Modern Resident - The newsletter of AAEM/RSA
December/January 2012
Volume 3: Issue 4


2011-2012 Leadership

President
Teresa M. Ross, MD

Vice President
Zachary Repanshek, MD

Secretary-Treasurer
Leana Wen, MD MSc

Immediate Past President
Ryan Shanahan, MD

At-large Board Members
Ali Farzad, MD
Stephanie Gardner, MD
Sarah Terez Malka, MD
Taylor McCormick, MD
Ketan Patel, MD

Medical Student Council President
Meaghan Mercer

Modern Resident Contributors

Copy Editor: Taylor McCormick, MD
Managing Editor: Jody Bath, AAEM/RSA Staff

Special thanks to this issue's contributors: Casey Grover, MD; McKaila Allcorn, DO; Jill Ward, MD; Veronica Tucci, MD JD; Michael Omori, MD FACEP; Michael Holman, MS4; Jeff Scott, MS4; Anthony L. Nguyen, MS2; and Christopher DeClue, MS1.

Interested in writing?

Email submissions to: info@aaemrsa.org

Please submit articles by February 15th for the February/March edition.

Opinions expressed are those of the authors and do not necessarily represent the official views of AAEM or AAEM/RSA.


ANNOUNCING NEW IN 2012: FREE EM:RAP SIGN UP WITH YOUR AAEM/RSA MEMBERSHIP!

The AAEM/RSA Membership Committee would like to extend the warmest wishes to you. We would also like to announce an exciting new benefit coming soon for paid AAEM/RSA members. All paid AAEM/RSA members will soon have access to Emergency Medicine: Reviews and Perspectives (EM:RAP) via their AAEM/RSA membership page http://www.aaemrsa.org/. This outstanding monthly educational audio program, which ordinarily costs a resident $195/year, will be free! Please watch for further updates on this new member benefit.

AAEM/RSA is committed to providing our members with comprehensive and up-to-date educational resources whether you are on shift, in the car or cramming for the boards. In addition to EM:RAP, we are in the process of making our texts accessible through mobile devices to ensure that AAEM/RSA will be "with you all the way!" Thank you for your membership and support, and we wish you all a great and prosperous 2012.


Why the AAEM Scientific Assembly?

As a student or resident, finances are tight, and days off are precious. What makes the AAEM Scientific Assembly a worthwhile use of that valuable time and cash?

For a refundable deposit, AAEM offers lectures of the highest academic quality. All physician lecturers have the same goal: presenting up-to-date, clinically relevant and academically excellent content. This year's list of speakers includes some of the specialty's most charismatic speakers and an array of topics from pediatrics to palliative care.

The RSA/YPS Track and Student Track enhance the didactic offerings with lectures and workshops oriented towards preparing you for your residency and career. Topics for the RSA/YPS Track will include finding your dream job, how to get the most out of your consultations, a fellowship panel and advice on how to prepare a professional application package. Topics for the Student Track will include pearls and pitfalls of EM, overview of EM, interesting cases in EM and toxicology, ultrasound in the ED, a military panel and a program director panel. The intimate size of these tracks allows plenty of time for questions and interaction with department chairs and program directors from across the country.

Of course, the Scientific Assembly allows multiple opportunities for networking and meeting your future colleagues. And best of all, the Scientific Assembly is free to AAEM members (refundable deposit required)!

We look forward to meeting you in sunny San Diego!


18th Annual Scientific Assembly

Did You Know?...Ketamine in Head Trauma
Casey Grover, MD
Stanford/Kaiser Emergency Medicine

We all learned in medical school that increased intracranial pressure is a contraindication to the use of ketamine...

Where does this come from?
The notion that ketamine increases intracranial pressure (ICP) comes from six studies published in the 1970s. These publications consist of a series of case reports and case control studies on a whopping 51 patients (mostly neurosurgical) in which the use of ketamine increased intracranial pressure. The concern about increased ICP is that it may reduce blood flow to the brain, damaging sensitive neuronal tissue. Interestingly, review of these studies demonstrates that cerebral perfusion pressure (mean arterial pressure minus ICP) actually increased in the majority of the patients who received ketamine.

