Modern Resident - The newsletter of AAEM/RSA
October/November 2013
Volume 5: Issue 3  |  FacebookTwitterLinkedIn

Your 2013-2014 Leaders:

Meaghan Mercer, DO

Vice President
Rachel Engle, DO

S. Terez Malka, MD

Immediate Past President
Leana Wen, MD MSc

At-Large Board Members
Michael Gottlieb, MD
Calvin Hwang, MD
Sean Kivlehan, MD
Nicole Piela, MD
Edward Siegel, MD
Victoria Weston, MD

Medical Student Council President
Mary Calderone

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

Modern Resident Contributors

Copy Editor: Victoria Weston, MD
Managing Editor: Lauren Johnson, AAEM/RSA Staff

Special thanks to this issue's contributors:
Stephen S. Austad, DO; Nicole Battaglioli, MD; Isaac Bruck, MD PhD; Thomas Doran, MSIV; Jenna Erickson, MSIII; Kaitlin Fries, MSIII; Ashley Grigsby, MSIV; Nathan Haas, MSIV; Geoff Jara-Almonte, MD; Joseph P. Marquardt, DO; Alexandra Murray, MSIII; Aaron Pannier, MD; Lauren Sims, MSII; Jennifer Stancati, MSII; and Susan M. Whitmer, MD

Interested in writing?

Email submissions to:

Please submit articles by November 26th for the December/January 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 mey 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:

Blunt Eye Trauma
Isaac S Bruck, MD PhD
Metropolitan Hospital/New York Medical College

Patient was a 36-year-old male who, while working on a construction site, was struck against the right eye by a piece of ejected reinforcement steel. He was wearing protective goggles at the time. Patient was brought to the ED via EMS complaining of right eye pain and loss of vision. Upon initial exam he was noted to have folding of the superior-lateral aspect of the iris, miosis and loss of visual acuity in the right eye. He was able to detect light sensation and had positive consensual accommodation. Seidel sign was negative as was fluorescein staining.

Figure 1.

Patient arrives to your ED following blunt force trauma to the right eye with pain and decreased vision. Examination reveals moderate periorbital swelling, conjunctival hemorrhage and pupil as seen in the image above. Visual acuity is 20/30 in the left eye and light perception only in the right eye. Which of the following is the most appropriate management?

  1. Ocular ultrasound and emergency ophthalmology consultation
  2. Measure intraocular pressure and emergent ophthalmology consultation
  3. Timolol drops, intravenous acetazolamide and emergent ophthalmology consultation
  4. Eye shield, CT scan of the orbit and emergent ophthalmology consultation

Blunt trauma causes scleral rupture by suddenly elevating intraocular pressure. Ruptures are most common at the insertions of the intraocular muscles or at the limbus, where the sclera is thinnest. The diagnosis of scleral rupture is obvious when intraocular contents are visualized; however, occult global rupture can be difficult to diagnose. Patients complain of eye pain and decreased vision. Examination may reveal a bloody chemosis or severe subconjunctival hemorrhage overlying the scleral rupture site. When the rupture occurs at the limbus, an irregularly shaped (teardrop) pupil may also be seen. Indicators of globe rupture include hyphema (blood in the anterior chamber), loss of anterior chamber depth or deviation of the pupil toward the laceration. Severe subconjunctival hemorrhage involving the area 360 degrees around the cornea is also highly suspicious for globe rupture.

Although a lower than normal intraocular pressure is a good indication of rupture, tonometry should not be performed in suspected globe rupture. Any maneuvers that increase intraocular pressure need to be avoided. A CT scan, ultrasonography and indirect ophthalmoscopy all play a role in the diagnosis of occult globe rupture, but may be left to the ophthalmologist. In studies conducted between 1998 and 2003 evaluating CT for detecting clinically occult open-globe injuries, the sensitivity varied from 56% to 68%, depending on the observer.

