Modern Resident - The newsletter of AAEM/RSA
April/May 2015
Volume 7: Issue 2 | Facebook  Twitter  LinkedIn

Inside This Issue

Clinical Pearl: A Parent’s Kiss for Nasal Foreign Body Removal
Ashley Grigsby, DO PGY-1
Indiana University Emergency Medicine/Pediatrics

Every little boy knows the best place for anything is up your nose. That is, until they show up in your emergency department (ED).

The Case:
Three-year-old previously healthy male presents after he put his older sister’s jewelry bead up his right nostril two hours ago. Vitals are normal. As you walk in the room, he is breathing comfortably and appears well, but his big brown eyes see you coming and immediately start welling up with tears. He’s sitting in his mom’s lap; he’s anxious and wants no part of you coming near him.

Now you start thinking to yourself, “How am I going to remove this bead from his nose without a giant screaming fit?” This is when you decide to employ the mother to perform the Parent’s Kiss.

The Parent’s Kiss is a technique that was first described in 1965 and there have been multiple case studies since then. The technique requires a parent, or trusted caregiver of the child, and careful instructions from the physician. You first council the parent on how to perform this technique, then you ask them to perform it. The parent should tell his or her child, “I’m going to give you a big kiss.” The parent then places his or her mouth over the child’s open mouth forming a seal and subsequently blows into the mouth until resistance is felt, then sharply exhales while occluding the unaffected nostril of the child.1 This puff of air should pass through the unoccluded nostril and expel the foreign body. It is important to explain the entire procedure to the adult prior to having them start the process with the child.

This process for removal is best for ages two to five years old or in children who cannot be coached to blow their own noses. It can serve as an invaluable tool in this age group, which is particularly useful as this age group can be the most difficult to gain trust from and to restrain. This technique also reduces the risk of tissue damage from instrumentation, especially in an uncooperative child.1

One study found this technique successful in 20 of 31 cases in children under age five years.2 A systematic review also found a similar success rate of 59.9% over multiple case series with no reported adverse effects.1 The systematic review did not find any difference in success based on the type of object that was lodged. There are some theoretical risks to this procedure, including barotrauma and ruptured tympanic membrane; however, none of these have ever been reported.1 The studies also suggest that its use as first line option may increase success rates with instrumentation if the Parent’s Kiss fails.2

Overall, the Parent’s Kiss can serve as a non-traumatic first step in the management of pediatric nasal foreign bodies. Next time that little boy is staring at you wide-eyed and tearful, give this clinical pearl a try.


  1. Cook S, Burton M, Glasziou P. Efficacy and safety of the “mother’s kiss” technique: A systematic review of case reports and case series. CMAJ. 2012 Nov 20; 184(17): E904–E912.
  2. Purohit N, Ray S, Wilson T, Chawla OP. The ‘parent’s kiss:’ An effective way to remove paediatric nasal foreign bodies. Ann R Coll Surg Engl. 2008 Jul; 90(5): 420–422.

Wilderness Medicine Update: Lyme Disease
Alexandra Murray, OMSIV
Ohio University Heritage College of Osteopathic Medicine

Since Lyme disease was first reported in Lyme, Connecticut, in 1977, the number of reported cases in the United States has skyrocketed. In 2013, more than 35,000 cases were reported to the Centers for Disease Control and Prevention (CDC), making Lyme disease the most commonly reported vector borne illness in the United States.1,2 Young males and children are disproportionately affected, with the majority of the reported cases concentrated along the northeast coast of the United States.2 Due to this dramatic increase in Lyme disease in a concentrated area, there has been a lot of interest in determining how to target the patient populations at greatest risk of Lyme disease from tick exposure.

The vague constitutional symptoms and multi-organ infection associated with B. burgdorferi infection can make Lyme disease difficult to diagnose. Fortunately, in approximately 70-80% of cases, patients develop a characteristic rash, known as erythema migrans (EM), within 30 days of infection.2-4 Despite this characteristic finding, a recent study by Knoll et al., reports that a large percentage of patients are unable to recognize the rash associated with Lyme disease.3 This study focused on 379 individuals who hiked the Appalachian Trail and had a high risk of Ixodes tick exposure. Of these hikers, 46% were unable to identify erythema migrans, leading to a delay in treatment.3

With the continued emergence of Lyme disease there is a critical need for patient education programs and tick bite prevention measures.2 Once recognized, Lyme disease can be diagnosed clinically based on physical exam and a history of probable exposure to infected ticks.4 Laboratory tests are not necessary or recommended to confirm diagnosis for patients with recent onset (two to three weeks) of a characteristic EM rash.5 If further testing is warranted, the CDC recommends using a two-tiered serologic test that can provide confirmation of infection in patients with musculoskeletal, neurologic or cardiac symptoms.2,6


  1. Centers for Disease Control and Prevention. Reported cases of Lyme disease by year, United States, 1995-2013. Lyme disease. Statistics. March 4, 2015.
  2. Bacon RM, et al. Surveillance for Lyme disease--United States, 1992-2006. MMWR Surveill Summ. 2008 Oct 3;57(10):1-9.
  3. Knoll JM et al. Appalachian trail hikers' ability to recognize Lyme disease by visual stimulus photographs. Wilderness Environ Med. 2014 Mar;25(1):24-8.
  4. Wormser GP, Dattwyler RJ, Shapiro ED, et al. The clinical assessment, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: Clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis. 2006;43:1089--134.
  5. American College of Physicians. Guidelines for laboratory evaluation in the diagnosis of Lyme disease. Ann Intern Med. 1997;127:1106--8.
  6. Centers for Disease Control and Prevention. Recommendations for test performance and interpretation from the Second National Conference on Serologic Diagnosis of Lyme Disease. MMWR Morb Mortal Wkly Rep. 1995 Aug 11;44(31):590-1.

