typically used in patients with hemophilia, has been raised as an option for non-hemophiliac patients with severe bleeding, but there are limited data supporting its use. Activated PCC (aPCC) also developed for hemophiliac patients, contains activated factors II, VII, IX and X, and has shown complete reversal of lab abnormalities.13 While there are dagibatran-specific reversal agents, they are currently being evaluated in clinical trials and are not yet available outside of study centers.14

In bleeding secondary to Factor Xa inhibitors, the mainstay of reversal is PCC’s. In one study, a single high dose of four factor PCC (factors II, VII, IX, X) reversed the PT prolongation caused by rivaroxaban.15 However, it is unclear if this reversal corresponds to a clinically significant reduction in hemorrhage. The half-lives of these agents may require repeat administration of PCC’s. Both three and four factor PCC’s are available in the U.S. and current data suggests four factor PCC’s may be more reliable in reversing coagulopathy; however, this data is primarily for warfarin reversal.16 There are limited, but promising data examining rVIIa in the reversal of lab abnormalities specifically due to rivaroxaban.17 While there are also specific antidotes currently being researched, none are currently available for commercial use in the U.S.


NOAC’s have significant therapeutic advantages over traditional warfarin therapy. However, these agents may cause life-threatening bleeding complications that are less easily reversed. When bleeding does occur, rapid stabilization, supportive care, and reversal of coagulopathy are the current mainstays of treatment.



References / Further Reading

  1. Wysowski DK, Nourjah P, Swartz L. Bleeding complications with warfarin use: a prevalent adverse effect resulting in regulatory action. Arch Intern Med 2007; 167:1414-19.
  2. Bruins Slot KM, Berge E. Factor Xa inhibitors versus vitamin K antagonists for preventing cerebral or systemic embolism in patients with atrial fibrillation. Cochrane Database Syst Rev 2013; 8:1-84.
  3. Mousa SA. Oral direct factor Xa inhibitors, with special emphasis on rivaroxaban. Anticoagulants, Antiplatelets, and Thrombolytics. Springer Science + Business Media 2010:181–201.
  4. Eikelboom JW, Weitz JI. New anticoagulants. Circulation 2010; 121:1523–32.
  5. Nisio MD, Middeldorp S, Buller HR. Direct thrombin inhibitors. N Engl J Med 2005; 353:1028-40.
  6. Cheng JW, Vu H. Dabigitran etexilate: an oral direct thrombin inhibitor for the management of thromboembolic disorders. Clin Ther 2012; 34:766-87.
  7. Samama MM. The mechanism of action of rivaroxaban — an oral, direct Factor Xa inhibitor — compared with other anticoagulants. Thromb Res 2011; 127:497-504.
  8. Haprer P, Young L, Merriman E. Bleeding risk with dabigatran in the frail elderly. N Eng J Med 2012; 366:864-66.
  9. van Ryn J, Stangier J, Haertter S. et al. Dabigatran exetilate-a novel, reversible, oral direct thrombin inhibitor: interpretation of coagulation assays and reversal of anticoagulant activity. Throb Haemost 2010; 103:1116-27.
  10. Samama MM, Contant G, Spiro TE, et al. Laboratory assessment of rivaroxaban: a review. Throm J 2013; 11:11.
  11. Siegal DM, Crowther MA. Acute management of bleeding in patients on novel oral anticoagulants. Eur Heart J 2013; 34:489-498b.
  12. Stangier J, Rathgen K, Stahle H, et al. Influence of renal impairment on the pharmacokinetics and pharmacodynamics of oral dabigatran etexilate: an open-label, parallel-group, single-centre study. Clin Pharmacokinet 2010; 49:259-268.
  13. Khoo TL, Weatherburn C, Kershaw G, et al. The use of FEIBA in the correction of coagulation abnormalities induced by dabigatran. Int J Lab Hematol 2013; 35:222-4
  14. Gomez-Outes A, Suarex-Gea ML, Lecumberri R, et al. Specific antidotes in development for reversal of novel anticoagulants: a review. Recent Pat Cardiovasc Drug Discov 2014; 9:2-10.
  15. Eerenberg ES, Kamphuisen PW, Sijpkens MK, et al. Reversal of rivaroxaban and dabigatran by prothrombin complex concentrate: a randomized, placebo-controlled, crossover study in healthy subjects. Circulation 2011; 124:1573-79.
  16. Voils SA, Baird B. Systematic review: 3-factor versus 4-factor prothrombin complex concentrate for warfarin reversal: does it matter? Thromb Res 2012; 130:833-40.
  17. Korber MK, Langer E, Ziemer S, et al. Measurement and reversal of prophylactic and therapeutic peak levels of rivaroxaban: an in vitro study. Clin Appl Thromb Hemost 2014; 20:735-40.

