UCONN Emergency Medicine Interest Group

Archive for October, 2011|Monthly archive page

Journal Article Synopsis: Apixaban and ACS

In JOURNAL CLUB on October 30, 2011 at 7:00 AM

Summary of “Apixaban with Antiplatelet Therapy after Acute Coronary Syndrome” by John Alexander et. al, New England Journal of Medicine ePub ahead of print: July 24th 2011: pp. 1-10

What is already known on this topic:
Patients with acute coronary syndromes frequently have recurrent ischemic events despite the use of currently recommended antiplatelet therapy, revascularization procedures, and other evidence based secondary preventative measures. Anticoagulation therapy with oral vitamin K antagonists reduces the recurrence of ischemic events following MI however, when added to aspirin or aspirin and clopidogrel combined it increases the risk of bleeding. Previous studies of the use of the factor Xa inhibitor apixiban were conducted in patients who had recent acute coronary syndrome and were receiving aspirin or aspirin and clopidogrel. Treatment with apixiban resulted in dose related increase in bleeding with a trend towards fewer ischemic events.

What question this study addressed:
Does the benefit of adding apixiban to standard acute coronary treatment outweigh the increased risk of bleeding in high-risk patients?

What was the study design:
The Apixiban for Prevention of Acute Ischemic Events 2 (APPRAISE-2) trial was a double blind, placebo-controlled, randomized clinical trial conducted at 858 sites in 39 countries. Patients included in this study must have had an acute coronary syndrome (myocardial infarction, with or without ST-segment elevation, or unstable angina) within the previous 7 days, with symptoms of myocardial ischemia lasting more than 10 minutes with the patient at rest plus either elevated cardiac biomarkers or dynamic ST-segment elevation or depression of 0.1mV or more. Patients meeting these criteria were eligible for the study if their condition was clinically stable and they were receiving standard treatment for acute coronary syndrome, including aspirin or aspirin and any P2Y12-receptor antagonist. Eligible patients were also required to have two high-risk characteristics which included: an age of at least 65 years, diabetes mellitus, MI within the previous 5 years, cerebrovascular disease, peripheral vascular disease, clinical heart failure or a left ventricular ejection fraction of less than 40% in association with the index event, impaired renal function with a calculated creatinine clearance of less than 60ml per minute, and no revascularization after the index event.

What this study adds to our knowledge:
Administration of apixiban at a dose of 5mg twice daily in high risk patients taking either aspirin or aspirin plus clopidogrel significantly increases bleeding events, including events of fatal and intracranial bleeding, without significant reduction in recurrent ischemic events.

How this is relevant to clinical practice:
The current standard of care for patients after acute coronary syndrome includes dual antiplatelet therapy, usually with aspirin and clopidogrel. Even with this aggressive antiplatelet therapy patients still frequently experience recurrent ischemic events. Newer P2Y12 antagonists are more potent and provide additional reductions in ischemic events and mortality but at the cost of increased risk of bleeding. The combination of antiplatelet and anticoagulant therapy seems attractive, yet it may pose an unacceptable risk of bleeding.

Other considerations:
The population included in the study comprised only high-risk patients, with large proportions of those patients having diabetes, heart failure, or renal insufficiency. The lack of significant reduction in recurrent ischemic events could partially be a product of such a high-risk population. As the authors noted, there may be other patient populations for which the results may be different.


Ultrasound Case #5

In RADIOLOGY on October 23, 2011 at 7:00 AM

Syndicated from the UCONN EM Residency website; credit to Dr. Russell and Dr. Kleinberg for cases and images.

Gallbladder wall

Common bile duct

CC: Abdominal pain – RUQ

HPI: 25 yo female with no PMH presents to the ED with nausea, vomiting and abdominal pain beginning the previous evening ½ hour after eating dinner.  Pain located in RUQ, 10/10 intermittent colicky pain.  Denies any fevers, chills, diarrhea, constipation, urinary symptoms or anorexia.

SH: Smokes 1.5 pack year history, denies other drugs or alcohol.

FH: DM2, HTN, Hyperlipidemia, Colon Cancer

PE: Afebrile, VSS
Abdomen is obese, soft, non-distended, tender in RUQ, + murphy’s sign, + bowel sounds

Labs: WBC’s14.9 with left shift.  H/H, Platelets and Chem7, AST, ALT, lipase and bilirubin within normal limits.  Alk Phos 141.

