Inside This Issue
Thank You for a Great Year!
Mike Wilk, MSIV
President, AAEM/RSA Medical Student Council
Dear AAEM/RSA Student Members,
Thank you for a wonderful past year. We had two great regional student symposiums at Loyola Chicago and Georgetown in addition to the student track at the Scientific Assembly in Austin, Texas. As always, keep in mind all of the resources AAEM/RSA has to offer. As an AAEM/RSA student member, be sure to take advantage of your free membership to the EM podcast, EM:RAP (Emergency Medicine: Reviews and Perspectives). Read through our book, Rules of the Road for Medical Students, to learn invaluable information on how to best navigate your way through medical school. Attend one of our regional medical student symposiums to hear from and network with residents and EM residency program directors. Registration for all of our conferences can be found on our website, www.aaemrsa.org. For the rising MSIVs, be sure to sign up for EM Select, our interactive residency database tool to help find the best residency for you.
For those interested in getting more involved and demonstrating your commitment to the field, AAEM/RSA has numerous opportunities for you. Become a site coordinator for your medical school or join one of the many committees (Publications, Advocacy, Communications, Education, International or Membership). Did you happen to see an interesting case while working or shadowing in the emergency department? Consider writing an article on it or anything EM related and publishing it here in Modern Resident or the AAEM/RSA blog. Apply to be a medical student ambassador and volunteer at the Annual Scientific Assembly next year in Las Vegas, February 17-21, 2016. Finally, keep an eye out for our new AAEM/RSA student podcasts!
It is my pleasure to introduce the new 2015-2016 members of the student board: Vice President Melanie Pollack (Western University of Health Sciences), Northeast Representative Aldo Manresa (Touro College of Osteopathic Medicine), Western Representative Amanda Purdy (University of California, Irvine School of Medicine), Midwest Representative Dan Holt (Loyola University Stritch School of Medicine), Southern Representative Aarian Afshari (Florida State University College of Medicine) and International Ex-Officio Member Matthew Camara (Ross University School of Medicine).
I encourage you to take advantage of these resources and all of the opportunities AAEM/RSA has to offer, no matter where you are on your journey through medical school. Keep an eye out for our upcoming conferences this year, including the Midwest Medical Student Symposium at Loyola (Chicago) on Saturday, September 26th. On behalf of the 2015-2016 board, we look forward to meeting and assisting you over the next year, and I look forward to continuing to serve you as president!
Alexandra Murray, DO PGY-1
Mercy St. Vincent Medical Center Emergency Medicine
A 45-year-old female presents to the emergency department with sudden onset shortness of breath and right-sided chest pain, which began while walking. The patient reports that she was hospitalized one month ago for a spontaneous pneumothorax that required a chest tube. She denies recent trauma, a history of pulmonary or pleural problems prior to one month ago, recent flu-like symptoms or cough. She takes no medications and states that she is generally healthy, with the exception of minor chronic anemia. The patient also reports that she had difficulty becoming pregnant but has one living child. The patient exercises frequently and denies use of tobacco or drugs. Her last menstrual period ended two days ago and was normal. CT and MRI of the chest show no signs of pulmonary blebs or any anatomical defects, but do demonstrate a spontaneous pneumothorax, for which a chest tube is placed. The patient is taken for exploratory laparoscopy and is found to have a diaphragmatic hole. Biopsy of the surrounding tissue reveals thoracic endometriosis.
Catamenial pneumothorax (CP) is a rare clinical condition in which women of reproductive age develop recurrent, spontaneous pneumothoraces in conjunction with their menstrual cycle. The etiology is not completely understood; however, in most cases it is associated with thoracic endometriosis resulting in endometrial tissue becoming embedded in the diaphragm. During the menstrual cycle the endometrial tissue sheds, leading to diaphragmatic fenestrations.1-5 The parietal pleura is the most common tissue affected, although the lung, visceral layer and more rarely the tracheobronchial tree can be involved.1-3
CP has previously been underdiagnosed, and the incidence of this condition remains unclear.1-5 Recent studies have shown that CP is responsible for 3-6% of spontaneous pneumothoraces among menstruating women and as high as 25-30% of women referred for surgery.1,2 Catamenial pneumothoraces generally occur on the right side (85-95%), but can be left sided or bilateral.1-3 CP usually affects women in the third or fourth decade of life, and typically occurs between 24 hours before to 72 hours after the onset of menses.1-5 Pelvic endometriosis is also documented in up to 30-51% of cases.1,2 The two main therapeutic options for thoracic endometriosis include hormonal suppressive therapy or surgical intervention.1-5
- Visouli AN, et al. Catamenial pneumothorax: A rare entity? Report of 5 cases and review of the literature. J Thorac Dis. 2012 Nov;4 Suppl 1:17-31.
