Community Case: Not Your Average Fainting Spell

A 36-year-old woman came into the ED by EMS with multiple ‘fainting spells’ throughout the day (her family thought it was because her blood sugar was low at 83 when they checked at home and treated with glucagon and candy).  I was handed this EKG by the receiving nurse:

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I walk into the Trauma Room to find a woman who is awake, alert, diaphoretic, and talking. I get handed this next EKG:

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Moments later the patient becomes suddenly unresponsive and this is what we see:

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Torsades de Pointes (TdP) = Polymorphic V Tach (PVT) + Long QT

So then what did we do?

*   Gave Magnesium 2 mg IV bolus x 2 immediately

*   iSTAT showed K 2.6 so started aggressive repletion, placed central venous access to increase rate of safe repletion

*   Started Magnesium drip, gave magnesium bolus PRN anytime there were prolonged runs of TdP

*   Gave lidocaine bolus 100 mg (dose can range from 0.5 to 0.75 mg.kg up to 1 to 1.5mg/kg)

*   Shocked patient three times (during prolonged runs of TdP associated with unresponsiveness):

Blue arrow indicates defibrillation; return of NSR afterward

Blue arrow indicates defibrillation; return of NSR afterward

*   Gave isoproterenol after confirming no history LQTS or prior prolonged QTc on prior EKGs (initial dose 0.05 to 0.1 mcg/kg/min in children and 2 mcg/min in adults)

*   She was transferred to the cardiology service in good condition, awake and alert

Torsades de Pointes ECG Pearls:

·      Long QT + PVT with characteristic morphology that seems to twist around isoelectric line

·      QT interval is inversely proportional to heart rate (HR)

o   The QT shortens at faster HR

o   The QT lengthens at shorter HR

o   There are formulas to calculate the QT interval (https://lifeinthefastlane.com/ecg-library/basics/qt_interval/)

·      TdP with HR >220 more likely to degenerate into VF

·      Bigeminy in a patient with known LQTS may herald imminent TdP:

This was the prehospital EKG

This was the prehospital EKG

Presence of abnormal giant T-U waves may also precede TdP.

Pathophysiology of TdP:

·      A prolonged QT reflects prolonged myocyte repolarization due to ion channel malfunction

·      This prolonged repolarization period also gives rise to early-after-depolarizations (EADs)

·      EADs may manifest on ECG as tall u waves; if these reach threshold amplitude, they may manifest as PVCs

·      TdP is initiated when a PVC occurs during a preceding T wave, known as ‘R-on-T’ phenomena

·      The onset of TdP is often preceded by a sequence of short-long-short PR intervals, so called ‘pause-dependent’ TdP with longer pauses associated with faster runs of VT

Clinical Significance:

·      TdP is often short lived and self-terminating, however can be associated with hemodynamic instability and ultimately may degenerate into ventricular fibrillation

·      If it does not spontaneously convert and the patient is unstable, it will need defibrillation

·      QT prolongation may be acquired and occur secondary to multiple drug effects, electrolyte abnormalities, medical conditions, or congenital long-QT syndrome (LQTS)

·      Recognizing the cause of TdP (acquired vs. congenital) allows initiation of specific treatment strategies

*   Defibrillation if unstable

*   Give magnesium (Mg 2-4 grams IV push followed by Mg drip of 3-10 mg/minute)

*   Removal of offending agent in acquired long QT

*   Correct any electrolyte abnormalities (especially hypoMg, hypoK, hypoCa)

*   Correct contributing factors such as respiratory alkalosis (which can worsen hypoK, etc)

*   Remove any offending agents (such as certain anti-arrhythmics, antibiotics, anti-emetics, psychotropics, or methadone)

*   Lidocaine may help because it can suppress PVCs, and therefore stop the R-on-T phenomena

*   Overdrive Pacing (usually at a rate of 100 bpm due to heart rate dependent effects of QT)