What have we since learned about ketamine?
Animal studies demonstrate that ketamine may be neuroprotective by reducing release of glutamate, a neurotoxic neurotransmitter. More importantly, we now have some higher quality evidence on the topic. Through the 1990s and 2000s, there have been four prospective, randomized, controlled trials on the use of ketamine in head trauma. In all but one, there was no significant increase in ICP in the ketamine group, and in the fourth study, the increase in ICP with ketamine was only about 2mmHg. Furthermore, in all four studies, cerebral perfusion pressure was either increased or unchanged in patients receiving ketamine. A 5th prospective study on the use of ketamine in neurosurgical patients in the 1990s actually showed a decrease in ICP with ketamine. It must be noted that these studies were somewhat limited by size, with a combined total of 134 patients between all five.

What does this mean?
There is significant evidence to suggest that ketamine may be safe in patients with head injury or suspected increased ICP.

References

  1. Filanovksy Y, Miller P, Kao J. Myth: Ketamine should not be used as an induction agent for intubation in patients with head injury. CJEM 2010; 12: 154-7.
  2. Himmelseher S, Durieux ME. Revising a dogma: Ketamine for patients with neurological injury? Anesth Analg 2005; 101: 524-34.

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Epistaxis
Michael Holman, MS4
Georgetown University School of Medicine

Epistaxis can be thought of as two separate entities, anterior and posterior, which differ in etiology, anatomy, treatment and disposition. After the patient is assessed for hemodynamic stability, have them blow out blood clots, apply an intranasal vasoconstrictor spray or soaked pledget, and apply pressure to the nasal ala for 10-15 minutes. A proper exam with a nasal speculum may then be performed to visualize the origin of the bleed.

Anterior bleeds are much more prevalent (90%) and occur from the septal vascular watershed area known as Kiesselbach's Area. Chemical cautery with silver nitrate may suffice for mild cases. Apply for ten seconds from the periphery to the center of the bleed, and look for the resultant white precipitate. Anterior nasal packing may be required for persistent bleeds. Nasal tampons or inflatable packs should be covered with topical antibiotic prior to insertion. The patient must return to have the packing removed after 24-48 hours; no systemic antibiotics are required.

Posterior bleeds are less common (10%) but are often more severe. They occur from the lateral wall's posterior branch of the sphenopalantine artery. Double balloon or Foley catheters should be inserted into the nasopharynx, inflated, and gently retracted to achieve tamponade. Be sure to protect the nasal ala from pressure necrosis as the device is secured. If the epistaxis persists, surgical embolization or ligation may be required. Although the existence of the nasopulmonary reflex has been debated, the risk of asphyxiation requires hospitalization while the posterior packing is in place. Amoxicillin/Clavulanate or a second-generation cephalosporin is recommended during the inpatient stay.

References

  1. Alter, Harrison. Approach to the Adult with Epistaxis. UpToDate. Waltham, MA, 2011.
  2. Marx, John A. (Ed). Rosen's Emergency Medicine, 7th ed. Mosby Elsevier, Philadelphia, PA 2010.
  3. Roberts, James and Hedges, Jerris. Roberts: Clinical Procedures in Emergency Medicine, 5th ed. Mosby Elsevier, Philadelphia, PA 2010.

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Medical and Surgical Emergencies in the Pregnant Patient
McKaila Allcorn, DO
Kent Hospital

For most of us, pregnant patients can be intimidating (and not just because of their hormones). While it would be nice to think that our obstetric colleagues can handle all emergencies that occur in pregnancy, it is important to remember that not all baby-bump wielding women present with a purely obstetric complaint. Here are just a few things to keep in mind!

Appendicitis is still the most common surgical emergency in pregnant patients. Incidence is the same in pregnant patients as it is in non-pregnant patients (7%). During the first 20 weeks, clinical findings are usually similar to that of the non-pregnant patient. The most constant feature in all gestational ages is right-sided abdominal pain (in only 23% of pregnant patients does the location of the appendix change from the RLQ). Management should include both OB and surgical consultation and judicious imaging with US or helical CT (with rectal contrast and limited study, only 300mrad fetal radiation exposure). MRI is emerging as a sensitive and low-risk alternative. However, laparoscopy or laparotomy is the diagnostic procedure of choice in these patients, and early exploration is encouraged. These procedures are relatively safe during pregnancy, especially in contrast to the risk of maternal morbidity from failure to diagnose and perforation.

