AAEM/RSA is proud to announce the 2011-2012 AAEM/RSA board of directors.
Click here for more information.
Teresa Ross, MD
Zachary Repanshek, MD
Leana Wen, MD MSc
Immediate Past President
Ryan Shanahan, MD
At-large Board Members
Ali Farzad, MD
Stephanie Gardner, MD
Taylor McCormick, MD
Ketan Patel, MD
Sarah Terez Malka, MD
Medical Student Council President
Copy Editor: Taylor McCormick, MD
Managing Editor: Jody Bath, AAEM/RSA Staff
Special thanks to this month's contributors: Stephanie Gardner, MD; Cassandra Bradby, MD; Stephanie Nicole Lewis, MD; Sundeep R. Bhat, MD; and Steven McGuire.
Opinions expressed are those of the authors and do not necessarily represent the official views of AAEM or AAEM/RSA.
President's Note: Hailing a New Year – RSA is With You All the Way!
For most of us, January 1 marks the New Year. However, when midsummer arrives, there’s another New Year to mark: the residency year. While our patients (and we, too!) may joke that July is no time to go to a hospital, the reality is that we’re all moving one step further in our career – and RSA is here to help!
Your new AAEM/RSA board of directors met at the SAEM Annual Meeting in Boston in early June. We revised our Vision and Mission Statements. Read them! They sum up to: we want our patients to HAVE the best emergency physicians, and we want you to BE the best emergency physician you can be.
We also want you – our cherished members – to know what outstanding resources AAEM/RSA has available. From the FREE EMedHome subscription to our essential AAEM/RSA Board Review Book, from the FREE AAEM/RSA Toxicology Handbook and level-specific Rules of the Road career guides to the FREE annual AAEM Scientific Assembly…and coming soon, our new pocket-sized can’t-live-without AAEM/RSA EM Survival Guide…RSA is with you all the way.
Stephanie Gardner, MD
Welcome to Advocacy 101, a bimonthly update on all things advocacy in emergency medicine. Advocacy is a hot topic right now in our specialty and the entire medical community. Some go so far as to call advocacy a core competency of medical training and push for its inclusion in formal student and resident education. But what exactly is advocacy? Is it a niche in which some physicians choose to specialize, like ultrasound and EMS, or an obligation for all physicians?
Advocacy is simply the act of supporting a cause, any cause, and like emergency medicine itself, the scope is broad. We advocate for our patients regarding issues surrounding their safety, access to care and health education. We advocate politically for our specialty in D.C. regarding health care reform, Medicare and the Sustainable Growth Rate and EMTALA related liability. We advocate for ourselves concerning loan forbearance through residency training, the integrity of board certification and equitable practice environments for all EM physicians. This is only the tip of the proverbial iceberg. With so many crucial issues to fight for, advocacy requires that we educate ourselves, speak up, get involved and take action.
This column will continue on a bimonthly basis to educate us to become more effective advocates. If you have any questions, concerns or a topic you would like to see addressed, email Stephanie Gardner, MD.
Clinical Pearl: Tube's in! High 5! Don't forget post-intubation sedation & analgesia!
Cassandra Bradby, MD
SUNY – HSC at Brooklyn, Downstate Medical Center
We obsess over pre-oxygentation, paralytic and induction agents, laryngoscope type and size, patient positioning, ET tube curvature and failed airway algorithms; but all too often we leave our intubated, paralyzed patients with insufficient sedation and analgesia. A staggering study from the University of Cincinnati showed 87 of 117 patients undergoing RSI in the ED received no or inadequate anxiolysis (74%, CI 65%-82%), and 88 of 117 received no or inadequate analgesia (75%, CI 66-83%). Take a brief moment to stick your finger down your throat – consider how uncomfortable that is. Now, imagine being intubated, paralyzed and unable to gag, yell or punch the doctor that did this to you.
Common medications used to maintain appropriate sedation and analgesia:
Sedation (*no analgesia)
Sedation (*no analgesia)
Sedation and Analgesia
Take Home Points
- Paralysis without sedation and analgesia is unacceptable.
- Post-intubation drugs should be ordered with RSI drugs.
- If there is a delay hanging drip, use IV pushes.
- Bonomo JB, Butler AS, Lindsell CJ, Venkat A. Inadequate provision of postintubation anxiolysis and analgesia in the ED. Am J Emerg Med. 2008 May;26(4):469-72. PubMed PMID: 18410818.
