Modern Resident - The newsletter of AAEM/RSA
August/September 2015
Volume 7: Issue 4 | Facebook  Twitter  LinkedIn

Inside This Issue

The Proper Start to Your Financial Journey
James M. Dahle, MD
Author of The White Coat Investor: A Doctorís Guide to Personal Finance and Investing

I’m occasionally asked to give very young physicians, i.e. students and residents, some financial advice. Typically these doctors have a low income, a dramatically negative net worth, little financial education and plenty of naiveté. In fact, I was recently questioned by a student how anyone could possibly spend more than $10,000 per month (to which I replied that I spent more than that on taxes alone.) The truth is that many of these physicians will find themselves spending more than $10,000 a month long before their net worth even reaches zero.

The most important advice I can give any student or resident is to LIVE LIKE A RESIDENT. That means not taking out additional loans during residency (you might be surprised how many of your peers cannot live on a resident’s income) as well as living a lifestyle similar to that of a resident for two to five years after residency. The slower you can grow into your attending physician income, the better off you will be financially. It is entirely possible to pay off your student loans, save up a big down payment for your dream house and be closing in on millionaire status within five years of residency completion. But most docs won’t be in that situation, and some docs will never get there, all because they grew into their peak income entirely too quickly. Make plans now to avoid being in this situation.

Managing student loans properly is also critical for the young physician. The two main options are to stay in the government programs (IBR or PAYE), planning to work at a 501(c)3 to hopefully qualify for Public Service Loan Forgiveness, or to refinance the loans as soon as possible and pay them off quickly. Recently, one private lender even started refinancing loans for residents while allowing them to make $100 a month payments until the completion of residency, saving many doctors tens of thousands in interest. At any rate, if you owe hundreds of thousands of dollars, you should become an expert in student loan management.

Many residents are severely underinsured. If people depend on you financially, you need a large quantity of term life insurance. Even if you cannot afford the $2-5 million a young physician family probably needs, at least buy a $1 million five year term policy and then upgrade when you finish residency. Disability insurance is similar. It will never be cheaper than during your residency and your need for it will never be greater. Try to buy as much as they will sell you as a resident, and then reevaluate your needs upon completion of training.

If you have children, you need a will that dictates who will care for them and who will manage your money for them in the event of your unexpected death. A simple will is inexpensive, whether done online as a do-it-yourself project or through a qualified attorney.

Start investing with your very first paycheck. Read the documents HR gives you and be sure to obtain any available match in your employer’s 401(k). You can also invest in a Roth IRA. Favor Roth (after-tax) accounts while in residency, as you are likely to never be in such a low tax bracket again.

Although you didn’t go into medicine for the money, if you fail to obtain a financial education early in your career and apply its lessons, you are likely to have significant regrets by mid to late career. Financial knowledge leads to financial freedom, and medicine is far more fun to practice when you no longer have to do it for financial reasons.

A Rare Cause of Altered Mental Status and Low Cardiac Output Shock
Linda Sanders, MD and Manish Garg, MD FAAEM
Temple University Hospital

Altered mental status (AMS) in the setting of low cardiac output shock represents one of the sickest patient encounters in any emergency department. In such cases, emergency physicians often hone in on the typical differential diagnoses: infection, toxic ingestion, neurogenic trauma, myocardial infarction and metabolic disorders. But it is important to keep a broader differential in these patients, including those rare cases of endocrine abnormalities if the history is suggestive of previous thyroid surgery or disorders.

Myxedema coma is the severest form of hypothyroidism with a mortality rate of 30-60%. Precipitants of this syndrome include infection, medications (amiodarone and lithium), cold weather, stroke, trauma and medication noncompliance.

Patients may present with depressed mental status, hypotension, bradycardia, bradypnea, hypothermia and skin changes such as pretibial edema. The diagnostic tests of choice are a TSH and free T4, but a concurrent altered mental status workup should occur for these patients. Labs often demonstrate leukocytosis, hyponatremia and hypoglycemia. An EKG is important in every AMS patient, and is pertinent in myxedema, which is associated with bradydysrhythmias and prolonged QT. Pericardial effusions can occur and can be diagnosed with a bedside ultrasound.

The initial management is supportive and includes airway management (airway edema can occur in myxedema patients), fluids and vasoactive drugs as needed, passive rewarming and dextrose. Thereafter, treatment with Levothyroxine should begin empirically and should not wait for a TSH result. Levotyhroxine is given initially as a bolus (300-500mcg) and then a daily dose (50-100mcg). Liothyronine, the T3 version, may also be considered because the conversion from T4 to its active T3 form is decreased in severe hypothyroidism. Steroids should be administered to avoid an adrenal crisis since hypothyroidism may be secondary to hypopituitarism (Hydrocortisone 100mg q8h). It is appropriate to obtain cultures and initiate empiric antibiotics while identifying any other underlying causes. The appropriate disposition for most of these patients is ICU admission.

