The Fast Track - Summer '15

The Fast Track

Summer 2015

The Fast Track

An Emergency Medicine Publication

Summer 2015 Issue

HOT, HOT

SUMMER get your fill of water, bugs, and drugs!

Jimson

WEED

Pg

08

an elusive diagnosis

intern

YEAR

reflections of the pivitol year in residency

SUMMER time water injuries!

Splish splash!

Pg

30

Pg

14

* --Spring Confer en Recap ce --------

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The Track The Fast Fast Track Editors-in-Chief Fall 2014

Tanner Gronowski, DO Veronica Coppersmith, DO Chris Swyers, OMS-IV Ariel Sindel, OMS-IV

Editors

Andy Little, DO Drew Kalnow, DO Jeremy Lacocque, DO Danielle Turrin, DO Erin Sernoffsky RC Board Members

Andy Little, DO President Joe Sorber, DO Vice President Drew Kalnow, DO Treasurer Tanner Gronowski, DO Secretary Veronica Coppersmith, DO Gina Moffa, DO Allison Remo, DO John Downing, DO Patrick Cary, DO Chase Ungs, DO Danielle Turrin, DO Daniel Engleberg, DO Steven Brandon, DO Past President

SC Board Members Cameron Meyer Sasha Rihter Timothy Bikman Jeffery Weeks

Deborah Rogers Michael Fucci Ariel Sindel Chris Swyers Chris Falslev Michelle Kinghorn Bryant Gray Kaitlin Fries, DO

President Vice President Treasurer Secretary

Letter from the Editor J

uly is a bittersweet month in the hospital. As we say congratulations and goodbye to our senior residents, we welcome in a new class of eager interns to the emergency department. The upper year residents realize how much they have learned, while the rising interns realize how very little they know about actually being a doctor.

My first day of residency felt about the same as my first day abroad in a country, where I didn’t speak the language; the “Oh no, I’m in way over my head, how am I ever going to make it through this?!”. I looked down at my scrubs that said “Veronica Coppersmith, DO - Resident” and felt my heart race. I tried to think through how my first patient would go, but my head felt completely blank. I walked in the ED doors and thought, “Well, it’s too late to quit this doctor thing now, you better figure it out.” My attending put me at ease saying, “Of course you’re going to be fine! You wouldn’t have gotten into med school if they didn’t believe you would make it. And we wouldn’t have picked you to be here if you weren’t going to be a great EM doctor!”

I began to realize through residency how dependent residents are on each other to make it through this crazy whirlwind life that is training to be a physician. My residency is a family, and we depend on each other heavily in and out of the hospital. I’m grateful to have my best friends by my side to help me through tough decisions, to watch me get berated by consultants, to see me at my best and my worst. They know when I’m having a bad day and how to make me feel better (usually snacks, doing push ups, or procedures). The hospital staff are to thank too. As I look back over who has helped me through to this point, it is everyone from the trauma surgeons who have taught me so much, my attendings who have analyzed how I learn and teach me as such, the cafeteria ladies who take the time to ask how I am doing and to get my favorite snacks when I need them, the nurses who have taught me proper ER etiquette, and obviously my fellow residents who have been there for me through it all. I feel so lucky to be in a residency where I can finally be myself and be surrounded by a supportive loving work family to help me through the best and the worst times.

As I began the job search process for after graduation, I began wondering if every ER is like mine.

Is every residency as lucky as St. Luke’s to have a loving work-family to help you through the worst times? I’ve been told that it wasn’t always this way, but everyone in the hospital put a lot of effort towards creating the family feel that the hospital has now. I’ve heard people describe my hospital saying “everyone is happy there, like there’s something in the water”. One of my dreams for emergency medicine is for every hospital to have this environment, where we actually want to go to work and we like learning medicine. Residency is hard enough as it is, I couldn’t imagine doing it without my hospital family, and I hope everyone has a similar experience in their residencies. If not, I encourage you to create it as we did here years ago - invite your co-residents out to happy hour, make work fun, take the time to ask how your co-workers are doing (and actually listen to the answer). Importantly, include the new interns.

I was devastated as I had to say goodbye to members of my residency family at graduation. Only put mildly at ease when a resident who had become a “big brother” to me told me that it was now my turn to be a “big sister” to all the new interns. That’s an awesome thing, the ability to be the helpful senior to those following you in training, just as your seniors were to you. Likewise, the new attendings are to the residents what their attendings were to them. So never forget who got you to where you are now, no one does residency alone, and everyone in the hospital helps shape you into the great physician you are becoming. You CAN and WILL make it, and everyone around you is there to help when you need it. But with that comes the duty to help the new interns, new med students, new attendings, or new hospital staff when they need it. Be humble enough to accept help and gracious enough to offer it, because no one is or should ever be on this bumpy rollercoaster of becoming an emergency physician alone.

Veronica Coppersmith, DO, FAWM

Past President

Printing of this issue sponsored by:

page Cover photo courtesy of Tanner Gronowski

Interested in contributing?

Let us know: FastTrack@ACOEP.org

CONTENTS Presidential Messages................................04 Rosh Review...................................................06

22

WILD MED get outdoors

Jimson Weed.................................................08 Tricks of the Trade.......................................13 Watersport Injuries......................................14 Networking......................................................17 ABG Interpretation......................................18

14

GHANA WATERSPORTS by Frederick Davis, DO injuries

Lyme Disease.................................................20 Wild Med .........................................................22 Submersion Injuries....................................24 Behind the Scenes.......................................28 What I Learned From Intern Year.........30

19

ABG HIGHLIGHTS

30

RHEUMATIC FEVER case study

Spring Conference Recap........................32 Rheumatic Fever...........................................34 Vagal Maneuvers..........................................38

The Fast Track Summer 2015

PRESIDENTIAL MESSAGE –

Resident Chapter

W

ith summer comes a time of thank yous and congratulations. A time when we thank our outgoing senior residents; for their years of service in our departments, being mentors to our residents, and leaders in our specialty. To our seniors we say thank you and good luck in your future endeavours. To the incoming interns, the recent medical school graduates, our newest members, we say welcome not only to the coolest specialty, but to your new extended emergency medicine family.

Over the next four years you will be put through a lot, so you need to make sure and take care of yourself, your entire self. For the rest of you I hope you remember a few things.

Remember it is ok to ask for help. Whether a new intern or new hire, there are plenty of people at your institution who can help you and who expect you to NOT know everything. So buddy up with your Chiefs, your new director and search to find a mentor in a fellow resident or colleague.

Remember to take time off to do something for you. I know over the next four years you will required to go to courses, and conferences, but please do not forget to spend at least 1 day a month and 1 week a year doing something completely selfish. This spring I had the opportunity to hike with my wife, my 8 year-old son and extended family in the Grand Canyon. Preparing for and doing this trip took a lot of my time away from residency, but I cannot express in words the satisfaction I had seeing my wife and son ascend the summit of the canyon walls (their first camping experience!) with smiles on their faces and having reached new heights.

Remember to take care of your health. The intern/new attending 15 is real (and is probably closer to 20, as I know from experience). So make sure to take the stairs at work and at the mall, find ways to pack snacks/ lunch when you’re on shift, and be a good patient and actually see your doctor.

Finally, remember that as new members of your prospective family’s (Resident/New Attending) that the ACOEP is here to help. If there is anything you need do not hesitate to call, email, or text myself or your other ACOEP officers.

Best Regards, Andy Little, DO ACOEP National Resident Chapter President ACOEP Board of Directors Emergency Medicine Resident Doctors Hospital

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PRESIDENTIAL MESSAGE –

Student Chapter

Summer 2015

The Fast Track

O

n behalf of the ACOEP-Student Chapter, I would like to congratulate all the recent medical school graduates. I would also like to congratulate those that were lucky enough to match in Emergency Medicine. EM is becoming more competitive every year and many qualified students don’t match into the field. The fear of not matching has lead to many sleepless nights for many of us.

To help give students an edge, however, the ACOEP-SC strives to give students the best opportunity to match in Emergency Medicine. There are many resources available to students, and below are a few of these resources that can potentially make the difference between matching and not matching.

The student membership page on the ACOEP website is full of valuable information to help students.

For example the website has a page to help students interested in doing research. It helps walk students through the process and helps them prepare to present their projects and case studies. Also on the website are downloadable recordings of lectures given at the various student conferences. Some of these lectures include was to improve your application and how to standout on interviews and rotations. A new addition to the website is a page that shows the location for each AOA-approved Emergency Medicine program, information about each program, and a link to each program’s website. These are only a few of the many great resources the ACOEP website has to offer.

However, the best resources available to students are the conferences and student symposiums. These events not only prepare students through great lectures and skills labs, but they also offer students a chance to meet residents and program directors from all across the country. Every year at the Fall Scientific Assembly the ACOEP-SC holds a residency expo with almost every osteopathic residency program in attendance. Last year, students received interviews that they would not have gotten if they had not attended the expo. Many students who got interviews from attending the expo ended up matching at those programs. Conference has proven to be a great asset to the students that attend.

Also coming up on September 12, 2015, we will be holding another regional symposium. It will be held at St. Joseph’s Regional Medical Center in Paterson, NJ. This will be open to all osteopathic medical students and will give students an introduction to the surrounding residency programs.

Over the years the ACOEP has shown that the students are a top priority to the college. They have supported the students in every way possible. I encourage you to take advantage of the resources they offer. Your active involvement could make the difference you need to get into the program of your dreams.

Best Regards, Cameron Meyer OMS-IV ACOEP National Student Chapter President West Virginia School of Osteopathic Medicine

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The Fast Track Summer 2015

Emergency Medicine Review with

Find more questions like these by visiting roshreview.com

1) A 10-year-old girl presents after a submersion incident at a nearby lake. She slipped on the dock, hit her head and fell in the water. She was extracted quickly and on reaching the dock, she coughed and then vomited clear fluid once. Since then, her only symptom has been an intermittent cough. Vital signs are normal. Physical examination reveals wheezing and a chest X-ray is normal. What management is indicated?

A) Admit and start antibiotics B) Discharge home on antibiotics C) Discharge home with incentive spirometer D) Observe for 4-6 hours with repeat chest X-ray

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2) A 23-year-old man presents unresponsive to the ED after being found in a park. His vital signs and finger stick glucose are normal. The physical examination is notable for the skin findings shown. What other examination finding would you expect to find?

A) Cataracts B) Compartment syndrome C) Irregularly irregular cardiac rhythm D) Tympanic membrane perforation 3) A 27-year-old man presents after being thrown a far distance off of a horse. Which of the following is consistent with an anterior cord syndrome?

A) Isolated motor function loss B) Loss of all motor and sensory function C) Loss of pain and temperature, loss of motor function D) Upper greater than lower motor weakness 4) A 21-year-old man presents with muscle cramps and a headache after a black widow spider bite. Vital signs are normal. What management is indicated?

A) Benzodiazipines and supportive care B) Black widow anitvenin C) Intravenous antibiotics D) Oral antibiotics

Find your Rosh Review Answers at the end of the issue

AIRWAY

SHOOTOUT

Summer 2015

The Fast Track

8 Residencies. 4 Airway Simulations. 1 Winner.

Eight residencies can select a team of four top airway gurus to compete against one another in the ultimate airway shootout! Each team member takes their shot at the airway simulation, but be careful of your choice of weapon because it can only be used once!

PRIZES FOR THE TOP 2 TEAMS! OCTOBER 18-22 Loews Portofino Bay Hotel Orlando, Florida Visit www.acoep.org/fall for more information ACOEP-RC

@acoeprc page 7

The Fast Track Summer 2015

Jimson Weed An Elusive Diagnosis Courtney Johnson D.O., Alec Bower D.O. Adena Regional Medical Center Department of Emergency Medicine It’s a beautiful August afternoon in your emergency department, when your nurse says, “Doc, I think you need to see this kid.” You pull back the curtain and see a 17-year-old male sitting on the bed, gripping the side rails like he’s on a rollercoaster. He can tell you his name but is otherwise speaking nonsensically. He is awake, alert and intermittently screaming. A friend dropped him off in the lobby and quickly left after telling the triage nurse, “he isn’t acting right.”

Initial vitals are BP 131/82, HR 122, RR 20, Temp 101.3, O2 98%. Pertinent physical exam findings include altered mental status, tachycardia, bilateral dilated and sluggish pupils, low-grade fever, and his skin is warm, flushed and dry. An IV is initiated and he’s placed on a cardiac monitor. EKG shows sinus tachycardia with a rate of 125 bpm. There is no significant widening of the QRS complex or prolongation of the QT interval.

By this time the patient is pacing around the room, swearing, agitated and delirious.

With limited information basic labs are ordered (CBC, CMP, acetaminophen and ASA) which are unremarkable.

Serum alcohol is undetectable. Unable to give a urine sample, a catheterized urine is obtained showing no protein, blood or signs of infection. Urine toxicology is positive only for marijuana. You suspect anticholinergic toxicity and you begin to rack your brain on what to do next.

At that moment, his mother frantically calls the ER looking for her son. She’s denies any past medical history, surgeries, medications or pertinent family history. She’s asked to look around the house for anything he may have taken. She finds what she describes as brown “spiky” pods with small black seeds laying on his desk. Because you are a well-read ER physician and an expert botanist you immediately diagnose Jimson weed anticholinergic toxicity and

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pat yourself on the back.

