Modern Resident - The newsletter of AAEM/RSA
December 2010/January 2011
Volume 2: Issue 4


Your Leadership

We welcome your comments and suggestions. Feel free to get in touch with your elected leaders:

President
Ryan Shanahan, MD

Vice President
Heather Jiménez, MD

Immediate Past-President
Michael Ybarra, MD

Secretary/Treasurer
Sandra Thomasian, MD

At-large Board Members
Melissa Halliday, DO
Ketan Patel, MD
Zachary Repanshek, MD
Teresa Ross, MD
Leana Wen, MD

Medical Student Council President
Brett Rosen

Modern Resident Contributors

Copy Editor: Teresa M. Ross, MD
Managing Editor: Jody Bath, AAEM/RSA Staff

Special thanks to this month's contributors: Heather Jiménez, MD; Michael Holman, MS III; Douglas Kuxhausen, DO; Meaghan Mercer, OMS III; Stephanie Nicole Lewis, MS IV; and Cameron McLaughlin, OMS IV.

Interested in writing?

Email submissions to: info@aaemrsa.org

Please submit articles by February 1st 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.


AAEM/RSA Board Updates

AAEM Scientific Assembly/Orlando, FL
February 28-March 2, 2011

The big event is fast approaching! Plan ahead now to attend this great educational opportunity at the Peabody in Orlando. Our specialized resident track of lectures is always a big hit.
http://www.aaem.org/education/scientificassembly/.

UPDATES: From Your Vice President's Council

  • Written Board Review Book: Give yourself a holiday treat by utilizing Emergency Medicine: A Focused Review of the Core Curriculum to study for your in-service this year. Check out our website for further information and pricing discounts.
  • Upcoming graduates: Take advantage of the CV/Cover Letter review service offered by the Young Physicians Section (YPS). By utilizing the review service, YPS will in turn extend a complimentary one-year YPS membership to you upon joining AAEM as an associate or full voting member following graduation. Furthermore, grab a newly published copy of the essential guidebook, Rules of the Road for Young Emergency Physicians. Interested in becoming involved with YPS now? 2011 graduates are invited to run for the YPS board of directors election. Nominations are being accepted December 17-30.
  • Advocacy in Action: Join our Advocacy Committee's efforts to monitor board certification issues at the state level. If you hear of any upcoming hearings in your state's medical board, please pass the information along to your VP Council representative so we can ensure AAEM's voice is heard. Email: Heather Jiménez, AAEM/RSA Vice President, at hlkuhlen@iupui.edu.

AAEM/RSA Exclusive - A Must Have!

Emergency Medicine: A Focused Review of the Core Curriculum
Emergency Medicine:
A Focused Review of the Core Curriculum

22 chapters, 225 board-style questions, 79 images...one way to excel!

To purchase this incredible new resource, visit http://www.aaemrsa.org/bookstore for your member discount!

Clinical Pearls - Board Review in Wilderness Medicine: High Altitude Headache Prophylaxis
Michael Holman, MS III
Georgetown University School of Medicine

Neurological symptoms of high altitude syndromes exist on a continuum: High Altitude Headache (HAH) – Acute Mountain Sickness (AMS) – High Altitude Cerebral Edema (HACE).

The International Headache Society defines HAH as:

  • Begins within 24 hours of ascent
  • Improves within 8 hours of descent
  • Includes two of the following: bilateral, frontal or frontotemporal, dull or pressing, mild to moderate intensity, aggravated by exertion, movement, straining, coughing or bending over

Although highly variable, the first symptoms begin when un-acclimated persons climb above 2,000–3,000 m (6,500–10,000 ft). Development of anorexia, fatigue, insomnia or dizziness suggests a progression to AMS.

Much of the pathophysiological mechanism of HAH remains unknown; however, it is well accepted that it is, in part, the result of cerebral hypoxia-induced compensatory changes. Endothelium-released nitric oxide dilates the cerebrovascular system, agitating the heavily-innervated meninges and activating the trigeminovascular system.

Acetazolamide remains the gold standard for the prophylaxis of HAH. It facilitates acclimatization by speeding renal clearance of bicarbonate, creating a metabolic acidosis that buffers the respiratory alkalosis of hyperventilation. However, a recent re-evaluation of ibuprofen showed it to be comparable to acetazolamide both in HAH prophylaxis and the prevention of subsequent AMS (Gertsch et al). The authors suggest that their outcome supports the theory of HAH being not just an hypoxia-induced acid-base issue, but perhaps also an inflammatory process. They do advise caution when recommending ibuprofen, as the preventive mechanism is not completely lucid and analgesics may simply mask the symptoms of a dangerous disease process.