Bedside U/S: see above images.

How would you describe the ultrasonographic findings?

Read the rest of this entry »

Upcoming meeting

In ANNOUNCEMENTS on October 19, 2011 at 11:49 AM

The next EMIG meeting has been scheduled for Monday, October 24th from 6-8 PM at Dr. Smalley’s. Further details available by contacting lburns@up.uchc.edu. Presenters will be Colin Huguenel, MSIV and Dr. LaSala.

Hazmat-Suit Up!

In DAY IN THE LIFE on October 18, 2011 at 8:18 PM

UCONN EM PGY 2’s train for potential hazardous exposure situations!

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Journal Article Synopsis: Vascular Access during Out-of-Hospital Cardiac Arrest

In JOURNAL CLUB on October 16, 2011 at 8:00 AM

Summary ofJournal Article Synopsis: Intraosseous Versus Intravenous Vascular Access During Out-of-Hospital Cardiac Arrest: A Randomized Controlled Trial,” Reades, Rosalyn, MD; Studnek, Jonathan R., PhD, NREMT-P; Vandeventer, Steven, EMT-P; Garret, John, MD.  Annals of Emergency Medicine. 2011 Aug 17. [Epub ahead of print]

What is already known on this topic:
Intraosseous vascular access was originally used mainly in children.  However, it has recently been shown that this method is also a rapid and effective way to obtain vascular access in the adult population, especially when a peripheral intravenous line fails.  Therefore, this technique is used commonly in out-of-hospital settings when rapid vascular access is needed during cardiac arrest.  Emergency Medical Services (EMS) protocols in the US list sternal, humeral, and tibial locations as available sites for intraosseous vascular access.

What question this study addressed:
The humeral and tibial locations are better sites during cardiac arrest due to constant chest compressions.  However, data regarding the effectiveness of the humeral site versus the tibial site are limited.  This study assessed the frequency of first-attempt success between humeral intraosseous, tibial intraosseous, and peripheral intravenous routes during out-of hospital cardiac arrest.

What was the study design:
This study was a prospective, nonblinded, triple-arm, randomized control trial of 182 adult patients over 18 years of age experiencing a non-traumatic out-of-hospital cardiac arrest in which resuscitation was initiated.  Patients were randomized to one of 3 vascular access routes: tibial intraosseous, humeral intraosseous, or peripheral intravenous.  Paramedics received extensive training in each method.  The outcome measure was first-attempt success, defined as secure needle position in the marrow cavity or a peripheral vein with normal fluid flow.  If a needle dislodged, it was considered a failure.

What this study adds to our knowledge:
Tibial intraosseous vascular access was determined to be the optimal method with regards to highest success rate and fastest time to access.  However, peripheral intravenous access was associated with a higher volume of infused fluid.

How this is relevant to clinical practice:
Tibial intraosseous vascular access is beneficial for patients in who are in cardiac arrest or unconscious and who are unlikely to need large-volume fluid resuscitation.  Its location is more removed from the primary site of resuscitation efforts, and is generally not beneath large amounts of soft tissue.

Other considerations:
The cost of intraosseous vascular access is much greater than the cost of peripheral intravenous vascular access.  Further studies should be conducted to determine the cost effectiveness of tibial intraosseous over peripheral intravenous access.

Book Review: Introduction to Clinical Emergency Medicine

In REVIEWS on October 9, 2011 at 8:00 AM

This review is for the book An Introduction to Clinical Emergency Medicine edited by S.V. Mahadevan and Gus M. Garmel, which can be purchased here. The reviewer has received no financial renumeration for this review.

I purchased this book and read it in its entirety prior to beginning my first EM rotation, with the thought that it would be a good and comprehensive overview of emergency medicine that would be more digestible than reading through Tintinalli or some other “classic” textbook. In addition, I was somewhat sucked in by the novel organization of the book with chapters based on complaint, rather than problem, with the idea that each chapter would give me a method of approaching a patient with said complaint. While the book did seem to accomplish these goals to some degree, I found a number of flaws that made me walk away wishing I had put in the extra time to just read Tintinalli’s instead.

