Modern Resident - The newsletter of AAEM/RSA
December 2014/January 2015
Volume 6: Issue 4 | Facebook  Twitter  LinkedIn

Inside This Issue

Bronchiolitis: Updated Guidelines
Ashley Grigsby, DO
Indiana University
Emergency Medicine/Pediatrics Residency

It’s that time of year again. Snow is starting to fall, holiday lights are going up and little babies are showing up wheezing in your emergency department. While babies sometimes make emergency physicians nervous, the treatment for bronchiolitis just got a little easier. The American Academy of Pediatrics recently updated their clinical practice guidelines; the last update prior to this was in 2006. These guidelines were updated to provide clinicians with the most recent evidence based management strategies.

Bronchiolitis is a viral illness caused by multiple viruses and occurs in 90% of children before the age of two. Bronchiolitis is a clinical diagnosis and as such, it does not require any testing to confirm diagnosis. Illness usually starts with rhinitis and cough, but can progress to respiratory distress.1 Exam frequently reveals tachypnea, mild retractions and expiratory wheezing.2 Patients with more severe disease can have grunting, nasal flaring or severe retractions.1 Assessment of these patients should include evaluation of hydration status, respiratory status, history of apnea, behavior changes and history of cyanosis.2

The new bronchiolitis management guidelines apply to patients aged one month through 23 months. They do not apply to immunocompromised patients, those with neonatal lung disease, cystic fibrosis, neuromuscular disease or congenital heart disease. Based on the new guidelines, clinicians should diagnose bronchiolitis based on history and physical examination, and assess risk factors for severe disease. These include less than 12 weeks of age, history of prematurity, comorbid conditions and immunodeficiency. If the diagnosis is made on a clinical basis, radiographic studies and laboratory studies should not be obtained.1

The new guidelines state that clinicians should not administer albuterol to infants with bronchiolitis nor should they administer nebulized epinephrine. Nebulized hypertonic saline can be administered in an inpatient setting, but should not be used in the emergency department. The use of systemic corticosteroids is also not recommended for clinical bronchiolitis.

In general, antibiotics should not be given to these infants, unless there is a strong suspicion of concomitant bacterial infection, which is rare. The risk of bacteremia or meningitis in febrile children with bronchiolitis is less than one percent.1

Supplemental oxygen is indicated if SpO2 is persistently below 90%. If SpO2 remains above 90%, and the child is able to feed, supplemental oxygen is not necessary.1 Nasal suctioning can provide temporary relief for these patients and allow them to feed properly. When making the decision to send these children home, teaching parents to perform saline nasal suctioning can be beneficial.3

Disposition decisions should take into account the child’s age, parent’s ability to care for the child, fluid status, ability to feed and respiratory status.3 If the child is able to go home, care return precautions and anticipatory guidance should be given. They should also be counseled on tobacco smoke exposure, which can increase the risk of severe disease.1


  1. Ralston SL, et al. “Clinical Practice Guideline: The diagnosis, management, and prevention of bronchiolitis.” Pediatrics. 2014;134:e1474-e1502.
  2. Piedra PA, Stark AR. “Bronchiolitis in infants and children: Clinical features and diagnosis.” Up to date. 2014. Accessed on 13 November 2014. Available from:
  3. Piedra PA, Stark AR. “Bronchiolitis in infants and children: treatment, outcome, and prevention.” Up to date. 2014. Access on 14 November 2014. Available from:

Journal Club - Ultrasonography Versus Computed Tomography for Suspected Nephrolithiasis
Alexandra Murray, OMSIV
Ohio University Heritage College of Osteopathic Medicine

Patients complaining of symptoms potentially related to "kidney stones" comprise a significant portion of people presenting to the emergency department (ED).1 Currently, computed tomography (CT) is the first line imaging study for urinary stone disease; however, it is unclear as to whether the ionizing radiation from CT is harmful to patients.2 In September 2014, the New England Journal of Medicine published the article "Ultrasonography versus Computed Tomography for Suspected Nephrolithiasis" based on the research of radiologist Dr. Rebecca Smith-Bindman and colleagues at the University of California, San Francisco. This study aimed to assess the effect of diagnostic imaging techniques on the outcomes of patients with suspected nephrolithiasis by conducting a multicenter, randomized trial comparing ultrasonography with CT.2

Within the study, 2,759 patients from 15 different EDs were randomized into three different groups:

  1. Diagnostic ultrasonography performed by an emergency physician proficient in ultrasound training as recommended by the American College of Emergency Physicians (point-of-care ultrasonography)
  2. Diagnostic ultrasonography performed by a radiologist (radiology ultrasonography)
  3. Abdominal CT

Results from the study showed that there were no significant differences in high-risk diagnoses with complications, total serious adverse events, related serious adverse events, pain scores, return ED visits or hospitalizations.2 Patient outcomes and diagnostic accuracy were also similar in the two ultrasonography groups, suggesting that ultrasound-trained emergency physicians are fully capable of detecting nephrolithiasis with point-of-care ultrasound.2 Serious adverse events occurred in 12.4% of the patients assigned to point-of-care ultrasonography, 10.8% of those assigned to radiology ultrasonography and 11.2% of those assigned to CT (P=0.50).2 In addition, the initial ultrasonography was associated with lower cumulative radiation exposure than initial CT.2

These results suggest that ultrasonography should be used as the initial diagnostic imaging test for urinary stone disease, with further imaging studies performed at the discretion of the physician on the basis of clinical judgment.2 Using ultrasound as a first-line diagnostic tool can ultimately reduce patient exposure to ionizing radiation without sacrificing the sensitivity of a CT.


