Modern Resident - The newsletter of AAEM/RSA
April/May 2016
Volume 8: Issue 4 | Facebook  Twitter  LinkedIn

Inside This Issue


SCUBA and Diving Injuries, Part 2
Daniel F. Leiva, MS OMSIV
Nova Southeastern University

Ambient pressure decreases when ascending from depth, causing gases to expand. This expansion can lead to various injuries including alternobaric vertigo, pulmonary barotrauma, aerogastralgia and arterial gas embolism. This mechanism of expansion also plays a role in these conditions due to inert gas dissolution (i.e., decompression sickness and nitrogen narcosis).1

Alternobaric vertigo is caused by air trapping within the middle ear. Trapped air expands causing the formation of a pressure differential. This induces symptoms of nausea, vomiting and vertigo. If this pressure is transmitted to the facial nerve as it travels through the middle ear and mastoid process, facial nerve palsy may occur.3 No treatment is necessary if nerve impingement has not occurred as alternobaric vertigo is typically temporary, and the gas will be absorbed by the surrounding soft tissues over time. If the nerve is affected, expert consultation should be sought.

Pulmonary barotrauma is pulmonary damage and possible rupture secondary to gas expansion within the lungs. Divers are taught to exhale during ascent in order to allow excess gas volume from gas expansion to vent from the body. Thus, this condition is more often seen in panicking divers. Holding one’s breath can lead to over-expansion lung injury including pneumomediastinum, pneumothorax and cerebral artery gas embolism. Symptoms may include chest pain, cough and hemoptysis but without neurologic findings. For minor cases supportive care is all that is required. Development of a pneumothorax typically requires drainage but does not require hyperbaric recompression unless a gas embolism has also formed, in which case the pneumothorax is drained beforehand. Neurologic symptoms should prompt evaluation for gas embolism or decompression sickness.

Arterial gas embolism in the setting of diving is most often secondary to pulmonary barotrauma, and typically occurs within two to ten minutes after surfacing.3 The most serious example is that of cerebral artery gas embolism (CAGE). Symptoms can include loss of consciousness, seizure, blindness, disorientation or hemiplegia. Signs and symptoms may seem disjointed in cases where a shower of bubbles has affected diverse areas of the brain. All cases of gas embolism require recompressive hyperbaric oxygen therapy as soon as possible. High flow supplemental oxygen should be administered in the interim (10L/min non-rebreather mask).

Decompression sickness (DCS) occurs when bodily fluids become saturated with an inert gas (i.e., nitrogen) during descent. During ascent, gas expansion causes bubble formation in bodily fluids and tissues leading to an inflammatory response with possible obstruction. Type I DCS is mild and involves the joints, extremities and skin, with the shoulders and elbows most commonly affected.3 The pain has typically been described as a dull ache but may be sharp or stabbing and exacerbated by movement. It may also radiate into the surrounding tissue. Type II DCS is more serious and can involve any combination of neurologic, cardiac, pulmonary, and vestibular dysfunction. Symptoms most often begin one to three hours after surfacing but one to two percent of people affected may have symptoms that appear 24-48 hours later. Hyperbaric recompression is essential in the treatment of DCS and, as above, high flow supplemental oxygen should also be administered. An IV infusion can be started to help flush the system of emboli obstruction.

For questions on medical care in the field, the Divers Alert Network (DAN) operates a medical emergency hotline that can be reached 24 hours a day at 919-684-9111.


  1. Tintinalli JE and Stapczynski JS. Chapter 208 Dysbarism and complications of diving. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York: McGraw-Hill, 2011. 1410-413. Print.
  2. Chandy D and Weinhouse GL. Complications of SCUBA diving. UpToDate, 10 Nov. 2014. Web. Accessed 07 Sept 2015.
  3. Auerbach PS. Chapter 27 diving medicine. Wilderness Medicine. 6th ed. Philadelphia: Mosby Elsevier, 2012. 1521-1542. Print.



Which Patients Should Have Blood Cultures Collected?
Linda Sanders, MD PGY3
Temple Unviersity Hospital

Patients with bacteremia have a mortality between 30 and 50%, thus obtaining culture data on these sick patients is critical.1 On the other hand, in the immunocompetent, non-septic patient, blood culture data rarely changes management, has a low yield, with a high rate of contamination and increases cost. False positive blood cultures increase length of stay by four to five days.2 In order to provide high quality, cost-effective care, emergency physicians need to know which patients benefit from blood cultures being collected.

Blood Cultures in Cellulitis, Pyelonephritis and Pneumonia
The yield of blood cultures in patients with cellulitis is only two percent.3,4 Meanwhile, the rates of contamination are equal to the rate of true positives and results rarely change antibiotic choice.3,4 This is true for complicated and uncomplicated cellulitis, ICU patients excluded.

In uncomplicated pyelonephritis, urine and blood cultures almost always grow out the same organisms (99.8%).5 In a study of 307 patients, none required a change in antibiotics.6 Urine cultures identify pathogens in pyelonephritis, and thus blood cultures likely provide no added value.

Multiple studies have demonstrated that blood cultures in immunocompetent patients with community-acquired pneumonia have a high false positive rate and have less than a one percent chance of affecting patient management.7,8 They are no longer recommended for admitted patients with community-acquired pneumonia according to the Centers for Medicaid and Medicare Services (CMS) and JCAHO, unless severe sepsis is present. Their low yield of 2-3% has been replicated in a pediatric population.9,10 As of the 2011 guidelines, the Infectious Disease Society of America and Pediatric Infectious Diseases Society recommend obtaining blood cultures in children with moderate to severe pneumonia.11

Risk Factors for Positive Blood Cultures
A meta-analysis by Coburn and an observational cohort study by Shapiro identified the following risk factors for true positive blood cultures: septic shock, an indwelling catheter, a fever greater than 103°F, shaking chills and suspicion for endocarditis.12,13 In a study of over 3,000 patients with about 10% positive cultures, bandemia was present in 80% of true positives and thus should be another trigger for obtaining blood cultures.14 Blood cultures should be considered in any immunocompromised patient with suspected infection.