In summary, consider myxedema coma and send thyroid studies on altered mental status patients who present in low cardiac output states. Initiate supportive care and administer early Levothyroxine and Hydrocortisone. Correct electrolyte abnormalities and passively rewarm. Investigate for pericardial effusions and prolonged QT. Identify the precipitant, send cultures, and treat empirically for infection.


  1. Tintinalli JE, Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, & Meckler GD. (2010). Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th Edition. New York: McGraw Hill, Medical Pub. Division.
  2. Dubbs SB, and Spangler R. (2014). Hypothyroidism: Causes, killers, and life-saving treatments. Emergency Medicine Clinics of North America 32, 303-317.

Carbon Monoxide Poisoning
Daniel F. Leiva, OMSIV
NOVA Southeastern University

Carbon monoxide (CO) exposure leads to between 40,000 and 50,000 emergency department visits and 5,000 to 6,000 deaths per year, and cases of intentional exposure outnumber unintentional exposures by as many as 10 to 1.1 In many cases, exposure goes unnoticed because CO is an odorless, tasteless, colorless and nonirritating gas. The risk for exposure is further increased as CO is a combustion product of many household objects including heaters, grills, camp stoves, generators and vehicle engines.

Toxicity occurs via inhalation, and potentially dangerous levels of exposure occur at concentrations of 1,200 ppm.2 Once inhaled, CO attaches to hemoglobin with an affinity 240 to 250 times that of oxygen, forming carboxyhemoglobin (COHb). Binding at one of four heme moieties has an allosteric effect that decreases the ability of other heme moieties to release oxygen. This shifts the oxygen-hemoglobin dissociation curve to the left, leading to a propensity towards tissue hypoxia. Other effects of CO include impairment of mitochondrial oxidative phosphorylation (particularly in cardiac tissue), inactivation of cytochrome oxidase and lipid peroxidation by reactive oxygen species generated by xanthine oxidase.2

Diagnosing CO toxicity is difficult because presentations are typically non-specific, and are commonly described as flu-like symptoms. The earliest and most common symptom is headache. Other symptoms may include nausea, vomiting, dizziness, myalgias and confusion. In the pediatric population, signs and symptoms may be more subtle, including fussiness and feeding difficulty. Of note, the commonly described “cherry-red” appearance of the mucous membranes is both insensitive and nonspecific.1

Long-term effects of exposure include myocardial injury, kidney injury and delayed neurologic sequelae (DNS). Myocardial injury, as demonstrated by ECG changes or elevated cardiac markers, predicts a two-fold increase in mortality.1 The development of DNS occurs between three and 240 days post exposure (mean 20 days) and may include changes in cognition including memory impairment, personality changes, movement disorders, focal neurologic deficits and dementia. The development of DNS does not correlate with measured serum COHb levels, although loss of consciousness at the time of exposure has been found to be an independent risk factor. Radiographic changes on CT and MRI are rare but may include hemorrhage into the globus pallidus.

Potential presentations of CO toxicity include an unconscious patient received from a house fire (who must also be evaluated for concomitant cyanide exposure), a patient with a headache and nausea who was working in an area with exposure to exhaust fumes (ie, a generator) or an elderly patient presenting with syncope and ischemic changes on ECG.3

The most important intervention is prompt administration of high-flow oxygen (100% O2 via a non-rebreather face mask or an endotracheal tube), which hastens the dissociation of CO from hemoglobin. For those with higher levels of exposure or patients who are more susceptible to CO toxicity, hyperbaric oxygen has been found to be effective if administered within 6 to 12 hours. Scenarios to consider hyperbaric oxygen for include CO level greater than 25%, CO level greater than 20% in a pregnant patient, loss of consciousness due to exposure, severe metabolic acidosis (pH less than 7.1) or evidence of end organ ischemia. As there are no strict guidelines regarding criteria for hyperbaric oxygen in cases of CO poisoning, it is recommended to consult a local hyperbaric oxygen provider. A list of such providers for each state can be found at the following link:


  1. Clardy PF, Manaker S, and Perry H. Carbon monoxide poisoning. Carbon Monoxide Poisoning. UpToDate, 27 Aug. 2014. Web. Accessed  07 July 2015.
  2. Harwood-Nuss A and Wolfson AB. Chapter 327 carbon monoxide. Harwood-Nuss' Clinical Practice of Emergency Medicine: 14th Ed. Philadelphia, Pa.: Lippincott, Williams & Wilkins, 2010. N. pag. Print.
  3. Tintinalli JE and Stapczynski JS. Chapter 217 Carbon Monoxide. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. 7th Ed. New York: McGraw-Hill, 2011. 1410-413. Print.