Thromboembolic disease is the leading cause of death in pregnancy. Pregnant women are six times more likely to develop venous thrombosis than non-pregnant women, most commonly six weeks pre- and post-partum. Lower extremity Doppler US is still the first-line test for DVT in pregnancy, but keep in mind that isolated iliac vein disease is common in pregnancy, and leg studies may be normal in such cases. Don't be afraid to scan these ladies! There is no known risk of fetal disability, anomaly or growth restriction at doses of radiation less than 5 rads. While there is still some debate as to which imaging modality is more sensitive in the pregnant patient, the average dose of radiation for a VQ scan (between 7-31mrad) or CT chest (30mrad) is well under the 5 rads recommendation. As you all remember, warfarin is contra-indicated in pregnancy, but heparin and low-molecular-weight heparin are both considered generally safe in pregnancy.

Reference

  1. Houry D, Bisan S. Rosen's Emergency Medicine: Concepts and Clinical Practice, Ch 176 Acute Complications of Pregnancy. 7th. 2. Philadelphia: Mosby Elsevier, 2010. 2279-2297.

Critical Care Pearl: Therapeutic Hypothermia
Jeff Scott, MS4
Saint Louis University School of Medicine

In the appropriate clinical setting, therapeutic hypothermia (TH) can be a life-saving procedure and the difference between severe brain damage and normal neurologic recovery. The American Heart Association and International Liaison Committee on Resuscitation both strongly encourage TH when appropriate, yet it remains underutilized among physicians and hospitals worldwide. Hypothermia protects brain tissue by inhibiting inflammation, free radical formation, apoptosis and edema. It also reduces intracranial pressure (ICP) and metabolic demand. Studies show dramatic improvement in neurological function and reduced mortality in patients who undergo TH in certain conditions, including refractory elevated ICP, neonatal asphyxiation encephalopathy and patients who remain unconscious after return of spontaneous circulation (ROSC) from shockable cardiac arrest (Vfib or pulseless Vtach). TH after non-shockable cardiac arrest (asystole or PEA) shows mixed data, but current recommendations encourage TH if these occur in-hospital. Data are lacking on pregnant patients, but successful fetal outcomes have been reported. Data for TH in liver failure encephalopathy is encouraging, but there are no official guidelines.

Following intubation, patients are quickly cooled to 32-34°C using ice packs, cooling devices, cold IV fluids, gastric lavage or a cooling cap in infants. TH is maintained for 12-24h in cardiac arrest and 72h for neonatal asphyxia to allow for reperfusion of ischemic tissue or until ICP is reduced in patients with refractory elevated ICP. Patients must be monitored closely for infection, seizures and coagulopathy. Electrolyte and glucose shifts should also be monitored and treated. Shivering is controlled with opioids, alpha-blockers and benzodiazepines. Warming skin surfaces with an air-circulation blanket while maintaining core temperature reduces the shivering threshold. Neuromuscular blockers are only used as a last resort. Rewarming should be done at 0.25-0.5°C/h being careful to avoid hyperkalemia, hypoglycemia and increased ICP.

References

  1. Granja et al. Improved survival with therapeutic hypothermia after cardiac arrest with cold saline and surfacing cooling: keep it simple. Emerg Med Int, 2011 April; 2011. Epub.
  2. Nichol et al. Regional systems of care for out-of-hospital cardiac arrest: a policy statement from the American Heart Association. Circulation. 2010;121(5):709–29.
  3. Neumar et al. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. A consensus statement from the International Liaison Committee on Resuscitation. Circulation. 2008;118(23):2452–83.

Advocacy 101: Drug Shortages...Advocate for Your Patient's Cure & Safety
Anthony L. Nguyen, MS2
University of Wisconsin School of Medicine & Public Health