- Visouli AN, et al. Catamenial pneumothorax. J Thorac Dis. 2014 Oct;6(Suppl 4):S448-60.
- Alifano M, et al. Catamenial and noncatamenial, endometriosis-related or nonendometriosis-related pneumothorax referred for surgery. Am J Respir Crit Care Med. 2007 Nov 15;176(10):1048-53.
- Alifano M. Catamenial pneumothorax. Curr Opin Pulm Med. 2010 Jul;16(4):381-6.
- Mikroulis DA, et al. Catamenial pneumothorax. Thorac Cardiovasc Surg. 2008 Sep;56(6):374-5.
Nathan Haas, MD
University of Michigan
In the United States, myocarditis is most commonly viral in nature, and only supportive management is typically warranted. However, many other etiologies of myocarditis exist including eosinophilic, toxic and systemic disorders (Celiac disease, Wegener’s Granulomatosis, inflammatory bowel disease, Kawasaki’s, SLE, Sarcoidosis, Thyrotoxicosis). Thus, the management of myocarditis hinges first on identifying the suspected underlying etiology.
Eosinophilic myocarditis can be precipitated by a number of underlying hypereosinophilic states. Most commonly, eosinophilia occurs secondary to hypersensitivity reactions. Common precipitants include antibiotics and anticonvulsants, but drugs ranging from triptans to diuretics have been implicated. Dobutamine infusions also commonly precipitate eosinophilia that can result in myocarditis, but this is thought to be secondary to the preservative used rather than the drug itself. In the appropriate geographical setting, parasitic infections should also be considered when evaluating eosinophilia. Lastly, malignancy or idiopathic hypereosinophilic syndrome have also been described as causes of eosinophilic myocarditis, and should thus also remain on the differential.
The diagnosis of eosinophilic myocarditis is typically made clinically, when signs and symptoms of myocarditis exist in the setting of marked eosinophilia. However, the diagnosis is often made via endomyocardial biopsy, and cases are often diagnosed post-mortem. If hypersensitivity is suspected, the underlying offending agent should be identified and removed as soon as possible. In one small case report, patients were managed with steroids, beta blockers and ACE inhibitors, and all responded well to treatment. If left untreated, eosinophilic myocarditis can rapidly progress to heart failure, arrhythmias or sudden cardiac death, and thus prompt recognition is crucial in management.
- Al Ali AM, Straatman LP, Allard MF, Ignaszewski AP. Eosinophilic myocarditis: Case series and review of literature. Canadian Journal of Cardiology. 22.14 (2006): 1233-237. Web.
- Weller PF, Klion AD. Approach to the patient with unexplained eosinophilia Uptodate. N.p., 24 Oct. 2014. Web. 28 May 2015.
Peds Tox Talk: Liquid Nicotine
Ashley Grigsby, DO PGY-1
Indiana University Emergency Medicine/Pediatrics
Nicotine toxicity is a well-described clinical entity that often occurs in children who accidentally ingest cigarette buds or nicotine patches. However, a new form of nicotine has the potential to cause serious clinical symptoms, including death.
E-cigarettes use a form of liquid nicotine of varying concentrations that come in individual vials. E-cigarette use is on the rise across the United States, and unfortunately, the liquid nicotine is both easily accessible and appealing to young children. These liquid cartridges are often packaged in a tempting way, with one such cartridge described as having a cartoon monkey holding grapes on the front. The packaging is not regulated by the FDA and therefore has no child proof regulations for packaging. The liquid itself is also appealing for young children, and flavors include cotton candy, bubble gum, fruit, mint and chocolate.1,2
The CDC reported a significant increase from 2010 to 2014 of calls to poison centers regarding nicotine exposure. They also reported that e-cigarette exposure compared to regular cigarette exposure was about 1.5 times more likely to cause an adverse health effect.1 Among the calls to poison centers during this time period, 51% involved young children.2
Symptoms of toxicity are dose dependent; however, a lethal dose of nicotine in children is estimated to be 1-13mg/kg depending on the route of nicotine exposure.3 Nicotine is readily absorbed in multiple ways, including the GI tract, mucous membranes, respiratory alveoli and skin.4 Nicotine concentrations in e-cigarette solutions vary widely across different manufacturers.1 One study found a range of concentrations from 6mg/mL to 36mg/mL across different manufacturers, with most solutions coming in five, 10 or 20mL vials. For example, if a 12kg child, the average weight of a two-year-old, were to drink a 10mL vial of 10mg/mL solution, they would have ingested 8mg/kg. This relatively small amount of solution could thus very well prove fatal.