Pediatric Dental Emergencies
Alexandra Murray, DO
Mercy St. Vincent Medical Center

In the United States, the emergency department functions as a substitute for dental services for a large population of children, especially minorities.1-3 Consequently, the emergency physician must be adept at identifying dental emergencies and providing care when possible. Most pediatric dental emergencies require little intervention while in the emergency department; however, there are specific situations where immediate intervention is required.1-3 Important dental emergencies to identify in the pediatric population include: tooth avulsion, subluxation, intrusion, extrusion, dental fractures and infection.4,5 All pediatric dental injuries must be seen by a dentist for definitive treatment within 24 hours. Without proper care, there can be devastating aesthetic, social and psychological effects to the child.1-6

One of the first steps in evaluating pediatric dental injuries is to determine if the tooth is a primary or permanent tooth.7 Adult incisors will have three small ridges (called mamelons) along the cutting edge as they erupt from the gum line. These ridges are quickly worn away with use, but if present, are useful in identifying an adult tooth.7 Avulsed permanent teeth should be replanted as soon as possible, whereas primary teeth are not replanted. Permanent teeth should only be manipulated by touching the crown, and if dirty, briefly washed with cold running water.4,5,8 The tooth should then be immediately placed back in the socket and the child should be instructed to bite down on a handkerchief to keep it in the correct position.5 If replantation is not possible, the patient should immediately seek medical treatment and transport the tooth in the patient’s own mouth between the gums and cheek.4 If the patient is unconscious or if there is any risk of aspiration, the tooth can be transported in milk.4,5,8 Once in the emergency department, the tooth can be transferred into an appropriate storage medium such as Hanks Balanced Salt Solution.4,5,8 Any tooth that is at risk of aspiration must be pulled in the emergency department. All other loose teeth or teeth that become intruded into the socket can be pulled if necessary by the dentist the following day.4,5

If a tooth is unstable to the point that there is at least 1mm of movement in any direction and the tooth is depressible in the socket, then splinting may be considered.4,5 Splinting teeth is difficult because it is challenging to create a dry surface for the splint to adhere.4,5 Typical splints found in the emergency department (self-cure composite, COE-PAK) can be used to anchor the loose tooth to the two teeth on each side of it.5 In the event of a dental fracture, it is most important to determine the depth of the fracture.4,5 If the enamel alone is affected, then no intervention is necessary in the ED. For fractures that extend into the dentin (appears yellow) or pulp (appears pink), calcium hydroxide paste should be used to seal the fracture until the patient sees the dentist the following day.5 Antibiotics (such as penicillin) may be given if the patient is unlikely to follow up with a dentist in a timely manner, since these fractures are vulnerable to bacterial infections.4,5 Pediatric dental fractures that involve the alveolar ridge will most likely need oral surgery under sedation. These injuries are time sensitive and an oral surgeon should be consulted as soon as possible.4,5


  1. Allareddy V, et al. Hospital-based emergency department visits with dental conditions among children in the United States: Nationwide epidemiological data. Pediatr Dent. 2014 Sep-Oct;36(5):393-9.
  2. Wagle E, Allred EN, Needleman HL. Time delays in treating dental trauma at a children's hospital and private pediatric dental practice. Pediatr Dent. 2014 May-Jun;36(3):216-21.
  3. Mitchell J, et al. Managing pediatric dental trauma in a hospital emergency department. Pediatr Dent. 2014 May-Jun;36(3):205-10.
  4. American Academy on Pediatric Dentistry Council on Clinical Affairs. Guideline on management of acute dental trauma. Pediatr Dent. 2008-2009;30(7 Suppl):175-83.
  5. Andersson L, et al. Guidelines for the management of traumatic dental injuries. II. Avulsion of permanent teeth. Dent Traumatol. 2012 Apr;28(2):88-96.
  6. Lee JY, Divaris K. Hidden consequences of dental trauma: The social and psychological effects. Pediatr Dent. 2009 Mar-Apr;31(2):96-101.
  7. Kumar PS. Dental anatomy and tooth morphology. Daryaganj, New Delhi: Jaypee Brothers Medical Publishers; 2007. Page 76.
  8. Poi WR,et al. Storage media for avulsed teeth: A literature review. Braz Dent J. 2013 Sep-Oct;24(5):437-45.

Did You Know? Broselow Pediatric Emergency Tape
Jenna Erickson, MD
Phoenix Childrenís Hospital/Maricopa Medical Center

In a pediatric trauma, one of the initial treatment steps is determination of a child’s “color.” This is referencing the Broselow Pediatric Emergency Tape, an old but widely accepted method of estimating a child’s weight based on length. Pediatric drug dosing is based on weight, therefore a fast, efficient way to calculate dosing is essential to reduce medical error and optimize patient outcomes. The Broselow Tape is a color-coded tape measurer consisting of nine color zones that group together pediatric medication doses and equipment sizes. When a child first arrives in a trauma bay he is measured with the tape from crown to heel. The color that is reached by the child’s heel indicates a weight estimate; this color is then used for a quick reference sheet of pre-calculated medication doses, voltages and equipment sizes. Resuscitation carts with color-coded drawers further simplify the process of selecting the correct supplies for pediatric patients, thus expediting treatment and minimizing error.