  1. Pearle MS, et al. Urologic diseases in America project: Urolithiasis. J Urol. 2005 Mar;173(3):848-57.
  2. Smith-Bindman R, et al. Ultrasonography versus computed tomography for suspected nephrolithiasis. N Engl J Med. 2014 Sep 18;371(12):1100-10.

Pediatric Emergencies Part 2: Abdominal Pain
Jenna Erickson, MSIV
Chicago Medical School

Abdominal pain in children is a difficult subject to tease apart as children often experience symptoms that they are unable to effectively communicate. The most common diagnoses of acute abdominal pain in pediatric patients are gastroenteritis, constipation, systemic viral illnesses, infections of non-gastrointestinal organs such as lower lobe pneumonia and mesenteric lymphadenitis. In the infant population, infantile colic is a common finding. The surgical diagnoses include acute appendicitis, intestinal obstruction (including volvulus and intussusception), bowel perforation and abdominal trauma. Although the surgical diagnoses are less common, it is essential to rule them out in an emergency setting utilizing history, physical exam, laboratory studies and if necessary, imaging.

The approach to differentiating causes of abdominal pain must begin with the consideration of age. Among the emergent conditions, neonates and infants are at the highest risk for incarcerated hernias, intussusception and volvulus. The school-age population is more likely to require emergent attention for appendicitis, and adolescent females become additionally at risk of gynecological emergencies such as ectopic pregnancy.

Other important components of the history can help localize the source of abdominal pain. Relief after bowel movement suggests a colonic source, whereas relief after vomiting is more indicative of small bowel disease. If vomiting precedes pain the source is likely medical; vomiting as a later symptom suggests a surgical abdomen. The emesis itself can help narrow the differential, as bilious emesis in infants and children is highly suspicious of bowel obstruction.

The physical exam must include heart, lungs and abdomen, as well as rectal and pelvic exams when indicated. One of the most important components of the exam is to observe whether the child is restless or still, which can indicate which nerve fibers are transmitting the pain. Visceral pain due to mechanical and chemical stimuli causes children to writhe in pain, constantly shifting positions to find relief. Activation of parietal receptors, however, produces a distinctly localized, intense, sharp sensation. These patients will resist movement, finding relief by lying still in a position that alleviates pressure on the affected area. The classic example contrasting visceral and parietal pain is the progression of appendicitis, which begins as poorly localized visceral pain and progresses to right-lower-quadrant (RLQ) parietal pain as the peritoneum becomes inflamed.

Unfortunately, pediatric patients do not always follow the typical picture of abdominal pain and can be difficult to diagnose without laboratory testing and imaging. Children presenting with abdominal pain and vomiting, with or without fever, must be considered for appendicitis. Initial laboratory evaluations include CBC, electrolytes, urinalysis and pregnancy testing in the adolescent female. These initial values help determine the necessity of imaging. In one retrospective study, a preoperative finding of leukocytosis correlated with a 92.5% positive predictive value of acute appendicitis in patients with RLQ pain. If imaging is necessary, plain radiographs are best when intestinal obstruction or perforation is suspected. When appendicitis is suspected the preferred imaging modality in pediatric patients is ultrasound. Although computed tomography is more accurate, it is typically a last resort for children due to high radiation exposure and cost.

Between the history, physical exam, laboratory testing and imaging, a diagnosis of pediatric acute abdominal pain can typically be reached in the emergency setting. The most important consideration of the emergency physician is to keep surgical causes high on the list of differential diagnoses, despite the potentially atypical presentations. Gathering all evidence and practicing caution will provide the best care in the ED setting for children who present with abdominal pain, especially those who present atypically.


  1. Kim JS, Acute Abdominal Pain in Children. Pediatr Gastroenterol Hepatol Nutr 2013; 16(4):219-224.
  2. Kamram H, Naveed D, Hameed M, Ahmed M, Khan U. Role of total leukocyte count in diagnosis of acute appendicitis. J Ayub Med Coll 2008; 20(3) 70-71.

Board Review: Bullous Myringitis
Kaitlin Fries, OMSIV
Ohio University Heritage College of Osteopathic Medicine

A 36-year-old male with a history of diabetes and hypertension presents to the ED complaining of one day of severe right ear pain. The patient states he recently had flu-like symptoms that improved with OTC medications. The ear pain is described as an “excruciating, throbbing” pain that keeps the patient awake at night. Associated symptoms include fullness and muffled hearing on the right side. The patient has no history of similar symptoms and denies fever, chills, ear drainage or tinnitus. The patient is afebrile on presentation and all other vitals are stable. On physical exam, the right ear canal has moderate erythema and the right TM has bullae throughout. There is also a white purulence covering one-third of the TM. There is no pain with tragus movement or tenderness to the mastoid noted. The patient is subsequently diagnosed with bullous myringitis.