Treatment in the ED for a known globe rupture includes avoidance of further examination or manipulation and the placement of a protective metal eye shield to prevent accidental pressure on the globe. The patient should be kept with nothing by mouth and a tetanus injection given as needed. Antiemetics should be given if the patient is nauseated. Broad-spectrum IV antibiotics should be instituted.

D is correct. The patient in the case scenario above had an acute posterior-lateral globe rupture identified on CT scan (Figure 2.). Negative Seidel sign misled the initial diagnosis. After dilation of the pupil by ophthalmology, the patient clearly had a “D-shaped or teardrop” pupil. Eye shield was placed, and the patient was taken to the operating room several hours later.

Figure 2.

Figure 2. CT scan of facial bones demonstrating retro-orbital fluid collection, decreased globe volume and irregular borders. These findings are consistent with globe rupture.


  1. Prabhat KP, Sanaz AL. Ocular emergencies. Am Fam Physician. 2007 Sep;76(6):829-36.
  2. Kubal WS. Imaging of orbital trauma. Radiographics. 2008 Oct;28(6):1729-39.
  3. Sharma R and Brunette DD in Marx JA, Hockberger RS, Walls RM, et al. (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 7. St. Louis, Mosby, Inc., 2010, Ch. 69: p 864.

Lesion of Merit
Stephen S. Austad, DO
Joseph P. Marquardt, DO
Aaron G. Pannier, MD
Susan M. Whitmer, MD
Naval Hospital Camp Pendleton

Twenty-two-year-old Caucasian male presents with a 10 week history of several skin lesions that appeared on his trunk and extremities. Lesions are 2mm to 2cm in diameter and are pruritic in nature. The patient initially attempted self-treatment with topical hydrocortisone with no improvement. The patient states this is the first episode of the lesions.

The patient’s vital signs are within normal limits. Physical exam is unremarkable except for his skin exam (images shown above). His medical history is remarkable for an upper respiratory infection prior to the onset of the rash, for which he did not seek medical treatment. His family history reveals a diagnosis of psoriasis in his mother and several second degree relatives. His only medication is the hydrocortisone he previously attempted, and has no known drug allergies.

What is the diagnosis?
Diagnosis: Guttate psoriasis

Psoriasis is a common skin disorder with a wide range of clinical manifestations. Variants of the disease include chronic plaque, erythrodermic, inverse, guttate, pustular and nail. The characteristic presentation is the development of inflammatory plaques of the skin. Guttate psoriasis (GP) is more prevalent in children and young adults, and many cases occur two to three weeks after streptococcal or viral upper respiratory infection.

Psoriasis affects 0.6-4.8 percent of the population, and less than 30 percent of these cases are GP. Guttate psoriasis is more common under age 30, and younger ages are more likely to be affected by the guttate variant. It affects both males and females with no general predominance.

GP normally presents with an acute onset of one to numerous well-demarcated, scaling, erythematous papules and plaques ranging in size from 2 to 15mm in diameter with a fine, adherent scale. “Guttate” refers to the discrete drop-like appearance of the lesions. It typically affects the trunk and proximal extremities, but can include the face, scalp, hands and feet. Generally, the palms of the hands and the soles of the feet are excluded. Lesions may or may not be pruritic.

The rash may present as a new disorder in patients without a history of psoriasis, or as a new presentation of the disease in patients with chronic plaque psoriasis. The diagnosis is made clinically, with biopsies occasionally used to confirm cases. There is no definitive serologic test for GP. Routine tests for streptococcal infection are controversial and may not be necessary without signs of strep infection. However, many patients do also have positive antistreptolysin O titers. Appropriate testing should be completed in patients with signs and symptoms of strep pharyngitis in order to treat the underlying condition.

Differential diagnosis for GP includes: nummular dermatitis, pityriasis lichen oides chronic, pityriasis rosea, small plaque parapsoriasis, secondary syphilis, tinea corporis, viral exanthems and morbilloform drug eruptions.