How did this method come to fruition, and why are we still using it?  In the late 1970s the first study correlating weight to length was published, and this data was then used to develop the Broselow Tape in 1985. Using 50th percentiles of weight for age, this method aims to predict the ideal body mass of children depending on their length. Although not without flaws, the Broselow Tape has been shown to determine medication doses and equipment that closely match doses calculated using actual weight. A 2012 review article published in the Journal of Pediatric Nursing compared 24 peer-reviewed articles analyzing the accuracy of this method. This review addressed many of the criticisms of the tape, including the inaccuracy of weight estimation in obese patients. However, the authors identified that in the setting of an acute trauma, excess adipose tissue plays little role in the efficacy of the drugs listed on the Broselow Tape. Furthermore, in most cases obesity does not play a role in selecting the proper equipment size. When the Broselow Tape was used as directed for children under 12 years of age and less than 80 pounds, this method estimated weight within 10% for nearly two-thirds of the patients tested.

There have been recent adaptations and numerous equations created aiming to increase accuracy of weight estimation in pediatric emergencies. However, in an acute trauma setting the simplicity of the Broselow Pediatric Emergency Tape and color-coded cart has allowed this method to remain a standard weight estimation tool. With its ease of use and relative accuracy, the Broselow Tape helps reduce medical error and facilitates swift resuscitation for the pediatric population.


  1. Heyming. T, Bosson N, Kurobe A, Kaji AH, and Gausche-Hill M. (2012) Accuracy of paramedic Broselow tape use in the prehospital setting. Prehosp Emerg Care, 16(3), 374-80.
  2. Luten RC, Zaritsky A, Wears R, and Broselow J. (2007). The use of the Broselow Tape in pediatric resuscitation. Academic Emergency Medicine, 14, 500–501.
  3. Meguerdichian MJ, and Clapper TC. (2012) The Broselow Tape as an effective medication dosing instrument: A review of the literature. Journal of Pediatric Nursing, 27, 416–420.

International Corner: Resident Feature with Vijay Kannan, MD
Amy Ho, MD
University of Chicago

Vijay Kannan is a PGY2 at Maricopa Medical Center in Phoenix, AZ, and is completing an internship at the World Health Organization Headquarters in Geneva, Switzerland.

First off, tell us about your experiences as a resident at the World Health Organization.
I am currently working in the Emergency, Trauma and Acute Care (ETA) program under program lead Dr. Teri Reynolds. Iím mainly working on the open-access WHO Basic Emergency Care Course. Itís meant to teach the approach to the acutely ill and injured patient to providers in low- and middle-income countries. Most of these are not specialists, and often not doctors, but still have to manage emergencies every day.

Our program is also tasked with defining a global emergency care framework. What exactly are the individual components and functions of an emergency care system? This is surprisingly difficult to answer because these systems have developed along very distinct arcs reflecting various geographical and financial conditions, as well as fundamental ideological differences. Without consensus on what exactly an emergency care system is, itís hard to advocate for its development.

This experience has been amazing. Iíve gained invaluable perspective and met some fantastic people. I also get assigned tasks that are way too cool for my pay grade. Right now Iím on a two-day trip to the Philippines for a strategic meeting on emergency care systems development in the Western Pacific Region. I. Love. This. Job.

What got you interested in international medicine in the first place?
Oddly enough, it came from my interest in rock climbing. I’ve traveled extensively for climbing, and along the way I’ve seen people in terrible situations that inspired me to act. I have to admit, my idea of what I want to do now is very different than what it was then. I thought international emergency medicine was going to be grabbing a penknife and duct tape and heroically saving the day. It’s not. It’s watching young people die who don’t have to, and trying to stop it from happening again.

Based on your work so far, how do you see emergency medicine shaping up globally? What are some of the bigger challenges for the field?
The biggest issue I see right now is funding. Most funding streams are disease-specific, which is understandable given the ease with which funders can appreciate the nature of a problem if they see a picture of a diseased patient and some striking statistics. It’s difficult to project the spectrum of acute care patients in the same way, as an explanation of exactly what we do is required to understand to whom the money would go. I think defining our role will be a large part of the solution.