BACKGROUND: Jimson weed (Datura stramonium) is a wild flowering plant that can be found across the United States and southern Canada typically growing along roadways, barnyards and pastures. The plant is a native to Asia but was introduced and naturalized throughout the U.S. 30, 31 Jimson weed is named after a case of human poisoning in 1697 when soldiers in Jamestown, Virginia allegedly ate the plant in a salad and then suffered extreme psychological effects including delirium and hallucinations31. Many names have been given to this plant including: Jimson Weed, Locoweed, Angel’s Trumpet, Thorn Apple, Devil’s Trumpet, Mad Apple, Stink Weed, Sacred Datura, Green Dragon, and Devil’s Trumpet30.

All parts of the plant are toxic and contain belladonna alkaloids (hyoscyamine, atropine and scopolamine)27.

Most of the human poisonings are through intentional ingestion of the plant’s seeds for its psychoactive properties. The alkaloids present in jimson weed have potent anticholinergic effects. An estimated 100 seeds contain approximately 6 mg of atropine, which if left untreated, can result in death 25.

Most cases are seen in the late summer and early fall when the seeds mature. Each pod, or capsule, can contain up to 100 seeds. The anticholinergic effects of Jimson weed cause delayed gastric emptying, which prolongs duration of action. Toxicity usually occurs within 60 minutes after ingestion and clinical symptoms may persist for 24 to 48 hour28.

Summer 2015

The Fast Track

CLINICAL FEATURES: Like any substance with anticholinergic properties, Jimson weed toxicity has a distinct clinical presentation.

Cutaneous vasodilation occurs secondary to hyperthermia and anhidrosis, as a means to dissipate heat. This gives the patient a “rose colored” appearance, terming the phrase “red as a beet”.

sphincter. This eventually leads to urinary retention (“full as a flask”).

Other features suggestive of Jimson weed (anticholinergic) ingestion are tachycardia secondary to antimuscarinic effects on the heart and decreased GI motility due to parasympathetic inhibition on the intestines.

DIAGNOSIS:

The antimuscarinic effects of anticholinergics cause an inhibition of sweat glands, thus giving patients dry skin (“dry as a bone”) despite hyperthermia.

Due to the patient’s hindered ability to dissipate heat through sweating, anhidrotic hyperthermia (“hot as a hare”) commonly develops.

Pupillary dilatation occurs due to parasympathetic inhibition of the antimuscarinic properties of Jimson weed and other anticholinergics. This mydriasis is unresponsive to light reflex causing an unaccommodating mydriasis, which leads to decreased visual acuity, thus terming the phrase “blind as a bat”.

Agitation and psychosis are a common manifestation of antimuscarinic effects on the CNS. Inhibition of anticholinergic receptors cause an increase in dopamine production leading to euphoria. However, too much of a good thing can be very bad. Many times this euphoria transitions into hallucinations and eventually psychosis. Hence the description “mad as a hatter”.

Detrusor muscle contraction within the bladder is also innervated by muscarinic receptors. Inhibition of these receptors leads to decreased contractility of the bladder and abnormal opening of the urethral

The diagnosis of anticholinergic toxicity is essentially made based on clinical findings. History is often unavailable or misleading. This is especially true of Jimson weed ingestions in adolescents, due to fear of retribution from family. Lab studies are of little value and are used in ruling out other causes of altered mentation. The same is true for imaging studies.

LABORATORY EVALUATION: Obtain the following studies in all patients suspected of overdose: Fingerstick glucose – hypoglycemia notoriously mimics numerous disease processes. Always obtain point of care (POC) glucose in all patients presenting with altered mentation.

Electrocardiogram (EKG) – anticholinergics have been known to prolong the QRS and QTc interval. This is also helpful in assessing for other co-ingested substances (i.e. TCA)2, 3.

Alcohol, Acetaminophen and salicylate levels – these are commonly co-ingested and carry higher morbidity and mortality if diagnosis is delayed.

Pregnancy test in all women of childbearing age – this page 9

The Fast Track Summer 2015

is an absolute can’t miss and spans beyond just the acutely intoxicated patient.

CONSIDERATIONS: Creatine Kinase (CK) – there have been case reports of rhabdomyolisis attributed to anticholinergic overdose, none of which have been directly linked to Jimson weed 4-7. More often, this is seen in those patients with severe psychosis and seizures.

Urine drug screen – positive and negative screens for drugs do not absolutely confirm or refute poisoning diagnoses and require further evaluation.

Comprehensive qualitative toxic screening is expensive, commonly requires upwards of six hours for results, often does not predict or define the severity of poisoning, detects unsuspected drugs in only a minority of patients, rarely leads to changes in patient management and disposition, and is unlikely to affect patient outcome21-24.

MANAGEMENT: Management of patients with Jimson weed toxicity is like that of any anticholinergic overdose. Begin with stabilization of the airway, breathing and circulation. In severe toxicity, seizures can occur causing patients to be at risk for airway obstruction. All but the most trivial ingestions should be placed on a

cardiac monitor and IV access should be obtained.

Patients demonstrating signs of psychosis or those with seizure activity should be treated with benzodiazepines.

Lorazepam 1-2 mg given IV (0.1 mg/kg IV for peds) as often as needed to control symptoms is effective, has a high safety threshold, and can be used in high doses to control symptoms. Alternatively if no IV is established, lorazepam can be given IM, or rectal diazepam is a good alternative.

Never use phenothiazines (i.e. Compazine™), and butyrophenones (i.e. haloperiodol and droperidol) to sedate patients with anticholinergic toxicity. They are themselves anticholinergic, and may exacerbate rather than improve symptoms.

Treatment of hyperthermia should begin with evaporative cooling measures [26]. To do this, expose the patient completely. Spray lukewarm water over exposed skin while using fans to blow air across moistened skin. This has been linked to decreased mortality in those with heat stroke and is extrapolated for uses in anticholinergic toxicity26.

While Jimson weed can be ingested in several different ways (smoked or brewed in tea), the most common form is to actually eat the seeds9-11. Depending on the timing of exposure, gastrointestinal decontamination should be performed. However, patient’s mental status must be intact and be cooperative before administering activated charcoal. Intubation is not indicated for the sole purpose of administering activated charcoal.

When indicated, give 1 g/kg of AC to a maximum dose of 50 g. Gastric lavage is rarely needed and induced emesis is no longer recommended.

ANTIDOTE: The majority of patients presenting with Jimson weed intoxication will do well with supportive care alone. Those experiencing moderate to severe peripheral and central toxicity may benefit from physostigmine therapy12. It should be noted that this treatment is controversial and debate still prevails among clinicians13, 14. There are no studies to date that have determined the safety or efficacy of physostigmine in Jimson weed toxicity or, for that matter, in anticholinergic overdose in general. However, select patients may benefit from its use it should be considered in cases of severe toxicity.

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Physostigmine inhibits acetylcholinesterase in the peripheral and central nervous system.

The latter differentiates it between neostigmine and pyridostigmine which do not cross the blood brain barrier. This makes it excellent at reversing

The Fast Track w i t h Summer 2015

anticholinergic effects.

Recommended dose for adults is 0.5-2 mg (0.02 mg/ kg IV). Smaller doses may be repeated after 20 to 30 minutes if delirium persists. It should be noted that, in one retrospective study, none of the 14 patient with anticholinergic toxicity required additional physostigmine more than 6.5 hours after the initial dose15. The drug should be given slowly over five minutes to avoid cholinergic symptoms or seizure.

Several situations exist in which physostigmine should be avoided.

Any situation in which there is not a clear history of pure anticholinergic overdose, physostigmine should not be given. This is especially true if there is concern for tricyclic antidepressant (TCA) co-ingestion. Several case reports of TCA-poisoned patients developed asystole following physostigmine administration17. If an anticholinergic agent is not the etiology of the patient’s presentation, cholinergic toxicity may result. In patients who develop cholinergic toxicity, administer atropine. Start with half the dose of physostigmine administered and titrate to clinical effect.

Physostigmine appears to be superior to benzodiazepines in the management of agitation and delirium due to anticholinergic toxicity. One study of 52 patients with anticholinergic poisoning, shows those treated with physostigmine were significantly more effective in controlling agitation and delirium than benzodiazepines13. Those treated with physostigmine experienced fewer complications and had shorter recovery times. Although it is reasonable to treat patients with very minor anticholinergic toxicity with small doses of benzodiazepines, those with moderate to severe agitation will likely respond better to physostigmine.

Because physostigmine is uncommonly used and unfamiliar to many practitioners, it is recommend it be given after consultation with a medical toxicologist or poison control center.

DISPOSITION Asymptomatic patients who have or are suspected of ingesting Jimson weed should receive gastrointestinal decontamination with activated charcoal and should be observed in the emergency department. If asymptomatic after six hours, they may be discharged.

Those with mild anticholinergic toxicity should receive gastrointestinal decontamination with activated charcoal (if possible). If necessary, they may be treated

benzodiazepines and observed for resolution of symptoms. If symptoms resolve within six hours they may be discharged. If not, they should be admitted for observation.

Patients exhibiting severe toxicity, and those treated with physostigmine, should be admitted to an intensive care unit for observation.

CASE OUTCOME: Despite repeated boluses of Ativan your patient becomes increasingly agitated, tachycardic and delirious. A large dose of Jimson weed is suspected with rapid progression of toxicity and the decision to administer physostigmine is made. Two milligrams of IV physostigmine is given with improvement in agitation, tachycardia and mental status. One hour after the first dose of physostigmine, the patient returns to his previous aggravated state and an additional 1mg dose is given with good response. The patient is admitted to the ICU for further monitoring. For the next 36 hours his symptoms are controlled with benzodiazepines and he recovered uneventfully. Upon discharge the patient admits to intentionally ingesting Jimson weed seeds in attempts to “hallucinate�.

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The Fast Track Summer 2015

Be the Next Big Thing in Rapid Fire Lectures!

The ACOEP RC invites you to apply for the chance to present a Rapid Fire Lecture at the upcoming Scientific Assembly.

SELECT Your Topic

CREATE Your Slides

PRESENT

at a National Conference

The top residents selected to present lectures Rapid Fire lecture style

Prizes for the three best speakers OCTOBER 18-22 Loews Portofino Bay Hotel Orlando, Florida page 12

Visit www.acoep.org/fall for more information

ACOEP-RC

@acoeprc

Tricks of the Trade

By Veronica Coppersmith, DO @ St. Lukes Hospital

Summer 2015

The Fast Track

Eye Exams Do you remember the last time you tried to do a fluorescein exam on a pediatric patient? Or even an adult who isn’t a contact lens wearer? You sometimes have to count your lucky stars that you are able to get a single drop of Proparacaine in some of your patient’s eyes, let alone trying to coordinate getting fluorescein in there, too. One trick of the trade to make eye exams easier: pull the back plunger off of a 10 mL saline flush, pour out 5mL of saline, drop the fluorescein strip into the syringe, and add 1-2 mL of Proparacaine as well. Now you just have to be lucky enough to get one squirt into the patient’s eye and you will have them numb and stained. Also, fluorescein strips themselves can cause minor abrasions if the strip itself comes in contact with the cornea, and this technique will avoid abrasions from the strips themselves. In addition, if your attending would like you to repeat the eye exam, or if another patient comes in with eye complaints later in your shift, you are all ready to do another exam.

Pregnancy Test when they can’t pee Knowing if a patient is pregnant is often a game changer in terms of differential diagnosis, imaging studies, and treatment. However getting urine in a timely fashion from a trauma patient, or from a patient who just refuses to urinate, or waiting for a bHCG quant can really slow down the process. But most urine pregnancy tests are approved for testing urine or blood! You can draw up some blood off a line or when doing a blood draw (not just blood from a finger stick unfortunately) and use this in the well of the pregnancy test instead of urine (see image). Be sure to check the package insert for your specific tests to ensure that blood can be used.

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The Fast Track Summer 2015

Watersport injuries

By Brian Lehnhof, DO - Kent Hospital, Rhode Island

I

t is that time of the year where those who have been hibernating for the long winter are venturing out and engaging in water based activities.

This makes for an exciting time for emergency providers. Inevitably the joyful activities of summer are going to create some work for us.

As a result of my passion for watersports I have experienced many water related injuries either directly or indirectly. Now, as I live in the “Ocean State”, the experiences continue. The types of injuries that can come from water sports and activities are nearly endless. The corresponding management of these injuries also varies widely. Tried and true ATLS and ACLS algorithms manage some of them and some require novel interventions. The key is to develop a broad differential and not get tunnel vision.

Interestingly over just the past couple months I have two patients brought into my ED for acute events while quahogging. What is quahogging you ask? This is a common activity in Rhode Island which is defined as “digging for the quahog clam”. While admittedly not an expert on quahogging, I still never thought of quahogging as a potential pathology provoker. Minor extremity trauma, sure? Hypothermia, possibly? Not the case, The first patient came in off the boat feeling intense shortness of breath and chest discomfort. He was diagnosed with a saddle pulmonary embolism. The second patient was brought in by EMS early one morning if full cardiopulmonary arrest after slumping over while working on a boat.