Bottom Line
Blood cultures are costly and often result in false positive results. They do not change management in immunocompetent non-ICU patients with cellulitis, pneumonia or pyelonephritis. They should be considered for immunocompromised patients, those with septic shock, suspected endocarditis, shaking chills, high fever, bandemia or indwelling catheters.


  1. Angus DC, Linde-Zwirble WT, Lidicker J, et al. Epidemiology of severe sepsis in the United States: Analysis of incidence, outcome, and associated costs of care. Crit Care Med 2001;29.
  2. Bates DW, Goldman L, Lee TH. Contaminant blood cultures and resource utilization. The true consequences of false-positive results. JAMA 1991;265:365–9.
  3. Mills AM, Chen EH. Are blood cultures necessary in adults with cellulitis? Ann Emerg Med. 2005 May;45(5):548-9.
  4. Paolo WF, Poreda AR, Grant W, Scordino D, Wojcik S. J Emerg Med. 2013 Aug;45(2):163-7.
  5. McMurray BR, Wrenn KD, Wright SW. Usefulness of blood cultures in pyelonephritis. Am J Emerg Med. 1997;15:137–40.
  6. Velasco M, Martinez JA, Moreno-Martinez A, Horcajada JP, Ruiz J, Barranco M, et al. Blood cultures for women with uncomplicated acute pyelonephritis: Are they necessary? Clin Infect Dis. 2003;37:1127–30.
  7. Benenson RS, Kepner AM, Pyle DN 2nd, Cavanaugh S. Selective use of blood cultures in emergency department pneumonia patients. J Emerg Med. 2007 Jul;33(1):1-8.
  8. Kennedy M, Bates DW, Wright SB, Ruiz R, Wolfe RE, Shapiro NI. Do emergency department blood cultures change practice in patients with pneumonia? Ann Emerg Med. 2005 Nov;46(5):393-400.
  9. Heine D, Cochran C, Moore M, Titus MO, Andrews AL. The prevalence of bacteremia in pediatric patients with community-acquired pneumonia: guidelines to reduce the frequency of obtaining blood cultures. Hosp Pediatr.2013 Apr; 3(2): 92-6.
  10. Shah SS, Dugan MH, Bell LM, Grundmeier RW, Florin TA, Hines EM, Metlay JP. Blood Cultures in the Emergency Department Evaluation of Childhood pneumonia. Pediatr Infect Dis J. 2011; 30(6):475-479.
  11. Williams DJ. Do all children hospitalized with community-acquired pneumonia require blood cultures? Hosp Pediatr. 2013 Apr;3(2):177-9.
  12. Coburn B, Morris AM, Tomlinson G, Detsky AS. Does this adult patient with suspected bacteremia require blood cultures? JAMA. 2012 Aug 1;308(5):502-11.
  13. Shapiro NI, Wolfe RE, Wright SB, Moore R, Bates DW. Who needs a blood culture? A prospectively derived and validated prediction rule. J Emerg Med. 2008 Oct;35(3):255-64.
  14. Siegel TA, Cocchi MN, Salciccioli J, Shapiro NI, Howell M, Tang A, Domnino MW. Inadequacy of temperature and white blood cell count in predicting bacteremia in patients with suspected infection. J Emerg Med. 2012 Mar;42(3):254-9.


Pediatric Toxicology: Rodenticides
Kaitlin Fries, DO PGY1
Doctors Hospital

A two-year-old female is brought to the emergency department by her parents after an accidental ingestion of rat poison. The parents report that the exterminator came the day before and removed all of the rodent traps from the home. This morning they let the child play in the family room unattended. They state they found the child holding a rodent trap with blue powder on her hands and surrounding her mouth. The parents washed the powder off the child’s hands and face prior to arrival. They state the child has been acting appropriately and playful since the event. They deny any active bleeding. You perform a thorough physical exam without any additional findings. After calling the poison center what is your final disposition for this child?

A. Admit for observation for 12-24 hours
B. Obtain a PT/INR to determine disposition
C. Discharge home with follow up without any further workup
D. Obtain a PT/INR then discharge home with follow up

Answer: C

Household rodenticide ingestions are most commonly accidental ingestions in children less than six years old. The bright colored bait and accessible location at ground level throughout the house can lure in the curious child. However, since the majority of ingestions occur in young children, the size of the ingested material tends to be minimal (typically less than one trap).6 This is much smaller than the estimated 30g of 0.005% rodenticide that would be required for coagulation to be prolonged.4

The majority of household rodenticides are made up of long-acting anticoagulants such as bromadiaolone, difenacoum, flocoumafen, 4-hydroxycoumarins brodifacoum, chlorophacinone and diphacinone.6 These drugs inhibit vitamin K and thus block the synthesis of clotting factors II, VII, IX and X.6 Large ingestions could cause bleeding such as epistaxis, gingival bleeding, hematomas, hematuria, menorrhagia or GI bleeds.6 Since the majority of the products on the market are made of long-acting anticoagulants, clinical signs of bleeding would not be present after the initial ingestion.