Since you’ve been in residency, what are some of the challenges you've faced in staying involved in international medicine? Any advice for people also wanting to get more involved?
Finding the time to go abroad is always challenging as a resident. I am fortunate to be at a program that prioritizes helping its residents develop their professional interests. I had to stack elective months together to meet the WHO’s minimum time commitment, and the rescheduling process couldn’t have been easier. My advice – don’t hesitate to submit proposals to residency leadership. If you’re truly passionate about a project it will show, and people are usually very responsive to that.

Funding is another challenge. There are a few grants available to residents, but for the most part we end up paying out of pocket. In the grand scheme of things, these opportunities are incredibly important in generating momentum toward our IEM careers. I don’t regret what I’ve spent so far, and I won’t hesitate to continue to invest in my future in this way.

A great resource for the budding IEMer will be the upcoming Nuts and Bolts of Global Emergency Medicine handbook, endorsed by AAEM, EMRA, ACEP and SAEM. Be on the lookout!

Board Review: Heat-Related Illnesses Part 2
Kaitlin Fries, DO
Doctors Hospital

Heat stroke is a life-threatening illness with a reported mortality rate as high as 80%, which left untreated is almost always fatal.1-4 It occurs due to a mechanical failure of the body’s thermoregulatory mechanisms, leading to hyperthermia and multi-system organ dysfunction.1-3 Heat stroke is a time sensitive medical emergency that should be considered in any patient presenting with hyperthermia and altered mental status in the context of a warm environment.

The defining difference between heat exhaustion and heat stroke is a change in mental status and/or CNS dysfunction.1-3 Patients are often combative, display bizarre behaviors, or present with ataxia.1,2 In heat stroke, core body temperatures are generally greater than 104°F.1-3  Heat stroke is further divided into two sub-types: classical and exertional.

Classical heat stroke is typically associated with a shorter course of illness and leads to fewer long-term complications.2 However, it does have a much higher mortality rate than exertional heat stroke.2 Classic heat stroke is commonly seen in the elderly population who do not have access to air conditioning during a heat wave.1,2 Often these patients present with dry skin and altered mental status.1,2 They may also be on medications that prevent heat dissipation.1

Exertional heat stroke is more common in young athletes. These patients will present with extreme dehydration and will usually be sweating profusely. Hypoglycemia is a common finding in these patients. Long-term complications such as liver failure, renal failure and DIC are often seen.2

Treatment of heat stroke is focused on the ABCs of resuscitation and rapid evaporative cooling. This can be accomplished by spraying water on the patient’s skin and fanning the patient. Other cooling options include ice packs to the neck/groin/axilla, cold water immersion and cold water lavage in intubated patients.1-4 It is important to avoid hypothermia by ceasing cooling efforts when the core temperature reaches 102°F.1-4

Excessive shivering can increase the time required to cool the patient; consider giving these individuals a short-acting benzodiazepine such as midazolam.2,4  It is recommended to rehydrate patients with Lactated Ringer’s solution or normal saline to maintain a MAP >60mmHg or a urine output of ≥0.5mL/kg/hr.4 It is imperative to avoid vasopressors if possible due to worsening ischemia and decreased heat exchange, and one should be cognizant that blood pressures will typically improve with cooling due to vasoconstriction.2 Seizures can be controlled with benzodiazepines, and antipyretics are contraindicated in the management of heat stroke. All patients with heat stroke should be admitted to the ICU for close observation and monitoring.


  1. Blok BK, Cheung DS, Platts-Mills TF. First aid for the emergency medicine boards. McGraw Hill; 2012. 13:723-725.
  2. Paquette R. Hippo Review: Heat cramps, heat exhaustion, heat syncope. 2015.
  3. Tintinalli JE. Tintinalli's emergency medicine: A comprehensive study guide. McGraw Hill; 2011. 16:1339-1341.
  4. Tintinalli JE. Tintinalli's emergency medicine: Just the facts. McGraw Hill; 2013. 13:424-425.

Board Review: Herpes Zoster
Sophia Johnson, DO and Shane Sergent, DO
Conemaugh Memorial Medical Center Emergency Medicine Residency

Herpes Zoster, commonly known as Shingles, is caused by a reactivation of the varicella virus that is latent in the dorsal root ganglia.1 It is more common with advancing age and in those who are immunocompromised, with a lifetime incidence of 10-20%.1,2 Any person who has previously been infected with varicella can present with herpes zoster.1 

The rash of herpes zoster is generally maculopapular and becomes vesicular within 24 to 48 hours.1,2  New lesions can continue to appear for up to seven days, with crusting occurring within 7 to 10 days.1  It can present along any dermatome, but is more common on the face and chest and does not cross midline.2  Prior to the rash erupting, patients may have malaise, headache and photophobia.2  Herpes zoster can be exquisitely painful and the patient may experience pain for several days prior to the rash appearing.1 A tzanck test can be used for diagnosis, but history and physical exam are generally sufficient.1