The text of the book is 752 pages (not including the index). It is divided into 4 main sections: Principles of Emergency Medicine (eg. airway management, shock, trauma, etc.), Primary Complaints, Unique Issues (eg. abuse, environmental emergencies, legal aspects), and Appendix (containing mostly information on common procedures done in the ED). More or less, each chapter is written by a different author (some authors contributed >1 chapter). This was a problem in the previous book review that I did due to lack of homogeneity between chapters, but in this book, there is a relatively rigid format with each chapter in Primary Complaints (which comprises the bulk of the text) describing the scope of the problem, relevant anatomy, approach to history (ie. what questions to ask and what they imply), physical exam, differential diagnosis, testing, treatment principles, special patients (eg. elderly, pediatric, and immunocompromised), disposition, and pearls/pitfalls. This format is followed by almost every chapter, and does make the book more consistent throughout. The material itself is quite basic, which you might take as a good thing or a bad thing, depending on what you are looking for. If you are truly looking for an introduction to emergency medicine, getting the basics is probably helpful. However, I found the lack of “new” information to me often frustrating, and I was frequently left wanting more. Another significant problem was the overuse of tables (a pet peeve of mine), and especially how general and lacking in detail the information therein provided was. This was a problem particularly in the differential diagnosis section, which relied heavily on the table format. Given that the actual book is mostly organized by complaint, rather than problem, there is very scant information about individual problems as a result of this; for example, identification and treatment of pulmonary embolism is treated only very superficially (which I’m not singling out- almost all disease in the book is described in the same manner).

Strengths of the book included the overall homogeneity of the book, excellent images, and the novel way in which emergency medicine is presented, as well as the relative brevity; individual chapters were generally less than 10 pages long. Weaknesses included the superficial treatment of individual diseases and overuse of tables and lists. I may have been somewhat biased in this review given that the book does present itself as an introductory text, rather than a comprehensive text, and thus if that is what you are looking for, this book may be a decent read. However, given that the book is 752 pages, and other introductory books targeted to medical students are significantly shorter (for instance, Blueprints is ~300 pages), while (if you restricted yourself to clinical topics only) other more definitive textbooks are not that far off in size, I feel this book occupies somewhat of a strained middle ground.

Overall score (out of 5 stars):

Pearl/Pitfall: Cyanide

In PEARL/PITFALL on October 2, 2011 at 8:00 AM

Based on discussion/lecture from Dr. O`Toole, Emergency Physician and Medical Toxicologist at Hartford Hospital:

In the case of a patient presenting with new onset seizures, tachycardia and hypotension with elevated lactate and acidosis, always consider cyanide poisoning as a potential etiology.

In brief, a lethal dose to adults of potassium cyanide is ~200 mg. Cyanide inhibits many enzymes, perhaps most importantly cytochrome oxidase at cytochrome a3 in the electron transport chain, inducing cellular asphyxia by preventing aerobic metabolism. This results in movement towards anaerobic metabolism, ultimately producing lactic acidosis.

Cyanide is also a neurotoxin by several mechanisms, including impairment of metabolism as above, as well as increased release of excitatory neurotransmiters and increasing/activation of NMDA receptor activity, producing a number of CNS s/s including seizures.

It should be noted that cyanide does cause variable cardiovascular effects depending on when in the course of the exposure the patient is observed. Initially, cyanide causes bradycardia and hypertension, followed by hypotension and reflex tachycardia, and finally, bradycardia and hypotension leading to death.

As there is now a very safe antidote, hydroxocobalamin available, which essentially binds cyanide to become cyanocobalamin (ie. vitamin B12), early recognition of this poisoning may be life-saving.


Hoffman, Robert. Goldfrank’s Manual of Toxicologic Emergencies. New York: McGraw-Hill, 2007.

Wilderness Medicine Symposium!

In ANNOUNCEMENTS on October 1, 2011 at 5:29 PM

Today the 11th annual UCONN Wilderness Medicine Symposium was held at Winding Trails and was a great success! Led by Katherine Farmer and Colin Huguenel (both MS4) with support from Dr. Regan, Dr. Gottschalk, and Jeff Hogan. Thanks to them and to all who showed up, as well as Winding Trails for letting us use their facilities.

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