Primary CNS Lymphoma
Sharina Mapleton, DO
Naresh Chandan, DO FACOI FACP
Riverside Medical Center

Jonathan Zygowiec, MSIV MPH MA
Midwestern University, Arizona College of Osteopathic Medicine

A 69-year-old Caucasian male with a past medical history significant for hypertension and severe rheumatoid arthritis presents with difficulty walking, headaches and fatigue for the past two weeks. He was referred to the ED after presenting to his PCP for these symptoms. He denies syncope, seizures, mood changes, memory loss or vision loss. His medications include Atenolol 50mg daily, Benicar 20mg daily, Folic acid 1mg daily, Methotrexate 12.5mg weekly and Etanercept 50mg weekly.

On physical exam, he is afebrile with a blood pressure of 148/84, pulse 64, respirations 16 and oxygen saturation 98% on room air. On neurological exam the patient is noted to have mild horizontal nystagmus on gaze to the right, decreased sensation to pain in the left foot and decreased strength 4/5 on the left side. Finger-to-nose and heel-to-shin testing are negative. Rapid alternating movements are negative. The patient’s gait is slow and unsteady.

A magnetic resonance image of the brain reveals ring-enhancing lesions in the right posterior frontal area with surrounding vasogenic edema. There are several other smaller lesions in the left frontal lobe as well as in the right frontal lobe. No midline shift is noted. The patient is admitted. Neurology and infectious disease are consulted.

Testing for infectious etiologies is negative. Computed Tomography of the chest, abdomen and pelvis are negative for primary malignancy. The patient undergoes a right parietal stereotactic brain biopsy, which reveals primary CNS lymphoma. There is a rapid neurological decline shortly after the biopsy. A repeat MRI is performed which reveals an acute infarct on the right thalamus, cerebral peduncle and pons with surrounding edema. The patient is placed into hospice care and subsequently expires not long after.

TNF blockers are effective medications for severe rheumatoid arthritis; however the adverse reactions to these drugs are severe and can be fatal. Lymphoma, although rare, is one fatal side effect of these drugs. Patients who are taking Etancercept in conjunction with Methotrexate are at an increased risk of malignancy.1,2



  1. Long-term effectiveness and safety of TNF-blocking agents in daily clinical practice: Results from the Dutch Rheumatoid Arthritis Monitoring Register. Rheumatology. 2011,50(1):196-203.doi:10.1093/rheumatology/keq325.
  2. Brown LS, Greene MH, et al. Tumor necrosis factor antagonist therapy and lymphoma development: Twenty six cases reported to the Food and Drug Administration. Arthritis & Rheumatism. 2002,46(12): 3151-3158.

Pediatric Emergencies Part 4: Asthma Exacerbation
Jenna Erickson, MSIV
Chicago Medical School

When a child presents to the ED with an asthma exacerbation, a series of events are performed to ensure patient safety. The stepwise approach to management is outlined by the National Heart, Lung and Blood Institute (NHLBI) 2007 Guidelines for the Diagnosis and Management of Asthma. The first step for children of all ages is a quick assessment by obtaining vitals and checking for overt signs of respiratory distress. Patients’ conditions are then classified as mild, moderate, severe or life-threatening. During a mild exacerbation the child will become dyspneic only with activity, sometimes detected solely by tachypnea. Mild exacerbations correlate with an FEV1 of 70% or greater and are usually successfully treated with home regimens. The majority of children presenting to the ED with asthma exacerbations will fall into the moderate or severe categories. For moderate exacerbations (FEV1 40-69%) dyspnea will begin to interfere with regular activities and treatment with a short-acting beta 2 agonist (SABA) is initiated in route to the clinic or ED. Children presenting in severe asthma exacerbation (FEV1 <40%) will show clear signs of respiratory distress including dyspnea at rest, retractions, inability to breathe while talking and low activity levels. Infants with severe exacerbations can rapidly deteriorate to life-threatening respiratory compromise and must be treated immediately upon arrival.

Assessment of asthma exacerbation severity in children can be particularly tricky. There is no well-established guideline for this population as a whole, though FEV1 measurements can be helpful in children over five-years-old. Pulse oximetry should be obtained as an initial assessment in all pediatric patients, especially infants as their ventilation-perfusion characteristics lead to hypoxemia at an accelerated rate. Scoring signs and symptoms by clinical presentation is a valuable tool for asthma assessment in pediatric patients. Children with moderate to severe exacerbations who continue to show signs of respiratory distress after one to two hours of treatment have an 84% chance of hospital admission.

Treatment can be initiated while obtaining the history and performing a physical exam. According to the NHLBI, patients of all ages presenting to the ED with moderate exacerbation should receive oxygen and SABA up to three times in the first hour. If presenting in severe exacerbation, patients require continuous SABA with ipratropium. In both cases, oral systemic corticosteroids are given if patients are not improving or if there is a history of recent use. Patients will then follow a series of assessments and treatments that ultimately determine if they are stable for home, require admission or are in need of close monitoring in the ICU. Patients in life-threatening states of respiratory arrest, however, must be intubated and administered SABA with ipratroprium, IV corticosteroids and admitted directly to the ICU.

After one hour of treatment in moderate and severe exacerbations, patients are reassessed for clinical improvement. These children can continue to receive SABA every 60 minutes for up to four hours in the ED, at which time a decision to admit or discharge must be made. If symptomatic improvement and FEV1 of >70% is achieved while in the ED patients are generally cleared for discharge. It should be noted, however, that in the pediatric population the decision to admit a patient can vary depending upon the reliability of caretakers. Pediatric patients cannot be assumed the primary party responsible for their own care, thus even patients meeting criteria for discharge may necessitate admission overnight for observation to ensure continuation of treatment.