Early symptoms of ingestion including nausea, vomiting, diarrhea and increased salivation.5 Nicotine’s toxic effects are a direct result of its mechanism of action as an agonist at nicotinic acetylcholine receptors.4 Severe toxicity can lead to symptoms similar to that of a cholinergic crisis with copious secretions (which may require atropine), respiratory muscle paralysis and seizures.3 Treatment of toxicity should be based on severity of symptoms. GI complaints are the most common, and as vomiting can help reduce the absorption of nicotine , anti-emetics are not recommended. Contaminated clothing should be removed as nicotine can be absorbed through the skin.4 Severe toxicity treatment is supportive with the addition of atropine as needed for secretions.
Most ingestions of liquid nicotine described in case reports have been mild, requiring only minimal observation in the emergency department. The half-life of nicotine is one to two hours allowing for only short observation in less severe cases.
As the use of these devices increases, clinicians should be aware of the clinical consequences of exposure. At this time, there are no FDA regulations on the solutions, packaging or devices. The amount of solution required to cause toxic results varies widely between manufacturers and clinical consequences can be difficult to predict based on volume ingested. Clinicians should be aware of these differences and clinical decisions should incorporate the above information .
- Cameron JM, Howel DN, White JR, et al. Variable and potentially fatal amounts of nicotine in e-cigarette nicotine solutions. Tob Control. 2014;23:77-78.
- Chatham-Stephnes K, et al. Notes from the field: Calls to poison centers for exposure to electronic cigarettes – United States, September 2010-February 2014. Center for Disease Control and Prevention. 2014. Available from: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6313a4.htm.
- Bassett RA, Osterhoudt K, Brabazon T. Nicotine poisoning in an infant. N Engl J Med. 2014 June;370;23.
- Gill N, et al. E-cigarette liquid nicotine ingestion in a child: Case report and discussion. CJEM. 2015;0(0).
- Gupta S, Gandhi A, Manikonda R. Accidental nicotine liquid ingestion: Emerging paediatric problem. Arch Dis Child. 2014;99:1149.
Board Review: Heat-Related Illnesses
Kaitlin Fries, DO PGY-1
Heat-related illnesses are responsible for approximately 400 U.S. deaths each year.4 Drastic spikes in mortality can be seen during severe droughts and heat waves, the latter of which is defined as temperatures greater than 90°F for three or more consecutive days.3,4 Those at greatest risk for heat-related emergencies are children, the elderly, people with certain predisposing medical conditions and those taking medications that interfere with the body’s thermoregulatory center.3,4 The spectrum of heat-related illnesses ranges from cramps, syncope and heat exhaustion to more serious conditions such as heat stroke. All of these conditions are easily preventable with public education and adequate access to hydration and cool shelters.
The main two cooling mechanisms used by the human body are radiation and evaporation.2,3,4 Radiation can account for up to 65% of total heat loss.4 However, radiation can only occur in a cool environment. Patients who do not have access to air-conditioning must rely on evaporation to dissipate heat by producing sweat, which then evaporates from the skin’s surface due to body heat.2 However, as atmospheric humidity increases, the effectiveness of evaporation decreases.2 Below is a brief review of the minor presentations of heat-related complaints.