Class I human leukocyte antigen HLA-Cw6 and beta hemolytic streptococci are the primary linked factors to the disease. New cases of GP are preceded by streptococcal pharyngitis in 56-97 percent of patients and can include perianal streptococcal infection in children. It typically shows up two to three weeks after these infections or other viral upper respiratory infections. This correlation is more common in new cases, but patients already affected by chronic plaque psoriasis can acquire GP. It can also occur after varicella, Pityrosporum folliculitis, at tattoo sites and after tumor necrosis factor alpha therapy.

Treatment for GP is similar to chronic plaque psoriasis. Spontaneous recovery may occur in weeks to months. Some patients may elect for no treatment. Phototherapy, including narrowband UVB, broadband UVB, psoralen plus UVA and even five to 10 minutes of prime outdoor sun exposure without sunblock can improve GP. Topical treatments include topical corticosteroids once to twice daily for two weeks, and vitamin D analogs, such as calitriol and calcipotriene. These treatments can be used alone or in conjunction. GP is more responsive to therapy than chronic plaque psoriasis. For patients with recurrent GP, tonsillectomy and chronic plaque psoriasis systemic immunomodulatory and immunosuppressive treatments have been used. Systemic therapy is the next line treatment if the above topical medications do not improve the condition. Antibiotics are controversial, and data to support their use is not sufficient. However, active streptococcal infections should be treated as indicated.


  1. Habif, TP. Clinical Dermatology: A Color Guide to Diagnosis and Therapy, 5th ed. Maryland Heights, MO: Mosby; 2010:212.
  2. Mehlis, S. Guttate Psoriasis. Up to Date. Topic 15280 Version 2.0. Accessed via the web at on July 26, 2013.

Ultrasound: Applications in a Resource Poor Setting
Lauren Sims, MSII
University of California Irvine School of Medicine

Ultrasound is used daily in emergency departments across the United States. Against a remote international backdrop, ultrasound can make an even greater impact when medical providers have no other means of viewing the internal anatomy of their patients. This setting often combines economic and geographic barriers that isolate patients from care. The portability of newer ultrasound models, the ease at which they can be used and the cost of each unit in contrast to other imaging options, makes these machines the perfect fit as the medical diagnostic technology of choice in a resource poor environment.1,2 Whether it is in the middle of sub-Saharan Africa or a secluded island off the coast of Panama, ultrasound can play a critical role in improving the standard of care for patients.

Over the past summer, I had the privilege of volunteering with Floating Doctors and saw first-hand how impactful ultrasound can be in a rural setting.3 Floating Doctors is a non-profit medical relief team with the mission of reducing the present and future burden of disease in the developing world. They are currently stationed in Bocas del Toro, Panama, and travel to remote islands in the area to provide medical care for the Ngobe-Bugle (indigenous Panamanians). On a typical clinic day, program volunteers travel via boat with a suitcase full of medications, a procedure bag and ultrasound machines. These machines will be relied upon to diagnose conditions ranging from a renal cyst in a chronically dehydrated farmer to congenital heart defects in a young child. They expand upon the level of care Floating Doctors can provide since they give medical providers insight into the underlying cause of the patient’s diagnosis. For a patient who cannot afford to travel to the closest hospital, which can be hours to days away, these portable ultrasound machines often prove to be life saving.

The majority of my time with Floating Doctors was spent developing and implementing an obstetric ultrasound-screening program with a group of UC Irvine medical students. Our program had two main goals. The first was to scan women in the communities for high-risk complications, notably placenta previa, fetal lie and polyhydraminos. In addition to scanning the women ourselves, we introduced parteras, traditional midwives, in the community to the basics of obstetric ultrasound. For pregnant women, who are a few days trip from a hospital that can perform a cesarean section, catching placenta previa or a breech birth can not only be life saving for them, but for their baby as well. Throughout the month I was in Panama, I witnessed and performed several ultrasound scans that were concerning. We warned these women to deliver at the hospital in order to avoid complications, and in a few cases, arranged for direct transport to the hospital. Complicated pregnancies and deliveries lead to maternal and infant death worldwide. For these women in Panama, an ultrasound machine changed a potentially poor outcome.