Herpes zoster ophthalmicus involves the trigeminal nerve and requires evaluation by an ophthalmologist; lesions on the tip of the nose are known as Hutchinson sign and are a clue to ophthalmic involvement.1,2 Herpes zoster oticus involves the seventh cranial nerve and may be indicated by lesions on the external ear or tympanic membrane.1,2  Ramsay Hunt syndrome involves the seventh cranial nerve and the patient presents with ipsilateral facial paralysis and auditory symptoms.1  In a young, otherwise healthy person, the presence of herpes zoster may indicate an immunocompromised state, such as HIV.2

It is important to initiate treatment within the first 24 to 72 hours with an antiviral such as acyclovir, valacyclovir or famciclovir.1 This helps reduce the duration of postherpetic neuralgia, decreases new lesion formation and hastens resolution.1 IV acyclovir is indicated for patients with disseminated herpes zoster, CNS involvement or an extreme immunosuppressed state.2 Valacyclovir or IV acyclovir is indicated for those with herpes zoster ophthalmicus.1,2

Herpes zoster can be very painful and patients may require opiate analgesics.1 NSAIDs, moist dressings and rest are also helpful.1 Postherpetic neuralgia can persist for months or years and is defined as pain that occurs for greater than 30 days.2 Patients should also be educated that zoster is contagious both prior to lesions appearing and until all lesions have crusted over, and direct contact with fluid in vesicles can lead to transmission.1,2


  1. Hess MR, Hess SP. Skin disorders common on the trunk. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. New York, NY: McGraw-Hill; 2011. Accessed July 15, 2015.
  2. Takhar SS, Moran GJ. Disseminated viral infections. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. New York, NY: McGraw-Hill; 2011. Accessed July 15, 2015.

Metformin-Associated Lactic Acidosis
Danielle Goodrich, MD and Nikita Joshi, MD
Stanford/Kaiser Emergency Medicine

Metformin is an oral hypoglycemic medication considered a first line agent for oral treatment of Type 2 Diabetes. It is a biguanide that functions by inhibiting hepatic gluconeogenesis and glucose absorption from the GI tract. It also increases the action of insulin in target organs.

Metformin use is associated with a rare type B lactic acidosis that can occur at therapeutic and toxic overdose levels. Unfortunately, the mechanism of action is not well understood. The current hypothesis is that the lactic acidosis is a result of suppression of hepatic gluconeogenesis resulting in lactate production, decreased lactate uptake by the liver and increased lactate production in the intestine.1 In severe cases, the metformin-associated lactic acidosis causes significant vasodilatation and depressed myocardial contractility leading to hypoperfusion and hypotension.

In addition to resuscitation, treatment includes addressing the toxicity through the use of activated charcoal and dialysis. However, in patients with lactic acidosis from chronic use, GI decontamination is unlikely to provide benefit. Since metformin is a small molecule and minimally protein bound, dialysis has been successfully used to clear both the metformin and the underlying lactic acid.2, 3 Indications for dialysis include severe metabolic acidosis (pH < 7.1), failure to improve with supportive care, and presence of renal insufficiency.4 In patients with hemodynamic instability, continuous renal replacement therapy has been shown to be effective.5

In summary, it is wise to always consider metformin as an etiology for a type B lactic acidosis. Activated charcoal may be useful for GI decontamination, and in severe cases, hemodialysis or continuous renal replacement therapy have been shown to be an effective treatment modality.


  1. Perrone J, Phillips C, and Gaieski D. Occult metformin toxicity in three patients with profound lactic acidosis. The Journal of Emergency Medicine 40.3 (2011): 271-75. Web.
  2. Rifkin SI, Mcfarren C, Juvvadi R, and Weinstein SS. Prolonged hemodialysis for severe metformin intoxication. Ren Fail Renal Failure 33.4 (2011): 459-61. Web.
  3. Kruse JA. Metformin-associated lactic acidosis. The Journal of Emergency Medicine 20.3 (2001): 267-72. Web.
  4. Chu J and Stolbach A. Metformin acidosis, In: UptoDate, Traub SJ(Ed), UpToDate, Waltham, MA. (Accessed on July 1, 2015)
  5. Alivanis P, Giannikouris I, Paliuras C, Arvanitis A, Volanaki M, and Zervos A. Metformin-associated lactic acidosis treated with continuous renal replacement therapy.Clinical Therapeutics 28.3 (2006): 396-400. Web.

New Onset Seizure in a 12-Year-Old Female
Phillip Fry, OMSIV
Midwestern University-Arizona College of Osteopathic Medicine

A 12-year-old Hispanic female presents to the emergency department after having seizure like activity while she was swimming at the beach. The patient was not actively seizing upon arrival to the ED, but her parents state that all four of her extremities were “jerking” for an unclear duration. The parents also note for the past week she has been complaining of a headache. She has no previous seizure history and her parents deny head trauma or toxic ingestions. She did travel to Mexico six months ago, and otherwise has no significant past medical or surgical history. Her parents do not endorse any relevant family history. The patient’s immunizations are up to date. The remainder of review of systems is non-contributory.