There are additional tests and treatment options exercised on a case-by-case basis. Adjunctive treatment with magnesium sulfate or heliox should be considered if patients are not responding to the standard treatment protocol. Once treatment has been initiated for the acute exacerbation further steps should be taken to identify coexisting conditions. In pediatric patients these most commonly include RSV infection, foreign body aspiration, history of prematurity (bronchopulmonary dysplasia) and cystic fibrosis. Additionally, imaging by chest X-ray may be obtained, though this decision is debatable. A 2014 study from the journal Asthma investigated the use of chest X-ray in pediatric patients presenting with asthma exacerbation. It was found that although 44% of subjects had a CXR performed, only 10% of those obtained had findings that influenced the treatment plan.

One of the most important factors of emergency care in asthmatics is proper education for the patient and family. Follow-up care should be initiated three to five days after discharge, with adjustments to the asthma action plan as necessary. Asthma is a controllable disease in most cases and emergency situations can often be prevented with the appropriate plan.


  1. Guidelines for the Diagnosis and Management of Asthma. National Heart, Lung, and Blood Institute, NIH Publication Number 08-5846, October 2007.
  2. Narayanan S et. al. Relevance of chest radiography in pediatric inpatients with asthma. J Asthma. 2014 Sep; 51(7): 751-5.

Board Review: Hypothermia/Cold Water Submersion
Kevin P. Beres, DO PGY-1
UTHealth Emergency Medicine Resident

Growing up in Wisconsin, one of the beloved New Year’s traditions was the polar bear plunge, which translates to a group of people jumping into the cold lakes on New Year’s Day. This event brings up two important concepts: cold water submersion and accidental hypothermia. Risk factors for accidental hypothermia include alcohol, AMS, behavior, extreme ages and certain comorbidities including peripheral vascular disease, trauma and diabetes mellitus.1,2

Cold Water Submersion:
When the body comes into contact with cold water, it leads to activation of the Mammalian diving reflex, resulting in bradycardia, shunting of blood to the CNS system and slow metabolism and may actually prolong survival.1 This reflex affects children more efficiently than adults. Alcohol has been shown to reduce this reflex.3  

Chilblains are red and/or blue edematous plaques and papules that appear on the distal extremities that occur secondary to prolonged cold exposure. A variety of sensory symptoms such as itching or burning can accompany the skin changes.1

Frostnip is very similar to chilblains; however, instead of a red or blue appearance, it results in a white appearance. Frostnip is caused by exposure to cold/damp conditions and is seen with the beginning stages of Hunter’s Reflex, which is vasoconstriction of the extremities to help maintain core temperature.1

In frostbite, cold exposure is so extreme that the tissue actually freezes.  Frostbite has two phases, the freezing of the tissue and the reperfusion phase. During the reperfusion phase, fluids — the arachidonic acid cascade, prostaglandin and thromboxanes — all cause changes that can lead to platelet aggregation and more vasoconstriction.1,4 This can ultimately result in hemorrhagic blisters and dry gangrene. Frostbite is graded just like burns: 1st and 2nd degrees involve the dermis, 3rd degree reaches into the subcutaneous tissue, and 4th degree involves muscle and/or bone. If treating personnel are unfamiliar with the management of frostbite, early transfer to the proper center is critical.1,2,5


Hypothermia Temp Cardiac Neurologic response EKG/Other
Mild   90-95° F Excitation response (HR, BP, RR) Shivering Mild confusion  
Moderate 86-90° F Slowing of all physiologic functions, negative inotropic effect Cessation of shivering, worsening ataxia, loss of papillary reflex EKG changes (Osborn waves)  
Severe <86° F Dysarrhythmia (Bradycardia > AF > VF > Asystole) Pupils fixed/dilated Cold Diuresis, bronchorrhea, absent gag

Treatment for Hypothermic Injuries:
Rapid rewarming in warm water (37-39° Celcius2,4) is ideal for the frostbite injuries. Whatever you do, do not rewarm if the area has potential to refreeze, as the results can be devastating.5 Analgesics are necessary, as rewarming is a very painful process.2,4 Affected areas are tetanus-prone, so vaccination status should be assessed and Tdap should be given if necessary.1,4  Debridement of blisters should occur only after the final demarcation is present. However, injuries are likely to expand.2,4 There are limited studies suggesting that TPA may have benefits.6 The coagulation process can be altered due to loss of enzyme function at lower temperature.1  For hypothermia alone, several rewarming approaches exist, including passive, active non-invasive and active invasive strategies. Passive rewarming is good for mild hypothermia.4,5 Shivering is thought to be beneficial as it helps raise the temperature more quickly.1 Do not place warm saline bags on the body, as this can lead to burns. Active non-invasive techniques include water bath, bair huggers and humidified air.1,4 Finally, active invasive warming includes lavages and ECMO.1,4,5,7 The key is to raise temperature above 30° degrees Celsius.1,4

1) A 24-year-old male with no PMH jumped into the cold water. His heart rate subsequently slowed due to

A. Partially freezing of the heart
B. Contact of the cold water with his face
C. Prior drug abuse
D. Cushing’s response from cerebral edema
E. Sepsis from exposure to cold

2) After successfully resuscitating a gentleman stranded in a car from mild hyperthermia, you note that his hands have clear blisters and the left index finger is turning purple. Your treatment plan for this patient is:

A. Debridement of clear blisters only, wrap in xeroform gauze and discharge with close follow up
B. Debridement of clear blisters, wrap in xeroform gauze and admit for observation
C. Debridement of clear and hemorrhagic blisters, wrap in xeroform gauze and discharge with follow up
D. Debridement of clear and hemorrhagic blisters, wrap in xeroform gauze and admit for observation
E. Transfer to the nearest burn center

Answers: B and E


  1. Tintinalli JE. Tintinalli's emergency medicine: A comprehensive study guide. McGraw Hill; 2011: Section 16.
  2. Knoop K. Environmental conditions. In:Atlas of emergency medicine 3rd ed. New York: McGraw Hill; 2010.
  3. Wittmers LE Jr, Pozos RS, Fall G, Beck L. Cardiovascular responses to face immersion (the diving reflex) in human beings after alcohol consumption. Ann Emerg Med. 1987 Sep;16(9):1031-6.
  4. Reichman E. Emergency medicine procedures; 2012: Chapter 189 Hypothermia Patient Management.
  5. Stone GK, Bowers,R. Current diagnosis and treatment. McGraw Hill; 2011:Chapter 46 Disorders Due to Physical and Environmental Agents.
  6. Johnson AR, Jensen HL, Peltier G, DelaCruz E. Efficacy of intravenous tissue plasminogen activator in frostbite patients and presentation of a treatment protocol for frostbite patients. 2011 Dec;4(6):344-8. doi: 10.1177/1938640011422596. Epub 2011 Sep 30.
  7. Turtiainen J, Halonen J, Syväoja S, Hakala T1.Rewarming a patient with accidental hypothermia and cardiac arrest using thoracic lavage.Ann Thorac Surg. 2014 Jun;97(6):2165-6. doi: 10.1016/j.athoracsur.2013.08.028.

When Back Pain is More Than Musculoskeletal: The Red Flags of Spinal Epidural Abscesses
Kaitlin M. Fries, OMSIV
Ohio University Heritage College of Osteopathic Medicine

As an emergency medicine physician it is important to always think about the worst-case scenario. What is the worst thing that could explain this patient’s symptoms? What could potentially kill this patient if not quickly identified and appropriately managed? For common complaints such as back pain, this mindset can easily be over looked. No matter how simple and straightforward a case of back pain may seem, it is still important to ensure there are no red flags. One of the most concerning worst-case scenarios of low back pain is that of a spinal epidural abscess.

Recent studies have shown that the number of cases of spinal epidural abscesses is rising due to an increase in IV drug abuse and spinal surgeries.2,3 If overlooked, this infection can cause a rapid decline and lead to sepsis, meningitis and permanent paralysis.3 With a mortality rate as high as 20%, it is vital to catch this infection on the patient’s first presentation.2,3 Diagnostic delays are far too common in these patients. In 2003, a retrospective study looked at 63 cases of spinal epidural abscesses. It was found that 75% of these cases had multiple ED visits or were admitted without a clear diagnosis.1

The classic triad of symptoms for a spinal epidural abscess is fever, back pain and neurological deficits.1,4 However, in the study mentioned above, 63 cases of spinal epidural abscess were studied and this classic triad was only seen in 13% of the patients.1,4 A more reliable predictor of the diagnosis was having one or more risk factors for spinal epidural abscess, which had a sensitivity of 98%.1,4 Consequently, it is important to ask about recent invasive procedures, immunocompromised states, spinal implants/devices, IV drug abuse, alcohol abuse, distant sites of infection, recent spine fracture, chronic renal failure or cancer.4 The first step when suspecting spinal epidural abscesses is to obtain an ESR level, as this is elevated in greater than 90% of cases.4 Next, or concurrently (depending on the degree of suspicion), order a MRI. This is the gold standard for diagnosis and will reveal the precise location of the infection.5 Treatment of choice in these individuals is emergent surgical consultation for decompression and debridement.5 Long-term antibiotic therapy directed at Staphylococcus aureus is also recommended.4


  1. Davis D, Wold R, Patel R, Tran A, Tokhi R, Chan T, Vilke G. (2003). The clinical presentation and impact of diagnostic delays on emergency department patients with spinal epidural abscess. The Journal of Emergency Medicine, 2003; 26(3), 285-291.
  2. Felton B, Dao T, Gerstner B, and Letarte S. Diagnosis of spinal epidural abscess by abdominal plain-film radiography. West J Emerg Med, 2014; 15(7), 885-886.
  3. Schoenfeld A, Hayward, R. Predictive modeling for epidural abscess: What we can, can't, and should do about it.The Spine Journal, 2014; 15(1), 102-104.
  4. Tintinalli J. Neck and back pain. Tintinalli's emergency medicine: A comprehensive study guide (7th ed.). New York: McGraw-Hill; 2011.
  5. Tompkins M, Panuncialman I, Lucas P, Palumbo M. Spinal Epidural Abscess. The Journal of Emergency Medicine, 2010; 39(3), 384-390. Retrieved March 15, 2015.

Phlegmasia Cerulea Dolens and the Spectrum of DVT
Nathan Haas, MD PGY-1 and Mary Haas, MD PGY-1
University of Michigan

Phlegmasia cerulea dolens is a rare but severe form of deep vein thrombosis (DVT). Early recognition in the ED is crucial, as treatment options often differ from those for an uncomplicated DVT. Venous thrombosis is a spectrum of disease that can progress from uncomplicated DVT to phlegmasia alba dolens, phlegmasia cerulea dolens and ultimately venous gangrene.

Phlegmasia alba dolens (PAD), which literally translates to “inflammation, white, painful,” refers to a DVT with complete deep venous occlusion, with venous drainage subsequently limited to only collateral veins of the superficial system. Venous outflow is decreased, but there is a lack of complete venous congestion given the patency of the superficial venous system. The pallor (which is part of the clinical syndrome of PAD) is believed to be secondary to subcutaneous edema.