Did quahogging directly cause these? Maybe not. These are not pathologies that I commonly associate with water sports, but it does illustrate that you cannot limit the scope of injuries that can occur in the water. Some things coincidentally occur in the water setting.

Some of the more common water sport related injuries I have encountered are trauma related. Triathlons can produce facial and ophthalmic injuries from contact with other swimmers. These injuries can be further complicated if they occur in contaminated water or if they fail to stop competing to address the wounds.

Motor boating involves many moving parts, high speed, and high tension. Such factors combined when a friend of mine was attempting to untangle the skier towrope. The rope quickly looped round his forearm and resulted in a degloving injury involving the majority of the upper extremity and a brachial artery disruption.

“...you cannot limit the scope of injuries that can occur in the water..”

Traumatic injuries such as my friend’s can be complicated when medical care is not readily available. While the etiology of the injuries may not change a lot about our management in the ED, it does affect whether or not the person even becomes an ED patient. Remoteness of locations of water activities is one of the most complicating factors. Such was the case with my friend who was in the middle of a large, remote lake with profound arterial bleeding. In these cases it is essential to identified resources

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Summer 2015

The Fast Track

QUAHOGGING early and activate them. Through early tourniquet application and air medical transport, my friend reached definitive medical care and ultimately made a full recovery.

Another complicating factor is continued exposure. Such was the case of a patient I had as a medical student. He was cliff jumping at Lake Havasu, AZ. While preparing to jump, he was struck from behind by a diamondback rattlesnake. Without much in the way of options and at risk for further strikes, he utilized his best option and jumped off the cliff. Once in the water he swam to the shore, got assistance from friends and then took a helicopter ride to the regional toxicology center.

The hard clam (Mercenaria mercenaria), also known as a quahog (or quahaug), round clam, or hard-shell (or hardshelled) clam, is an edible marine bivalve mollusk that is native to the eastern shores of North America.

Above Quahogs

The fact that an otherwise minor injury occurs in water can complicate it immensely. My wife was on a boating trip in high school when their boat was struck by another boat. A friend who had been positioned in the bow was thrown from the boat. She had some minor orthopedic injuries, but her primary issue became the head trauma she experienced. She lost consciousness and was thrown from the boat; she landed in the water unresponsive. This was not immediately known and before she was found she had died due to drowning.

We as emergency medicine providers cannot control much of what occurs prior to arrival, we can prepare ourselves to perform the best care upon their arrival. We prepare tediously for managing the trauma and medical resuscitations that some of these cases will require. In addition to these core competencies, there are some pathologies that require specific management that we need to be aware of.

Submersion injuries have had recent changes in nomenclature and classification but the management remains the same. Drowning is defined by the WHO as “the process of experiencing respiratory impairment from submersion in a liquid. ” Death is not a requirement.

WHO urges: “Drowning outcomes should be classified as: death, morbidity, and no morbidity.” Management of drowning victims will often require aggressive resuscitation; the history may reveal specific measures needed to optimize your resuscitation measures.

First, hypothermia may play a large role in pathophysiology. A patient does not have to be immersed in frigid water to be hypothermic.

Prolonged exposures to less than physiologic temps of any degree can be sufficient exposure to produce hypothermia. Aggressive measures for core rewarming are needed. A core temp of 32-35°C should be obtained prior to terminating resuscitation efforts.

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The Fast Track Summer 2015

Second, consider secondary injuries that could be contributing to the primary respiratory failure. Diving can produce cervical spine injuries that could greatly alter management of the patient. Toxicologic issues create confounding metabolic and neurologic states that limit or at least alter the efficacy of your resuscitation efforts.

Another water sport related injury that requires specific intervention is decompression sickness (DCS), AKA “the bends�. I have the luxury of working at an institution that has a hyperbaric center so we may see a larger volume of these cases, but these patients can present anywhere. Scuba diving has become an increasingly popular activity and people are diving in all areas of the world now, even in landlocked states. Additionally people may not become symptomatic until returning home from their dive trip and then present to your ED. DCS results from the formation of nitrogen gas bubbles during ascent. On descent, increasing pressure causes gases to be dissolved at varying rates depending on the gas. Likewise during ascent these gases are released back into the bloodstream. If pressure is altered too quickly from rapid ascent, the gases do not have a chance to return to the normal concentration mixture or to be filtered out in the lung. Consequently these air bubbles can become pathologic to tissue and organ systems. The white matter of CNS is particularly fond of these fat soluble nitrogen gases, and thus at risk for disproportionately worse damage.

In addition to a history of rapid ascent while diving, there are some other important points in the history that may help make the diagnosis of DCS. Males are at over 2 times greater risk of developing DCS. Night dives, cold-water dives, recent illness, heavy exertion, and air travel soon after diving can all increase the risk of developing DCS. The length of dive increases the risk of developing DCS. PFO has been identified as another common risk factors; and is found in approx 65% of serious DCS patients.

The manifestations of DCS almost always present in the first 24 hours with vast majority presenting within 1 hour of resurfacing. The most common and earliest symptom is typically periarticular pain affecting all the extremities. One approach to differentiating this pain is to place a BP cuff on an affected limb and inflate to approx 150-200mmHg. If DCS is the etiology, this maneuver will often relieve the pain. Additional symptoms are numbness, paresthesias, dizziness, motor weakness, skin mottling/marbling, and mental status changes.

Patients with DCS need to have their body returned to the same pressurized environment that created their symptoms. This is done utilizing a decompression chamber. The pressure environment is recreated and then slowly reduced simulating a slow ascent. This allows the gas bubbles to re-balance and be eliminated properly.

Summer is a great time of year. A lot of fun can be had and lot of pathology can occur. No matter the location of your department you are going to see water related injuries. It is crucial in these cases to keep in mind some of the potential complications that could be occurring related to the water exposure and incorporate this into your management plan.

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ACOEP-RC

@acoeprc

By: Jeffrey R. Weeks, OMS-III, MBA, Georgia-PCOM

B

efore I quit my job to become a doctor, I was crunching numbers, sitting behind a desk in a hospital. One night while working on a time study in the ED, there was a terrible car wreck on the interstate near the hospital. The events I witnessed that evening left me wondering which things I had learned in business school would have the biggest impact in healthcare if doctors learned them as well. One of the biggest differences between two of the physicians I noticed that night was the networks the two different doctors had formed. Not the type of network that involves getting computers and programs to communicate between hospitals and offices, but the kind that comes from interacting with other physicians.

That night in the ED, one of the patients needed to be transferred to a larger hospital with more resources. There were two different calls made to a larger facility a couple hours down the road and the two conversations were strikingly different. The first conversation went something like this: “Dr. Smith, this is Dr. Wilson from Community Hospital ED, I have a patient who was in an MVA and is going to need to see a neurosurgeon before ours is back in town on Monday. I was hoping I could send him to you…”

Dr. Smith went into much more detail about the patient’s condition as well as his rationale for wanting to send him to this particular hospital and was eventually put on hold while they checked to see if they could take the patient. The call got disconnected and before Dr. Smith could call back, another doctor from the ED at Community Hospital found out what had happened in the first conversation. He offered to see if he could help. His conversations went more like this: “Jim, hey this is Frank, I’ve got a patient here who was just brought in from an MVA. We have him stabilized but he is going to need more care than we can provide for him here….. ok, great I’ll let the pilot here know and they should arrive within the hour.”

Both physicians from Community Hospital called the same larger hospital. The difference between the two calls came from the fact that while Dr. Smith and Dr. Wilson were simply two ED doctors doing their job and attempting to gain all the information needed to determine if the transfer to this particular hospital was in the patient’s best interest, Frank was part of Jim’s medical network. Jim and Frank had attended medical school together and Frank trusted Jim’s judgment. He knew that if Jim thought the patient should be transferred to his hospital, it was the right thing to do.

In business school, I was taught accounting, finance, investing etc. There are other skills that are encouraged but not explicitly taught as a class; networking is one such skill. We were taught

the proper etiquette on handling business cards and we were encouraged to attend all career fairs. Even if we were not interested in working for any of the companies represented at the fair or already had a job waiting for us upon graduation, attendance was a way to expand our business networks. It was also strongly recommended that we join a social networking web site for professionals such as LinkedIn. In the business world, networking is about making connections for both short and long-term opportunities

Summer 2015

Can Networking Save Lives?

The Fast Track

In healthcare, networking has many of the same benefits for the physician; but more importantly, it can help improve patient care. Fellow physicians can be invaluable in helping to develop treatment plans for difficult cases long after school and residency have become a distant memory. With an aging population, a greater number of my future patients will be seeing multiple doctors. The better I am able to communicate with these other doctors, the better the care for my patient will be. In the case described, networking allowed patient care to be expedited when every second counted.

As a medical student, I have continued to approach networking in much the same way I did in the business world. Every doctor I encounter, both current and future, has the potential to become a part of my professional medical network. The classmates with whom I spent two years of my life as well as those in the classes ahead of and behind mine form the foundation of my network.

While many saw clubs, volunteer activities and social event as an opportunity to unwind or give back to the community, they were also excellent opportunities to get to know other future doctors and expand my network. The preceptors and other students I have met while on rotations are helping to grow my network even further. As I prepare to enter into the next phase of my training and begin residency, my network will grow even larger and stronger. This very type of networking is one of the factors which leads many doctors to stay in the area where they complete their training. Through residency, they have already established relationships with many of the doctors to whom they will be referring patients as well as from whom they will be accepting referrals.

The best way I have found to network on a larger, broader scale is to attend conferences. Conferences have allowed me to not only meet doctors from all over the country, but they have also given me the opportunity to hear how medicine is practiced in parts of the country very different from my own. I have no doubt that one day soon I will encounter a patient with a problem not normally seen in my part of the country. I may not know exactly how to help my patient; but because of the network I have built, I will be able to quickly get in touch with another doctor who treats this type of problem on a regular basis.

To claim that networking can save lives may be a little presumptuous; but it can improve the quality and the delivery

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The Fast Track Summer 2015

ABG Interpretation Cody Reynolds, DO, PGY-3 Marietta Memorial Hospital, Marietta, OH

Early in our careers, nothing can be a more intimidating task than interpreting an arterial blood gas, or ABG. There’s really no wiggle room and if you don’t have a solid, stepwise approach for reading them, you may find yourself struggling to accurately diagnose and treat your patient. There are many ways approach the determination of the patient’s status, but I will list the way I was taught, which has always worked well for me. This is a brief overview about the basics of interpretation and doesn’t encompass all aspects of AcidBase topics.

Step 1: Analyze the pH First and foremost, you have to look at the pH. You initially must determine if you are dealing with an acidic pH or one that is alkaline. A normal pH ranges from 7.35-7.45. Values less than 7.35 are considered acidic and those greater than 7.45 are termed alkalotic. Simple, right?

Step 2: Determine the primary disturbance Disturbance

Mechanism

PH

PCO2 Level

Acidosis Acidosis Alkalosis Alkalosis

Metabolic Respiratory Metabolic Respiratory

pH pH pH pH

PaCO2 PaCO2 PaCO2 PaCO2

Now, there’s a trick to the next part and remembering it will make your job a lot easier, but it’s not essential to understanding the ABG concept. Take a look at the carbon dioxide level. The normal levels are 3545. The easiest way to determine what is going on from here is to see if the CO2 level is moving the same direction as the pH. In metabolic disturbances, the pH and CO2 levels move in the same direction.

If they move in opposite directions, the primary disturbance is respiratory. Make sense? When your acute opioid overdose is breathing 10 times per minute, with a pH of 7.2 and a PaCO2 of 65, you’ll know that’s a respiratory acidosis! page 18

Step 3: Is there a compensation present?

This can get tricky, but stay with me. First, we figure out whether there is either compensation or there isn’t. If the pH is normal, there must be compensation. When the pH is not normal, then we must determine if the suffering system is working. Remember, the body will never overcompensate. Let’s say we go back to our overdose patient. If his HCO3 is normal, he has not compensated for his acidosis. The body should increase his HCO3 to compensate for the acidosis caused by his decreased respiration rate.

Summer 2015

The Fast Track

Step 4: Analyze the PaO2 The normal levels for your dissolved oxygen are 80-100. If you have a value less than 80, you have a hypoxemic patient. It is really that simple!

Putting it all all together: Let’s put everything together with a real-world example. Say we have a patient presenting to the ED with intractable vomiting for the past three days. We draw an ABG that looks like this: pH: 7.51 CO2: 47 HCO3: 36 pH >7.45 tells us we’re dealing with alkalosis. The CO2 is in the same direction as the pH so I know this is a metabolic alkalosis (a high CO2 otherwise would cause acidosis). The elevated CO2 level is compensating for the increase bicarb level. Therefore, we have a metabolic alkalosis with partial compensation.

Like any skill, ABG interpretation takes time and practice. If you keep these simple steps in mind the next time someone hands you the ABG on a crashing patient, it just might save a life!