Portable ultrasound machines can transform the care provided by medical providers in a resource poor international setting. For the patients, who often find themselves isolated from the healthcare they need, these machines can prove to be life saving.


  1. Nelson BP, Melnick ER, Li J. Portable ultrasound for remote environments, part II: current indications. The Journal of Emergency Medicine. 2011 March; 40(3): 313-321.
  2. Smith-Rohrberg M, Duncan, Schwarz R. Turning a blind eye: the mobilization of radiology services in resource-poor regions. Globalization and Health. 2010; 6(18).
  3. Floating Doctors:

Treatment of Jellyfish Stings
Nicole Battaglioli, MD
York Hospital

Jellyfish stings cause an estimated 150 million envenomations per year. The tentacles of the jellyfish contain venom-encapsulating stingers called nematocysts. When these specialized appendages come into contact with skin, they release enzymes and polypeptides into the body causing both local and systemic effects. The initial reaction to a jellyfish sting typically involves redness, itching, numbness and tingling at the site, as well as pustules or a rash forming in the pattern of tentacle exposure. Systemic effects can occur, resulting in muscle pain, vomiting, sweating, agitation, hypertension, chest pain and abdominal pain.

Various species of box jellyfish can cause a medical condition known as Irukandji syndrome, which is associated with major systemic effects. These envenomations usually occur off the coast of Australia but have been reported in Papua New Guinea, Hawaii, Fiji, Japan and China. The venom contains a sodium channel modulator, which causes systemic and pulmonary hypertension and increases cardiac output. Hypertension may also be related to catecholamine release after envenomation resulting in a “stress cardiomyopathy.” A second phase can occur after the initial envenomation 6-18 hours later resulting in cardiac failure with pulmonary edema. This may require treatment with diuretics, vasodilators, CPAP/mechanical ventilation and inotropes. In a retrospective evaluation of 12 cases of Irukandji syndrome, pulmonary edema was a common feature occurring at a mean time of 14 hours post-envenomation.

Many first aid remedies have been proposed to relieve the initial symptoms of jellyfish stings including: vinegar, warm urine, ammonia, hot water, sodium bicarbonate, meat tenderizer and cold water. A systematic review of treatment studies suggests that hot water/heat packs commonly decrease the symptoms of envenomation, predominately the perception of pain. Meat tenderizers such as papain or bromelain, as well as freshwater, saltwater and urea have generally shown to have no effect on symptoms. Studies suggest that methanol/ethanol, ammonia and acetic acid may increase symptoms of pain sensation. Topical lidocaine (4%) may help with symptom relief, and pain lasting more than a couple of days can be treated with topical steroids.

Attempted removal of tentacles may cause discharge of nematocysts, which would increase envenomation and symptoms. Nematocysts can often be “deactivated” with a vinegar rinse. Sea nettles and Portuguese man-of-wars can often be deactivated with a paste made of baking soda and salt water. After deactivation, stingers can be scraped off with a flat object, such as a credit card. The treatment of jellyfish stings is a topic of emergency medicine that providers should be aware of in a time when travel to warm water destinations is common and easy.


  1. Boulware DR. A randomized, controlled field trial for the prevention of jellyfish stings with topical sting inhibitor. J Travel Med. 2006 May-June; 13(3): 166-71.
  2. Little et al. Severe cardiac failure associated with preseumed jellyfish sting. Irukandji syndrome? Anaesth Insens Care. 2003; 31: 642-47.
  3. Tibballs et al. Australian carybdeid jellyfish causing “Irukandji syndrome.” Toxicon. 2012; 59: 617-25.
  4. Ward et al. Evidence-based treatment of jellyfish stings in North America and Hawaii. Annals of Emergency Med. 2012; 60(4): 399-414.