Phlegmasia cerulea dolens (PCD) which translates literally to “inflammation, blue, painful,” refers to a DVT with complete deep and collateral (superficial) venous occlusion. It is pathophysiologically distinguished from PAD by occlusion of the collateral veins, resulting in venous congestion of the extremity and blue discoloration. If the clot burden progresses to involve the capillary beds in addition to the deep and superficial venous systems, venous gangrene results.

Ultrasound is the imaging modality of choice in diagnosing DVT. However, if pallor, blue discoloration, pain out of proportion to exam or significant edema are present, CT venogram (or occasionally MR venogram) is the non-invasive test of choice to evaluate for more severe forms of VTE, such as PAD and PCD. CT venogram allows visualization of the extent and chronicity of the thrombus and can be helpful when considering more invasive treatment measures such as thrombolysis.

PCD is typically managed with guidance from vascular surgery and/or interventional radiology. Thus, suspicion of the diagnosis should prompt early consultation. Treatment options (in addition to systemic anticoagulation) include venous thrombectomy, systemic thrombolytic therapy or catheter-directed thrombolytic therapy.

In summary, if a DVT is accompanied by blue discoloration of the limb, pain out of proportion to exam or significant edema, the diagnosis of PCD should be considered. CT venogram can establish a diagnosis and vascular surgery and/or interventional radiology should be consulted early to aid in management.


  1. Hoffer, et al. Imaging in Deep venous thrombosis of the lower extremity. Accessed 1/20/15
  2. Life in the fast lane: Phlegmasia cerulea dolens. Accessed 1/20/15
  3. Juhn P, Herbert M. HIPPO reviews: Phlegmasia. EM:RAP.
  4. Dardik, et al. Phlegmasia alba and cerulea dolens. Accessed 1/10/2015

Dude, My Chest Hurts
Nicholas Pettit, PhD OMSIII
Ohio University Heritage College of Osteopathic Medicine

A 26-year-old male presents to the local community ED with a one hour history of left-sided chest pain. He describes the chest pain as sharp, constant and worse with deep inspiration. He said the pain came on while driving to work at 5 AM, has never happened previously and is associated with shortness of breath. He has no significant past medical history and past surgical history, nor does he endorse any relevant family history. Social history is positive for one pack of cigarettes per day and one “joint” per day of marijuana. Remainder of review of systems is non-contributory.

Physical exam
Afebrile, pulse 85, 120/75, respiratory rate of 12, 75 inches tall, 75kg. Patient appears uncomfortable preferring an upright position, with shallow breaths. Other than some slight tenderness to palpation and discomfort on deep inspiration in the upper left thorax, the remainder of his exam is normal.

Given this patient’s presentation what is the most likely diagnosis:

  1. Pneumonia
  2. Acute myocardial infarction
  3. Pericarditis
  4. Costochondritis
  5. Tension pneumothorax
  6. Spontaneous pneumothorax

Answer: F
Given the patient’s age, vital signs, body size/habitus and social history, F is the most likely answer. In this case, chest X-ray was performed and subsequently demonstrated a large spontaneous pneumothorax.

While this patient appeared to be the prototypical tall, skinny, male that presents with a spontaneous pneumothorax, his social history also revealed recent marijuana use. Per the literature, there are numerous case reports of frequent marijuana users presenting with subsequent complications such as pneumothorax, airflow obstruction and chronic bronchitis.1 One such example is where a 28-year-old smoker developed a pneumothorax following a breath holding competition.2 Other examples include the development of pneumothorax, pneumomediastinum and pneumopericardium following a Valsalva maneuver during marijuana smoking.3 Lastly, a relatively recent article demonstrated a connection between marijuana use and spontaneous pneumothorax.4  

Current treatment of most spontaneous pneumothorax includes a chest tube or needle aspiration, followed by a short-term stay in the hospital. A recent research article is challenging this paradigm by developing a protocol in the emergency department that treats large, spontaneous, pneumothoraces with pigtail catheters along with ambulatory management.5 Patients were managed with pigtail catheters with a one-way valve, immediately discharged and subsequently evaluated every two days according to their algorithm. They demonstrated a cost savings of $3,350 per patient, assuming a four-day hospital admission. They observed a 78% ambulatory success rate by implementing their ambulatory protocol.


  1. Joshi M, Joshi A, Barrtter T. Marijuana and lung diseases. Current Opinion in Pulmonary Medicine. 2014; 20:173-179.
  2. Aujayeb A, Donald C, Doe S. Breath-holding in a marijuana smoker. Respiratory Medicine Case Reports. 2012; 5:69-72.
  3. Birrer RB, Calderon J. Pneumothorax, pneumomediastinum, and pneumopericardium following Valsalva’s maneuver during marijuana smoking. New York State Journal of Medicine. 1984; 84:619-620.
  4. Jakab L, Szanto Z, et al. Etiopathogenesis of spontaneous primary pneumothorax. Marijuana: Cause or a blame? Magy Seb. 2012; 65:421-425.
  5. Voisin F, Sohier L, et al. Ambulatory management of large spontaneous pneumothorax with pigtail catheters. Annals of Emerg Med. 2014; 64:222-228.

Pediatric Pearl – Acute Ischemic Stroke
Randy Kring, MS-IV
Tufts University School of Medicine

Acute ischemic stroke is a disease every EP must be prepared to manage. But what about stroke in kids? How often do children have acute ischemic strokes? Are risk factors for stroke the same in kids as they are in adults? How should pediatric stroke be managed? This segment will review key aspects of pediatric acute ischemic stroke to prepare you for the next time a child with a stroke comes into your ED.