Question: What is bullous myringitis?
Bullous myringitis is a sudden onset of severe pain caused by bullae formation due to direct inflammation and infection of the tympanic membrane. Infection can be due to bacterial or viral causes. According to Tintinalli, “The blisters are believed to be between the highly innervated outer epithelium and inner fibrous layers of the tympanic membrane, thus explaining the severe otalgia.”5 These blisters may be filled with blood, serious or serosanguineous fluid.5 The onset is generally preceded by a URI. Commonly, an associated otitis media with effusion is also present with the bullae.3,5

Question: Which bacteria are most commonly responsible for this condition?
The most common bacteria are those seen in otitis media (Streptococcus pneumonia, beta-hemolytic Streptococcus, and Haemophilus influenza).3 It was previously believed that there was a strong connection between bullous myringitis and Mycoplasma pneumoniae.4,5 However, recent literature has disproved this theory.

Question: What is the recommended treatment for this patient?
Most episodes of bullous myringitis resolve spontaneously. However, pain control and symptomatic relief with warm compresses and oral decongestants is favored.3 Oral antibiotics will be needed if a concomitant otitis media is present.5 Otic antibiotic drops can help prevent super-infection if the bullae rupture. Be sure to instruct the patient that they may see purulent drainage or bleeding from the ear canal if this occurs.3 If sensorineural hearing loss is present, it is important to arrange ENT follow up for audiometry evaluation.2

Question: Should steroids be given to patients with associated sensorineural hearing loss?
In 2011, the British ENT Journal published a study that looked at adding steroids to the treatment plan for those individuals that experienced hearing loss while suffering from bullous myringitis. The study design administered antibiotics to the first group while the second received antibiotics plus corticosteroids. The results showed no significant difference in the number of patients whose hearing returned nor the rate of hearing recovery.1

Clinical Pearl: Herpes zoster oticus is a more serious condition that can present very similarly to bullous myringitis. Herpes zoster can lead to cranial neuropathy and requires antiviral treatment.3 The key distinguishing characteristic is that bullous myringitis is limited to only TM involvement.5


  1. Ciorba A, Bovo R. Are systemic oral steroids effective for sensorineural hearing loss in bullous myringitis?. B-ENT. 2011; 7(2):111-4.
  2. Drendel M, Yakirevitch A, Hearing loss in bullous myringitis. AN Larynx. 2012 Feb; 39(1):28-30.
  3. Knoop K, Ear, nose, and throat conditions. Atlas of Emergency Medicine. Ch. 5. 2009 August.
  4. Limb C, Lawerence L. Acute otitis media in adults. UpToDate.
  5. Tintinalli J. Common disorders of the external, middle, and inner ear. Tintinalli’s Emergency Medicine Manual. Ch. 237.

Antibiotics in Cardiac Arrest
Nathan Haas, MD
University of Michigan

Out of hospital cardiac arrest (OHCA) is a relatively common occurrence, and accounts for a large number of emergency department (ED) presentations nationwide. The initial presentation and management is often anxiety-provoking, exhilarating, procedure-ridden and (occasionally) satisfying when return of spontaneous circulation is achieved. However, what emergency physicians often fail to consider while focusing on regaining pulses is the precipitating cause of the arrest.

It is well known that early antibiotics improve mortality in sepsis.1 Sepsis often leads to significant morbidity and mortality via vastly differing presentations, including cardiac arrest. Thus, it has been speculated that early antibiotics in cardiac arrest may improve outcomes by the transitive property.

One recent study aimed to establish the prevalence of bacteremia in OHCA patients, prospectively studying 173 patients.2 Of OHCA patients undergoing Advanced Cardiac Life Support (ACLS) in the ED, 38% were found to be bacteremic even after excluding likely contaminates. Bacteremic patients had a significantly higher mortality in the ED (75% vs. 60%) than did the non-bacteremic patients; 28-day mortality was similar between the two groups.

The clinical significance of this bacteremia remains to be seen. It is unclear whether the arrests were infection-driven, or if infection was introduced post-arrest, such as via CPR, intubation or insertion of lines. A low flow shock state, such as cardiac arrest, may also lead to ischemic bowel with subsequent migration of bowel flora into the bloodstream. Regardless of why these patients are bacteremic, do antibiotics help?

One retrospective ICU-based study from the United Kingdom suggests that early antibiotics may be of benefit for these patients.3 The authors conclude that patients receiving antibiotics within the first seven days of ICU admission following OHCA had a significantly lower hospital mortality rate than did those not receiving antibiotics (57% vs. 75%).

A direct correlation between early antibiotic administration in the ED and survival of OHCA is yet to be demonstrated. Recent literature has suggested there may be some benefit to doing so, although this has not been directly studied.