The American Association of Poison Control Centers studied these long-acting anticoagulant ingestions over a twelve year period (1993-2004), and out of 191,036 reported cases, 89% were unintentional and involved children less than six years of age.5 None of the children in this age group died from their ingestion.5 Ingels et al. performed a prospective poison center study involving the same age group and found that those children who ingested less than one box were rarely symptomatic.1 Two other similar studies supported that children exposed to rodenticides in the home developed few symptoms without any significant long-term effects when followed for a four year period.2,3 Thus, data supports that children less than six years old who ingest a small amount of rodenticide without any symptoms do not require any further testing or INR measurement.6 If there is concern for a large exposure, INR should be measured at presentation and again at 36-48 hours.6 If the INR is less than four and there is no active bleeding, no further action is required.6 In the few cases where the INR is greater than or equal to four, phytomenadione is indicated.6 If the INR is greater than four and active bleeding is present, then prothrombin complex concentrate, recombinant activated factor VII or fresh frozen plasma and phytomenadione should be administered.6 Any patient who receives anticoagulation reversal should have a repeat INR drawn in two weeks.


  1. Ingels M, Lai C, Tai W, et al. A prospective study of acute, unintentional, pediatric superwarfarin ingestions managed without decontamination. Ann Emerg Med. 2002; 40:73-8.
  2. Mullins ME, Brands CL, Daya MR. Unintentional pediatric superwarfarin exposures: do we really need a prothrombin time? Pediatrics. 2000; 105: 402-4.
  3. Parsons BJ, Day LM, Ozanne-Smith J, et al. Rodenticide poisoning among children. Aust N Z J Public Health. 1996; 20: 488-92.
  4. Smolinske SC, Scherger DL, Kearns PS, et al. Superwarfarin poisoning in children: a prospective study. Pediatrics. 1989; 84: 490-4.
  5. Watson WA, Litovitz TL, Rodgers GC, et al. 2004 Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. M J Emerg Med. 2005; 23: 586-666.
  6. Watt BE, Proudfoot AT, Bradberry SM, Vale JA. Anticoagulation Rodenticides. Toxicology Review. 2005; 24(4), 259-69.

Board Review: Pheochromocytomas
Danielle Goodrich, MD PGY3
Stanford/Kaiser Emergency Medicine Residency

Pheochromocytomas are catecholamine-secreting tumors that cause paroxysmal episodes of headache, diaphoresis and hypertension. Although it is present in less than 0.2 percent of patients with hypertension, it is an important diagnosis to consider and test for in the appropriate situation.1 Without correct management, these patients may present with malignant hypertension and subsequent complications. Occurring equally in both men and women, pheochromocytomas commonly present in the fourth to fifth decades of life. The annual incidence is approximately 0.8 per 100,000 person-years. Thirty percent of patients with pheochromocytomas have the disease as part of a familial disorder, and these tumors are more likely to be bilateral and present at a younger age. These familial disorders include Multiple Endocrine Neoplasia Type 2, von Hippel-Lindau Syndrome and Neurofibromatosis.1

The classic triad of symptoms includes episodic headache, diaphoresis, and tachycardia. Hypertension is the most common sign of a pheochromocytoma. Fifty percent of patients have primary hypertension, and 50% have paroxysmal hypertension. In addition, patients may present with elevations of blood pressure induced by foods or medications such as metoclopramide.

The diagnosis of pheochromocytoma is made by urinary and plasma fractionated metanephrine and catecholamine levels. A 24-hour urinary fractionated catecholamine and metanephrine level is the recommended first test in patients with resistant hypertension and hyperadrenegic spells.2

The preferred first-line agent for outpatient treatment is phenoxybenzamine, as it is an irreversible and nonspecific alpha-adrenergic blocking agent. It is important to avoid pure beta-blockade, as this would result in unopposed alpha activity from circulating catecholamines. An urgent referral to appropriate specialists is indicated.

Though pheochromocytomas are rare, it is an important cause of hypertension that needs to be identified and managed carefully.

Board Review
1. A 34-year-old female presents to the emergency department with headache and palpitations. She is sweating profusely and appears tremulous on exam. Vital signs are as follows: HR 120, BP 190/110, RR 18, O2 99% on room air and Temp 37°C. She has a family history of pheochromocytomas. Which of the following medical regimens is contraindicated as a first-line therapy in this patient?

A. Phenoxybenzamine
B. Hydralazine
C. Labetalol
D. Lisinopril

2. A 49-year-old-male presents to the emergency department with multiple episodes of severe headache, sudden anxiety and a "racing heart.” He was diagnosed with anxiety; however, these episodes are becoming more frequent and severe. Laboratory evaluation during such an episode reveals elevated plasma free metanephrines. Which of the following additional findings in this patient is most likely?

A. Episodic hypertension
B. Anhidrosis
C. Diarrhea
D. Hypoglycemia

1. C
2. A


  1. Young WF and Kaplan NM. Clinical presentation and diagnosis of Pheochromocytoma. In Post TW, Lacroix A, Martin A (Eds.). 2016 Uptodate.
  2. Levy PD. Hypertension. Rosen’s Emergency Medicine. 8th ed. Saunders, 2014. 1113-1123. Print.

Mid-Marathon CPR
Joel Betcher, MD and Al Majkrzak, MD
University of Michigan

I remember our conversation as we entered mile nine of the Detroit Half Marathon, a lighthearted argument over our college football cheering interests. People screamed and cheered from the sidewalks as we curved through the streets of Detroit. In the midst of this discussion, my co-chief resident and I looked over towards the edge of the race at a small gathering of people, with someone clearly in distress.

We came upon a middle-aged gentleman who was down, pale and unconscious, with no pulses to be found. We signaled for someone to call EMS and started compressions right there on the road, with runners whizzing by left and right. With some additional help, we continued to do round after round of compressions, but continually lost pulses after each check. With no medications, no supplies and nothing to monitor but a pulse and his mental status, we were a little outside of our usual comfort zone. By the fourth or fifth round of CPR, though, the patient started to awaken. “It’s either a ventricular rhythm or asystole,” noted my co-chief, given his loss of pulses after each round.