- EMCrit Podcast 21 – A Bad Sedation Package Leaves your Patient Trapped in a Nightmare - Feb 21, 2010. <http://emcrit.org/podcasts/post-intubation-sedation/>.
Critical Care Pearl: "Near Drowning"
Stephanie Nicole Lewis, MD
UMKC - Truman Medical Center
Traditionally, near drowning is referred to as survival >24 hours after a submersion event. In 2005, the World Health Organization (WHO) redefined drowning as “the process of experiencing respiratory impairment from submersion/immersion in liquid,” doing away with the term near-drowning and abandoning the association between drowning and fatality.
Unfavorable prognostic factors include prolonged submersion (>5min) or time from rescue to CPR (>10min), severe acidosis, hypothermia, unreactive pupils, GCS of 3 and ongoing CPR upon arrival to the ED. However, neurologically intact survival has been reported in patients with each of these factors, including functional recovery for victims submerged for 66 minutes!
- Assess ABCs.
- IV, O2, cardiac monitoring, pulse oximetry, core temperature measurement and C-spine immobilization should be immediately established.
- Check blood sugar and consider empiric naloxone administration.
- For the hypothermic patient, initiate warmed IV normal saline and warming adjuncts.
- Patients unable to maintain an O2 sat >90% or PaO2 >60mmHg on high-flow oxygen require positive pressure ventilation via BiPAP/CPAP for alert and cooperative patients or endotracheal intubation for patients at risk of aspiration.
Patients who are asymptomatic on arrival who maintain normal vitals (including 02 sat) can be observed for six hours then safely discharged home.
Prophylactic antibiotics are not indicated except in the setting of grossly contaminated water. “Brain resuscitation” methods such as hypertonic saline, loop diuretics and barbiturate coma have shown no benefit.
Hypothermic victims from cold water submersion arriving in cardiac arrest should undergo prolonged and aggressive resuscitation until they are normothermic or not viable. Remember, the patient is not dead until they are warm and dead!
- Ma OJ, Cline DM. Emergency Medicine Manual, 6th edition. Copyright The McGraw-Hill Companies 2004.
- Kellum JA, Gunn SR, Singer M, Webb A. Oxford American Handbook of Critical Care. Oxford University Press (2008).
- Marx, J. Rosen’s Emergency Medicine, 7th Edition, (2010).
Image of the Month #1
Sundeep R. Bhat, MD
Stanford/Kaiser Emergency Medicine Residency
A 22 year-old male is brought in by ambulance after being a restrained driver in a high-speed motor vehicle accident. He is alert with GCS 15, airway is patent, but has decreased breath sounds on the left. His initial vital signs are BP 137/56, SpO2 98% on room air, but shortly after ED arrival his BP drops to 95/50, and he requires a NRB to maintain SpO2 above 92%. A chest radiograph (CXR) is obtained. What is your diagnosis?
A) Tension Hemo-Pneumothorax
B) Diaphragmatic Rupture
C) Tension Pneumoperitoneum
D) Hemorrhagic Shock
E) Traumatic Aortic Injury
Image #2 of the Month
Steven McGuire, MSIII
University of New England COM
K is an obese 31 yo female with no medical history presenting to the emergency department (ED) via EMS complaining of a week-long illness. It began as aches and pains, then nausea and vomiting, and now dry retching. She denies hematochezia, hemoptysis or abdominal pain but has had occasional diarrhea. Today she fell while returning to bed from the bathroom, and neither she nor her wheelchair-bound boyfriend were able to get her up so 911 was called. Upon arrival to the ED she was afebrile, normotensive, tachypneic, with a normal sinus rhythm. She was somnolent with an odd, slow affect but answered all questions appropriately. Her boyfriend stated that her behavior over the last few weeks had been ‘weird,’ including auditory hallucinations and episodes of internal preoccupation. She has not had similar symptoms before.
Labs showed mildly abnormal LFTs (bili 1.5, AST 21, ALT 32, AlkPhos 123, albumin 4), CBC showed Hb 16.2, WBC 12.7 (88% PMN, 3% Lymphs, 3% Monos). Chemistry was within normal limits. CSF studies show oligoclonal bands (OCB). HIV was negative.
After CT showed multiple lesions, and an MRI was ordered. A few representative slices are shown below.