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Cardiac Output by Echo

Author: Tom Rozen
Peer reviewer: Lloyd Roberts

Measuring the cardiac output is straightforward, and relies on a few simple concepts which we review here:

  1. The Left Ventricular Outflow Tract (LVOT) is assumed to be roughly circular. Measure a diameter and you can calculate the area of the circle.
  2. Pulsed Wave Doppler (PW) through the same point, in the centre of the LVOT tells us how fast that blood is travelling at any  time.
  3. The area under the curve then tells us how far the column of blood has been pushed. (Y axis is in m/sec, X axis in seconds, so the area under the curve will tell us how far the blood has moved travelling at these velocities for this amount of time.)
  4. Work out the volume of the cylinder – Multiply the area of the LVOT (a circle) by the length the blood travels and you get the stroke volume (ie volume ejected per beat)
  5. The stroke volume multiplied by the heart rate gives us the cardiac output (expressed as L/Min).
  6. Divide the cardiac output by the body surface area and we get the Cardiac Index.

Summary of the required echo steps

Step 1

Measure the LVOT diameter (Parasternal long axis, 2D). Zoom in to be accurate. Measure up to 0.5cm back from the aortic valve leaflet insertion points (on the ventricular side).

Step 2

Using pulse wave Doppler (PW) line up the LVOT in the apical views, using either the apical 5 chamber or the apical 3 chamber.  Aim to be as close as possible to the aortic valve, but not into the area of flow acceleration. The flow of blood is laminar through the PW gate, which is why the all the velocities follow a narrow band and the PW waveform is not “filled in”. The PW gate should be 2-4mm.

Step 3

Obtain the PW waveform.  To get the most accurate reading, move sample volume toward aortic valve until flow accelerates. Then move sample volumes slightly away from the aortic valve, toward apex until laminar flow returns.

In a surface echo, the blood flows through the LVOT away from the probe so the curve is below the line. It should look hollow if the blood has laminar flow. Trace along the edge of the modal velocity (the outside of the chin, not the beard of the waveform) to measure the area under the curve (the Velocity Time Integral – VTI expressed in cm).


(First published on Echopraxis by Tom Rozen on 20/02/2014; reviewed by Lloyd Roberts)

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Subarachnoid Hemorrhage with Increased Intracranial Pressure

This case was written by Dr. Martin Kuuskne from McGill University. Dr. Kuuskne is a PGY4 Emergency Medicine resident and one of the editors-in-chief at EMSimCases.

Why it Matters

This case highlights three important aspects of the management of a subarachnoid hemorrhage:

  • Blood pressure control in an undifferentiated neurologic catastrophe
  • Safe approaches to intubating a patient with possible acute hydrocephalus
  • Management of a patient demonstrating signs of increased intracranial pressure

Clinical Vignette

You are working an evening shift at a tertiary care centre emergency department with full surgical capabilities. A patient is brought into the resuscitation area by ambulance with decreased mental status. The patient was at the gym lifting weights; he complained of an acute headache to his friend and suddenly fell to the ground. The patient remained unconscious with sonorous breathing. The ambulance was called.

Case Summary

A 45-year-old male who suffered an aneurysmal subarachnoid hemorrhage while weightlifting presents to the emergency department requiring intubation for airway protection and develops acute hydrocephalus requiring ICP lowering maneuvers before definitive surgical management.

Download the case here: SAH Case

ECG for case found here:

Deep cerebral t-wave inversions

(ECG source:

CXR for case found here:

Post Intubation

Post Intubation CXR

(CXR source:

Swollen finger? Take a bath!

Dr. Gordon presents a case of a swollen finger worth reviewing.

POCUS is becoming extremely useful at investigating these patients as it allows great visualization of the tendon and sheath showing lacerations, foreign bodies and infection.  Being a dynamic exam, you can have the patient move their digits and watch the tendons slide.

An important trick is to consider use of a water bath to immerse the affected area.  The probe is then floated in the water above.  This provides an acoustic “step off” for improved image quality and the patient can easily move the finger while the probe hovers above.


This young man probably had micropunctures with sharp plastic at work 2 days ago. He presented with a painful, somewhat red, swollen finger mainly proximally near the PIP joint. Movement and pressure were painful. Sounds like tenosynovitis. Still it can’t hurt (me) to look. POCUS revealed no joint fluid but did reveal fluid along the flexor tendons. So it looks like flexor tenosynoivitis, too.


For bonus points can anyone identify what is likely the A3 pulley/annular ligament?FlexTend