ACO EP FA L L S C IENT IFIC A S S EM B LY Oct 18-22, 2015 Loews Portofino Bay Hotel Universal Studios, Orlando, Florida

Come join ACOEP at their flagship conference in the brilliant and exciting Universal Studios! Get ready for rapid fire lectures, hot topics, and big name lecturers for one of the premier Emergency Medicine Conferences in the country! Visit www.acoep. org for more information and registration!

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The Fast Track Summer 2015

Summertime with Lyme Jessica Biller, OMS-I GA-PCOM

A

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s the beginning of summer rolls around, we must remain conscientious of the incidence of Lyme disease in the northeast and upper midwest.

According to the CDC, Lyme disease is the most commonly reported vectorborne illness in the United States. The incidence of Lyme over the years has steadily increased, which could either be due to the spread of the disease or the increase in public awareness. The disease is caused by the spirochete Borrelia burgdorferi and transferred to humans by the blacklegged tick (Ixodes scapularis). The small size of the ticks is the reason why so many bites go unnoticed. The majority of bites during the summer months are by the nymphal ticks, which are approximately the size of a poppy seed or pinhead. Because the majority of patients cannot recall if they were bitten, we must rely heavily on the travel and environmental exposure history and physical exam to make a diagnosis. There are three stages of Lyme disease.

thirds of patients who develop the rash go on to develop stage two and even stage-three symptoms.

S tage 1: E arly localized

S tage 3: L ate / chronic

This stage usually occurs within four weeks of the tick bite. Erythema migrans, the classic, oval, bull’s-eye rash of Lyme disease, only occurs in two thirds of patients. The rash typically appears seven or more days after the tick bite and may be asymptomatic or itchy. Some patients may have multiple rashes due to hematogenous spread and shouldn’t be mistaken for Tinea corporis.

Flu-like symptoms are reported in approximately half of patients, along with fatigue, myalgia, arthralgia, headache and neck stiffness. Two

The late or chronic stage of Lyme disease can occur months to years after the infection. Symptoms of this stage are primarily rheumatologic or neurologic. Most of the patients who have reached this stage did not present with erythema migrans because they likely would have had earlier intervention. Arthritis is largely involved in stage-three Lyme disease and almost always involves the knees. It must be differentiated from arthralgia, which is more common in the earliest stage. Neurologic involvement involves the central

S tage 2: E arly disseminated This stage usually begins three to 10 weeks after the bite. Common manifestations at this stage are musculoskeletal, neurological, cutaneous and ocular. The most common musculoskeletal complaint is intermittent inflammatory arthritis, which can last up to 10 years but typically becomes less severe as time goes on. Neurologic involvement, also known as Lyme neuroborreliosis, includes cranial neuropathies (Bell’s palsy most common), meningitis and encephalopathy. The encephalopathy presents with cognitive disturbances and can occur months to years after the infection. Ocular manifestations include diplopia due to cranial neuropathies or blurred vision, eye pain or unilateral blindness due to inflammation of different ocular structures.

and peripheral nervous systems and must be differentiated from fibromyalgia and acute disc disease.

Borrelia encephalomyelitis is rare but involves hemiparesis, ataxia, seizures, cognitive impairment, bladder dysfunction and hearing loss.

Myelitis occurs in half of patients with neuroborreliosis and presents with paresis.

P ost - treatment L yme disease syndrome In approximately one fifth of patients, symptoms of Lyme persist even after treatment with antibiotics. Lingering symptoms include fatigue, pain, joint and muscle aches. Often called “chronic Lyme disease”, it is more accurately known as “post-treatment Lyme disease syndrome” (PTLDS).

Many believe this occurs as a result of tissue damage by the bacteria and the body’s immune response. Many patients believe they feel better with a continuous course of antibiotics but studies show that there is no benefit and that continued treatment can actually be detrimental to the patient.

C o - infections Some ticks carry more than one disease, which can result in coinfections. Symptoms of patients with co-infections are usually non-specific, making diagnosis much more difficult.

When patients with Lyme disease don’t respond to treatment, a coinfection should be considered. Other organisms sometimes associated with Lyme are Babesia, Ehrlichia and Bartonella.

Symptoms of babesiosis are similar to Lyme disease but more often start with a high fever and other flu-like symptoms.

Ehrlichiosis symptoms are also flulike with high fever, fatigue,

muscle aches and headache. Clinical manifestations of bartonellosis are also fever, fatigue, headache, but also include a streaked rash and swollen glands. Most of these co-infections are mild but can be severe in the elderly or immunocompromised.

Summer 2015

The Fast Track

S outhern tick - associated rash illness In the southern region of the United States is another tick, Amblyomma americanum, also known as the lone star tick. The rash resulting from a lone star tick bite is very similar to Erythema migrans. Along with the rash, patients may present with fatigue, fever, headache, muscle and joint pains. This condition has been called “southern tick-associated rash illness” (STARI). The cause for STARI is unknown but can be diagnosed based on geographical location, symptoms and history. Patients with STARI are more likely to remember being bit by a tick than patients with Lyme. Most patients with STARI end up being treated with antibiotics for Lyme even though symptoms of STARI are self limiting.

The biggest steps we can take towards combating Lyme disease as medical professionals is by educating our patients. With more awareness comes more detection and ultimately less complications from the disease.

It is important to not only educate patients on identifying different ticks but also to teach how to prevent tick bites and how to properly remove ticks if they are bitten.

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The Fast Track

Summer 2015

KEEPING MEDICAL SCHOOL WILD Jake Current, OMS-III, OUHCOM

S

truggling to catch my breath and the rest of my team, I was realizing just how out of shape I had become. A few months of endless studying and minimal physical activity culminating in a weeklong marathon cram for the ENT final was not the ideal preparation for an adventure/wilderness medicine race.

Man, I wish I could breathe, or take this pack off, or maybe just remember how the hell to read a compass again.

"Medical school is not the end to all things wild and exciting" My two buddies and I were in Tennessee for the MedWAR medical wilderness adventure race. The MedWAR events focus around handling medical emergencies in the wild with minimal equipment while simultaneously hiking, running, biking, and navigating over miles of harsh terrain. Our day consisted of 12 miles of racing

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up and down the mountains of the Cumberland Gap handling everything from MIs and crush injuries to heat stroke and a tension pneumo. Both medical and wilderness survival- based skills are tested with a team’s performance based on a combination of the two.

With a little luck, the cumulative knowledge of a few second years,

Summer 2015

The Fast Track

and a lot of sweaty and winded miles, our team Wild Heritage managed to eke out a second place.

Results aside, the true highlight of the day was how much fun our team had during the race.

Regardless of the mental and physical exhaustion of the race, we laughed and smiled from start to finish. This sort of type two fun combined with a post-race beer, BBQ, and a campfire made for an unforgettable weekend. Contrary to what the typical adventurer will say, medical school is not the end to all things wild and exciting. Yes, the nights spent out under the stars and the weekends spent chasing epic [insert hobby here] conditions are fewer and farther between, but medical school still allows for some awesome experiences. I mean, how often do you get to spend the day flying downhill on a mountain bike, pop a chest, trail run across mountains, sew up lacerations, climb a ropes course, and splint a broken femur?

MedWARs is the perfect marriage of my former wilderness- based life and current medical skill set in development. My backpack used to be stuffed with ice axes, carabiners, and ultralight alpine gear, but now I haul around Pathoma, First Aid for

USMLE, and a DIT Step 1 Study Guide. One of my biggest struggles has been trying to find a new balance in life between the long hours of studying and taking time off for the adventures that keep my spirit strong and my sanity intact. This, I am certain, is no different than what my senior colleagues (and inevitably my future self) also work to maintain. I constantly remind myself that medical school is no different than developing any other wilderness skill set. It takes many years of hard work and commitment before climbing tough routes in the Yosemite valley, paddling huge rapids on the Colorado River, or sinking my ice axes and crampons into sheer vertical ice. Medicine is no different. Luckily for me, I found my niche in the world of wilderness medicine, and with events like MedWARs I have the opportunity to work on all these passions both new and old at the same time.

I cannot wait for the next MedWAR race coming in the fall, but for now the primary objective is to survive Step 1. Then I’ll get back to figuring out that compass thing.

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The Fast Track Summer 2015

Winter coats are back in the closet. The season of bikinis and cold lemonade is finally here. The kids are taking full advantage of the warm weather, cooling off in pools, lakes, rivers, and the ocean.

Hand and hand with all the joy associated with water play comes the unfortunate truth that many kids in the United States will die or have significant morbidity Michael Hong, DO and Terrance McGovern, DO MPH each year from drowning.

St Joseph’s Regional Medical Center, Paterson, NJ In fact, according to CDC statistics, drowning is the leading cause of death among children aged 1 to 4 only trumped by congenital anomalies. Among those ages 1 through 14 , drowning paves the way as the second most common unintentional injury-related death behind motor vehicle accidents.1 It’s inevitable as an emergency physician that you’re going to encounter submersion injuries a submersion injury and it’s important that you know how to manage them it when the time comes.

There has been a wide range of nomenclature used to describe the different extents of submersion injuries. According to experts, confusion in terminology contributed to underestimation and inaccurate number of drowning victims. In 2002, The World Congress on Drowning (WCOD) met in Amsterdam, Netherlands in an effort to come up with a new definition that would improve surveillance of drowning victims. The definitions adopted by attendees of conference and The World Health Organization (WHO) in 2002 is as follows: “Drowning is the process of experiencing respiratory impairment from submersion/ immersion in liquid.” Furthermore, “Drowning outcomes should be classified as: death, morbidity, and no morbidity…the terms wet, dry, active, passive, silent, and secondary drowning should no longer be used.”2 Using the more clearly defined definitions will provide a more accurate representation of the true extent of drowning victims.

Pathophysiology of Drowning

Among those ages 1-14, drowning paves the way as the second most common unintentional injury related death

The first sequence of drowning occurs when the airway is submerged in a liquid medium, usually water. The sudden, unexpected submersion causes the victim to panic and attempt to struggle out of the water. Water is then both voluntarily and involuntarily swallowed, asand the victim attempts to hold his or her breath. This breath-holding usually lasts less than one minute (even less for children) and hypercarbia soon triggers inspiratory drive at an attempt to inhale oxygen. Aspiration of water into airway leads to coughing and reflexive laryngospasm, and as a consequence, no oxygen is exchanged due to obstruction at the level of the larynx. As the arterial oxygen tension drops further, the victim rapidly loses consciousness and becomes apneic, systemic hypoxemia ensues and results in multi-organ failure.2,3 page 24

Hypoxia is the primary driving force in the pathophysiology of drowning. Lack of adequate ventilation

to the lungs and a liquid medium in the alveoli disrupts the alveolar capillary membrane along with surfactant washout. This leads to intrapulmonary shunting, alveolar collapse, ventilation perfusion mismatch and ultimately thus, inadequate diffusion of oxygen into systemic circulation. Hypoxemia soon causes a loss of consciousness that leads to apnea. If the victim is not rapidly rescued, cardiovascular dysfunction will occur soon ensues due to hypoxia, acidosis and hypothermia. The most likely sequence of dysrhythmia is tachycardia, bradycardia, pulseless electrical activity then finally, asystole. This downward spiral, which begins with hypoxia, ultimately leads to coma, respiratory failure, cardiac arrest, and death.

Pre-hospital and ED Management The single most important factor for the survival of a drowning victim is the extent and duration of hypoxia. Therefore, the most important intervention for drowning victims is restoration of ventilation. For that reason, in these cases we revert back to the A-B-C’s of CPR as opposed to the newly adopted C-A-B algorithm from the 2010 AHA guidelines.4 There is no need for clearance of water from airway as majority of drowning victims aspirate less than 3-4ml per kg of water and attempts such as Heimlich maneuvers should be avoided as regurgitation and aspiration of gastric content can further worsen ventilation.5 Drowning victims will typically respond to rescue breaths. If the patient does not respond to initial rescue breath, CPR should be started immediately, along with the removal of wet clothing and passive rewarming.

The goal does not change in the emergency department. Adequate oxygenation and ventilation

takes priority in drowning victims. Drowning victims arrive in a spectrum of clinical presentations. For patients with little to no symptoms and oxygen saturation >95%, a quick chest X-ray and monitoring of their oxygen saturation for 4-6 hours may suffice for management.In For more symptomatic patients, endotracheal intubation may be warranted to reverse the patient’s hypoxemia and also prevent further aspiration of stomach content. Since most drowning victims are hypothermic, both passive and active rewarming is recommended depending on the severity of hypothermia. In cases of severe hypothermia, where core body temperature is <30oC, extracorporeal membrane oxygenation may be another possibility in capable facilities.

Resuscitation should be continued until the body temperature is at least 32 – 34oC. Although occurrence of C-spine injuries in submersion victims is relatively low, if there are clinical signs of trauma, history of diving, or if history of intoxication, one must still consider the possibility of a traumatic injury and therefore must adhere to cervical spine precautions.6

Summer 2015

The Fast Track

It is far too easy to blame a drowning incident on a young child’s imperfect doggy paddle, or that the discovery of a child at the bottom of the pool was “just a failed attempt at the deep end.” Once the patient is resuscitated, it’s important to explore the possibility of an underlying condition that may have precipitated the accident. One of the more concerning potential medical etiologies is epilepsy.