*   Only in acquired long QT: beta-adrenergic stimulation with isoproterenol

*   Only in LQTS: give beta-blockade (start with esmolol, then propranolol if not effective)

*   Patients with LQTS may require permanent pacing and ICD

*   Amiodarone may be harmful because it lengthens the QT interval and can possibly cause PVCs (although amiodarone has never been specifically shown to cause Torsades)

ACC/AHA/ESC Guidelines:

The 2006 American College of Cardiology/American Heart Association/European Society of Cardiology (ACC/AHA/ESC) guidelines for the management of ventricular arrhythmias and the prevention of SCD addressed the management of TdP in the setting of acquired LQTS:

*   Intravenous magnesium

*   Temporary pacing

*   Isoproterenol

References:

· Up To Date: https://www.uptodate.com/contents/acquired-long-qt-syndrome?source=search_result&search=torsades%20de%20pointes&selectedTitle=1~150

· Life In the Fast Lane: https://lifeinthefastlane.com/ecg-library/basics/qt_interval/

· HQMedEd:   http://hqmeded-ecg.blogspot.com/2013/10/polymorphic-ventricular-tachycardia.html

https://en.wikipedia.org/wiki/Torsades_de_pointes

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Faculty Reviewer: Dr. Kristina McAteer

AEM Early Access 06: Gender and Racial Disparities Among Academic Emergency Medicine Physicians

Welcome to the sixth episode of AEM Early Access, a FOAMed podcast collaboration between the Academic Emergency Medicine Journal and Brown Emergency Medicine. Each month, we'll give you digital open access to an AEM Article in Press, with an author interview podcast and suggested supportive educational materials for EM learners.

Find this podcast series on iTunes here.

           A FOAM Collaboration: Academic Emergency Medicine Journal and Brown EM

           A FOAM Collaboration: Academic Emergency Medicine Journal and Brown EM

LISTEN NOW: Author INTERVIEW WITH DR. TRACY MADSEN

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Dr. Tracy Madsen

Assistant Professor, Division of Sex and Gender in Emergency Medicine (SGEM)

Department of Emergency Medicine

Alpert Medical School, Brown University

Full text of this month's article (open access through November 1, 2017): Click below

Tracy E. Madsen, et al., “Current Status of Gender and Racial/Ethnic Disparities Among Academic Emergency Medicine Physicians,” A Joint 2015 Report by Academy for Women in Academic Emergency Medicine (AWAEM), Academy for Diversity & Inclusion in Emergency Medicine (ADIEM) and Academy of Administrators in Academic Emergency Medicine (AAAEM).

ARTICLE SUMMARY:

Objective: A 2010 survey identified disparities in salaries by gender and underrepresented minorities.  With an increase in the EM workforce since, the authors aimed to 1) describe the current status of academic EM workforce by gender, race and rank, and 2) evaluate if disparities still exist in salary or rank by gender.

Methods: Information on demographics, rank, clinical commitment, and base and total annual salary for full-time faculty members in U.S. academic EDs was collected in 2015 by the Academy of Administrators in Academic Emergency Medicine (AAAEM) Salary Survey.  Multiple linear regression was used to compare salary by gender while controlling for confounders.

Results:

  • Response rate was 47% for 1371 full-time faculty

  • 33% were women

  • 78% White, 4% Black, 5% Asian, 3% Asian Indian, 4% other, and 7% unknown race

  • White vs nonwhite race:

    • 62% vs 69% instructor/assistant

    • 23% vs 20% associate

    • 15% vs 10% full professors

  • Women vs men (p<0.05):

    • 74% vs 59% instructor/assistant

    • 19% vs 24% associate

    • 7% vs 17% full professors

    • 37% vs 31% fellowship trained

    • 59% vs 64% Core Faculty

    • 47% vs 57% had administrative roles

    • 1069 vs 1051 clinical hours worked

  • 15% of 113 Chair/Vice-Chair positions were women, 18% were nonwhite race

  • Mean salary: $278,631

    • Mean salary of women was $19,418 less (SD +/- $3,736, p<0.001) even after adjusting for race, region, rank, years of experience, clinical hours, core faculty status, administrative roles, board certification, and fellowship training

Conclusions: In 2015, disparities in salary and rank persist among full-time U.S. academic EM faculty, even after controlling for key factors that have been speculated to contribute to salary differences, such as rank, clinical hours, and training.  There were also gender and underrepresented minority disparities in rank and leadership positions.  Future efforts should focus on evaluating salary data by race and developing system-wide practices to eliminate disparities.