Heat cramps are painful, involuntary skeletal muscle spasms most commonly seen in the lower extremities.2,3,4 Patients typically experience these muscle contractions during or several hours after vigorous physical activities.3 This is thought to be secondary to dilutional hyponatremia and can be prevented by drinking electrolyte based sports drinks instead of water.1,4 Treatment includes rest and salt replacement with an electrolyte-based solution.1-4 In severe cases, IV rehydration with normal saline may be required.3
Heat syncope is another minor form of heat-related illness most commonly seen in non-acclimatized individuals, especially the elderly.3 While standing in the heat, vasodilation causes blood to pool in peripheral vasculature, thus decreasing preload.2 As the environmental temperature continues to increase, volume depletion is further worsened and eventually causes decreased vasomotor tone. Treatment consists of removing the patient from the warm environment, rest and oral/IV hydration.1-4 If the patient fell, it is important to assess for any traumatic injuries.4 It is also important to simultaneously rule out other serious causes of syncope in the elderly population.3,4
Heat exhaustion is the most commonly seen heat-related illness.1 It is caused by a combination of volume and salt depletion.1,2,3 Once again, it is most commonly seen in the elderly and individuals working in warm environments.3 These patients can present with any combination of the following complaints: headache, dizziness, weakness, nausea, vomiting, diaphoresis, myalgia, syncope, tachypnea, tachycardia and orthostatic hypotension.1-4 It is important to note that in heat exhaustion core body temperature will not exceed 104°F.1,2 Also, a key distinguishing factor between exhaustion and heat stroke is in heat exhaustion the patient will have a normal neurological exam.1,2 Laboratory values may show hemoconcentration and/or electrolyte abnormalities; however, liver function should be normal.1,3 Treatment should consist of rest, oral/IV rehydration and electrolyte replacement as needed.1-4 The majority of these patients can be discharged home. However, heat exhaustion can turn into heat stroke, so these patients should be observed until their symptoms have completely resolved.3,4 Patients with a history of congestive heart failure or with serious electrolyte abnormalities may need admission for more aggressive rehydration.3
Stay tuned for the next issue to review heat stroke!
- Ahmadi M. Environmental emergencies in: Blok BK, Cheung DS, Platts-Mills TF, eds. First aid for the emergency medicine boards. McGraw Hill; 2012. 13:723-725.
- Paquette R. Hippo Review: Heat cramps, heat exhaustion, heat syncope. 2015.
- Tintinalli JE. Tintinalli's emergency medicine: A comprehensive study guide. McGraw Hill; 2011. 16:1339-1341.
- Tintinalli JE. Tintinalli's emergency medicine: Just the facts. McGraw Hill; 2013. 13:424-425.
Pediatric Emergencies Part 5: Forearm Fractures of Abuse
Jenna Erickson, MSIV
Chicago Medical School
Child abuse is a sobering subject, but it remains one of the most important topics of education for emergency physicians. To underscore the importance of this issue, consider the following facts about child abuse in the United States:
- 6.3 million children are referred to child protective services each year
- On average four to seven children die per day from abuse or neglect
- Over 70% of victims are under two years old
Unfortunately, when considering child abuse in the emergency room setting there are no clear cut answers. The most important fact to keep in mind is that any injury in a child could be an indication of abuse, whether it follows a well-documented abuse pattern or not. As child abuse is a vast subject, the following article will focus on one often overlooked chief complaint: forearm fractures.
Fractures are a frequent finding in abuse victims, second only to bruising. Eighty percent of these cases are in children under 18 months of age. Although not typically associated with child abuse, fractures of the radius and ulna are the most common types in children. In fact, these fractures comprise nearly 40% of all fractures in children under three years. With the frequency of forearm fractures observed, especially in emergency medicine, a correlation between forearm fractures and child abuse is of extreme importance.
A team of researchers in two Chicago area hospitals investigated this correlation. A retrospective study currently in press compared the characteristics and mechanisms of forearm fractures in children under 18 months. Cohorts of patients with accidental radial and ulnar fractures were compared to non-accidental injury (NAI) fracture patients over a five year time span. The most common radial and ulnar fracture characteristics observed were buccal and transverse. Buccal fractures are caused by axial loading, in children usually from falling at standing height directly onto an outstretched arm. Transverse fractures are a result of perpendicular force on the bone, often seen in children falling from a bed or couch. Interestingly, among the 137 cases reviewed, there was no significant difference between the mechanisms of forearm fractures in accidental versus NAI groups.
Although these results do not conveniently outline a red flag of potential abuse cases, this study underlines one very important fact. The most common fracture in children under three years old will usually look the same in innocent fall cases as it does in a victim of child abuse. Emergency physicians must approach forearm fractures in young children with extreme caution. Proper attention to detail by the physician in these cases could save a child’s life.
- Flaherty E, et al. Evaluating children with fractures for child physical abuse. Pediatrics. 2014;133(2).
- Pressel D. Evaluation of physical abuse in children. Am Fam Physician 2000; 61(10)3057-64.
- Ryznar E, et al. Understanding forearm fractures in young children: Abuse or not abuse? Child Abuse and Neglect (epub ahead of print) April 2015.