Diekema et al found in a retrospective cohort study that pediatric patients with epilepsy had a relative risk of drowning in a bathtub of 96 (95% CI: 33275) and 23.4 (95% CI: 7.1-77.1) in a pool.7 In the undiagnosed epileptic child these numbers can be intimidating; however, in a separate study of witnessed submersion events in epileptic children,

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The Fast Track Summer 2015

all children survived, demonstrating that with proper supervision these patients are at no higher risk of death in these accidents than their seemingly healthy peers.8 Another possible underlying cause is undiagnosed cardiac abnormalities, such as congenital long QT syndrome (LQTS) or catecholaminergic polymorphic ventricular tachycardia (CPVT). For both of these conditions the patientâ&#x20AC;&#x2122;s heart is structurally sound, but they are prone to potentially fatal dysrhythmias that present with syncope, seizures, or sudden cardiac death. LQTS and CPVT can both be exacerbated by a triggering event, such as swimming.9,10,11 In a post-mortem evaluation, it was found that approximately 30% of unexplained swimmingrelated drowning patients had cardiac channel mutations that were indicative of LQTS and CPVT.12 A pediatric death is undeniably tragic, but knowing about this inheritable channelopathy may save the lives of surviving relatives. We must also consider the unfortunate possibility that an apparent drowning was not an accident. Further investigation into potential non-accidental trauma may be necessary if the parentâ&#x20AC;&#x2122;s stories are not aligning, there are additional signs of abuse, a previous history of abuse or delayed presentation for medical care.

Disposition Obviously, the patients that present to the emergency department after receiving CPR, rescue breaths, or are exhibiting unstable vital signs are going to be admitted to an intensive care unit, but what about the essentially asymptomatic or mildly symptomatic children

page 26

after a submersion injury? Causey et al delved into this in a retrospective cohort study that .

They reviewed 48 pediatric patients who had a near-drowning episode and who presented to the ED with a GCS >= 13, without receiving any advanced life support;. Tthey found that patients within this cohort that had a normal physical exam and normal room air oxygen saturation between 4-6 hours after ED admission could be safely discharged home with outpatient follow up.13 In the emergent care of a pediatric submersion injury we are essentially providing secondary prevention, attempting to reduce the impact of the hypoxic/ischemic event that has already occurred. Ideally, we could provide primary injury prevention by stopping the event from occurring.

Prevent the incident from even happening in the first place, also known as primary prevention.

There are numerous interventions to help reduce the amount of submersion injuries, including: four-sided pool fencing, swimming lessons, adult supervision, CPR training for supervisors, swimming in life-guarded areas, flotation devices, hot tub covers and general awareness of bath tub and bucket drownings.14 While it may not seem in the scope of our practice, it is worthwhile to incorporate even the smallest warning to parents about the dangers of drowning, especially in the summer months during our daily interactions with them in the emergency department. In addition to providing the best care during these unfortunate cases of drowning, letâ&#x20AC;&#x2122;s also do our part to prevent them from ever occurring.

Summer 2015

The Fast Track

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The Fast Track Summer 2015

Deborah Rogers, OMS-IV, LMU-DCOM Mike Fucci, OMS-IV, WVU-SOM

Behind the scenes of the student conference P

lanning conference is more than just scheduling speakers and preparing labs; it’s an experience of a lifetime. From day one as conference committee co-chairs we were excited to plan the best conference possible.

We chose to run for this position to gain experience in planning large EM events, and to get an inside view of how the ACOEP functions.

We both ran for the conference committee, and were elected, as third years. However, you can run for the position any year of medical school. By being in this position we have come to know some great people in our osteopathic emergency medicine family, and have built friendships that will last a lifetime.

To plan a ACOEP- SC conference several factors have to play in to make it an enjoyable experience for all. The location and dates are predetermined by our parent chapter. The speakers, the labs, and their content are all subject to change to be the best fit for each conference. Being able to

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work as a team is imperative for conference planning, and being able to delegate tasks is crucial.

Organization is key to staying sane, and to keep everyone on the same page. Flexibility and adaptability are mandatory qualities of emergency physicians, and as a conference committee planner you get to hone these skills. Last-minute schedule changes, delayed flights, and stolen cars happen. You must be able to think on your feet, adapt and overcome.

Actually preparing for conference involves a lot of emails. The resident chapter physicians are great resources for lecturers. They are very approachable, down to earth, and a wealth of knowledge. The ACOEP has many great speakers in the parent chapter as well. The hardest part is making sure that everyone’s schedules line up and the topics all fit together well. Finding qualified speakers that are free from other conference obligations, and scheduling them in advance allows for less stress when it’s show time.

Preparing for the two labs is more time consuming than scheduling the lectures. Generally, we have to

contact a whole residency program and review potential topics. The next step is making sure all of the materials for the lab are transported to the conference location. The labs require several people to be able to help with each table or section, so often a little more time is put into preparation for the labs.

The day of the conference is go time! Prepping for the day starts an hour before, and goes until the last student leaves. You are required to introduce each speaker without butchering their name, and help labs flow with ease. Attendance has to be taken, and gifts have to be given. Luckily, you have several other board members that are there to help keep everything rolling. We are lucky as students in the ACOEP; we have several amazing DO’s that are willing to help out during last minute conflicts to ensure we put on a great conference. Whether its from the parent chapter or the resident chapter, we are guided by the best around.

After the conference is over we meet with the rest of the student board to discuss what went well

and what we can improve on for the next conference. Everyone shares ideas about future conferences and what we can do to make them more engaging. By the time conference has ended, we have met with key members from the resident chapter and created a tentative schedule far in advance so that we have a framework to build upon. In addition to all of this, we send out a post-conference survey to help us gather direct feedback while the conference is still fresh in everyoneâ&#x20AC;&#x2122;s minds. Our predecessors have created a process which works like a well-oiled machine, and ensures that we do not miss any crucial steps in planning for the future.

Thinking about running for conference committee co-chair, or any position for that matter? Letâ&#x20AC;&#x2122;s discuss some reasons that you may not want to run for national leadership. If your goal is to add another checkmark on your curriculum vitae without dedicating a significant amount of time, this is not the right choice for you.. There are many avenues through which you can explore emergency medicine or even another unrelated field which can make you a more well rounded individual and potentially a more desirable residency applicant.

Planning a conference requires dedication, and a love for the profession. It will show poorly if your heartâ&#x20AC;&#x2122;s not in the right place.

There are many reasons to serve on the ACOEP- SC board. One obvious advantage of being in a leadership position is gaining organizational and leadership experience. After serving as committee chairs, we find ourselves more willing to ask questions, assert our opinions, and get more involved on our third year rotations. One of the things that surprised us the most about this position was the camaraderie on the student board.

Communicating through email, having discussions on the phone, and spending time together during and outside of conference has helped us to forge a strong bond with each other. The first couple years of medical school are very busy, and this can make it difficult to communicate with students from other schools on a regular basis. The exposure to a diverse group of quality students who each have different perspectives on school, residency, and life is an often overlooked benefit of having this position. Our discussions about how to best tackle the process of setting up rotations, finding a residency that is a good fit, and being a successful student have been invaluable.

Part of the job requires that we work with emergency medicine residents and attendings, and this has given us the opportunity to build friendships with some incredible people who offer great advice. Going to conference

Summer 2015

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The Fast Track

allows you to meet people who have already accomplished what we are striving for. Interacting with them is an amazing opportunity to glean some wisdom and knowledge about how they overcame certain obstacles to get where they are today. Attending conference provides attendees with a significant advantage over other students because of the cutting edge lectures and labs. For example, the airway and ultrasound labs gave us a strong foundation as a medical student before even starting our emergency medicine rotations. We were able to perform intubations, FAST exams, and central lines relatively early in our rotations because of the confidence gained from previous instruction at national conference.

Serving as committee co-chair has been a great experience that has helped us learn more about current topics in emergency medicine, forge lasting friendships, and provide access to priceless information from colleagues and mentors. We are fortunate to have a parent chapter and staff who are so supportive of the students and who allow us to organize incredible conferences. We encourage you to not only attend, but to actively participate in these conferences so that you can gain the knowledge, confidence and resources to become an outstanding student and emergency medicine physician.

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The Fast Track What I Learned Intern Year

(and why I could never be a pediatrician) Summer 2015

By Ken Argo, DO

E

arly in my medical training I considered the possibility of specializing in pediatrics. The first physician I shadowed was a pediatrician. This particular pediatrician, Dr. McQuillen, was a seasoned, old-school doctor with decades of experience. He easily recognized how much I enjoyed his patients and how effortlessly I interacted with them. I confided in Dr. McQuillen that I had a soft spot for kids, especially babies. He said with a wry grin, “I’d have never guessed.” Then sarcastically, “It’s not like you have much experience with them anyway.” I rolled my eyes at him with a half smile of my own. His statement was entirely ironic because I’m a father of four, and Dr. McQuillen had been caring for my children since each of them was born.

The smile faded from Dr. McQuillen’s face as he thought for a moment. In a more serious tone he said, “You know it’s good that you like kids, but you have to be careful that you don’t get too attached because it might affect your objectivity.” I nodded. I may have looked a little deflated because he quickly added, “I understand how you feel. I’ve been doing this a long time. I still love coming to work because I enjoy my patients, but at the end of the day I’m the

doctor not the parent.”

By the time I started medical school, emergency medicine had caught my eye. Ok, it had more than caught my eye. The more I learned about EM the more I liked, and it was not long until I knew EM was what I had to do. I am not going to use this article as a forum to catalog the virtues of being an emergency physician for fear that it would end up looking like some cliché personal statement.

Instead, I’ll keep to the topic at hand: kiddos! On any given shift, I estimate that 10 percent of the patients I see in the ER are of the short, snotty-nosed variety, known to some with more discriminating vocabulary as rugrats. I don’t have any hard statistics (or any statistics at all for that matter), but I imagine that other ERs around the country see roughly similar numbers of pediatric patients. It’s like a little bonus when I walk into a peds encounter.

I’m not suggesting that my shift just drags until I see a kid. There’s plenty more to like about what I do. Going to work in the ER is like putting on your favorite pair of jeans. They’re comfortable, they fit just right, and damn they make you look good. Finding a twenty in your favorite pair of jeans, that’s my Peds encounter.

Intern year is coming to an end for

me. It’s been a rough ride as I’m sure it is for every intern. I love being on-service in the ER, but some of my off-service months weren’t so fun. At my program every other month is spent in the emergency department. The off-service months for intern year include medicine, ICU, surgery, OB, night house officer and pediatrics. My first off-service rotation was internal medicine, and although I learned a lot, the pain to gain ratio was high. I was always happy when the off-service month was over and could return back to the emergency department.

It was toward the end of intern year when I started my pediatric month. The rotation is located at a children’s hospital in the same city as our home hospital. The children’s hospital accepts neonatal and pediatric patients from the surrounding area, so the pediatric census is high most of the time. Most pediatric patients at my home ER fall within the category of minor acute illness. We do not see many chronic or serious acute cases, and of those cases all are transferred because our pediatric unit closed in a recent merger. As I began my rotation I realized that the cases seen at the children’s hospital were far different from those in my own ER.

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I was surprised to learn how often chronic constipation in pediatric patients result in hospitalization. Among those hospitalized, several were anemic, dehydrated and suffered protein calorie malnutrition. These were children with a primary diagnosis of chronic constipation; they had no other comorbidities. I was amazed how constipation could be a problem with major sequelae in severe pediatric cases. Many cases experienced were

Summer 2015

The Fast Track e d. u s to m c c a s a to a i l u re t e r f that I w r u o e f i l i i t te d al m tly af e t ypic te admr care shor etails to h a t n o m e o an n d nt fr e fo s t e volved placed in ely vague oncluding th f d i f fe r e n i e s a o i s s uals t wa ning urpo uch c One s . This infanave been prious individ t the begin t in the t h r i ve b o r n . I h y m i t y o f v a i s p a t i e n t a m u c h we i g h a s we l l being t the anon signed to th not gained ral aversioning was protec t. I was as patient had atient had o lacia. Feed ards. I patientation. The ir th. The p lar yngoma vomit after we room the ro following bon risk and ient would staying in th gs. Yet w e e k s i l d a s p i r a t i m e s t h e p a t t i e n t o f t e n w i t h fe e d i n a m e o r a s a m l t. O f te n t i i t h t h i s p a i n g to h e l p e m a i n t h e s l e m e nt d i f f i c u e x t r a t i m e wre a t t e m p t h t wo u l d r c e d t o s u p p o vo m i t spent hour or mo tient ’s weigube was pla continued t . After a fo r a n d a y t h i s p a a s o g a s t r i c t t t h e p a t i e n t f fe c t i v e n e s s y t u b e ever y lightly. A n helped, bu ion of the e s gastrostom as the d ro p s e d i n g s. T h i s a t i n g a p o r t n d a t i o n w a o n . A s s o o n ro c e e d. o r a l fe e e d i n g s n e g e r e c o m m e u n d o p l i c a t i e r y w o u l d p t o m e e t a f t e r f r y c o n s u l t t h o n c u r re n t f t , t h e s u rg e re u n a b l e u l t , t h e y surge ent with c arget weigharetakers wild. As a res placemt reached t e patient ’s c s of the ch ER patientunately, th anding need fo r a n e d n a , m r onth d ho U n fo s i n g l y d e m t i o n . n t i re m e. I re t u r n e w n w i t h e n a i n c re a e d t h e p o s i r o m s e fo oss t l i fe t i ed re s i g n ild’s caseem like a mained acr ally I follow ad h c s i h e can ed t iodic me r er y h I followian a monthtle piece of about. Per case. Surg t. I was h t c t i p hy s i E R , b u t a l n o t fo r g e c i a n o n t h e g a i n w e i g s t i l l a n to the life I could ding physi s star ting tor, there was s of Dr. a littleth the atten patient wa s; howeve e wise word e to be up wi well and the e good newuld hear th , “…you hav was too gone to hear th ment. I co ears earlier ached…” I t ere was happye with placeom many y get too att ttached; th nvolved issu Quillen fr you don’t already a o longer i d. My M c eful that as n was s chil gh. I do that. I wl care of thi . car u o h t l a t e w ay t o u n e m e d i c a w a s o ve r I no w i fe, n y i n t h e p hy s i c i a n l y t c m e r a i i h d s th wit hy s i c time a e a k i n g at te n d i n g p a d t a k e n p s r Af te c te d t h e i e nt t h at h e a r t . I c o n t a h e t i ny p a t e i n my h of t cial plac if the a spe d him that e i n fo r m

patient was not placed at the time of discharge, I would be happy to provide a home. I had never done anything like this before, and wasn’t even sure if it was possible. After a couple of nerve-wracking weeks wrought with paperwork, home inspections and soul-searching, we finally received an answer. The child would be temporarily placed in our care.