These demyelinating lesions are most likely caused by:
A) Progressive Multifocal Leukoencephalopathy (PML)
B) Acute Disseminated Encephalomyelitis (ADEM)
C) Primary Progressive Multiple Sclerosis (PPMS)
D) Acute Hemorrhagic Leukoencephalopathy (AHL)
Image #1 of the Month
This image demonstrates traumatic diaphragmatic rupture with corresponding compression atelectasis of the left lung and rightward mediastinal shift. The tension physiology created by the herniation of abdominal contents into the thoracic cavity explains the patient’s hypotension and hypoxia. The patient was treated with aggressive fluid resuscitation and was transferred immediately to the operating room where he underwent reduction of the abdominal contents and primary repair of his diaphragm. A post-operative CXR is provided below.
Diaphragmatic injury can be seen in blunt and penetrating abdominal trauma but is often diagnosed late due to delayed symptoms. Estimates of incidence range from 0.6% to 1.2% of all trauma presentations.1 Among blunt abdominal trauma, left sided diaphragmatic rupture is more common due to the protective effect of the liver on the right. Presentation is described in three phases: an acute phase due to herniation causing hemodynamic compromise, respiratory distress and CXR abnormalities; a latent phase during which there may be intermittent herniation of visceral organs causing vague abdominal pain, belching and nausea; and an obstructive phase that can occur months to years later and at which point herniation with incarceration or bowel obstruction may be seen.1,2
Radiographic diagnosis is challenging; studies have shown up to 50% of initial CXRs are read as normal.1 Diagnosis can be made based on CXR findings, computed tomography, and often a rupture is found only during exploratory laparoscopy or laparotomy with direct visualization of the diaphragm. There is poor consensus on reliable CXR signs to diagnose diaphragmatic rupture, but a few pathognomonic signs have been proposed: nasogastric tube visualized curled in the thorax; bowel loops seen in the chest; a “collar” sign with a band-like compression of bowel and mesentery that have herniated into the chest; and/or hepatic displacement. Other less specific findings include irregularity of the diaphragmatic contour, lower lobe atelectasis or mediastinal shift.1
- Morgan BS, Watchyn-Jones T, Garner JP. Traumatic Diaphragmatic Injury. JR Army Med Corps 2010 September, 156(3): 139-149.
- Rosen CL, Legome EL, Wolfe RE. Adams JG et. al. Blunt Abdominal Trauma. Emergency Medicine (ed 1), 2008 Saunders-Elsevier, Inc, Philadelphia, PA. pp 827-40.
Image #2 of the Month
PPMS is the presentation of MS in 10-15% of cases. PPMS typically causes fewer CNS lesions than relapsing-remitting MS. OCBs are found in up to 90% of MS patients.
A. PML is associated with the JC virus, especially in an immunocompromised host (HIV/AIDS, post-transplant, and multiple sclerosis patients on immunosuppressants). The lesions tend to be larger, confluent, granular, whereas MS lesions are more likely to be ring enhancing and periventricular (Dawson’s Fingers).
B. ADEM lesions can be difficult to distinguish from the initial MS flare. However, ADEM typically shows no CSF OCBs and often occurs post vaccination (esp. rabies) or post infection (esp. measles).
D. AHL is thought to be a hyperacute more fulminant form of ADEM and therefore appears similar to ADEM on MRI. However, as the name suggests, you will likely find areas of hemorrhage on brain imaging.
- Bennetto L, Scolding N. Inﬂammatory/post-infectious encephalomyelitis. J Neurol Neurosurg Psychiatry (2004) 75:i22–i2.
- Boster A, et al. Progressive Multifocal Leukoencephalopathy and Relapsing-Remitting Multiple Sclerosis: A Comparative Study. Arch Neurol, May 2009; 66: 593-599.
- Kremenchutzky M, D Lee D, Rice G P A, Ebers G C. Diagnostic brain MRI findings in primary progressive multiple sclerosis. Mult Scler April 2000 6: 81-85,doi:10.1177/135245850000600205.
- Pinto P S, Taipa R, Moreira B, Correia C, Melo-Pires M. Acute hemorrhagic leukoencephalitis with severe brainstem and spinal cord involvement: MRI features with neuropathological confirmation. Journal of Magnetic Resonance Imaging (2011), 33: 957–961. doi: 10.1002/jmri.22505.