On exam, the patient is afebrile, heart rate 72, BP 110/68, respiratory rate 12. Her height is 59” and weight is 45kg. The patient appears drowsy, but there are no focal neurologic deficits, and the remainder of the physical exam is normal. A CT scan of her head demonstrates multiple parenchymal cysts with some calcified granulomas found in the cerebral cortex.

What is the most likely cause of this patient's seizure?

  1. Febrile seizure
  2. Toxic ingestion
  3. Neurocysticercosis
  4. Head Injury
  5. Brain Tumor

Answer:  C

Neurocysticercosis is caused by ingestion of the tapeworm Taenia Solium, which is typically found in raw pork. Mexico has traditionally been an endemic area of the disease; however neurocysticercosis is becoming more prevalent in the United States because of increased migration and travel.1 The cysticerci in the tissue develop over a period of three to eight weeks, usually do not cause significant inflammation, and thus are able to remain asymptomatic for a period of years. The clinical manifestations of the disease depend on the location and number of parasites, with seizures being the most common clinical manifestations.2

The diagnosis of neurocysticercosis is based largely on clinical presentation and imaging. Serologic tests are also available; however negative serology testing does not exclude the diagnosis.3 It is important for antiepileptic therapy to be started as soon as possible, with commonly used agents including phenytoin or carbamazepine.4 Treatment for multiple cysts, such as this case, includes albendazole and corticosteroids.5


  1. Garcia HH, Coyle CM, White AC Jr. Cysticercosis. In: Tropical Infectious Diseases: Principles, Pathogens, and Practice, Guerrant RL, Walker DH, Weller PF. (Eds), Churchil-Livingstone, Philadelphia 2011. p.815.
  2. Nash TE, Del Brutto OH, Butman JA, et al. Calcific neurocysticercosis and epileptogenesis. Neurology. 2004; 62(11):1934.
  3. Nash TE, Garcia HH. Diagnosis and treatment of neurocysticercosis. Nat Rev Neurol. 2011 Oct; 7(10):584-94. Epub 2011 Sep 13.
  4. Kaushal S, Rani A, Chopra SC, Singh G. Safety and efficacy of clobazam versus phenytoin-sodium in the antiepileptic drug treatment of solitary cysticercus granulomas. Neurol India. 2006; 54 (2):157.
  5. Vazquez V, Sotelo J. N Engl J Med 1992; 327:696-701. September 3, 1992

Notes from the Field: Uncontrolled Hemorrhage
Chris Winstead-Derlega, MSIV
University of Virginia School of Medicine

While hiking, travelling or vacationing, many medical providers carry first aid kits and basic medical supplies well suited for management of low acuity injuries such as sprains, strains or bruises. However, the leading cause of traumatic death in the austere environment is uncontrolled hemorrhage. A recent review of management can be found in Drs. Drew, Bennett and Littlejohn’s 2015 Application of Current Hemorrhage Control Techniques for Backcountry Care.1,2

This two part series assesses recent literature on controlling life-threatening bleeds in austere environments. The first article highlights the importance of direct manual pressure followed by the early application of a tourniquet, as opposed to traditional teachings of utilizing pressure points and extremity elevation.1 A prospective military observational study by Kragh et al., found a 90% vs 10% survival rate (p<0.001) when shock was absent versus when shock was present before tourniquet application, suggesting benefit from early application of a tourniquet.3 The review continues by highlighting the four commercially available tourniquets approved by the Committee on Tactical Combat Casualty Care and the new junction axilla or inguinal area hemorrhage control devices.1 Despite ongoing debate on tourniquet use and the fear of complications, when applied for less than two hours, tourniquets have been demonstrated to pose little to no harm.1, 3 When faced with a life threatening bleed, the benefits of hemorrhage control outweigh the potential risks of pain or limb loss.

To review the technique of tourniquet placement, first assure that the tourniquet is easily accessible. In a life or limb situation, place a tourniquet early to control massive hemorrhage. Place the tourniquet two to three inches proximal to the wound, and tighten until distal pulses are absent.
Part two in the series discusses hemostatic dressings, pelvic bindings and the prehospital use of transexamic acid (TXA).2 While personal use of hemostatic dressings and TXA may sound far fetched, consider the availability of hemostatic dressings for purchase on the internet. In addition, pelvic fracture stabilization is a simple technique with life saving effects. With a simple bed sheet or article of clothing, external splinting with the goal of compressing internal hemorrhage may be life saving in an austere environment. Unfortunately, neither article discusses the utility of improvised tourniquets, which the layperson without access to a commercial tourniquet may employ in a “life or limb scenario.”4

Before your next summer adventure, review your medical kit and consider the inclusion of a tourniquet or other hemorrhage control device for the above reasons.