Bear in mind that this patient was a special case; and while my wife often tells people that this is the reason I can’t be a pediatrician (or a veterinarian), I feel that this once-in-a-lifetime opportunity would not have arisen any other way. I don’t intend to foster the world, nor do I think situations like this are for everyone.

Regardless, I am grateful for the experiences my intern year has brought me, including one that has already changed my heart in a way I could never have predicted.

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The Fast Track Summer 2015

SUNNY BEACHES & SPRING CONFERENCE Christopher Falslev, OMS-II, WVSOM ACOEP-SC GME Chair COEP Spring conference was held at Marriott Harbor Beach Hotel in Fort Lauderdale, Florida. The student programming,organized by the ACOEP Student Chapter, was a great success, with over 100 students from 22 different medical schools in attendance. The conference kicked off Tuesday night with â&#x20AC;&#x153;A Taste of Paradiseâ&#x20AC;? opening reception. Students had the opportunity to mingle with emergency physicians, residents and fellow students from across the United States.

Wednesday morning sprang into action as the participants awoke early to compete in the first part of the Leadership Academy, a team building scavenger hunt. The Leadership Academy provides a yearly opportunity for students to hone their leadership skills.

The forty participants were divided up into eight teams competing in a two-part workshop. In part one, teams competed on foot through the streets of Ft Lauderdale for a timed scavenger hunt.

The teams faced challenges together as they raced page to acquire points, while 32

A

networking with their peers.

The scavenger hunt ranged from challenges such as photoops with strangers to videos of the team breakdancing on the sidewalks. The top three teams took home prizes such as a GoPro, FitBit, and Skullcandy wireless headphones.

In part two the teams and an Attending Physician mentor worked together on how to organize a medical station for a Boy Scouts of America National jamboree.

They presented their plan to a panel of judges. The Leadership academy is only offered at the spring conference, so be sure

Summer 2015

The Fast Track

to sign up early to secure a spot in this unique the progress of emergency medicine over time event. and the future of the profession.

The Conference also included events offered to all attendees. The ultrasound lab put on by the Resident Chapter was a particular success.

Students obtained hands-on opportunities to practice ultrasound skills that can be used on rotation. Following the ultrasound lab were the popular Rapid Fire lectures on topics such as EKG’s, concussions, airplane emergencies, and management of critical care patients. In addition, an informative lecture was given with tips from a program coordinator about the “dos” and “don’ts” during rotations to help obtain a residency spot. Dr Mark Mitchell, ACOEP president, wrapped up the lectures, discussing

The evenings were spent enjoying social events where the residents and students mingled at events hosted by EMP and TeamHealth.

Students were able to relax and gain tips from residents and program directors during this time.

As the rays settled on the sandy beaches of Fort Lauderdale, those in attendance walked away with increased knowledge, skills and friendships. We encourage all those that were not able make it down to the April conference to join us this fall in Orlando!

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The Fast Track Summer 2015

Demand Ischemia, Acute Right Ventricular Strain, and Pulmonary Artery Hypertension Secondary To Severe Rheumatic Mitral Stenosis Dhimitri Nikolla, DO, Saint Vincent Hospital, Erie PA Eric Garfinkel, OMS IV, LECOM, Erie PA Bryan Doverspike, DO, Memorial Hospital, York PA

INTRODUCTION:

A 31-year-old Cambodian female presents to the emergency department, complaining Rheumatic heart disease is a common cause of of morbidity and mortality in developing nations.

Screening echocardiography has revealed a higher prevalence than substernal, left-sided chest pain and previously thought: about 21.5 to 30.4 cases shortness of breath that woke her up per 1000 in Cambodia and Mozambique, from sleep. She describes the pain as a respectively. About 87.3% to 98.4% of the â&#x20AC;&#x153;pressureâ&#x20AC;? that is constant, non-radiating cases in these countries involved the and worse with exertion. Nothing makes mitral valve [1]. Nevertheless, it is not a the pain better. She admits to having had common cause of chest pain in American mild chest pain for the last two years when emergency departments. Here, we present she exerts herself. She denies palpitations, a case of acute chest pain caused by lightheadedness, syncope, nausea, and demand ischemia and right ventricular vomiting.

(RV) strain secondary to severe rheumatic mitral stenosis.

Her past medical history includes rheumatic fever and mitral stenosis. She denies any CASE: surgical history and takes metoprolol for her mitral stenosis. She has no known allergies.

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Figure 1 - Our patientâ&#x20AC;&#x2122;s electrocardiogram showing a normal sinus rhythm with first-degree AV block, right axis deviation, biatrial abnormality, and RV hypertrophy with strain pattern.

She consumes alcohol one to two times per year and has never smoked. Her family history is significant for hypertension and myocardial infarction in her father at age 56.

Physical exam reveals: temperature 97.7°F, heart rate 83 bpm, respiratory rate 21 breaths/min, blood pressure 118/101 mmHg, and SpO2 99%

Figure 3A

Figure 3B

cyanosis, no clubbing of the digits, normal chest wall expansion, no accessory muscle use, and clear lung sounds. Cardiovascular exam reveals no peripheral edema, strong distal pulses, and heart sounds that have a regular rate, regular rhythm, a

on room air. She is in no apparent distress and is alert and oriented to person, place, and time.

Respiratory exam reveals midline trachea, no

Figure 3C

Figure 3D page 35

The Fast Track Summer 2015

prominent S1, and a diastolic opening snap best appreciated at the cardiac apex.

Figure 2 displays our patientâ&#x20AC;&#x2122;s chest x-ray showing widening of the left, middle mediastinum.

Figure 3 A-D displays images from our patientâ&#x20AC;&#x2122;s computed tomography angiography scan of her chest showing no evidence of pulmonary embolism, but cardiomegaly and a left atrial mass or thrombus.

An electrocardiogram shows a normal sinus rhythm with first-degree AV block, and largely signs of right heart strain: right axis deviation, biatrial abnormality, and RV hypertrophy with strain pattern (Figure 1 and Table 1). A chest x-ray reveals widening of the left middle mediastinum (Figure 2). Her Troponin I is elevated at 0.228 ng/mL, B Type Natriuretic Peptide at 554.5 pg/mL, and lactic acid at 2.4 mmol/L. Computed tomography angiography of the chest is performed which shows no evidence of pulmonary embolism, but cardiomegaly and a left atrial mass or thrombus (Figure 3).

We diagnose our patient with demand ischemia and acute, RV strain likely secondary to type-2 pulmonary artery hypertension (PAH) caused by her severe rheumatic mitral stenosis. Her pain is controlled with morphine as well as nitroglycerin. She is continued on her metoprolol, and we began a heparin drip for her left atrial mass that was concerning for a thrombus.

The following day, she undergoes a transesophageal echocardiogram showing moderate RV hypertrophy, severe PAH

page 36

with a pressure of 55mmHg, normal left ventricular ejection fraction, severe left atrial enlargement, severe mitral stenosis with a pressure gradient of 19/14mmHg, and a large 1.5 x 3cm homogenous mass in the left atrium, likely a blood clot. Cardiac catheterization is performed which corroborates the echocardiographic findings with normal epicardial coronary arteries. The cardiologist recommends surgical intervention and she is transferred to another facility for mitral valve replacement and extirpation of the left atrial thrombus.

DISCUSSION: Besides the unique experience of evaluating a patient with severe rheumatic mitral stenosis, this case illustrates several important teaching points pertaining to cardiac ischemia and PAH. Although our patient had a very typical presentation of acute coronary syndrome, with anginal chest pain, elevated troponins, and ST segment depressions, her pain was not caused by acute coronary syndrome. Her heart was stressed by an acutely elevated pulmonary artery pressure causing demand ischemia.

Demand ischemia is a supply and demand mismatch of oxygen to the myocardium that can be precipitated in many clinical conditions including sepsis, hypotension, severe anemia, severe aortic stenosis, and tachyarrhythmias [3,4]. If infarction occurs secondary to demand ischemia in the absence of coronary artery disease, it is deemed a type-2 myocardial infarction by the Universal Classification of Myocardial Infarction (Table 2) [4]. In a country rampant with coronary artery disease, it is natural to assume someone with anginal symptoms, elevated troponins, and ST depressions are experiencing an acute coronary syndrome. However, it is essential to also consider demand ischemia as a

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Summer 2015

The Fast Track Core Faculty Academic and Research Skills Development Course

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The Fast Track Summer 2015

Vagal Maneuvers A Review, and a Uniquely Osteopathic Addition to the ACLS Armament

Richard M. Pescatore II(a), Benjamin N. Abo(c), Matthew C. Ruppel(b), Jessica M Smolar(a), Robert M. Sklar(b), Stephen A. Pulley(b) (a) Dept of Emergency Medicine, Cooper University Hospital, Camden, NJ

(b) Dept of Emergency Medicine, Philadelphia College of Osteopathic Medicine, Philadelphia, PA (c) Dept of Emergency Medicine, Mount Sinai Medical Center, Miami Beach, FL

Introduction

In the United States, there are more than half a million people diagnosed with supraventricular tachycardia (SVT). There are approximately 89,000 new presentations of SVT per year. Many of them present to emergency departments for initial management of their tachydysrhythmia. In the emergency setting, treatment of hemodynamically stable patients proceeds along the widely accepted Advanced Cardiovascular Life Support (ACLS) pathway, and can include physical maneuvers, pharmacologic intervention, or electrical cardioversion. Since the introduction of adenosine, a primary medication for the treatment of SVT, emergency physicians have tended to neglect physical maneuvers due to assumed time cost and unfamiliarity. Vagal maneuvers, however, represent an effective and safe method for termination of superventricular tachycardias. The purpose of this article is to describe the wide range of effective techniques for the initial non-pharmacologic management of supraventricular tachycardia, and to discuss their mechanisms of action and potential drawbacks. Additionally, we will introduce a commonly used Osteopathic Manipulative Therapy as a potential first-line treatment option for hemodynamically stable SVT. The â&#x20AC;&#x153;V-Spreadâ&#x20AC;? technique presents a potentially effective and particularly safe initial intervention and could be added to the treatment algorithm for stable, narrow-complex tachydysrhythmias in the emergent setting.

page 38

Discussion

SVT is a general term, and its common use within the ACLS guidelines and introductory cardiology literature often creates confusion for students and practitioners. Dysrhythmias such as sinus tachycardia and atrial fibrillation represent distinct etiologies. Their treatment pathways differ from accepted treatment of regular, narrow-complex tachycardias. We have excluded their discussion from this article. It is important to note that treatment of supraventricular tachycardia, as it is defined within American Heart Association (AHA) recommendations, focuses on the management of the most common form of SVT—atrioventricular (AV) nodal reentrant tachycardia (AVNRT).

AVNRT is a consequence of a dual AV nodal physiology created when two competing pathways for electrical conduction arise between the atria and ventricles. Aberrant conduction can cause a reentrant circuit within the AV node. This can cause patients to present to the emergency department with symptoms that may include palpitations, chest pain, dyspnea, anxiety, lightheadeness, weakness, and diaphoresis. The condition is more common in women (75%) than men. Most patients seek emergency medical care during the fourth or fifth decade of life.

After identification of AVNRT, the most recent American Heart Association ACLS guidelines provide for the use of vagal maneuvers in the initial management of a hemodynamically stable patient. Recommended maneuvers include carotid massage and the Valsalva maneuver. As up to 27% of SVT presentations may convert with such simple maneuvers alone, it is nearly certain that use of vagal techniques as primary interventions will remain.