Critical Sample Collection in Pediatric Hypoglycemia
Nathan Haas, MSIV
Loyola University Chicago Stritch School of Medicine

A four-year-old boy with no significant past medical history is brought to the ED by his parents for “not acting right.” The boy was reportedly “slumped over his desk” at pre-school, and was complaining of feeling “jittery.” Upon examination, the child is alert with age appropriate behaviors, but appears diaphoretic and anxious. Vital signs are normal with the exception of tachycardia, and a thorough physical examination is otherwise within normal limits. A fingerstick blood glucose is 39mg/dL. What is your approach to managing this patient?

The definition of hypoglycemia remains controversial, with accepted blood glucose levels ranging from 40-75mg/dL. Signs and symptoms of hypoglycemia can be broadly characterized into autonomic symptoms (tachycardia, diaphoresis, tremulousness) and neuroglycopenic symptoms (confusion, lethargy, seizure, coma). The differential diagnosis for pediatric hypoglycemia is quite broad, and includes metabolic disorders, diabetes mellitus, ingestion (beta blockers, oral hypoglycemics, alcohol), hormone deficiencies, heart disease and recent surgery. The initial management of hypoglycemia at any age includes prompt reversal of hypoglycemia with identification and correction of an underlying cause.

However, pediatric patients with hypoglycemia present an interesting dilemma, and should be managed slightly differently. The critical sample is a laboratory panel that is essential to proper identification and diagnosis of an underlying cause of hypoglycemia. If at all possible, the critical sample should be drawn prior to reversal of hypoglycemia to provide the most diagnostic value. Typically, drawing an extra 5-10cc syringe of blood prior to administration of a reversal agent is sufficient.

The critical sample should be run for a variety of key substrates and glucoregulatory hormones, including glucose, insulin, free fatty acids, beta-hydroxybutyrate, lactate, carnitine, acylcarnitines, C-peptide, growth hormone, ammonia, amino acids and cortisol.

In addition, the first available voided urine sample is essential for diagnosis of an underlying etiology. Urine is typically tested for ketones, reducing substances, organic acids and toxicological screens. The remainder of the initial urine sample should be preserved and frozen, as further testing of the initial void is often warranted.

It is essential for the emergency physician to recognize that collection of the critical sample prior to reversal is invaluable in the diagnosis of neonatal or pediatric hypoglycemia. The differential diagnosis is expansive, and the underlying cause is often unidentifiable without proper laboratory evaluation. If the critical sample is not collected, the child often must fast in a controlled environment to “recreate” the hypoglycemic event so that a critical sample can be drawn at that time.

In a pediatric patient with hypoglycemia without a known underlying cause, draw an extra 5-10cc syringe of blood prior to reversing the hypoglycemia in order to run the critical sample. Promptly collecting a urine sample also provides invaluable diagnostic evidence.


  1. Critical Sample for Hypoglycemia. University of Minnesota Department of Pediatrics, Division of Endocrinology, n.d. Web. 22 Sept. 2013.
  2. Sunehag, Agneta, and Morey W. Haymond. Etiology of Hypoglycemia in Infants and Children. UpToDate, 2013. Web. 22 Sept. 2013.

Clinical Pearl: Valacyclovir Neurotoxicity
Jennifer Stancati, MSII
Loyola University Chicago Stritch School of Medicine

A 73-year-old woman with a history of ESRD developed a rash from herpes zoster three days ago and began treatment. She now presents to the ED with acute onset of visual hallucinations, agitation, confusion and disorientation. Studies include: unremarkable CBC and urinalysis, and head CT with no abnormalities.

What do you think is the cause of her altered mental status?