  1. Drew B, Bennett BL, Littlejohn L. Application of current hemorrhage control techniques for backcountry care: Part one, tourniquets and hemorrhage control adjuncts. Wilderness Environ Med. 2015 Jun;26(2):236-245. doi: 10.1016/j.wem.2014.08.016.
  2. Littlejohn L, Bennett BL, Drew B. Application of current hemorrhage control techniques for backcountry care: Part two, hemostatic dressings and other adjuncts. Wilderness Environ Med. 2015 Jun;26(2):246-254. doi: 10.1016/j.wem.2014.08.018.
  3. Kragh JF, Walters TJ, Baer DG, et al. Survival with emergency tourniquet use to stop bleeding in major limb trauma. Ann Surg. 2009;249:1–7.
  4. Stewart SK, Duchesne JC, Khan MA. Improvised tourniquets: Obsolete or obligatory? J Trauma Acute Care Surg. 2015 Jan;78(1):178-83. doi: 10.1097/TA.0000000000000485.

Imaging a Maxillofacial Foreign Body
Erica Schramm, MSIV and Gururaj Shan, MSIV
Cooper Medical School of Rowan University

Detection of maxillofacial foreign bodies can prove challenging in the emergency department, especially when there is a high suspicion of contamination without a grossly visible foreign body on exam. Wounds with a high potential of contamination include wounds sustained via objects that splinter or shatter and patient perception of a foreign body in the wound. When a foreign body is not grossly visible in a wound that is potentially contaminated, the location and composition of the object become key to detection.

The authors of one comparative in vitro study sought to determine the optimal imaging modality for detection of various materials in maxillofacial tissues - specifically on bone, in muscle and in air space using a sheep model.1 Foreign bodies were composed of metal, glass, stone, wood, acrylic, graphite or Bakelite. Imaging modalities used to detect the objects were plain films, CT and ultrasound. Images were read by six independent observers, and visibility of objects was rated on a four-point scale.

The authors determined that the selection of an ideal imaging modality should take into account both the potential position and the composition of a foreign body. Metal, glass and stone foreign bodies could be reliably detected with all imaging modalities in all tissue zones. Radiolucent materials (wood, acrylic, graphite and Bakelite) posed a greater challenge. Wood, acrylic and Bakelite could not be visualized on plain films, and graphite was only visible in muscle on plain films. CT imaging of wood, acrylic and Bakelite showed that these materials were less visible or undetectable in muscle and on bone. Graphite however was detectable on CT in all tissue zones. Overall, ultrasound was superior to CT and plain films for detecting radiolucent materials. However, ultrasound did not detect any foreign body materials in air. All foreign bodies were visible in air on CT.

This study was limited by in vitro collection of data, as foreign bodies of standardized dimensions were artificially inserted into a sheep’s head. The study did not take into account very small foreign bodies < 1cm x 1cm x 0.1cm or multiple foreign bodies of different composition, as may occur in clinical scenarios. However, in vivo data comparing standardized foreign body size and tissue location would be very difficult to collect.  Results of this study can be interpreted clinically to select an ideal imaging modality based on suspected foreign body material and location, but variability of interpreter and/or operator skill should also be taken into account.


  1. Aras MH, Miloglu O, Barutcugil C, Kantarci M, Ozcan E, and Harorli A. Comparison of the sensitivity for detecting foreign bodies among conventional plain radiography, computed tomography and ultrasonography. Dentomaxillofacial Radiology; 2010. 39:2, 72-78.

Your 2015-2016 Leaders:

Victoria Weston, MD

Vice President
Michael Gottlieb, MD

Nicole Battaglioli, MD

Immediate Past President
Meaghan Mercer, DO

At-Large Board Members
Phillip Dixon, MD
Mary Haas, MD
Nathan Haas, MD
Amy Ho, MD
Megan McKay, MD
Greg Wanner, DO

Medical Student Council President
Michael Wilk

Modern Resident Contributors

Copy Editor: Nathan Haas, MD

Managing Editor:
Madeleine Montony, MSM

Special thanks to this issue's contributors:

James M. Dahle, MD; Jenna Erickson, MD; Kaitlin Fries, DO; Phillip Fry, OMSIV; Manish Garg, MD FAAEM; Danielle Goodrich, MD; Amy Ho, MD; Sophia Johnson, DO; Nikita Joshi, MD; Daniel F. Leiva, OMSIV; Alexandra Murray, DO; Linda Sanders, MD; Erica Schramm, MSIV; Shane Sergent, DO; Gururaj Shan, MSIV; Chris Winstead-Derlega, MSIV

Interested in writing?

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Please submit articles by September 15th for the October/November 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:


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