To begin, it’s important to remember that ischemic stroke in children is significantly different from ischemic stroke in adults. Not surprisingly, ischemic stroke is much less common in kids. Estimates of incidence range from 0.6 to 7.9 strokes per 100,000 children, compared to 88 to 191 strokes per 100,000 adults in the U.S.1-3 Furthermore, pediatric stroke is typically not caused by hypertension, hyperlipidemia, diabetes or smoking, as children rarely have these stroke risk factors. Instead, pediatric stroke is often caused by congenital heart disease, prothrombotic disorders, sickle cell disease, trauma, infection or drugs like cocaine or amphetamines.4 Presentation of pediatric stroke varies depending on the etiology, but the most common presentation is hemiparesis or focal neurological deficit. 4

Management of pediatric stroke is challenging, since there are few studies to support management decisions.5 Guidelines published in 2004 by the Royal College of Physicians (RCP) and the American College of Chest Physicians (ACCP) are based only on consensus and expert opinion. For acute management of pediatric stroke in the ED, the RCP recommends fever control and supplemental oxygen as needed, but offers no recommendations on glucose or blood pressure control. For acute anticoagulation, the RCP recommends initial treatment with aspirin 5mg/kg/day, excluding patients with evidence of hemorrhage or sickle cell disease.6 The ACCP, in contrast, recommends treatment with unfractionated heparin or low molecular weight heparin (LMWH) for five to seven days and until vascular dissection or cardioembolism have been excluded.7 The most controversial question is when tPA should be given. Neither the RCP nor the ACCP offer specific guidelines regarding tPA use or mechanical intra-arterial thrombolysis, stating that the risk/benefit ratio is unknown.6,7

In summary, remember that pediatric stroke is not the same as adult stroke. Kids are not little adults! Pediatric ischemic stroke is much less common and often harder to recognize than adult ischemic stroke and thus the EP’s index of suspicion for pediatric stroke must be high. Acute management of pediatric ischemic stroke can include supportive care, anticoagulation and thrombolysis, although evidence-based guidelines for these therapies are limited.


  1. Giroud M, Lemesle M, Gouyon JB, et al. Cerebrovascular disease in children under 16 years of age in the city of Dijon, France: A study of incidence and clinical features from 1985 to 1993. J Clin Epidemiol. 1995;48(11):1343.
  2. Earley CJ, Kittner SJ, Feeser BR, et al. Stroke in children and sickle-cell disease: Baltimore-Washington Cooperative Young Stroke Study. Neurology. 1998;51(1):169.
  3. White H, Boden-Albala B, Wang C, et al. Ischemic stroke subtype incidence among whites, blacks, and hispanics: The Northern Manhattan Study. Circulation. 2005;111(10):1327.
  4. Tsze DS, Valente JH. Pediatric stroke: A review. Emerg Med Int, 2011.
  5. Benard TJ, Goldenberg NA, Armstrong-Wells J, et al. Treatment of childhood arterial ischemic stroke. Ann Neurol. 2008; 63: 679-696.
  6. Royal College of Physicians, Pediatric Stroke Working Group. Stroke in childhood: clinical guidelines for diagnosis, management and rehabilitation, 2004.
  7. Monagle P, Chan A, Massicotte P, et al. Antithrombotic therapy in children: The seventh ACCP conference on antithrombotic and thrombolytic therapy. Chest. 2004;126:645S– 687S.

Board Review: Atrial Fibrillation  
By Sophia Johnson, DO and Shane Sergent, DO
Conemaugh Memorial Medical Center

The most common persistent arrhythmia in adults is atrial fibrillation.It is associated with many conditions including rheumatic heart disease, valvular disease, chronic hypertension, ischemic heart disease, cardiomyopathy and thyrotoxicosis.1,2  Atrial fibrillation may also be seen in chronic lung disease, myocarditis, pericarditis, excess caffeine intake, acute alcohol intoxication, pulmonary embolus, hypoxia and congenital heart disease.1,2  It can present in those without any underlying heart disease.1  In patients with pre-existing left ventricular failure, the presence of atrial fibrillation can cause heart failure.2

On EKG, atrial fibrillation is a narrow complex, irregular rhythm.2 There are fibrillatory waves with no distinct p waves and an irregularly irregular ventricular response.1,2 Fibrillatory waves are best visualized in leads V1, V2, V3, and AVF.2   The atrial rate is usually 300-650 beats per minute and the ventricular response is 170-180 beats per minute in patients with a healthy AV node.1,2  

Treatment is aimed at rhythm and rate control and anticoagulation to prevent thromboembolic events.1,2  In unstable patients, including unstable pregnant patients, synchronized cardioversion is the first line treatment, starting with 100-200 J biphasic.1,2  If a patient is stable and exhibiting a rapid ventricular response, rate control should be the first goal in treatment.2  First line therapies for rate control are Diltiazem, 0.25mg/kg IV over two minutes followed by an infusion of 4-20mg/hour; Metoprolol 5mg IV every 5 minutes up to 15mg, Esmolol, or Propanolol.2 Second line therapies include Digoxin, Amiodarone, Procainamide, or Ibutilide.1,2  Beta blockers should not be used in those with accessory pathways, severe CHF, COPD or asthma, hypotension or ventricular tachyarrythmias.2 Digoxin can be helpful in those with LV dysfunction and beta blockers can be helpful in those with atrial fibrillation caused by hyperthyroidism.1

Anticoagulation is important as patients with nonvalvular atrial fibrillation are at an increased risk of thromboembolic events, with an approximately 5% yearly incidence of stroke.1,2  Just as the incidence of atrial fibrillation increases with age, so does the yearly incidence of thromboembolic events.1  According to CURRENT Diagnosis & Treatment Emergency Medicine, the prevalence of atrial fibrillation approaches 10% in those over 80 and the annual thromboembolic risk is around 30% in patients who are 80-89 years old.1