  1. Gaieski, DF, Mikkelsen ME, Band RA, et al. Impact of time to antibiotics on survival in patients with severe sepsis or septic shock in whom early goal-directed therapy was initiated in the emergency department. Critical Care Medicine 38.4 (2010):1045-053. Web.
  2. Coba V, Jaehne AK, Suarez A, et al. "The incidence and significance of bacteremia in out of hospital cardiac arrest." Resuscitation 85.2 (2014):196-202. Web.
  3. Davies K., Walters JH, Kerslake IM, et al. "Early antibiotics improve survival following out-of hospital cardiac arrest." Resuscitation 84.5 (2013):616-19. Web.

The Surgical Airway and Application in the ED
Nicholas Pettit, PhD OMSIII
Ohio University Heritage College of Osteopathic Medicine

Scenario: It is about 3am and you are on your first shift in the ED as an intern. A patient rolls into your ED with a gunshot wound to the face. At the same time, your attending is busy running a code, and thus you and your handy-dandy medical student are responsible for the airway of this trauma patient. After four unsuccessful attempts at securing the airway with an endotracheal tube, the patient crashes and eventually dies due to hypoxia and arrest. While this situation is completely hypothetical, a lesson to be learned is that we should always be prepared to obtain a secure airway via a surgical airway in the ED.

To quote the very talented Dr. Scott Weingart (the author and creator of the EMCrit blog and podcasts), during a talk from SMACC Gold regarding the surgical airway, “If you do it now the patient will never critically desaturate, and they will never have a cardiac arrest. If you wait until you are forced, it’s too late.”1 Emergency physicians are responsible for some of the most difficult airways, some of which cannot be accomplished without a surgical intervention via a cricothyroidotomy.2 There have been instances where poor outcomes have occurred due to inappropriately delaying or attempting to avoid a surgical airway. To share another relevant quote from the EMCrit blog, “In appropriate circumstances, prophylactic cricothyrotomy has numerous advantages, not least the potential to secure and check the ‘rescue airway’ in a calm, unhurried manner, without hypoxia, before an emergency arises – NAP4 Study.”1

Many practitioners may not feel fully comfortable with the surgical airway techniques (especially on live patients), as demonstrated by a recent survey which showed that only 22% of surveyed residents performed a cricothyrotomy on a patient.3 While a larger proportion of respondents, 68.1% of residents, practiced on recently deceased patients, there is still varying levels of confidence among residents about their ability to perform this procedure. There are a few basic tidbits that can help the next time (or for the first time) you need to perform a cricothyrotomy. If you need help or information regarding the technique, I highly encourage checking out the EMCrit blog/podcast, or, a site designed by airway guru Dr. Rich Levitan.


  • Have the kit visible at all times
  • In “high risk” patients, have the kit open and neck prepared
  • Don’t worry about blood, the patient won’t exsanguinate
  • Protect yourself and your team
  • Keep in mind that the patient needs air, and prolonging hypoxia with multiple failed intubation attempts leads to an increased risk of arrest.


  1. Weingart S. EMCrit Podcast 131 – Cut to Air: Surgical Airway from SMACC Gold. Audio blog post. EM CRIT. N.p., n.d. Web. <>.
  2. Wong E, Ng YY. The difficult airway in the emergency department. J Emerg Med. 2008; 1(2); 107-111 doi: 10.1007/s12245-008-0030-6.
  3. Makowski, AL. A survey of graduating emergency medicine residents’ experience with cricothyrotomy. West J Emerg Med. 2013: 14(6): 654-661. Doi: 10.5811/westjem.2013.7.18183.

The Other ACS: Abdominal Compartment Syndrome
Randy Kring, MSIV
Tufts University School of Medicine

In the emergency department (ED), Acute Coronary Syndrome (ACS) is always a topic on our minds. But there’s another ACS out there that is important to be aware of as well: Abdominal Compartment Syndrome.

Consider this patient presentation: Mr. M is a 47-year-old man with a history of alcohol abuse who presents to the ED with sudden onset abdominal pain. Workup reveals a white blood cell count of 20,200, Lipase of 1,283 and CT of the abdomen/pelvis consistent with acute pancreatitis. He is admitted for supportive care and pain control, and on hospital day #2 his abdomen is noted to become increasingly tense. Someone mentions the possibility of Abdominal Compartment Syndrome (ACS). What is this “other” ACS, and what should you do about it?

In ACS, acutely elevated intra-abdominal pressure (IAP) reduces blood flow to the abdominal viscera. Elevated IAP can be caused by conditions such as pancreatitis, intra-abdominal hemorrhage, massive ascites, or large volume resuscitation in trauma patients. When IAP exceeds around 20mmHg, patients begin to experience organ dysfunction which is diagnostic of Abdominal Compartment Syndrome.1 Patients can present with abdominal pain and distension, hypotension and tachycardia, tachypnea, oligura, and lactic acidosis. However, studies have shown that abdominal exam is only about 50% sensitive for recognizing ACS, so a high index of suspicion is necessary.2 Diagnosis is typically made by measuring bladder pressure, which closely approximates IAP.3 Bladder pressures greater than 20mmHg are concerning for ACS in the appropriate clinical context. Once ACS is diagnosed, intra-abdominal pressure can be decreased by placing an NG tube to suction, starting a bowel regimen, decreasing the tidal volume in ventilated patients, and increasing abdominal wall compliance through sedation and/or pharmacological paralysis. Definitive treatment often involves percutaneous drainage of ascites or hematoma if present, or surgical decompression.4 Untreated ACS can ultimately result in ischemia of multiple intra-abdominal organs, cardiopulmonary collapse and death.