After only 10 minutes, but what felt like an eternity, EMS arrived. Sure enough, the pads strapped across his chest showed ventricular fibrillation. I’m fairly used to yelling “clear” and pressing the shock button in front of a large crowd in a resuscitation bay, but doing it on the road with a thousand onlookers is a bit of a surreal experience.

After the shock was delivered, we saw a resulting sinus rhythm on the monitor, with the large ST elevations that were to blame for the patient’s situation. Lights and sirens blaring, EMS promptly took him to the local emergency department. We looked around at each other after the dust had settled. There was no note to sign, no attending to discuss the case with, no ICU to call for admission. It all felt very familiar, yet very foreign at the same time.

I think I learned two things from this experience. The first should almost go without saying, but CPR really works. Although seemingly obvious, experiencing the success of CPR firsthand in someone who has recently collapsed is something to behold. We watched as the patient’s perfusion improved after each round of CPR. By the end, he was stating between each compression “You’re…hurting…me…ouch…my…chest…that…hurts,” but would continue to go unresponsive with each pulse check. He would follow simple commands to squeeze our fingers with compressions even while in ventricular fibrillation. If dozens of rounds of what feels like futile CPR in the resuscitation bay have jaded me, then this experience certainly re-demonstrated the importance of high quality CPR.

The second thing I took away was the surprising response from the crowd and my colleagues. Following completion of the race and once people found out about our story, we were proclaimed heroes! Heroes? I know for a fact that I performed CPR three times earlier that week in my own emergency department, certainly with no such proclamation. We only did at that race what any nurse, paramedic or doctor would have done in our situation. I know this to be true because we turned away dozens of people who offered to help amidst the CPR, and who often only added to the chaos. We already had our impromptu team of two emergency medicine residents, a surgical resident from a local Detroit residency and an emergency department nurse at the patient’s side. With all the negativity that we might read in the newspaper, or see on television today, there was an overabundance of people wanting to offer help when a stranger was in distress.

I’ve never felt so much adrenaline to finish a race as I did that day. The final four miles seemed to fly by. And our patient? He made a full recovery, and returned to work full time only ten days later. As for my co-chief and I, the Ann Arbor Half Marathon is only a few short months away, so training (and a brief ACLS review) starts soon.

Interstitial versus Cornual Pregnancies:
There is a Difference
Megan Litzau, MD
Indiana University

Commonly the terms interstitial and cornual pregnancies are used interchangeably. However, these are two distinct entities, and are managed differently.1 An interstitial pregnancy occurs when there is implantation in the proximal intramural portion of the fallopian tube. A cornual pregnancy is when there is implantation in the lateral portion of the uterus.

An interstitial pregnancy is an emergency. There has been recent discussion on whether interstitial pregnancies tend to rupture at a later gestational date; however the typical period for rupture of an ectopic interstitial pregnancy is between 7-16 weeks.2 An interstitial pregnancy is located near the uterine artery and therefore carries a high risk of rapid hemorrhage should the interstitial pregnancy rupture.3 In contrast, a cornual pregnancy is located in the intrauterine cavity and can be a viable pregnancy.

Since the outcomes of these two are distinctly different, it is important to distinguish between the two. When using ultrasound to attempt to locate an intrauterine pregnancy, suspicion should be raised if there is an eccentric gestational sac located in the uterus. Once this concern is raised, a measurement should be taken of the myometrial mantle. If the myometrial mantle is less than 8mm, it is concerning for an interstitial pregnancy, and an emergent OB/GYN consultation should be obtained. If the myometrial mantle is greater than 8mm, it is less likely that the eccentrically placed pregnancy is interstitial. Though a cornual pregnancy can be a viable pregnancy, a consultation with OB/GYN to discuss the case and arrange for follow up is still recommended as the patient will need to be carefully monitored.4


  1. Lewiss R, Shaukat N, Saul T. The endomyometrial thickness measurement for abnormal implantation evaluation by pelvic sonography. J Ultrasound Med. 2014; 33 (7): 1143-1146. Doi: 10.7863/ultra.33.7.1143.
  2. Noble V, Liteplo A, Miller R, Murray A, Villen T. Cornual ectopic pregnancy diagnosed by emergency physician-performed bedside ultrasound in the emergency department. J Emerg Med.2008; 40 (4) e81-82. Doi:10.1016/j.emermed.2008.04.033.
  3. Malinowski A, Bates SK. Semantics and pitfalls in the diagnosis of cornual/interstitial pregnancy. Fertil Steril. 2006; 86 (6). Doi:10.1016/j.fertnstert.2006.03.073.
  4. Goudie A. Ultrasound features of interstitial ectopic pregnancy: The role of the non expert emergency medicine sinologist. Emerg Med Australas. 2012; 24: 480-481. Doi:10.111/j.1742-6723.2012.01606x.

EMS Specialty Update: Backboards & Cervical Collars
Alexandra Murray, DO PGY1
Mercy St. Vincent Medical Center Emergency Medicine Residency

The practice of immobilizing patients has varied widely over the past several decades. Prior to 1995, the only patients that were immobilized were those who had neurologic deficits or a concerning mechanism of injury. Secondary to the fear of paralyzing neck injuries, in 1995 the EMS curriculum was streamlined so that every patient suspected of having any sort of trauma was placed in a c-collar and on a backboard.1 Despite good intentions, review of the literature shows very little support for either the cervical collar or the backboard. In fact, there is no evidence that supports that the cervical collar limits any significant range of motion at the neck. Immobilization has been shown to increase intracranial pressure, impede respiratory function, limit opening of the mouth during intubation, cause pressure ulcers and cause distraction of C1-C2 injuries.1-6 In comparison, countries who do not use any type of immobilization (i.e., Malaysia) have better outcomes when comparing similar injuries.7 The literature also shows that mortality doubles with immobilization in penetrating trauma.8 Furthermore, video capture analysis found that conventional extrication techniques with a backboard result in more cervical spinal movement than allowing the patient to self-extricate.9,10

The culture of backboards and cervical collars has been heavily engrained in the EMS and emergency medicine world. There may be a role for these devices in particular situations; however, we need to ask ourselves if we are doing more harm than good.