- Shelmerdine S, et al. Who are we missing? Too few skeletal surveys for children with humeral and femoral fractures. Clin Radiology. 2014;60,e512-e516.
Drug Choice for Procedural Sedation: Propofol vs. Ketamine
Randy Kring, MSIV
Tufts University School of Medicine
Procedural sedation is frequently performed in the emergency department, whether it is for electrical cardioversion, closed joint reduction or abscess incision and drainage. Although the focus in these cases is often on the procedure, smart preparation for procedural sedation and an understanding of the different strategies that can be used is vitally important.
The goal of procedural sedation is to provide moderate sedation and analgesia while preserving the patient’s protective airway reflexes, adequate ventilation and cardiovascular function. Relative contraindications for procedural sedation may include advanced age, significant medical comorbidities such as CHF or COPD or signs of a difficult airway.1 Recent food intake is not a contraindication for procedural sedation, but aspiration risk should be assessed and minimized whenever possible.2 Many drugs can be used for procedural sedation, including midazolam, etomidate, propofol and ketamine. Which drug is “the best?”
Propofol, a sedative and amnestic, has onset in about 40 seconds and duration of action of about six minutes. Common side effects include pain at the injection site, hypotension and respiratory depression.3 Ketamine, a dissociative anesthetic that provides sedation, amnesia and analgesia, has onset in about 30 seconds and duration of action of about 10 to 20 minutes. Common side effects include agitation on emergence, nausea and (rarely) tachycardia and hypertension.4
Several studies have compared propofol and ketamine. One non-blinded randomized trial (n=97) found that compared with ketamine, propofol is associated with a shorter time to return to baseline mental status, and reduced agitation during recovery.5 Another non-blinded randomized trial (n=60) found that patients sedated with a combination of ketamine and midazolam took longer to return to baseline mental status than patients sedated with propofol.6
Yet another option for procedural sedation is what has been dubbed “ketofol,” a 1:1 combination of ketamine and propofol. The theory behind this formulation is that using lower doses of each medication imparts fewer side effects while reaching the same level of sedation. However, studies of ketofol to date have not found it to be safer or more effective than propofol alone.7
- Frank RL. Procedural sedation in adults. UpToDate. Last updated July 2, 2014. http://www.uptodate.com/contents/procedural-sedation-in-adults.
- Godwin SA, Caro DA, Wolf SJ, et al. Clinical policy: Procedural sedation and analgesia in the emergency department. Ann Emerg Med. 2005;45(2):177.
- Miner JR, Burton JH. Clinical practice advisory: Emergency department procedural sedation with propofol. Ann Emerg Med. 2007;50(2):182.
- Brown TB, Lovato LM, Parker D. Procedural sedation in the acute care setting. Am Fam Physician. 2005;71(1):85.
- Miner JR, Gray RO, Bahr J, et al. Randomized clinical trial of propofol versus ketamine for procedural sedation in the emergency department. Acad Emerg Med. 2010;17(6):604.
- Uri O, Behrbalk E, Haim A, et al. Procedural sedation with propofol for painful orthopaedic manipulation in the emergency department expedites patient management compared with a midazolam/ketamine regimen. Journal of Bone & Joint Surgery. 2011;93:2255-62.
- David H, Shipp J. A randomized controlled trial of ketamine/propofol versus propofol alone for emergency department procedural sedation. Ann Emerg Med. 2011;57(5):435.
Board Review: Appendicitis
Shane Sergent, DO and Sophia Johnson, DO
Conemaugh Memorial Medical Center
Appendicitis occurs most frequently in the second and third decades of life, with an incidence of approximately 233/100,000. It occurs more commonly in males, with a male to female ratio of 1.4:1.1 The pathogenesis of appendicitis is linked to bacterial overgrowth and/or intraluminal bacteria which infect the appendiceal wall. The first organisms to predominate are aerobic organisms, followed by a mixed infection. The immunological response to this bacterial overgrowth is the activation of B and T lymphoid cells, and the secondary reaction is lymphoid hyperplasia and possible obstruction.2 Late findings include gangrenous and perforated appendicitis.
The most predictive findings that support acute appendicitis include the following: pain in the right lower quadrant, abdominal rigidity and migration of pain from the periumbilical region to the right lower quadrant.3 In one study, Wagner, et al., found that the onset of pain before vomiting had 100% sensitivity, while the Psoas sign had 95% specificity.4 Appendicitis can also present less typically, such as right upper quadrant pain during pregnancy, or right flank pain with retrocecal appendicitis.