In sum, ACS is an organ dysfunction caused by intra-abdominal hypertension, most commonly in the setting of trauma, pancreatitis, or massive ascites. Measuring bladder pressure aids in the diagnosis of ACS. Bladder pressure greater than 20mmHg suggests ACS, and should prompt a surgery consult for possible surgical decompression.


  1. Malbrain MLNG, Cheatham ML, Kirkpatrick A, et al. Results from the international conference of experts on intra-abdominal hypertension and abdominal compartment syndrome. Part I: definitions. Intensive Care Med. 2006;3211:1722-1732.
  2. Kirkpatrick AW, Brenneman FD, McLean RF, et al. Is clinical examination an accurate indicator of raised intra-abdominal pressure in critically injured patients? Can J Surg 2000; 43:207.
  3. Fusco MA, Martin RS, Chang MC. Estimation of intra-abdominal pressure by bladder pressure measurement: validity and methodology. J Trauma 2001; 50:297.
  4. Cheatham ML, Malbrain MLNG, Kirkpatrick A, et al. Results from the international conference of experts on intra-abdominal hypertension and abdominal compartment syndrome. Part II: recommendations. Intensive Care Med. 2007; 336:951-962.

Psychiatric Patients Parked in California EDs
Tatiana Ramage, MSIII
UC Irvine School of Medicine

A lack of psychiatric hospital beds and limited alternatives has turned the ED into virtual “holding pens” for psychiatric patients.

Psychiatric boarding is the process by which psychiatric patients are admitted but remain in the ED for prolonged time (hours to days) until psychiatric beds become available. The rising prevalence of this practice has emerged as a growing problem in overstretched emergency departments. In California, there has been a devastating drop of psychiatric beds over the past 15 years. As of 2011 data, California lost close to 32% of the beds present in 1995, a drop of nearly 3,000 beds.1

The reduction of psychiatric beds is having a significant impact on emergency medicine. One hundred twenty-three ED directors from 42 of California’s 58 counties recently reported that average wait times for adult patients with a primary psychiatric diagnosis in the ED was 10.05 hours once the decision to admit was made until placement. The most common reason reported for extended ED stays for this population was lack of inpatient psychiatry beds.2

Prolonged boarding in the ED for psychiatric patients results in lower quality care. The loud and often chaotic environment in EDs is toxic for patients who are struggling with suicidal ideation, paranoia or drug withdrawal. Violent behavior by patients has always been a challenge for EDs, and the frustration of long wait times exacerbates this problem. In addition, long wait times consume ED resources, leaving EDs with less capacity to see and treat new patients. Most importantly, those individuals suffering from acute mental distress are failing to receive the treatment they need. Being “parked” in the ED is far short of being examined by psychiatrists in a specialized setting.

Solutions to the problem
Hospitals are devising innovative solutions to manage mental health patients who come to the ED rather than “boarding” them. A number of possible solutions have been proposed, including increasing hospital inpatient staffing and capacity, the use of telemedicine or telepsychiatry to enable psychiatrists to perform evaluations and screenings from a remote location, and even the elimination of in-network insurance requirements to reduce the challenge of finding an appropriate bed. One solution already proven effective is called the Alameda Model.

The Alameda Model is an alternative emergency care design where patients are transferred from general hospital EDs to a “regional dedicated emergency psychiatric facility” that serves to evaluate and treat all mental health patients for a given area. A recent study evaluated the Alameda Model on boarding times and hospitalization rates for psychiatric patients in area EDs. The results demonstrated the average boarding time was approximately 1 hour and 48 minutes. This translates to a greater than 80 percent reduction in boarding times for patients awaiting psychiatric care versus comparable state ED averages.3 Whether other counties will adopt this model remains to be seen. What is evident is that a solution to improve timely access to care that addresses the safety and well-being of our psychiatric patients is imperative.


  1. California’s acute psychiatric bed loss. California Hospital Association; Sep, 2013. Available at:
  2. Stone A, Rogers D, Kruckenberg S, et al. Impact of the mental health care delivery system on California emergency departments. West J Emerg Med. 2012;13(1):51–56.
  3. Zeller SL, Calma NM, Stone A. Effect of a regional dedicated psychiatric emergency service on boarding and hospitalization of psychiatric patients in area emergency departments. West J Emerg Med. 2013.

Compartment Syndrome
Terren R Trott, MD
University of Kentucky

Compartment syndrome is notorious for being insidious in onset and obscure in prevalence. It is frequently considered as part of a differential, yet rarely diagnosed. At is imperative to have a high index of suspicion in appropriate cases given that missing this diagnosis is fraught with catastrophic consequences, including permanent disability and possibly litigation.