  1. White CC, et al. EMS spinal precautions and the use of the long backboard - resource document to the position statement of the National Association of EMS Physicians and the American College of Surgeons Committee on Trauma. Prehosp Emerg Care. 2014 Apr-Jun;18(2):306-14.
  2. Haut,ER, et al. Spine immobilization in penetrating trauma: More harm than good? J Trauma. 2010 Jan; 68(1):115-20. PMID: 20065766.
  3. Ben-Galim P, et al. Extrication collars can result in abnormal separation between vertebrae in the presence of a dissociative injury. J Trauma. 2010 Aug;69(2):447-50. PMID: 20093981.
  4. Vanderlan WB, et al. Increased risk of death with cervical spine immobilization in penetrating cervical trauma. Injury. 2009 Aug;40(8):880-3. PMID: 19524236.
  5. Goutcher CM, et al. Reduction in mouth opening with semi-rigid cervical collars. Br J Anaesth. 2005 Sep; 95(3):344-8. PMID: 16006487.
  6. Gaither JB, et al. Prevalence of difficult airway predictors in cases of failed prehospital endotracheal intubation. J Emerg Med. 2014 Sep;47(3):294-300. PMID: 24906900.
  7. Hauswald M, et al. Out-of-hospital spinal immobilization: Its effect on neurologic injury. Acad Emerg Med. 1998 Mar;5(3):214-9. PMID: 9523928.
  8. Oteir AO, et al. Should suspected cervical spinal cord injury be immobilised?: A systematic review. Injury. 2015 Apr;46(4):528-35.
  9. Engsberg JR, et al. Cervical spine motion during extrication. J Emerg Med. 2013 Jan;44(1):122-7.
  10. Dixon M, et al. Biomechanical analysis of spinal immobilization during prehospital extrication: A proof of concept study. Emerg Me J. 2014 Sep;31(9):745-9. PMID: 23811859.

Relevance of New CDC Opiate Guidelines for Emergency Physicians
Samuel Bergin, MSIV, Uniformed Services University of the Health Sciences
Chad Roberts, MSII and Scott Pew, MPH Candidate
University of Utah

While the CDC was compiling data from 1999 to 2014, more than 165,000 people in the US died from overdoses linked to prescription opioids.1 The opioids most commonly prescribed include methadone, oxycodone and hydrocodone. From 2004 to 2010, ED visits due to abuse of prescription drugs increased 115% while visits due to illicit drugs increased 18%.2 Currently up to 1,000 people per day are treated in emergency departments for misusing prescription opioids. While emergency physicians are responsible for less than 5% of immediate and extended-release opiate prescriptions, they prescribe opiates for 17% of ED discharges.4 Reasons for ED opioid prescriptions most commonly include back pain, abdominal pain and fractures/sprains.4 We are in a position to help play a pivotal role in prescriptions, addictions and treating overdoses.3

Click to view larger image.

CDC Recommendations
The new CDC Guideline for Prescribing Opioids for Chronic Pain — United States, 2016 are generally directed at primary care physicians and evaluates three broad categories: (1) when to initiate and continue opioids for chronic pain, (2) opioid selection, dosage, duration, follow up and discontinuation, and (3) assessing risk and addressing harms. Spanning these broad categories are 12 recommendations to guide appropriate opioid prescription. These recommendations include:

  1. Starting with non-pharmaceutical & non-opioid management for chronic pain
  2. Setting & keeping goals
  3. Patient education of risks & benefits
  4. Immediate-release formulations instead of extended release
  5. Lowest effective dose & taking care to assess the morphine milligram equivalents
  6. Acute pain treated with lowest effective dose for three to seven days
  7. Frequent follow up
  8. Evaluating risk factors for abuse and harm
  9. Using state Prescription Drug Monitoring Programs (PDMP’s)
  10. Using urine drug screens to assess compliance
  11. Avoiding co-prescribing opioids and benzodiazepines
  12. Use of evidence-based medicine for opioid use disorder

Two recommendations are particularly applicable to emergency medicine.

Recommendation #6 states: “When opioids are used for acute pain, clinicians should prescribe the lowest effective dose of immediate-release opioids and should prescribe no greater quantity than needed for the expected duration of pain severe enough to require opioids. Three days or less will often be sufficient; more than seven days will rarely be needed.” The authors note that “just in case” opioids should not be prescribed.

Recommendation #9 states: “Clinicians should review the patient’s history of controlled substance prescriptions using state prescription drug monitoring program (PDMP) data to determine whether the patient is receiving opioid dosages or dangerous combinations that put him or her at high risk for overdose…” Application of these two recommendations may help reduce the likelihood of opioid-naïve patients becoming dependent and can help prompt intervention for opioid-dependent patients.