Valsalva Maneuver The Valsalva Maneuver should be performed with the patient in the supine position.6, The patient is asked to forcibly exhale against a closed mouth or by asking the patient to bear down, both for at least 15 seconds. Ideally, the intrathoracic pressure should be measured, though this is impractical in the emergency setting. Exhalation against a closed glottis causes an increase in intrathoracic pressure that incites a sequence of rapid changes in preload and afterload stress. As preload and venous return fall, stroke volume follows suit via the Frank-

Starling mechanism. Pressure on the thoracic aorta induces a baroreceptor reflex that transiently slows the heart rate during the maneuver. On release of intrathoracic pressure, sudden increase in diastolic filling and concomitant stroke volume increase induces an arterial pressure overshoot and a relative compensatory bradycardia. The efficacy of the Valsalva Maneuver is variable, with four small studies reporting reversion success rates ranging from 6-54%. Part of this variability may be patient effort dependent. One technique to judge the patient’s effort is to place the practitioner’s fist into the patient’s abdomen and have the patient hold their breath and push their abdominal musculature against the fist. A weak effort can be detected and the patient coached to increase the effort. This method also gives the patient a focus for their effort. Despite a potentially low success rate, the Valsalva Maneuver is safe and takes little time with correct application.

Summer 2015

The Fast Track

Carotid Massage Perhaps the most utilized vagal maneuver, carotid massage consists of five seconds of circular massage on the carotid artery at the level of the carotid bulb. Pressure at this location is thought to cause baroreceptor stimulation, which is transmitted via cranial nerve IX, the glossopharyngeal nerve, to the solitary nucleus (NTS) embedded within the medulla oblongata. The NTS in turn modulates autonomic input to the viscera, and causes parasympathetic impulses to be conducted via cranial nerve X, the vagus nerve. Vagal innervation of the atrioventricular node is inhibitory, and causes variable rates of obliteration of AVNRT. It has been known since the early part of this century that the autonomic nervous system can profoundly affect AV conduction, and it has been demonstrated that the nerves on the left side primarily control AV conduction, whereas those on the right govern SA rate. As such, it is a reasonable practice in efficacy for the emergency physician to direct carotid massage efforts to the patient’s left side. Waxmen et al showed a 48.5% conversion rate of SVT with carotid massage, however additional studies have reported efficacy between 11.8-22%.6, Carotid massage is not without risk. The most common adverse effect of the maneuver is hypotension. Although the incidence of hypotension is relatively rare (<1%), other adverse events associated with carotid massage include page 39

The Fast Track Summer 2015

ventricular tachycardia, hemiplegia, coronary artery spasm, thromboembolic stroke, prolonged asystole, and ventricular fibrillation.15 While current ACLS teachings warn students to use caution when performing carotid massage in patients greater than 55 years old, it is clear that the procedure still carries some small risk to a patient already in extremis. The absence of carotid bruits should always be noted and documented.

Facial Immersion Facial immersion in ice water represents a lessstudied and far less frequently used treatment option for initial management of stable tachydysrhythmias. Figure 1.V-Spread Technique applied to the Also known as the â&#x20AC;&#x153;Diving Reflex,â&#x20AC;? facial immersion occipitomastoid suture of a healthy volunteer nurse. induces a profound bradycardia and peripheral Digital Rectal Massage vasoconstriction. The reflex is thought to be Digital Rectal Massage (DRM) is an efficacious initiated by stimulation of afferent nerve endings and rapid technique that may be employed in in the mouth and nose which induces sympathetic the termination of SVT. The rectum is supplied stimulation of peripheral vessels and a significant with parasympathetic nerve fibers from the simultaneous vagal stimulation to the heart. second, third, and fourth sacral segments.23 Previous small investigations have demonstrated Afferent impulses stimulated via rectal massage that ice water applied to the face of a pediatric are transmitted through the pelvic splanchnic patient for five seconds can result in up to a 96% nerves and to secondary afferents en route to the conversion rate. While the application of ice water brainstem and thalamus via the sacral segments. is safe and potentially effective, it presents technical Once the thalamus is signaled, vagal stimulation challenges to adequately perform. Additionally, is accomplished via efferent signaling through the more research, particularly in the adult population, anterior and medial hypothalamus. DRM may be is needed. preferable to other techniques due to its low risk for the complications associated with other vagal Ocular Pressure maneuvers.

The vagal effect of ocular pressure is caused by stimulation of the extraocular muscles. Direct V-Spread Technique pressure on the globe induces an oculocardiac The V-Spread Technique represents a long-taught reflex mediated by the vagus nerve via the technique in osteopathic medical schools where trigeminal nerve, CN V. While ocular pressure has a traction force is applied across the diameter shown efficacy in mediating vagal tone, its use in of the occipitomastoid grooves bilaterally in an the management of SVT has waned due to concerns attempt to relieve myofascial restriction. Release over retinal detachment., of the occipitomastoid suture induces a direct Figure 2. Before-and-after pulse oximetry device readings after five seconds of V-Spread

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In contrast to carotid massage, the V-Spread Technique directly impacts the vagus nerve at its eruption from the jugular foramen, enabling the practitioner to address the parasympathetic malignment of AVNRT. No studies yet exist quantifying the effectiveness of the V-Spread technique in the emergent management of ANVRT; however, the anatomic and physiologic basis for its implementation is sound, and the procedure is well-tolerated by patients with little of the risk encountered with the use of carotid massage.

At the time of publication, no strong studies exist that quantify the effectiveness of the VSpread Technique for treatment of stable narrow complex tachycardias, and evidence of the procedure’s efficacy remains hypothetical and anecdotal. V-Spread and occipitomastoid suture manipulation represent a safe and potentially effective initial intervention in cardiovascular life support and further investigations are warranted regarding its use in the emergency setting.

Summer 2015

parasympathetic reflex by the vagus nerve to influence the cardiac rate.

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FAsT FACTs EmErgEnCy mEdiCinE BOArd rEviEw Conclusion The prevalence of supraventricular tachycardias and the incidence of their presentation to emergency centers across the United States pose an opportunity for non-pharmacologic healing and demands familiarity with those techniques.

Understanding the anatomy and pathophysiology of SVTs, particularly AVNRT, allows the emergency practitioner to intervene quickly and safely with the most basic of tools. Carotid massage, Valsalva maneuver, facial immersion in ice water, ocular pressure and digital rectal massage are excellent and accepted techniques for initial intervention. V-Spread Technique represents a potential additional primary treatment of stable supraventricular tachycardia.

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The Fast Track Summer 2015

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page 42

1) ANSWER: D. This patient presents with a submersion incident and near drowning and likely has experienced aspiration of water leading to pneumonitis. Pneumonitis or inflammation of the lung does not require antibiotics.

Drowning is a common cause of accidental death in the US. Submersion injuries can occur in homes (swimming pools, bathtubs, etc.) and in natural bodies of water. In adults, drowning and submersion are frequently associated with ethanol consumption. Typically, only small amounts of water are aspirated during drowning (about 4 ml/kg) due to closure of the glottis and laryngospasm. Patients who have severe symptoms should be admitted for observation. However, patients who are mildly symptomatic or asymptomatic on presentation with normal saturation and normal chest X-ray should be observed for 4-6 hours to make sure there is no decline in respiratory status. A repeat chest X-ray to look for the development of infiltrates.

Antibiotics (A and B) are not required in patients with pneumonitis. Although the patient has minimal symptoms on presentation, immediate discharge (C) is not recommended as delayed decline has been described.

Summer 2015

Review Answers

The Fast Track

One Step Further: What is the importance of the type of fluid medium (fresh vs. salt water) in submersion injury?

Answer: The type of fluid does not have a clinical relevance 2) ANSWER: D. The photograph shows a “feathering burn” or “ferning.” This pattern of injury is pathognomonic for lightning strike. The lesions are superficial burns caused by the steam production of the flashover phenomenon that occurs when lightning strikes the body. Tympanic membrane rupture is common after lightning strikes resulting either from the shock wave, a direct burn, or basilar skull fracture when the victim falls to the ground.

Deep burns are rare after lightning occurring less than 5% of the time.

Cataracts (A) develop after both electrical and lightning injuries. However, this is a late complication and is not present on initial evaluation. Compartment syndrome (B) is much more common after an electrical injury. High voltage electrical injuries may cause muscle necrosis leading to vascular ischemia and muscle edema. As pressures increase from the edema, compartment syndrome occurs. Lightning injuries may cause transient vasospasm leading to a mottled or pulseless extremity without tense compartments. The vasospasm from lightning usually resolves in several hours. In fatal lightning injuries, cardiac asystole is the most common cause of death from the massive direct current exposure.An irregularly irregular cardiac rhythm (C) is characteristic of atrial fibrillation. Lightning injuries may cause ventricular arrhythmia or prolongation of the QT interval, but atrial fibrillation is not common.

One Step Further: What is the name of transient paralysis of the extremities caused by vasospasm after a lightning strike?

Answer: Keraunoparalysis.

3) ANSWER: C. In order to fully understand the different syndromes of injuries to the spinal cord, it is imperative to understand the location of the tracts of the cord. The posterior columns carry tracts responsible for ipsilateral position and vibratory sensation. The lateral spinothalamic tract carries fibers for contralateral pain and temperature. The lateral corticospinal tract is responsible for ipsilateral motor function. Syndromes may be incomplete depending on how much of the cord is affected by the injury. In the anterior spinal cord syndrome, just the posterior columns are preserved and sopatients lose all pain and temperature sensation as well as motor function. Most cases of anterior cord syndrome follow aortic surgery, but it has also been reported in the setting of hypotension, infection, vasospasm, or anterior spinal artery ischemia or infarct. In trauma, typically hyperflexion of the cervical spine causes the injury to the spinal cord.

Loss of all motor and sensory function (B) occurs with a complete transection of the spinal cord. Most commonly this occurs after a significant trauma. Isolated motor function loss (A) is not a classic syndrome and would result from a small area of injury on the cord just involving the corticospinal tract. Upper greater than lower motor weakness occurs (D) with a central cord syndrome. Sensory involvement is variable although burning dysesthesias in the upper extremities may occur. Most commonly the syndrome occurs after a fall or motor vehicle accident.

4) ANSWER: A. Latrodectus mactans (the black widow spider) is found throughout the US and southern Canada.

Only the female spider, with its telltale bright red, hourglass marking on its abdomen, is venomous. Patients who are bitten will usually experience a pinprick sensation followed by local swelling and redness. Over the subsequent hour, cramping develops near the site and then spreads and becomes generalized. Severe, cramping abdominal pain may ensue and the abdominal examination can mimic that of an acute surgical abdomen. Other associated symptoms include dizziness, headache, ptosis, nausea, vomiting, pruritus, dyspnea, weakness and anxiety. Symptoms may abate on their own in hours and will typically resolve completely within 2-3 days. Supportive care and page the administration of benzodiazepinescan control the majority of symptoms.

43

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REFERENCES Jimsome Weed 1. Glatstein MM, Alabdulrazzaq F, Garcia-Bournissen F, Scolnik D. Use of physostigmine for hallucinogenic plant poisoning in a teenager: case report and review of the literature. Am J Ther 2012; 19:384.

2. Wiley JF 2nd, Gelber ML, Henretig FM, et al. Cardiotoxic effects of astemizole overdose in children. J Pediatr 1992; 120:799.

3. Hasan RA, Zureikat GY, Nolan BM. Torsade de pointes associated with Astemizole overdose treated with magnesium sulfate. Pediatr Emerg Care 1993; 9:23.

4. Mendoza FS, Atiba JO, Krensky AM, Scannell LM. Rhabdomyolysis complicating doxylamine overdose. Clin Pediatr (Phila) 1987; 26:595.

5. Soto LF, Miller CH, Ognibere AJ. Severe rhabdomyolysis after doxylamine overdose. Postgrad Med 1993; 93:227.

6. Frankel D, Dolgin J, Murray BM. Non-traumatic rhabdomyolysis complicating antihistamine overdose. J Toxicol Clin Toxicol 1993; 31:493.

7. Leybishkis B, Fasseas P, Ryan KF. Doxylamine overdose as a potential cause of rhabdomyolysis. Am J Med Sci 2001; 322:48.

8. Clark RF, Vance MV. Massive diphenhydramine poisoning resulting in a wide-complex tachycardia: successful treatment with sodium bicarbonate. Ann Emerg Med 1992; 21:318.

9. Sharma AN, Hexdall AH, Chang EK, et al. Diphenhydramine-induced wide complex dysrhythmia responds to treatment with sodium bicarbonate. Am J Emerg Med 2003; 21:212.

10. Reilly JF Jr, Weisse ME. Topically induced diphenhydramine toxicity. J Emerg Med 1990; 8:59.

11. Bernhardt DT. Topical diphenhydramine toxicity. Wis Med J 1991; 90:469.

12. Thompson HS. Cornpicker’s pupil: Jimson weed mydriasis. J Iowa Med Soc 1971; 61:475.

13. Beaver KM, Gavin TJ. Treatment of acute anticholinergic poisoning with physostigmine. Am J Emerg Med 1998; 16:505.

14. Burns MJ, Linden CH, Graudins A, et al. A comparison of physostigmine and benzodiazepines for the treatment of anticholinergic poisoning. Ann Emerg Med 2000; 35:374.