Compartment syndrome is the result of a confined swelling within a sealed space. Edema may result from a crush injury, fracture, hematoma or even third spacing. One of the most common sites, the anterior compartment of the lower leg, is bound by minimally elastic fascial planes thus preventing any expansion to accommodate the excess volume. As swelling increases, venous and lymphatic return decrease, which leads to a further increase in interstitial pressures. Ischemia ultimately occurs when compartment pressure surpasses the arterial pressure. At this point, irreversible nerve and muscle damage are inevitable without relief of the compartmental pressures. Normal capillary hydrostatic pressure is usually well below 10mmHg with upper limits being near 30mmHg.

Up to 69% percent of recorded compartment syndrome presentations occur secondary to a fracture and 40% of those fractures occur in the tibia. Tibial fractures have such a high incidence of associated compartment syndrome (PPV of 1-11%), that it should always be considered with these types of fractures. The lower extremity is by no means the sole location for a potential compartment syndrome; forearm fractures comprise approximately 18% of the population who ultimately receive a diagnosis of compartment syndrome. Other less common sites for elevated compartment pressures after fracture are the thigh, foot, buttock and even hand. Do not limit your suspicions for compartment syndrome to those with concomitant fracture. Those patients with pain out of proportion or pain with passive range of motion and volume overload are at extreme risk to acquire this disease. Patients who have recently undergone strenuous exercise alone may present with a compartment syndrome.

Diagnosis can be very difficult because of the poor sensitivity of associated exam findings early in the course of the disease. Several studies have demonstrated the poor predictive value of the “6 P’s” (Pain, Pallor, Paresthesias, Pulselessness, Paralysis, Poikilothermia) of compartment syndrome. Pain is subjective to say the least. It may be difficult to differentiate pain caused by a fracture from the pain of increasing compartmental pressures. Pain with passive stretch (range of motion) is thought to be the most sensitive predictor of impending compartment syndrome and any pain with passive exam should be followed by an immediate surgical consult. Paresthesia carries a much lower sensitivity and positive predictive value (0.13 and 0.15 respectively) and is usually a later finding. Pallor and paresis are findings suggestive of arterial occlusion and nerve ischemia. Both of these are exceptionally late findings and often the result of delayed presentation or a delay in diagnosis. Laboratory studies are not helpful. While lactic acid, urine myoglobin and creatinine kinase may be elevated, the practitioner that waits on these studies in the face of pain with passive range of motion sentences the patient to a potential for lifelong disability.

When to intervene when the diagnosis of compartment syndrome is suspected is also a topic for debate. Direct pressures can be measured using commercially available pressure testing kits. Traditionally, compartment pressures greater than 30mmHg were thought to be consistent with compartment syndrome. In an effort to increase sensitivity and decrease morbidity, an alternative method for diagnosis has been suggested. By calculating the delta between the diastolic blood pressure and the measured compartment pressure, some patients have been spared from fasciotomy. This can be reflected in the hypotensive patient, who will have less pressure perfusing an extremity and thus will need a lower compartmental pressure to overcome blood flow.

The use of delta pressures was supported by the work of McQueen et al. In a prospective trial evaluating one hundred sixteen patients with clinical concern for compartment syndrome, a device was placed to continually monitor compartment pressures over a twenty-four hour period. In the first twelve hours of monitoring, twelve patients had absolute pressures greater than 30mmHG, thirty patients had absolute pressures greater than 40mmHg and four patients had absolute pressures greater than 50mmHg. The decision to perform fasciotomy was based soley on the delta pressures obtained.  Only one patient was taken for fasciotomy. All enrolled patients were then monitored for an additional twelve hours. They were then seen again at a six month outpatient follow up and none had associated morbidity or complications from withholding fasciotomy. By convention, 75% of the patients monitored would have required fasciotomy by absolute pressure. None of the patients who had normal deltas and abnormal absolute pressures had any associated morbidity at follow up.

As emergency medicine providers, we must have a high degree of suspicion and make an accurate diagnosis of compartment syndrome when the situation presents as the results of missed diagnosis are catastrophic. The work up involves obtaining compartment pressures and surgical consultation early for patients exhibiting pain with passive range of motion.


  1. McQueen, et al. Compartment monitoring in tibial fractures. J Bone Joint Surg. 1996;78-B:99-104.
  2. Murdoch M, Murdoch M. Compartment syndrome: A review of the literature. Clin Podiatr Med Surg. 2012. 29:301-310.
  3. Ulmer T. The clinical diagnosis of compartment syndrome of the lower leg: are clinical findings predictive of the disorder? J Ortho Surg. 2002; 16, 8:572-577.

Simulation Based Learning: The Real Deal in Emergency Medicine Training
Martha M. Masters, MD
University of Wisconsin Hospital and Clinics

Your heart is racing almost as fast as the patient’s, and your mind is running through the differential and the treatment plan. One resident is working on the airway, another obtaining a history from the distraught family member at bedside. The clock keeps ticking as labs and imaging start to return. Finally, you get the patient stabilized and you call the ICU for transfer.

There’s no training quite like a life or death situation – except your patient is neither alive nor dead. It is a high fidelity manikin, complete with reactive pupils, perioral cyanosis, coarse breath sounds and a thready pulse.