  1. Dowell D, Haegerich TM, Chou R. CDC guideline for prescribing opioids for chronic pain—United States, 2016. JAMA. doi:10.1001/jama.2016.1464.
  2. Drug Abuse Fact Sheet. ACEP News. American College of Emergency Physicians. Accessed on 22 March 2016.
  3. Governale L. Outpatient prescription opioid utilization in the U.S., Years 2000–2009. Presented at the Joint Meeting of the Anesthetic and Life Support Advisory Committee and the Drug Safety and Risk Management Advisory Committee, Adelphi, Maryland, 22–23 July 2010. Accessed at (slide 16) on 22 March 2016.
  4. Hoppe JA, Nelson LS, Perrone J, et al. Opioid prescribing in a cross section of US emergency departments. Ann Emerg Med. 2015;6:253–259.
  5. Phillips DM. Joint Commission on Accreditation of Healthcare Organizations. JCAHO pain management standards are unveiled. JAMA. 2000;284(4):428-429.

Health Policy Corner:
New CDC Opioid Prescribing Guidelines

Heather Boynton, MD
UC San Diego Health System

On March 15, 2016, the Centers for Disease Control and Prevention (CDC) released a new set of guidelines for prescribing opioids for chronic, non-cancer pain. The guidelines are intended to provide specific guidance for primary care providers, and are based on updated information from a 2014 systematic review. What do these guidelines mean for emergency physicians?

As AAEM’s own clinical practice statement on prescribing opioids points out, pain is one of the most common presenting complaints in the emergency department, accounting for at least half of all visits. Emergency physicians have a clear mandate to address acute pain in the emergency setting, and pain management is closely correlated with patient satisfaction. On the other hand, patients presenting with chronic pain report weeks, months and even years of intractable pain. Long-term use of opioid pain medication has increased their tolerance far beyond the lowest effective dose for an opioid-naive individual. Many patients with chronic pain will request refills of home medication or specific IV medications by name and dose.

The CDC’s prescribing guidelines address five key questions. Researchers conclude it is unclear if opioid versus non-opioid therapy or placebo results in any long-term (>1 year) difference in pain, function or quality of life. Additionally, opioid therapy is associated with a significantly increased likelihood of long-term use, even when initiated for acute pain.

The CDC also makes 12 recommendations about when and how to prescribe pain medication. One is to review patients’ use of controlled substances via a state prescription monitoring program for multiple prescribers or dangerous combinations (ie, with benzodiazepines). For acute pain, three days of home pain medication has been shown to be “sufficient,” with a maximum of seven days advised. Patients at greatest risk of overdose include those with sleep apnea, kidney disease or liver disease, older than 65, pregnant or have a history of mental health problems or substance abuse.

Discussing these new guidelines with patients underscores the evidence basis of our medical decision making. It may also help offload some of the charge that builds up in a “request-denial” dichotomy between patient and physician. Referrals to appropriate prescribers, including primary care physicians and pain clinics, can add value to an ED visit. For under- or uninsured patients, it can be helpful to offer a list of community clinics as well.


  1. Dowell D, Haegerich TM, Chou R. CDC guideline for prescribing opioids for chronic pain — United States, 2016. MMWR Recomm Rep. ePub: 15 March 2016. DOI:
  2. Emergency department opioid prescribing guidelines for the treatment of non cancer related pain. AAEM Board of Directors Nov 12, 2013.
  3. Clinical policy: Critical issues in the prescribing of opioids for adult patients in the emergency department. Annals of Emergency Medicine Volume 60, No.4: Oct 2012.


Clinical Pearl: Procalcitonin and Lower Respiratory Tract Infections
Jordan Kaylor, MD PGY4
Northwestern/McGaw Medical Center

Procalcitonin (PCT) is a serum biomarker that, when paired with clinical judgment, may help guide management of lower respiratory tract infections (LRTIs) in the emergency department (ED). Procalcitonin levels can help clinicians distinguish between bacterial and viral infections and might subsequently guide decisions to initiate or discontinue antibiotics. Procalcitonin is a prohormone of calcitonin. It is an acute-phase reactant synthesized in many tissues and released in response to cytokines such as interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)-α.1 Normal serum concentrations are <0.05ng/mL, but in bacterial infections, PCT increases to detectable levels within three to four hours (earlier than ESR or CRP).1 Elevations are not seen in noninfectious inflammatory conditions or viral infections, but are possible in Addisonian crises, malaria, severe fungal infections and medullary thyroid carcinoma.1 In viral infections, interferon (INF)-ɣ probably decreases PCT release, leading to lower or undetectable serum levels.2

Although PCT interpretation depends on the specific assay used, in general, along with clinical judgment, a PCT ≤0.1mcg/L (also expressed as 0.1ng/mL) may be able to exclude bacterial infection as a cause of LRTIs. Values of 0.1-0.25mcg/L make bacterial infection unlikely. Values of 0.25-0.5mcg/L suggest possible bacterial infection, and levels ≥0.5mcg/L indicate probable bacterial infection.3 When PCT drops to < 0.25mcg/L, antibiotics may be discontinued. In Switzerland, among patients presenting to multiple EDs with symptoms of LRTIs (including those with community-acquired pneumonia, chronic obstructive pulmonary disease [COPD] and acute bronchitis), using a PCT algorithm in addition to clinical judgment safely decreased both antibiotic usage and duration of antibiotic therapy without increasing mortality.4 These results were supported by a 2012 Cochrane review of 14 trials in various clinical settings, although most were done in Europe or China.5 Additionally, PCT use has been evaluated in the ED workup of heart failure and may identify concomitant bacterial pneumonia or distinguish between bacterial pneumonia and heart failure.6 It may also identify patients with COPD exacerbations who will benefit from antibiotic therapy.7 Of note, trials have generally excluded patients with more severe medical comorbidities, such as HIV with a CD4 count <200, active tuberculosis, neutropenia, history of stem cell transplant, cystic fibrosis, hospital-acquired/healthcare-associated pneumonia or those requiring ICU admission.