Although laboratory findings are not diagnostic, approximately 80% of patients demonstrate mild leukocytosis.5 There is also a correlation between high white blood cell counts and gangrenous or perforated appendicitis.6 Mild elevations in serum bilirubin have been demonstrated in appendiceal perforation (sensitivity 70%, specificity 86%).7 Other findings include elevated CRP and sterile pyuria from ureteral irritation.6
Diagnostic imaging is a useful adjunct to the clinical examination, in one study the sensitivity of ultrasound was 99% and specificity of 76.1%.7Ultrasound (US) is recommended for children and during pregnancy to avoid radiation, and has demonstrated a sensitivity of 99.1% and specificity of 91.7%.7 US has also been found to have desirable positive and negative predictive values in trained hands.8 When using US, an appendiceal diameter of >6mm is highly suggestive of acute appendicitis.8 Computerized tomography (CT) is often helpful when the appendix is not visualized using US, and has a sensitivity of 96.4% and specificity of 95.4%.7 CT findings can include appendiceal diameter >6mm, wall thickening >2mm, periappendiceal fat stranding, obstruction or appendicolith. MRI can also be a useful adjunct, particularly in children or during pregnancy.
Treatment includes IV fluids, antibiotics, pain control and surgery. Some international communities prefer antibiotic treatment alone, while surgery is typically the preferred treatment modality in the United States.9 In acute non-perforated appendicitis, recent literature demonstrates treatment efficacy of 90.8% for antibiotic therapy and 89.2% for surgery.10 The current acceptable rate of negative appendectomy is approximately 15% (20% in women).11 This number has been unchanged even with the introduction of CT, US and laparoscopy.12
- Addiss DG, Shaffer N, Fowler BS, Tauxe RV. The epidemiology of appendicitis and appendectomy in the United States. Am J Epidemiol. 1990; 132:910.
- Lau WY, Teoh-Chan CH, Fan ST, et al. The bacteriology and septic complication of patients with appendicitis. Ann Surg. 1984; 200:576.
- Paulson EK et al. Suspected Appendicitis. New England Journal of Medicine. 2003; 348:236-242.
- Wagner JM, McKinney WP, Carpenter JL. Does this patient have appendicitis? JAMA. 1996 Nov 20;276(19):1589-94.
- Silen, W. Cope's early diagnosis of the acute abdomen, 19th edition, Oxford University Press 1996. p.70.
- Guraya SY, Al-Tuwaijri TA, Khairy GA, Murshid KR. Validity of leukocyte count to predict the severity of acute appendicitis. Saudi Med J. 2005; 26:1945.
- Park JS, Jeong JH, Lee JI, et al. Accuracies of diagnostic methods for acute appendicitis. Am Surg. 2013; 79:101.
- Kessler N, Cyteval C, Gallix B, et al. Appendicitis: Evaluation of sensitivity, specificity, and predictive values of US, doppler US, and laboratory findings. Radiology. 2004; 230:472. 43.
- Tugnoli G, Giorgini E, Biscardi A, et al. The NOTA study: Non-operative treatment for acute appendicitis: Prospective study on the efficacy and safety of antibiotic treatment (amoxicillin and clavulanic acid) in patients with right sided lower abdominal pain. BMJ Open 2011;1:e000006.
- Hansson J, Körner U, Khorram-Manesh A, Solberg A, Lundholm K. Randomized clinical trial of antibiotic therapy versus appendicectomy as primary treatment of acute appendicitis in unselected patients. Br J Surg. 96: 473–481. doi: 10.1002/bjs.6482
- Flum DR, Morris A, Koepsell T, Dellinger EP. Has misdiagnosis of appendicitis decreased over time? A population-based analysis. Journal of the American College of Surgeons. Oct 2001; 286:14.
- Andersson RE, Hugander AP, Ghazi SH, et al. Diagnostic value of disease history, clinical presentation, and inflammatory parameters of appendicitis. World J Surg.1999; 23:133. 24.
Making the Most of Audition Season
Nicholas Pettit, PhD OMSIV
Ohio University Heritage College of Osteopathic Medicine
If you are in the midst of auditions or will be applying for auditions in the near future, especially in emergency medicine, this article may be for you! Audition season is an especially hectic time, one that can make or break many dreams of obtaining that ideal residency spot. Here are some tips that I learned while going through the process:
- Auditions prior to the submission of residency applications are great for obtaining letters of recommendation, especially a Standard Letter of Evaluation (SLOE).