Simulation training, long part of other industries such as aviation, is also part of the core training for physicians and other health care providers. Emergency medicine is at the forefront of this style of learning, as EM providers have to be prepared to manage rare and complex cases, even without prior practical experience. Simulation labs are increasingly integrated into hospitals and academic departments, and simulation cases have become a growing part of the didactic curriculum.

At the University of Wisconsin Hospital, the Clinical Simulation Program hosts the ED faculty and residents every month, with multiple scenarios. Furthermore, the medical student EM curriculum is entirely simulation based, presenting a unique training opportunity that is highly rated by the students. The current EM Simulation fellow, Dr. Ryan Thompson, describes the importance of simulation training and its growing ubiquity, from EMS, to helicopter medicine, to disaster drills. He points out that it’s not only useful and proven as an education tool, but that it’s a great opportunity to “stress the system” in a controlled environment – identifying delays to diagnosis and treatments - thus being a useful method for quality improvement. Dr. Thompson mentions how simulation training has been utilized in light of the need for Ebola training, as well as other scenarios too intricate or cost prohibitive to otherwise recreate.

Simulation allows the learner to gain experience managing difficult situations without risk to the patient. These scenarios also provide a level of stress that doesn’t exist inside textbooks and lecture halls. From personal experience, this kind of learning reinforces lessons in an effective, lasting way. Each case comes with a ‘de-brief’ session, allowing the team to troubleshoot the process, identifying strengths and weaknesses in an effort to make future patient encounters more efficient and effective.

Furthermore, it’s an excellent arena for inter-disciplinary practice. With nurses and residents working together in the lab, closed loop communication grows routine, and an enhanced appreciation for the different positions is born of the shared experience. When multiple services, such as Trauma Surgery and Emergency Medicine, train in the lab, there is a better mutual understanding of the roles and capabilities, and far more clarity about the process of treating a flesh and blood patient.

Gradually, simulation training is leaving the lab and finding its way into the sphere of patient care. In situ learning is occurring in the trauma bays and other care areas, with teams using the existing stock of supplies to manage the simulation case.

As a field, simulation training has advanced exponentially from the CPR manikins on which learners once practiced. While it will never replace the ‘real thing,’ it will increasingly be the way that trainees and providers expand their knowledge base and refine their skills.

Delirium in the Elderly: An Emergency Department Approach
Jennifer Reink, OMSIII
Ohio University Heritage College of Osteopathic Medicine

Delirium is a concern for geriatric patients seen in the emergency department (ED). As many as 8-10% of patients age 65 and older will either present with or become delirious during their ED stay, with physicians missing nearly 75% of the diagnoses.1 Delirium is considered an acute change in cognition and attention that cannot be accounted for by preexisting dementia.2 Being aware of the risk factors, and using simple depression, dementia, and delirium screenings can assist in identifying treatable causes.3 Some of the risk factors associated with the onset of delirium include:2,4

  • Demographics (advanced age, male gender)
  • Sensory impairments (hearing or vision)
  • Poor mobility (catheters, multiple IVs, or physical impairments)
  • Medications and polypharmacy (sedative hypnotics, narcotics, benzodiazepines, anticholinergics, corticosteroids, withdrawal of alcohol or other drugs)
  • Acute neurological diseases
  • Concurrent illness (infections, anemia, dehydration, poor nutritional status, depression, fracture or trauma)
  • Metabolic derangement (electrolyte disturbances, thyroid dysfunction, hepatic or renal failure, hypoglycemia or hyperglycemia)
  • Recent surgery (hip fracture repairs and emergency operations)
  • Unfamiliar environments
  • Pain
  • Emotional distress
  • Sleep deprivation

Older adults discharged from EDs are known to be at higher risk of adverse outcomes, such as functional decline, readmission, hospitalization, death, and institutionalization.5 To aid in the prevention of these concerning issues, many hospitals now have specialized geriatric EDs or protocols tailored to the needs of patients age 65+. Even if your hospital is not equipped with its own special unit or protocol, some simple measures can be taken to improve the quality of care and outcomes for your patients:3,6

  • Use non-glare lighting or dim surrounding lights
  • Reduce noise wherever possible; designating a corner of the ED for geriatric patients may suffice
  • Provide private or semi-private rooms
  • Use extra padded beds to prevent bed sores and keep them more comfortable; this can be accomplished by adding egg crate foam to a traditional gurney
  • Have patients repeat back information to ensure understanding
  • Provide large print information pamphlets or print-outs
  • Know BEERs Criteria for Potentially Inappropriate Medication Use in Older Adults guidelines to avoid stopping or starting potentially harmful medications
  • Conduct depression, dementia, and delirium screens
  • Consult family members about changes in patients mental status
  • Consult case managers and social workers

Geriatric care can be as much about the psychosocial factors as it is the physiological ones. By implementing some of these strategies, you can make sure your patients are getting the support services and care they need to stay out of the hospital.