Based on the available data, it is hard to say if PCT is ready for routine use when evaluating LRTIs in the ED. Although existing literature suggests PCT values are helpful when combined with clinical judgment, patients from North America and those with multiple medical comorbidities are noticeably absent from current publications. Therefore, it is difficult to infer sensitivities and specificities for PCT’s use in ruling out bacterial LRTIs among medically complex patients in EDs across the United States. More research is necessary before we can routinely initiate or withhold antibiotics based on PCT values.


  1. Markanday A. Acute phase reactants in infections: Evidence-based review and a guide for clinicians. Open Forum Infect Dis. 2015;2(3):1-7.
  2. Gilbert DN. Procalcitonin as a biomarker in respiratory tract infection. Clin Infect Dis. 2011;52 Suppl 4:S346-50.
  3. Christ-Crain M, Jaccard-Stolz D, Bingisser R, Gencay MM, Huber PR, Tamm M, et al. Effect of procalcitonin-guided treatment on antibiotic use and outcome in lower respiratory tract infections: Cluster-randomised, single-blinded intervention trial. Lancet. 2004;363(9409):600-7.
  4. Schuetz P, Christ-Crain M, Thomann R, Falconnier C, Wolbers M, Widmer I, et al. Effect of procalcitonin-based guidelines vs standard guidelines on antibiotic use in lower respiratory tract infections: The ProHOSP randomized controlled trial. JAMA. 2009;302(10):1059-66.
  5. Schuetz P, Muller B, Christ-Crain M, Stolz D, Tamm M, Bouadma L, et al. Procalcitonin to initiate or discontinue antibiotics in acute respiratory tract infections. Cochrane Database Syst Rev. 2012;9:CD007498.
  6. Stolz D, Christ-Crain M, Bingisser R, Leuppi J, Miedinger D, Muller C, et al. Antibiotic treatment of exacerbations of COPD: A randomized, controlled trial comparing procalcitonin-guidance with standard therapy. Chest. 2007;131(1):9-19.
  7. Alba GA, Truong QA, Gaggin HK, Gandhi PU, De Berardinis B, Magrini L, et al. Diagnostic and prognostic utility of Procalcitonin in patients presenting to the emergency department with Dyspnea. Am J Med. 2016;129(1):96-104 e7.


Tox Talk: Calcium Channel Blocker Overdose
Erica Schramm, MS4
Cooper Medical School of Rowan University

Calcium channel blockers (CCBs) are used to treat a variety of common conditions such as hypertension, cardiac dysrhythmias and headaches. But use of CCBs is not without risk, particularly in cases of toxicity and overdose. CCBs are the ninth most widely prescribed class of drugs in the United States, accounting for an estimated 92 million prescriptions filled per year. The American Association of Poison Control Centers’ 2008 data noted over 10,000 human exposures to CCBs and 60 deaths associated with CCB overdose.1

What are the Signs of CCB Overdose?
The most common signs of CCB overdose are hypotension, sinus bradycardia, and shock. Other associated signs of overdose are hyperglycemia, pulmonary edema, myoclonus, dizziness, syncope, seizures, nausea, vomiting and acute kidney injury. Sustained release formulations can cause initial signs of overdose up to 12 hours post-ingestion. Diagnosis is clinical and thorough history taking is key to identifying CCB overdose. Patients taking CCBs who present with signs of toxicity should be questioned about intentional or unintentional overdose. Physicians should also inquire about details of how and when the patients take their medication to identify potential overdose.1

Differential diagnosis of CCB overdose may include: beta blocker overdose, tricyclic antidepressant overdose, acute coronary syndromes and sepsis. Recommended testing is focused on clinical management of the systemic manifestations of overdose and hypoperfusion - including 12 lead ECG, chest x-ray, arterial blood gas, serum electrolytes, BUN and creatinine.1,2

How is CCB Overdose Treated?
General management includes continuous cardiac monitoring, airway management, fluid resuscitation and GI decontamination. Initial treatment of symptomatic bradycardia and atrioventricular block can be attempted with atropine, and external or internal pacemaker therapy may be required. If capture is achieved, heart rate should be set at 60 bpm.1 Administration of calcium solutions (10% calcium chloride 10-20mL IV or 10% calcium gluconate 30-60mL IV followed by repeated boluses or continuous infusion) is also recommended for CCB overdose.2,3 Glucagon is used to treat bradycardia as well as hypotension. The recommended initial dose of glucagon is 2-5mg IV, followed by repeated boluses, up to a total of 10mg.2 In cases of severe CCB overdose, insulin-euglycemia therapy may be initiated with initial bolus of 1unit/kg of regular insulin along with 0.5g/kg of dextrose, followed by an infusion of regular insulin at 1.0units/kg/h with continuous dextrose infusion, beginning at 0.5g/kg/h. Blood glucose should be monitored every 30 minutes and insulin titrated to maintain euglycemia.3 Vasopressor therapy may be necessary for an unstable patient with persistent hypotension not responding to the above interventions.3


  1. Brooks DE, Katz KD. Calcium channel blocker toxicity. In: Vincent JL, Abraham E, Moore FA, Kochanek PM, and Fink M, eds. Textbook of Critical Care. 6th ed. Philadelphia, PA: Elsevier Saunders; 2011.
  2. Morgan DL, Borys DJ. Poisoning. In: Stone CK, Humphries RL, eds. Current Diagnosis and Treatment in Emergency Medicine. 7th ed. McGraw-Hill: 2011.
  3. Jang DH, DeRoos FJ. Calcium Channel Blockers. In: Hoffman RS, Howland MA, Lewin NA, Nelson LS, Goldfrank LR, eds. Goldfrank's Toxicologic Emergencies. 10th ed. McGraw-Hill: 2015.