15. Schneir AB, Offerman SR, Ly BT, et al. Complications of diagnostic physostigmine administration to emergency department patients.

Ann Emerg Med 2003; 42:14.

16. Rosenbaum C, Bird SB. Timing and frequency of physostigmine redosing for antimuscarinic toxicity. J Med Toxicol 2010; 6:386.

17. Pentel P, Peterson CD. Asystole complicating physostigmine treatment of tricyclic antidepressant overdose. Ann Emerg Med 1980; 9:588.

18. Suchard JR. Assessing physostigmine’s contraindication in cyclic antidepressant ingestions. J Emerg Med 2003; 25:185.

19. Shervette RE 3rd, Schydlower M, Lampe RM, Fearnow RG. Jimson “loco” weed abuse in adolescents. Pediatrics 1979; 63:520.

20. Sorisky A, Watson DC. Positive diphenhydramine interference in the EMIT-st assay for tricyclic antidepressants in serum. Clin Chem 1986; 32:715.

21. Pohjola-Sintonen S, Kivistö KT, Vuori E, et al. Identification of drugs ingested in acute poisoning: correlation of patient history with drug analyses. Ther Drug Monit 2000; 22:749.

22. Brett AS. Implications of discordance between clinical impression and toxicology analysis in drug overdose. Arch Intern Med 1988; 148:437.

23. Kellermann AL, Fihn SD, LoGerfo JP, Copass MK. Impact of drug screening in suspected overdose. Ann Emerg Med 1987; 16:1206.

24. Hammett-Stabler CA, Pesce AJ, Cannon DJ. Urine drug screening in the medical setting. Clin Chim Acta 2002; 315:125.

25. Boumba VA, Mitselou A, Vougioklakis T. Fatal poisoning from ingestion of Datura stramonium seeds. Vet Hum Toxicol. 2004;46:8182 26. Bouchama A, Dehbi M, Chaves-Carballo E. Cooling and hemodynamic management in heatstroke: practical

recommendations. Crit Care 2007; 11:R54.

27. Tintinalli, Judith E. Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 7th ed.: The McGraw-Hill Companies, 2011. 1402.

28. Spina, Sean P., and Anthony Taddei. “Teenagers with Jimson Weed (Datura stramonium) Poisoning.” CJEM 2007, 9.6: 467-69 29. Arnett, Amy M. “Jimson Weed (Datura stramonium) Poisoning.”

Clinical Toxicology Review 18.3 (1995).

30. Howell, Catherine H. National Geographic Pocket Guide to Wildflowers of North America. N.p.: National Geographic Society, 2014 p.145.

Photo credit to Wikipedia.com, pictures approved for noncommercial reuse.

Vagal Maneuvers 1. LA Orejarena, H Vidaillet, F DeStefanoet al., Paroxysmal supraventricular tachycardia in the general population. Am CollCardiol, 31 (1998), pp. 150-157 2. Taylor DMcD, Auble TF, Yealy DM. First-line management of paroxysmal supraventricular tachycardia. Letter to editor, Am J Emerg Med. 1999; 17:214 3. Muller G, Deal B, Benson DW. “Vagal Maneuvers” and adenosine for termination of atrioventricular reentrant tachycardia. Am J Cardiol.

1994 Sept;1(74):500-3.

4. Ganz LI, Friedman PL. Supraventricular tachycardia, N Engl J Med, 332 (1995), pp. 162-173.

5. Akhtar M, Jazayeri MR, Sra J, Blanck Z, Deshpande S, Dhala A. Atrioventricular nodal reentry: clinical, electrophysiological, and therapeutic considerations. Circulation 1993; 88: 282-295.6. Neumar RW, Otto CW, Link MS, et al., Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.

Circulation. 2010;122(suppl 3):S729-S767.

7. Lim S, Anantharaman V, Teo W, Goh P, Tan A. Comparison of treatment of supraventricular tachycardia by Valsalva maneuver and carotid sinus massage.Annals of Emergency Medicine. January 1998; 31 (1):30-35.

8. Incorrect instruction in the use of the Valsalva maneuver for paroxysmal supra-ventricular tachycardia is common. Emerg Med Australas. 2004 Aug; 16(4):284-7.

9. Porth CJ, Bamrah VS, Tristani FE, Smith JJ. The Valsalva maneuver: mechanisms and clinical implications. Heart Lung. 1984 Sep;13(5):507-18.

10. Junqueira, LF. Teaching cardiac autonomic function dynamics employing the Valsalva (Valsalva-Weber) maneuver. AdvPhysiol Educ.

2008 Mar; 32 (1):100-106 11. Smith G. Management of supraventricular tachycardia using the Valsalva maneuver: a historical review and summary of published evidence. Euro J Emerg Med. 2012 Dec; 19(6):346-352.

12. Rothberger CJ, Winterberg H. UberdieBeziehungen der Herznervenzuratrioventrikularenautomatie (nodal rhythm). Arch Ges Physiol. 1910; (135) 559-604.

13. Martin, P. The Influence of the Parasympathetic Nervous System on Atrioventricular Conduction.Circulation Research. 1988;41:593599.

14. Waxman MB, Wald RB, Sharma AD, et al: Vagal techniques for termination of paroxysmal supraventricular tachycardia. Am J Cardiol 1980;46:655-664.

15. Ornato JP, Hallagan LF, Reese WA, et al. Treatment of paroxysmal supraventricular tachycardia in the emergency department by clinical decision analysis. Am J Emerg Med 1988;6:555-560.

16. Richardson DA, Bexton R, Shaw FE, Sten N, Bond J, Kenny RA. Complications of carotid sinus massage—a prospective study of older patients. Age and Ageing, 2000 (29), pp. 413-417.

17. Matthews, OA. Ventricular tachycardia induced by carotid sinus stimulation. J Maine Med Assoc, 60 (1969),pp 135-136.

18. Askey, JM. Monoplegia following carotid sinus massage. J Intern

Summer 2015

The Fast Track

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The Fast Track Summer 2015

Med, 235 (1994),pp379-381.

19. Nishizaki M, Yamawake N, Arita M. Coronary artery spasm induced by carotid massage. Heart. 2000. 84, pE2.

20. Finley JP, Bonet JF, Waxman MB. Autonomic pathways responsible for bradycardia on facial immersion. Journal of Applied Physiology.1979; 47:1218-1222.

21. Aydin M, Baysal K, Kucukoduk S, Cetinkaya F, Yaman S. Application of ice water to the face in initial treatment of supraventricular tachycardia. Turk J Pediatr. 1995 Jan-Mar;37(1):15-7.

22. Arnold, Robert W. The human heart rate response profiles to five vagal maneuvers. Yale Journal of Biology and Medicine, 1999; 72: 237-244.

23. Yamashita, M. Oculocardiac reflex and the anesthesiologist.

Mideast J. Anesthesiology, 1986; 8:399-415.

24. Bolton, EC. Dysrhythmias, in Rosen P, Baker F, Braen RE, et al (eds): Emergency Medicine: Concepts and Clinical Practice. St Louis, CV Mosby CO, 1983, p 887-916.

25. Silverman ME: Recognition and treatment of arrhythmias, in Schwartz GR, Safar P, Stone JH et al (eds): Principles and Practice of Emergency Medicine. Philadelphia, WB Saunders CO, 1978, p891-921.

26. Roberge R, Anderson E, MacMath T, Rudoff J, Luten R. Termination of Paroxysmal Supraventricular Tachycardia by Digital Rectal Massage. Annals of Emergency Medicine, 1987; 16: 139-141.

27. Adams RD, Victor M. Principles of Neurology, ed 2. New York, McGraw-Hill, 1981; 363-383.

28. Dejong RN. The Neurologic Examination, ed 4. Philadelphia: Harper and Row, 1979; 507.

29. Nicholas A, Nicholas E. Occipitomastoid Suture Pressure, in Atlas of Osteopathic Techniques. Philadelphia: Lippincott Williams & Wilkins, 2008; 398.

Rheumatic Mitral Stenosis: 1. Marijon E, Ou P, Celermajer D, et al. Prevalence of Rheumatic Heart Disease Detected by Echocardiographic Screening. N Engl J Med. 2007;357:470-6.

2. Taylor GJ. 150 Practice ECGs: Interpretation and Review, Third Edition. Blackwell Publishing Ltd: 2006.

3. Gibson CM and Morrow DA. Elevated cardiac troponin concentration in the absence of an acute coronary syndrome.

UpToDate. http://www.uptodate.com/contents/elevated-cardiactroponin-concentration-in-the-absence-of-an-acute-coronarysyndrome. Published July 10, 2014. Accessed October 7, 2014.

4. Thygesen K, Alpert JS, Jaffe AS, et al. Third Universal Definition of Myocardial Infarction. Circulation. 2012;126(16):2020-2035.

5. Simonneau G, Galie N, Rubin L, et al. Clinical Classification of Pulmonary Hypertension. J Am Coll Cardiol. 2004 Jun 16;43(12 Suppl S):5S-12S. 6. Nishimura R, Otto C, Bonow R, et al. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease. Circulation.

2014;129:e552-e558.

Drowning: 1.

Centers for Disease Control and Prevention, National Center for Injury Prevention and Control. Web-based Injury Statistics Query and Reporting System (WISQARS) [online]. [cited 2012 May 3].

Available from: URL: http://www.cdc.gov/injury/wisqars.

2.

Van Beeck EF, Branche CM, Szpilman D, Modell JH, Bierens JJLM. A new definition of drowning: towards documentation and prevention of a global public health problem. Bull World Health Organ 2005;83:853-856 3.

Szpilman, D.; Bierens, J.J.L.M.; Handley, A.J.; Orlowski, J.P. Drowning. Drowning. N. Engl. J. Med. 2012; 366:2102–2110 4.

Vanden Hoek TL, Morrison LJ, Shuster M, et al. Part 12: cardiac arrest in special situations—2010 American Heart Association guidelines for car- diopulmonary resuscitation and emergency cardiovascular care. Circulation. 2010;122(18, suppl 3):S829-S861.

5.

Chandy D, Weinhouse G. Submersion injuries (near-

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drowning). UpToDate. 2009. Accessed 9/23/2009.

6.

Watson RS, Cummings P, Quan L, Bratton S, Weiss NS. Cervical spine injuries among submersion victims. J Trauma. 2001; 51(4): 658-62 7.

Diekema DS, Quan L, Holt VL. Epilepsy as a risk factor for submersion injury in children. Pediatrics. 1993; 91(3): 612-6.

8.

Kemp AM, Sibert JR. Epilepsy in children and the risk of drowning. Arch Dis Child. 1993; 68(5):684-685 9.

Ackerman MJ, Tester DJ, Porter CJ. Swimming, a genespecific arrhythmogenic trigger for inherited long QT syndrome. Mayo Clin Proc. 1999: 74:1088-1094 10.

Moss AJ, Robinson JL, Gessman L, et al. Comparison of clinical and genetic variables of cardiac events associated with loud noise versus swimming among subjects with long QT syndrome. Am J Cardiol. 1999;84:876-879.

11.

Schwartz PJ, Priori SG, Spazzolini C, et al. Genotypephenotype correlation in the long-QT syndrome: gene-specific triggers for life-threatening arrhythmias. Circulation. 2001;103:89-95.

12.

Tester DJ, Domingo AM, Will M, et al. Unexplained drownings and the cardiac channelopathies: a molecular autopsy series. Mayo Clin Pro. 2011; 86(10): 941-7.

13.

Causey AL, Tilelli JA, Swanson ME. Predicting discharge in uncomplicated near-drowning. Am J Emerg Med. 2000; 18(1): 9-11.

14.

Semple-Hess J, Campwala R. Pediatric Submersion Injuries: Emergency Care and Resuscitation. Pediatric Emergency Medicine Practice. EBMedicine.net June 2014. 11(6).

Tick Bites: References 1. Ixodes scapularis (n.d.). In TickEncounter Resource Center.

Retrieved May 10, 2015, from http://www.tickencounter.org/tick_ identification/deer_tick 2. Lyme Disease Data and Statistics (n.d.). In Centers for Disease Control and Prevention. Retrieved May 10, 2015, from http://www. cdc.gov/Lyme/stats/index.html 3. Meyerhoff, J. O. (n.d.). Lyme Disease Clinical Presentation. In Medscape. Retrieved May 10, 2015, from http://emedicine.medscape. com/article/330178-clinical 4. Co-infection (n.d.). In Lymedisease.org. Retrieved from http:// www.Lymedisease.org/Lyme101/coinfections/coinfection.html 5. Southern Tick – Associated Rash Illness (n.d.). In Centers for Disease Control and Prevention. Retrieved May 10, 2015, from http:// www.cdc.gov/stari/index.html 6. Amblyomma americanum (Lone Star ticks) (n.d.). In TickEncounter Resource Center. Retrieved May 10, 2015, from http:// www.tickencounter.org/tick_identification/lone_star_tick CONEMAUGH HEALTH SYSTEM

Conemaugh Memorial Medical Center, Johnstown, PA, is seeking an

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