One potential use for ibuprofen includes short stays at high elevations. In the continental U.S., the highest peak is about 4,500 m (14,500 ft), and the highest ski-friendly terrain is about 4,000 m (13,000 ft). These elevations are not hospitable for more than momentary stays. Therefore, ibuprofen may be an easy and safe option for HAH prophylaxis.

Recommendations:

  1. Climb high and sleep low. Go slow.
  2. Avoid alcohol. Stay hydrated.
  3. Consume a carbohydrate-heavy diet before ascent.
  4. Ibuprofen 600 mg TID or Acetzolamide 5 mg/kg/day for 24 hours before ascent and continued while at elevation.

References:

  1. Gertsch, Jeffrey H., et al. Prospective, Double-Blind, Randomized, Placebo-Controlled Comparison of Acetazolamide Versus Ibuprofen for Prophylaxis Against High Altitude Headache: The Headache Evaluation at Altitude Trial (HEAT). Wilderness and Environmental Medicine. 2010; 21:236-243.
  2. Serrano-Duenas, M. High Altitude Headache. A prospective Study of its Clinical Characteristics. Cephalalgia. 2005; 25: 1110-1116.
  3. Wilderness Medicine, 5th Ed, [edited by] Paul S. Auerbach. Elsevier Inc. 2010.

A Day in the ER: A Tale of Two Ectopic Pregnancies
Douglas Kuxhausen, DO
Tufts Medical Center

I had two cases in consecutive days of ectopic pregnancy, but each presentation was extremely different. It is important to realize that there are many ways for this problem to present itself, but the diagnosis needs to be made as quickly as possible.

The first case presented by EMS was a 30-year old female who was in severe distress and had a systolic blood pressure of 60 on arrival. The patient was pale, diaphoretic and complaining of right lower quadrant pain. She was known to be six weeks pregnant. We started two large bore IVs and began to resuscitate, so I grabbed the ultrasound machine and performed a FAST exam. The ultrasound revealed fluid in Morrison's pouch. OB was called, and the patient went to the OR very quickly. This is the classic case we all hear about with ectopic pregnancy.

The second patient presented as a walk-in also with a chief complaint of right lower quadrant pain. She was in no distress and stated that the pain was mild. She had normal vital signs and stated, "There is no chance I am pregnant." On exam she had no rebound or guarding but mild tenderness in the right lower quadrant. Labs were sent including, of course, a pregnancy test. The pregnancy test came back positive, and a formal transvaginal ultrasound was ordered. I also performed a FAST exam on this patient, and it revealed fluid in Morrison's pouch. This patient never had any changes in vitals but almost the exact same ultrasound results as the first patient. OB was called, and this patient was also taken to the OR.

I thought this was very interesting since both had fluid in Morrison's pouch, and it was a large amount of fluid. But one patient was in severe distress with terrible vital signs, and the other never had any problem with her vital signs. In my opinion, the best thing to take from these cases is to always have ectopic pregnancy in the differential, and just because the patient looks stable does not mean they do not have a ruptured ectopic.


New In Medicine: Intravenous Acetaminophen Approved
Meaghan Mercer, OMS III
Western University School of Osteopathic Medicine

The FDA approves OFIRMEV – an acetaminophen injection for the treatment and management of pain and fever. Ofirmev is indicated for the reduction of fever, to manage mild to moderate pain, or for the management of moderate to severe pain in conjunction with opioid analgesics. In a study where volunteers were induced with fever, a single dose of 1 gm IV Ofirmev demonstrated a significant reduction of fever in six hours (p<0.01).

In two clinical studies evaluating postoperative patients that underwent orthopedic procedures (hip or knee surgery) and those who underwent abdominal laparoscopic surgery where patients received Ofirmev 1 gm IV q6, there was a statistically significant reduction in pain when compared to the placebo group (p<0.01 and p<0.02). Ofirmev should only be given as a 15 minute intravenous infusion and should not exceed the maximum recommended daily dose of 4 grams. Side effects currently do not appear to be different than the oral formula, and cautions associated with acetaminophen should be considered for both modes of administration. "With the approval of Ofirmev, clinicians will now be better able to use a multi-modal approach to pain management in the hospital setting, when oral medication can't be used."