  1. Han JH, Shintani AE, Eden S, et al. Delirium in the emergency department: an independent predictor of death within six months. Ann of Emerg Med. 2010; 56(3): 244-252.
  2. Fong TG, Tulebaev SR, Inouye SK. Delirium in elderly adults: diagnosis, prevention, and treatment. Nat Rev Neuro. 2009 (4); 5: 210-220.
  3. Geriatric Emergency Department Guidelines. Society for Academic Emergency Medicine. Accessed October 28, 2014.
  4. Han JH, Wilson A, Ely EW. Delirium in the older emergency department patient – a quiet epidemic. Emerg Med Clin North Am. 2010; 28(3): 611-631.
  5. Martin-Khan M, Burkett E, Gray LC, et al. Methodology for developing quality indicators for the care of older people in the emergency department. BMC Emerg Med. 2013; 13: 23.
  6. Welch, Shari. The geriatric emergency department. American College of Emergency Physicians. October 28, 2014.

Expanding the Differential: What Else Can an Elevated Troponin Signify?
Shyam Sivasankar, MD
Stanford-Kaiser Emergency Medicine

We often underestimate the utility of modern laboratory technology—we become shortsighted and we forget that a lab value can tell us more than what we are naturally used to it representing. One such lab value is cardiac troponin.

Instinctively, we assume that an elevated troponin is a sign of a myocardial infarction (MI), but that is not always the case. Troponin is released by cardiac muscle fibers in the setting of irreversible cell injury.

Occasionally, we can be fooled into thinking that all chest pain with an elevated troponin is a definitive diagnosis of MI, but other life-threatening causes of chest pain such as pulmonary embolism (PE) or aortic dissection can also present with an elevated troponin. The ‘troponin leak’ from PE results from right-sided heart strain and from direct myocardial injury in dissection. Elevated troponin can also be seen in pericarditis (which can also present with ST segment changes), myocarditis, blunt chest trauma and arrhythmias. Patients who have suffered from cardiac arrest and undergone CPR can also have elevated troponin levels.

Besides diseases that primarily involve the heart, sepsis can also present with elevated troponins. Although underlying cardiovascular disease can have an impact on the elevation of troponin, the mechanism underlying troponin elevations in sepsis is not very well understood. Chronic diseases may also present with baseline elevations in troponins, such as amyloidosis, chronic kidney disease, renal failure and congestive heart failure (CHF).
The mechanism of troponin elevation in patients with renal failure is still a widely debated topic, but the general consensus is that troponin levels increase secondary to a combination of reduced renal clearance of troponin and troponin leak secondary to uremic muscle tissue. Elevations of troponin in this group should not be ignored, as this population is a particularly high-risk group. Accordingly, these values should be compared to a patient’s baseline and most importantly, be placed into clinical context. The mechanism behind higher than normal troponin levels in CHF is thought to be due to pressure induced ischemia or inflammation. Long-standing disease such as left ventricular hypertrophy and systemic hypertension can also present a rise in troponin levels.

Common causes of elevations in troponin besides acute coronary syndromes (ACS):

  • Pericarditis
  • Pulmonary Embolism
  • Aortic Dissection
  • Heart Failure
  • Myocarditis
  • Blunt Chest Trauma
  • Sepsis/SIRS
  • Renal Failure
  • Strenuous Exercise
  • Upper GI Bleed
  • LVH
  • Systemic Hypertension
  • Medication Induced (Cardiotoxic Drugs, such as chemotherapeutic agents)

The bottom line? Not all troponin elevations are due to an MI and when chest pain is the presenting chief complaint, we must rely on the entire clinical picture in addition to an EKG, troponin, and other adjunct studies to make a diagnosis and potentially, to save a life. For example, in the patient with an acute aortic dissection, a diagnosis of ACS based on chest pain with an elevated troponin can be deadly when anticoagulation is initiated. This is by no means an extensive or exhaustive list, but encompasses some of the major alternative diagnosis to consider.


  1. Januzzi JL. Cardiac biomarkers. Cardiac Biomarkers. CardioSource, 08 Sept. 2010. Web. 16 Oct. 2014.
  2. Korff S. Differential diagnosis of elevated troponins. Heart 92.7 (2006): 987-93. Web.
  3. Roongsritong C. Common causes of troponin elevations in the absence of acute myocardial infarction: incidence and clinical significance." Chest 125.5 (2004): 1877-884. Web.

Your 2014-2015 Leaders:

Meaghan Mercer, DO

Vice President
Victoria Weston, MD

Edward Siegel, MD

Past President
Teresa Ross, MD FAAEM

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

Medical Student Council President
Michael Wilk

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

Copy Editor: Mary Calderone, MD

Managing Editor:
Madeleine Montony, MSM

Modern Resident Contributors

Special thanks to this issue's contributors:

Jenna Erickson, MSIV; Kaitlin Fries, OMSIV; Ashley Grigsby, DO; Nathan Haas, MD; Randy Kring, MSIV; Martha M. Masters, MD; Alexandra Murray, OMSIV; Nicholas Pettit, Phd OMSIII; Tatiana Ramage, MSIII; Jennifer Reink, OMSIII; Syam Sivasankar, MD; Terren R. Trott, MD

Interested in writing?

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Please submit articles by Jan 15th for the February/March 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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