Patients who are discovered to be in new onset atrial fibrillation often require hospitalization for both rate control and anticoagulation.1  If it is unclear how long the patient has been in atrial fibrillation or it is determined to have started over 48 hours ago, it is recommended to anticoagulate for three weeks prior to proceeding with elective cardioversion.1  Those with chronic atrial fibrillation that is rate controlled do not require hospitalization.1  Stable patients whose atrial fibrillation is determined to be less than 48 hours duration can be considered for electrical or chemical cardioversion in the ED.1  Agents for chemical cardioversion include Amiodarone, Procainamide and Sotalol.1 Anticoagulation is not recommended in those patients whose atrial fibrillation has been present for less than 48 hours.1


  1. Heidenreich J. Chapter 35. Cardiac arrhythmias. In: Stone C, Humphries RL. Stone C, Humphries R.L. Eds. C. Keith Stone, and Roger L. Humphries. CURRENT Diagnosis & Treatment Emergency Medicine, 7e. New York, NY: McGraw-Hill; 2011. Accessed March 15, 2015.
  1. Piktel JS. Cardiac rhythm disturbances. In: Tintinalli JE, Stapczynski J, Ma O, Cline DM, Cydulka RK, Meckler GD, T. Tintinalli J.E., Stapczynski J, Ma O, Cline DM, Cydulka RK, Meckler GD, T Eds. Judith E. Tintinalli, et al. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. New York, NY: McGraw-Hill; 2011. Accessed March 15, 2015.

21 Days Until The 2015 Match
Sumit Patel, OMSIV
Temple University School of Medicine

What were you doing on Wednesday, February 25th, 2015  at 9:00pm EST? Were you taking a bath? Were you having a meal? Maybe you were at the gym, running errands or grabbing a drink with a friend? On Wednesday at 9:00pm, most people in the country were probably watching their favorite television show, having quality time with their families, considering how they will push through the rest of the week or reflecting on the day’s happenings. However, just under 20,000 people1 in the United States collectively held their breath at 9:00pm EST on Wednesday, February 25th, 2015. Who are these people? They’re senior medical students who had just submitted their official rank lists for the 2015 residency match through the National Resident Matching Program.

What is “the Match?” It’s a service which allows medical students and residency programs to submit their preferences for each other. The service then runs a complicated computer algorithm to pair up medical students with their highest preferred, most closely ranked residency program. To the general population, it may seem strange, complicated or irrelevant. But for medical students, besides studying for and taking the MCAT, and actually getting into medical school in the first place, “the Match” is arguably the most important event of our medical careers.

How did I end up at this point? I can recall the specific moment at the age of 14 when I decided I wanted to become a doctor. It always felt like something I needed to do. I knew at that point that physicians worked hard to take care of their patients, and I wanted to do the same. Despite plenty of people who told me I was making a mistake or that I could not achieve this goal, I set out to become a doctor.

I took my SATs, graduated from Townsend Harris High School and moved to Binghamton, NY, to pursue a Bachelor of Arts in Biology at Binghamton University. There, I joined the student run volunteer ambulance service, Harpur’s Ferry SVAS. Through my time there, I met some of the most amazing and selfless people I have ever met. There were countless volunteer firefighters, paramedics, police officers and other vital servants. Many of them had second and third jobs to pay bills but worked tirelessly and without recognition to care for the people of the region and to educate me. They joked with me about my goals to attend medical school, the path that lay ahead of me, but almost universally encouraged me and motivated me to continue moving forward. It was in the squad room of Broome Volunteer Emergency Squad, on the morning of March 18, 2011, that I received my acceptance email from Temple University School of Medicine. You cannot imagine the joy that filled my heart upon reading the few short sentences in that email.

Finally, after all that I had endured and achieved, I had gotten accepted into a medical school. Needless to say, I was thrilled and moved to Philadelphia that summer and embarked on what has been an amazing, challenging, reality-check inducing and ridiculous four years. I could not possibly describe in words what it has felt like to get through medical school and get to this stage in my life.

During the past four years, I have lost important loved ones. I have met and proposed to my now fiancée, who is truly the most remarkable person I have ever met and who never ceases to blow my mind with her love, passion and laughter. I have put 60,000 miles on a Mazda CX-5 that I bought only two years ago. I have traveled across the country for conferences and residency interviews. I have met people from all the corners of the world. I have worked the front desk of a Philadelphia hotel to help pay some bills. I have been teaching aspiring medical students how to master the MCAT for four years. I have sewn together horrible wounds, performed countless rounds of CPR and even intubated patients to ensure they are able to breathe. I have seen nurses, physicians, technicians and all forms of staff and volunteers take the burden of healing squarely upon their shoulders. I have seen people make some of the hardest decisions imaginable in deciding how to spend their time and money. I have seen people put life on hold so they could finally achieve their goals of becoming a physician.

For senior medical students, the journey to Match Day has been a long, grueling, arduous process, full of sacrifice, challenges, struggles and hardships. Most of us have spent four years in high school, four years in undergraduate education, and now are completing our fourth and final year of medical school. However, plenty of graduating medical students took time off due to personal or family commitments or setbacks. A portion worked in a different industry prior to attending medical school, founded companies, which were then sold, or spent years caring for family members with chronic illness before coming to medical school. For these students, Match Day and graduation mark the beginning of an even more difficult next chapter.

It is hard to convey in words what it takes to become a physician in America today. Perhaps this bullet point list of statistics based on my own experience will illustrate the funny and not so funny realities of what medical students have almost accomplished. Keep in mind these statistics begin with the start of high school.