International Patient Transports
Amy Ho, MD
University of Chicago

International transports and repatriation is a part of flight medicine and emergency medicine that the University of Chicago Emergency Medicine residency has taken special focus on. Its residents have dedicated time for these experiences, working as flight doctors for international repatriation of patients who fall ill and require stabilization in a foreign country but then desire to seek the remainder of their care in their home country. Here we interview the Chief Residents of the program responsible for running these opportunities, Drs. Chali Mulenga (CM) and Kelvin Adjei-Twum (KA), on their insight into these programs.

What are some of the international medical organizations you work with?

KA: One of the organizations we work with is Fox Flight, based in Toronto, Canada. It is an air ambulance company focused on critically ill international patient transfers. Teams include ACLS trained physicians (such as ourselves), nurses, respiratory therapists (RT) and paramedics. Critically ill patients are transferred on Learjets that are configured into mini-ICUs. More stable patients have medical escorts through commercial flights. These escorts carry with them medications and equipment to assist with active patient needs and management.

Who are the patients and how are they funded?

KA: There are an array of patients who use these organizations for their repatriation. Most are people who have travelled from their native country due to business or other employment opportunities, and have fallen to illness. Some patients are simply away for vacation or personal reasons. Our patients also include students who are studying abroad. Services are usually covered via medical travel insurance fees that patients have opted to pay into.

How do they find doctors and staff?

KA: A medical doctor contracted by the company reviews each case and deems whether the patient will require a non-medical escort, nurse escort, physician escort or some combination. Nurses and RTs are hired and work for each company on a call basis. Physicians, such as ourselves, are reached out to when a patient is medically cleared for flight. If the physician is available, travel arrangements and information on the patient are made available as soon as possible. Typical repatriation flights take approximately three to four days.

How do you see these experiences lend hand to the education of residents or attendings?

CM: As emergency physicians, we seldom get the chance to really sit down and connect with patients and their families given time constraints. Patient transports have afforded me the opportunity to spend several hours with patients and their loved ones. I have come to learn how far the little things we do for otherwise stable patients can go in earning their respect, trust and admiration, and frankly I have been incorporating that more and more in the ED.

KA: As emergency physicians, we will be faced with an array of patient disease presentations and backgrounds. Being a part of an international team gives you some insight into how other countries approach different disease processes. You also continue to learn about emergency medicine from a non-traditional care setting. This requires using some out of the box techniques with limited resources. All in all, this enables us to be better prepared to handle stressful situations in an environment we may not be use to.

Any interesting or memorable transport stories?

KA: We just recently had a really interesting case where one of our residents, Dr. Eric Toone, MD MBA, was the flight physician for a repatriation for a patient from Japan back to the states. This patient had severe necrotizing fasciitis requiring amputation of an upper extremity, including clavicle and scapula. Not only was the patient critically ill, requiring a flight nurse and Dr. Toone as the physician escort, but their trip included stopping for fuel at a WWII army base in Kamchatka, Russia!

We also get an opportunity to learn about different cultures and spend time with groups of people we may never meet for a span of three days. I had the opportunity to transport a patient back to his native Lima, Peru. He had been teaching Japanese in Peru for over five years. I had a great time listening to different experiences he had in Peru, prior to his unfortunate NSTEMI requiring multiple stent placements.

CM: I recently helped with the repatriation of an elderly male who had recently had a spontaneous subarachnoid hemorrhage needing surgical evacuation. We flew from Uruguay to Paris and then to Tokyo. We were together for over 24 hours. His wife and a translator accompanied us. He probably went to the bathroom every two hours and I ensured I helped every time. I administered subQ meds, offered to get him food and water and conversed with him and the wife wherever and whenever I could. When all was said and done, I was exhausted, but almost brought to tears by how much the little I had done meant to the wife and the patient. They had the kindest things to say about me and were simply overwhelmed with gratitude. Since then, I've made more of a conscious effort to graciously help with the little things in the ED, even with our very stable patients and their loved ones. I'll help move a patient, find a chair for a loved one, help the nurses put in difficult IVs more readily, grab a boxed lunch, etc. Never would I have imagined gaining so much perspective from caring for a stable patient all the while getting to see Montevideo and Tokyo and flying business class. It really is a beneficial part of our training.

Pros and Cons of having these opportunities as part of residency?


  1. You get to travel the world! We've had residents go to Japan, Spain, Scotland, China, Trinidad & Tobago, Canada, London, France and many more places.
  2. Build great relationships with patients and their families.
  3. Opportunity to take care of people (isn't that what EM is about!) in a non-traditional role.


  1. Your everyday shift doesn't feel quite the same after a transport.
  2. If you have a fear of flying, this won't be an experience you may be looking forward to!

Caption: Recent flight By Dr. Chali Mulenga to Surabaya, Indonesia. “The kindness of the locals was a true highlight. I am already keeping in touch with some of the people I met. Such wonderful people.”

Your 2015-2016 Leaders:

Victoria Weston, MD

Vice President
Michael Gottlieb, MD

Nicole Battaglioli, MD

Immediate Past President
Meaghan Mercer, DO

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

Medical Student Council President
Michael Wilk

Copy Editor:
Nathan Haas, MD

Managing Editor:
Madeleine Hanan,

Modern Resident Contributors

Special thanks to this issue's contributors:

Samuel Bergin; Joel Betcher, MD; Heather Boynton, MD; Kaitlin Fries, DO; Danielle Goodrich, MD; Amy Ho, MD; Jordan Kaylor, MD; Daniel Leiva; Megan Litzau, MD; Al Majkrzak, MD; Alexandra Murray, DO; Scott Pew; Chad Roberts; Linda Sanders, MD; Erica Schramm.

Interested in writing?
Email submissions to:

Please submit articles by May 15th for the June/July 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.

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