References:
1) "Cadence Pharmaceuticals Announces FDA Approval of OFIRMEVTM (acetaminophen) injection for the Management of Pain and Fever." PR Newswire [San Diego, CA] 02 Nov. 2010.

2) Waknine, Yael. "FDA Approves First Intravenous Formulation of Acetaminophen." Medscape Medical News 04 Nov. 2010.


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Critical Care Pearl: Atelectasis and Pulmonary Collapse

Stephanie Nicole Lewis, MS IV
Meharry Medical College

What is atelectasis? Atelectasis is a collapsed lobe or segment usually seen on CXR. Macroatelectasis can be seen as volume loss. Microatelectasis may present normal on CXR, but alveolar-arterial oxygen difference will be high.

Why is it important? Atelectasis reduces lung compliance and PaO2 (arterial oxygen) and increases the work of breathing. This may result in poor gas exchange, increases airway pressure, reduced VT (tidal volume), and if severe, circulatory collapse.

Causes: An entire collapsed lobe or segment is caused by bronchial obstruction (sputum retention**, foreign body blood clot, vomitus, misplaced endotracheal tube). Macroatelectasis is air space compression by heavy, edematous lung tissue, external compression (pleural effusion, hemothorax), and sputum retention. Microatelectasis results from inadequate depth of respiration, nitrogen washout by 100% oxygen with subsequent absorption of oxygen occurring at a rate greater than replenishment.

Prevention:

  • Sputum hydration: Nebulized saline/bronchodilators, heated water bath or heat-moisture exchange filter.
  • Cough: By encouraging inspiration to near-total lung capacity, then expulsion of the sputum. This technique is simple but of limited use if total lung capacity is reduced; abdominal muscles are weak, pain limits contraction, or small airways collapse on expiration. Patients can flex the abdomen on coughing by drawing the knees up to help limit pain from an upper abdominal wound.
  • Physiotherapy: Via postural drainage, percussion and vibration, hyperinflation, intermittent positive-pressure breathing, incentive spirometry or manual hyperinflation.
  • Maintenance of lung volumes: Use increased VT, CPAP, PEEP and positioning to reduce compression of lung tissue by edema.

Management: Management depends on the cause and should be corrective, while continuing measures for prevention. If there is lobar or segmental collapse with obstruction of proximal airways, bronchoscopy may be useful to allow direct suction, foreign body removal and saline instillation. Patients with a high FiO2 may deteriorate from the effects of excessive lavage or suction reducing minute ventilation.

**Excess mucous normally stimulates coughing; however, sputum retention can occur if ciliary clearance is reduced (smoking, sedatives), mucous volume is excessive (asthma, bronchiectasis, cystic fibrosis, chronic bronchitis), there is inadequate coughing (COPD, pain, neuromuscular disease) or increased mucous viscosity (hypovolemia, inadequate humidification of inspired gas).

Reference:
1. Kellum JA, Gunn SR, Singer M, Webb A. Oxford American Handbook of Critical Care. Oxford University Press (2008).


Clinical Pearl: Managing Hypoglycemia in Acute Renal Failure
Cameron McLaughlin, OMS IV
Arizona College of Osteopathic Medicine

Recently, I saw a patient in the ED who was hyperkalemic and hypoglycemic. The patient was in acute renal failure secondary to Bactrim (TMP-SMX) use for cellulitis. During the first 24 hours of her stay in the hospital, she continued to experience episodes of hypoglycemia. In cases like this, it is important to remember the underlying physiology of renal failure before automatically treating hyperkalemia with standard protocols. (Standard treatment is "C BIG KA," or calcium, bicarbonate, insulin with glucose, kayexalate and albuterol).

Why? Sure, insulin is one of the early treatments for hyperkalemia, and usually we give it with some glucose. However, it is important to remember that the kidneys are a major site of insulin clearance from the body. In acute kidney injury, the glomerular filtration rate is assumed to be less than 10 mL/min, so not only is potassium clearance reduced (leading to hyperkalemia), but the insulin clearance is greatly reduced, too. This leads to insulin retention, and, even in an obese, diabetic female, can cause severe hypoglycemia. Most protocols for hyperkalemia call for 1 amp of D50 along with the standard 10 units of insulin, but patients in severe renal failure may need significantly more glucose if they continue to retain insulin. Be aware of the physiology of hypoglycemia in renal failure, order frequent blood glucose monitoring, and give additional glucose as needed.