Suggestions for further reading:

Jena AB, Olenski AR, Blumenthal DM, A S, P U, R J. Sex Differences in Physician Salary in US Public Medical Schools. JAMA Intern Med. 2016;176(9):1294. 

Heron SL, Lovell EO, Wang E, Bowman SH. Promoting Diversity in Emergency Medicine: Summary Recommendations from the 2008 Council of Emergency Medicine Residency Directors (CORD) Academic Assembly Diversity Workgroup. Acad Emerg Med. 2009;16(5):450-453. 

Choo EK, Kass D, Westergaard M, et al. The Development of Best Practice Recommendations to Support the Hiring, Recruitment and Advancement of Women Physicians in Emergency Medicine. Pines JM, ed. Acad Emerg Med. June 2016. 

Faculty Editor/Reviewer: Dr. Gita Pensa 

Podcast credits: Intro/exit music by Scott Holmes and freemusicarchive.org. Also featuring "Money", Pink Floyd, from The Dark Side of the Moon.

Ultrasound Case of the Month

Case: Submitted by Dr. Sam Goldman

This is an 83-year old woman with a history of prior abdominal surgeries presenting to the ED as a transfer from her SNF with increasing abdominal distention. Patient has not had a bowel movement in four days although endorses passing occasional flatus. She denies emesis though endorses nausea, hiccupping, and burping. She denies any abdominal pain, fevers, chills, dysuria or urinary frequency. 

Diagnosis:

Small Bowel Obstruction

Image was acquired with the curvilinear probe, but any high penetration probe (eg curvilinear of phased array probe) can also be used.  Multiple regions of the abdomen should be interrogated when evaluating for SBO.

What are we looking for with abdominal US for SBO?

When evaluating for an SBO, we are looking for fluid filled small bowel loops >2.5-3cm in width. You maybe more likely to see an increase in intestinal contents (fluid and echogenic materials) and you may see to-and-fro or whirling of the intestinal contents. In more severe cases, you may see bowel wall thickening (greater than 3mm) and free fluid which is extraluminal. pSBO may be more difficult to evaluate with the US machine.   

What do we see in this video?

  • Dilated loops of bowel > 2.5cm measured outer wall to outer wall (most sensitive and specific finding). 
  • Bidirectional flow of bowel contents (to and fro or whirling)
  • Visualization of plicae circularis (“keyboard sign”)

How good is U/S for Detecting SBO?

Ultrasound is superior to abdominal plain films and approaches the sensitivity and specificity of CT scan in many cases. 

Sensitvity Specificity
Abdominal Films 66-77% 50-57%
CT 92% 93%
Ultrasound 88% 96%

Faculty Reviewer: Dr. Kristen Dwyer

References

(Mallo RD, et al. Computed tomography diagnosis of ischemia and complete obstruction in small bowel obstruction: a systematic review. Journal Gastrointestinal Surgery. 2005. May-Jun;9(5):690-4.)

(Ogtata M, et al. Prospective Evaluation of Abdominal Sonography for the Diagnosis of Small Bowel Obstruction. Annals of Surgery. 1996. 23(3):237-241.) 

Additional resources:

Podcast on US of SBO from www.ultrasoundpodcast.com: Episode 36 - Small Bowel Obstruction - Ultrasound Podcast

Great view of Plicae Circularis (“Keyboard Sign”) from Emory University