  • Number of Years in School: 12
  • Number of Significant Family Events Missed (weddings, funerals, birthdays, vacations, etc): 60
  • Number of Textbooks Purchased: 80
  • Number of Exams Taken: 240
  • Number of 8 Ounce Cups of Coffee Drank: 5,200
  • Number of Hours Spent Studying: 11,000

* Please sit down for the next one, especially if you’re the parent or guardian of a pre-med student, and note that I attended a state undergraduate institution. These values are conservative.*

  • Number of Dollars Spent on Tuition, Textbooks, Exam Fees, Applications, Interviews & Other Mandatory Fees: $553,050

On March 20, 2015, at 1:00pm EST, medical students all around the country will enter the electronic “Registration, Ranking, and Results” system (R3) and, quite simply, lose their minds as they stare at which hospital they will be moving to for the next three to five years to complete their training. There will be lots of screaming. There will be lots of crying. There will be innumerable hugs, congratulations and kisses. Family members, spouses, partners, friends, classmates, educators and staff will be present to share in this exciting event. There will be laughter, balloons, food and drink. There will be falling over on top of each other or tackling your best friend. There will be frantic calls, sloppy posts on Facebook, Twitter and social media all over the world. Passersby might wonder if the people inside may have contracted some type of zombie doomsday infection. Even describing it right now is causing an adrenaline rush for me.

On March 20, 2015, at 1:00pm EST, I don’t know where you will be. I don’t know if you will be at work, finishing up your lunch, getting ready for a weekend getaway, making a phone call, reading a post on Twitter, posting a photo to Facebook, daydreaming in a bus or train or doing nothing. But I can tell you what I’ll be doing.

I’ll be standing in the main lobby of the Medical Research and Education Building at Temple University School of Medicine’s health science campus in North Philadelphia. I’ll be holding my phone in my hand with Safari navigated to the R3 system. I’ll be holding my fiancée’s hand. I’ll be looking nervously at my friends, thinking of my mom and dad who have invested their entire lives to nurture and care for me up until this stage. I’ll be thinking of all the hours I spent studying in labs, long after every other student left to go eat or relax. I’ll be thinking of the years of sacrifice that I made, that my parents and brother made, that my fiancée has made, that my friends made. I’ll be thinking of the winter I lived in the HFSVAS squadroom and a closed down dormitory so I could attend my EMT Critical Care shifts and field time. I’ll be thinking of all of the times I cried in the arms of someone I cared about because I doubted whether I could do this. I’ll be thinking of all of the times someone told me I wasn’t capable of becoming a physician. I’ll be thinking of all those people I have met in hospitals all over the country, in doctor’s offices, all of the nurses, advanced practitioners and technicians, who have patiently trained me to become a soon-to-be-physician. I’ll be thinking of all the times I had to stay up for three days straight because of mandatory classes, shifts and personal commitments. I’ll be thinking of all the times I had to tell people I loved and wanted to spend time with that I had to go to the hospital or the office, that I had to go to the library to study, that I had to miss out on the events of our lives because I had a larger cause.

I’ll be thinking of the non-healthcare related individuals as well. The patient’s daughter, the patient’s grandfather, the patient’s employer, the patient’s nurse, the patient’s pharmacist, the patient’s dog and cat and the patient’s spouse. Most of all, I’ll be thinking of my patient, the single most important person who will ever exist in my world from this day forward.

Ready or not, here I come!

Update: Sumit matched at the University of Maryland Medical Center and is looking forward to starting his emergency medicine residency there this summer.

Your 2014-2015 Leaders:

Meaghan Mercer, DO

Vice President
Victoria Weston, MD

Edward Siegel, MD

Past President
Teresa Ross, MD FAAEM

At-Large Board Members
Nicole Battaglioli, MD
Mary Haas, MD
Michael Gottlieb, MD
Sean Kivlehan, MD
Amrita Lalvani, MD
Andrew Phillips, MD

Medical Student Council President
Michael Wilk

Publications Advisor - Ex-Officio Board Member
Joel Schofer, MD MBA CPE FAAEM

Modern Resident Contributors

Copy Editor: Mary Haas, MD

Managing Editor:
Madeleine Montony, MSM

Special thanks to this issue's contributors:

Kevin Beres, DO; Naresh Chandan, DO; Jenna Erickson, MSIV; Kaitlin Fries, OMSIV; Ashley Grigsby, DO; Mary Haas, MD; Nathan Haas, MD; Sophia Johnson, DO; Randy Kring, MSIV; Sharina Mapleton, DO; Alexandra Murray, OMSIV; Sumit Patel, MSIV; Nicholas Pettit, Phd OMSIII; Shane Sergent, DO; Jonathan Zygowiec, MSIV

Interested in writing?

Email submissions to:

Please submit articles by May 15th for the June/July edition.

Articles appearing in Modern Resident are intended for the individual use of AAEM members. Opinions expressed are those of the authors and do not necessarily represent the official views of AAEM/RSA. Articles may not be duplicated or distributed without the explicit permission of AAEM/RSA. Permission is granted in some instances in the interest of public education. Requests for reprints should be directed to the AAEM/RSA, 555 East Wells Street, Suite 1100, Milwaukee, WI 53202, Tel (800) 884-2236; Fax: (414) 276-3349, Email:


AAEM/RSA  |  555 East Wells Street, Suite 1100  |  Milwaukee, WI 53202
Tel: (800) 884-2236  |  Fax: (414) 276-3349  |  Email:

You have received this message because you have had previous contact with American Academy of Emergency Medicine Resident and Student Association. If you do not wish to be included in our mailing list, please forward this message to