- Auditions after your ERAS submission should not be used to obtain a SLOE, but should be for prospective programs that you may want to attend.
- Waiting for VSAS, the Visiting Student Application Service, to open may be too late to obtain your desired date and location. Many programs avoid using VSAS all together, and some even preauthorize spots prior to VSAS opening, thereby using VSAS as a simple formality.
- Do not create more work for the residents while on auditions. Your goal is not to know every answer or technique, but instead it is to be a hard working team player that is an asset to the emergency department.
- Find out where the supply cart is and have things ready to go to make everyone’s job easier.
- Attendings see two to three patients per hour. Do not try to manage three or more patients, which inadvertently creates more work for the staff. Know your two to three patients very well and you will be just fine.
- Request a shift with the program director and/or a chief resident.
- Have fun!
Kevin Beres, DO
UT Health Emergency Medicine Residency
A 62-year-old African American male with a history of hypertension and significant freebase crack cocaine abuse (the patient estimated $200,000 worth per year) presented to the emergency department in acute respiratory failure. He complained of a fever for three days, hemoptysis for two days and left sided chest pain. An ECG demonstrated biatrial enlargement and was otherwise unremarkable. Troponin, CBC and metabolic panel were all unremarkable. Sputum cultures, acid-fast bacilli smears, HIV and Influenza PCR were all negative. A chest X-ray demonstrated a diffuse, hazy appearance of the right lung and left lower lung. Chest CTA demonstrated ground-glass opacities with no evidence of a pulmonary embolism, but possible edema or hemorrhage. A bedside transthoracic echocardiogram demonstrated a normal ejection fraction. The patient was admitted to the ICU for continued positive pressure ventilation, where a bronchoscopy demonstrated alveolar hemorrhage and eosinophilia. The patient was diagnosed with Cocaine-Induced Pneumonitis or Crack Lung.
Cocaine is the fourth most abused drug in the United States.1 One of the complications of freebase cocaine abuse is an acute pulmonary syndrome, known as Crack Lung.2,3 Though still not fully understood, the pathophysiology is most likely due to the high temperature of volatilized cocaine and impurities that induce alveolar damage.4 Common presentations include acute respiratory failure, fever and hemoptysis.5 Imaging typically demonstrates ground-glass opacities with lymphadenopathy. Bronchoscopy often demonstrates no endobronchial lesions, abnormal secretions or mucosal abnormalities, although there is frequently alveolar hemorrhage and an eosinophilic predominance.2 In general, pulmonary infiltrates will resolve spontaneously within 36 hours after cessation of cocaine use and after administration of corticosteroids. The disease, however, can rapidly progress to Acute Respiratory Distress Syndrome and requires aggressive respiratory support.
Figure 1: Portable AP Chest X-ray demonstrating diffuse hazy appearance concerning for pneumonia, aspiration or pulmonary edema
Figure 2: CTA chest, coronal image, demonstrating diffuse ground-glass opacities
Figure 3: CTA chest, axial image, demonstrating diffuse ground-glass opacities and interlobular thickening, concerning for edema or acute hemorrhage
- US. Department of Health and Human Services. Results from the 2013 National survey on drug use and health: Summary of national findings. 2013; 1-170.
- Forrester JM, Steele AW, Waldron JA, Parsons PE. Crack lung: An acute pulmonary syndrome with a spectrum of clinical and histopathologic findings. Am Rev Respir Dis. 1990; 142(2): 462-467.
- Perper JA, Van Thiel DH. Respiratory complications of cocaine abuse. Respiratory complications of cocaine abuse. Recent Dev Alcohol. 1992; 10: 363-377.
- Mégarbane B, Chevillard L. The large spectrum of pulmonary complications following illicit drug use: Features and mechanisms. Chem Biol Interact. 2013; 206(3): 444-451.
- Hirche TO, Lambrecht E, Wagner TO. Crack-syndrome: The pulmonary complications of inhaled cocaine. A review a propos a case report. Pneumologie. 2002; 56(11): 684-688.
- Kissner DG, Lawrence WD, Selis JE, Flint A. Crack lung: Pulmonary disease caused by cocaine abuse. Am Rev Respir Dis. 1987; 136(5): 1250-1252.