What do epinephrine, succinylcholine, naxolone hydrochloride, calcium gluconate, propofol and more than 140 other drugs have in common? They have all been in short supply this past year. Especially critical to emergency physicians are sterile injectables on the American Society of Health System Pharmacists' drug shortage list (http://www.ashp.org/DrugShortages/Current/). A drug shortage is a supply and demand mismatch that affects how physicians and pharmacists prepare and dispense a drug product, often forcing physicians to use alternative drugs or delay treatment. While many emergency physicians have not yet experienced the effects of these shortages, thanks to pharmacists scrambling to find stock, adverse effects on patient care will be felt soon. This crisis gained publicity as the American Hospital Association's July 2011 survey of 820 hospitals found that 91% experienced drug shortages in emergency care within the last six months. Additionally, 62% of hospitals delayed treatment, and 58% prescribed a less effective alternative drug. Drug shortages often force physicians and pharmacists to use alternative drugs and to make mixtures and solutions that are unfamiliar. For example, pre-filled syringes of epinephrine .1mg/mL were in short supply in 2010, forcing pharmacies to make kits with 1mg/mL ampules, which increased the risk of overdose. The changes in packaging and concentration of substitute drugs can put patients at higher risk for mistakes and adverse reactions. Overdoses, underdoses, misidentification of IV bags and treatment delays have all occurred recently because the health care teams were unfamiliar with these substitutes and their appropriate dosages. Furthermore, shortages drive up costs in hospital pharmacies by forcing pharmacists to order drugs outside existing contracts through "gray market" suppliers who charge over 1000 percent of the drug's original price.

There is no single reason for drug shortages. The drug manufacturers' reasons for shortages are often unclear citing "manufacturing difficulties." Many economic factors including FDA regulations, supply of raw materials, manufacturing problems and cost pressures prevent adequate production of critical drugs. The drug industry also continues to consolidate, meaning fewer drug companies are providing raw material and manufacturing drugs. Few companies make sterile injectables, because most injectables are generic, leading to low profit margins. Also, up to 80% of raw drug ingredients come from foreign sources. Therefore, raw ingredient supply can be at the whim of political sentiment and natural disasters. If one manufacturer ceases production, this places stress on the supply from other manufacturers and on alternative drugs, further exacerbating the shortage. Surprisingly, the FDA has little power to improve the situation. FDA regulation violations and product recalls can cease production. Additionally, the FDA requires notice at least six months prior to a manufacturing disturbance of a "medically necessary" drug, but this rule is not often followed or enforced. Unfortunately, while the FDA can control distribution and evaluate the data of alternatives, it cannot force companies to increase production or to manufacture discontinued drugs.

But don't lose hope! Emergency physicians can work to prevent adverse outcomes due to drug shortages on a hospital and systematic level. Proper planning, good communication, and clear guidelines can reduce negative consequences on patient care. Physicians should be in close communication with the pharmacy to be quickly notified of potential limited supply. Additionally, physicians should serve on Pharmacy & Therapeutic (P&T) Committees and work closely with pharmacists to develop plans on managing shortages, finding appropriate substitutes, and forming guidelines to ensure equitable patient care. Stockpiling drugs should not be practiced. If a shortage directly affects patient care, physicians should document the event in the patient's chart, inform the treatment team, and report it to hospital risk management. On a system wide level, emergency physicians can work with AAEM/RSA Advocacy Committee and contact their congressperson to inform their representatives about the scope and human impact of the problem. Currently, the AAEM/RSA Advocacy Committee is working on collaborating with other professional organizations to raise awareness. Additionally, Senator Orrin Hatch (R-Utah) of the Senate Finance Committee has recently introduced this issue to the Senate, and we hope to work closely with him on his efforts in the near future. The AAEM/RSA Advocacy Committee welcomes your suggestions and participation in raising awareness of this issue and in advocating for quality patient care and safety.

References

  1. Fox, E. R., & Tyler, L. S. (2004). Measuring the impact of drug shortages. American Journal of Health-System Pharmacy : AJHP : Official Journal of the American Society of Health-System Pharmacists, 61(19), 2009.
  2. Mitka, M. (2011). FDA, US hospital and pharmacy groups report drug shortages a growing problem. JAMA : The Journal of the American Medical Association, 306(10), 1069-1070.
  3. McKenna, M. (2011). Hospital pharmacists scrambling amid vast drug shortages: Emergency

Beta-Blocker Overdose in Children: A Threat?
Jill Ward, MD
Florida Hospital Emergency Medicine Program

An 18-month old toddler is brought to the ED after swallowing one or two of his grandma's pills while her back was turned. Grandma tells you that the pill was metoprolol, which she takes twice daily, but she cannot remember the dose and did not bring the bottle with her. The child is well appearing with a heart rate of 130 beats/min and blood pressure of 90/60 mmHg. She asks you if her grandson will be okay and when they can go home...

Accidental ingestion of beta-blockers by children is common and increasing due to the escalating usage of beta-blockers in adults. There are no documented cases of serious cardiovascular morbidity or death in children less than 6 years old who have ingested 1-2 tablets of a beta-blocker. Hypoglycemia is the most common side effect in children. Glucose infusion and glucagon are normally sufficient for maintaining euglycemia. While serious complications are rare, CNS, cardiac and metabolic toxicities can be similar to adults in higher dosages. Six hours of observation for mild hypotension and bradycardia is recommended for an asymptomatic child with low suspicion for toxicity. High-risk ingestions (multiple tablets, extended release formulations, or co-ingestions) may need 24 hours of observation.

References

  1. Love, J and Sikka N. "Are 1–2 tablets dangerous? Beta-blocker exposure in toddlers." J of Emer Med. April 2004: 26(3), pgs. 309-314.
  2. Roberts DJ. Cardiovascular Drugs. In: Marx JA, et al. Rosen's Emergency Medicine: Concepts and Clinical Practice. 7th ed. Philadelphia, PA: Mosby Elsevier; 2010: Vol 2, pg. 1985.

'Tis the Season to Investigate Holiday Plant Myths
Christopher DeClue, MS1
Veronica Tucci, MD JD
Michael Omori, MD FACEP
University of South Florida Emergency Medicine

Contrary to popular belief, the poinsettia (Euphorbia pulcherrima) is not a toxic plant. This misconception began as an urban legend dating back to 1919 when the two year old son of an Army officer stationed in Hawaii reportedly died of poisoning from what was believed to be a poinsettia leaf. Even though the story was later retracted, the poinsettia leaf had been incorrectly identified as the cause of death. Modern research has worked to prove that there is no validity to these toxicity claims. After reviewing over 22,793 cases of poinsettia poisoning, investigators from the Children's Hospital of Pittsburgh and Pittsburgh Poison Center reported no deaths from exposure and cited mild to moderate gastrointestinal tract irritation as the only adverse effects. They also described how 92.4% of cases didn't develop any symptoms related to exposure and how 96.1% of cases weren't even treated in a health care facility. In addition, POISINDEX claims that it would take over 500 poinsettia leaves for a 50lb child to reach a potentially toxic dose of the plant. Not only does this research debunk the myth regarding poinsettia toxicity, but it also allows the poinsettia to remain a safe and prominent emblem throughout the holiday season.

Exposure to mistletoe may not prove to be as forgiving. Mistletoe is the common name given to over 1,400 species of plants belonging to the order Santales. Although European mistletoe (Viscum album) and North American mistletoe (Phoradendron serotinum) are the two species sold commercially during the holiday season, they each contain different compounds that can alter major biological functions. Structural variance accounts for the similarities and differences in toxicity between the European mistletoe and North American mistletoe. While ingestion of North American mistletoe can lead to gastroenteritis, exposure to concentrated extracts of European mistletoe can result in severe toxic effects such as seizures, hallucinations and anaphylaxis. Additionally, both species contain toxins that have also been proven to produce hypotension, bradycardia, as well as have a negative ionotropic effect on the heart. Therefore, the degree of mistletoe toxicity is dependent upon both the type and quantitiy of mistletoe that has been ingested.

Holly is another holiday plant that can be toxic and even lethal at high doses. Belonging to the family Aquifoliaceae, holly is part of the genus Ilex that contains over 600 different species of the plant. Most species of holly contain both tannins and saponins: two compounds which lead to toxicity when ingested. While tannins are polyphenolic compounds that interfere with the normal absorption of proteins, saponins are amphipathic glycosides that confer toxicity via sterol complexation. Both tannins and saponins contribute to gastroenteritis that develops upon ingestion of holly. Not only does this lead to vomiting and diarrhea, but it also results in dehydration and electrolyte imbalances as well. The more severe toxic effects that are related to higher doses of holly ingestion can be attributed to tannins. Aside from irritating the gastrointestinal tract, tannins have also been found to be responsible for kidney irritation and liver damage that could prove to be fatal.

References

  1. Arena, JA. "Questions and answers: are holly berries toxic?" JAMA (1979): 242 (21): 2341.
  2. Bauer, C et. al. "Anaphylaxis to viscotoxins of mistletoe (Viscum album) extracts." Ann Allergy Asthma Immunology (2005): 94 (1), 86- 89.
  3. Brunvand, Jan Harold. The Big Book of Urban Legends. New York, NY: Paradox Press, 1994.