  1. Herpes encephalitis
  2. Valacyclovir neurotoxicity
  3. Urinary tract infection
  4. Alzheimer’s dementia
  5. Lewy body dementia

B is correct. Valacyclovir neurotoxicity (VAN) is a side effect seen in patients, especially the elderly or those with renal dysfunction, within 72 hours of initiation of treatment with valacyclovir. Valacyclovir is a prodrug of acyclovir that achieves higher serum concentrations more rapidly than acyclovir. It is often preferred to acyclovir because it is effective with less frequent administration. The dose at which valacyclovir is typically prescribed for herpes zoster can be as high as 4000 mg/day.

VAN has a number of different symptoms, including: disturbance of consciousness, hallucinations, confusion, ataxia, dysarthria, disorientation, delirium, unresponsiveness, agitation, irrational behavior, myoclonus, coma, obtundation, seizure, death delusions and photophobia.

Populations that are predisposed to VAN are elderly patients and patients with renal impairment, although cases have been seen in patients without renal impairment. Acute renal failure can also be caused by valacyclovir, further elevating blood levels and increasing the chance of VAN. In patients with preexisting renal impairment, dose adjustment of valacyclovir is recommended.

Recovery from VAN usually occurs within four days after cessation, although full recovery may take as long as two weeks. Treatment of VAN is primarily to stop valacyclovir. In extreme cases, hemodialysis may speed recovery if necessary.

VAN can be distinguished from option A, herpes encephalitis, because herpes encephalitis presents one week after the rash and is accompanied by headache, fever, and cranial nerve abnormalities. Option C, urinary tract infection (UTI), can present in the elderly with mental status changes; however, the UA and CBC in this patient were normal. Option D, Alzheimer’s dementia, would not have acute onset, as seen in this patient. Option E, Lewy body dementia, presents with symptoms of dementia, cognitive fluctuations, visual hallucinations and Parkinsonism, which is incorrect due to the lack of Parkinsonian symptoms and acute onset.

It is important that we keep VAN in mind when evaluating certain at-risk patients with altered mental status. Although VAN is very rare, with about 20 reported cases in the medical literature, shingles occurs in nearly one million individuals annually and is often treated with valacyclovir.


  1. Asahi T, Tsutsui M, Wakasugi M et al. Valacyclovir neurotoxicity: clinical experience and review of the literature. European Journal of Neurology. 2009; 16: 457-460.
  2. Kambhampati G, Pakkivenkata U, Kazory A. Valacyclovir neurotoxicity can be effectively managed by hemodialysis. European Journal of Neurology. 2011; 18: 33.
  3. Strumia S, De Mitri P, Bionda E. Neurotoxicity of acyclovir and valacyclovir in a hemodialyzed patient. European Journal of Neurology. 2004; 11: 67-70.
  4. Yawn BP, Saddier P, Wollan PC, St Sauver JL, Kurland MJ, Sy LS. A population-based study of the incidence and complication rates of herpes zoster before zoster vaccine introduction. Mayo Clin Proc. 2007; 82: 1341-9.

Foreign Body Ingestion
Alexandra Murray, OMSIII
Ohio University College of Osteopathic Medicine

Complications from foreign body ingestion affect thousands of people each year and are responsible for approximately 1,500 deaths annually.1,2 Foreign bodies can create a unique set of problems depending on whether they become lodged in the airway or GI tract. The course of treatment varies depending on the type of object ingested, the size of the foreign body and the patient’s age.

Aspirated Objects
Of aspirated foreign bodies, 80-90% become lodged in the bronchi whereas larger objects tend to become lodged in the larynx or trachea.3 The location of the obstruction can sometimes be deciphered by certain clinical cues. Laryngeal foreign bodies can present with hoarseness or aphonia, whereas tracheal obstructions may present with asthma-like wheezing. Patients with foreign bodies in the bronchus typically demonstrate cough, unilateral wheezing and/or decreased breath sounds.3

GI Foreign Bodies
Foreign bodies that are swallowed may become lodged at any point in the GI tract. Most foreign bodies that are identified in the esophagus must be removed, as well as foreign bodies that are too large to pass through the pyloric sphincter. Objects that reach the stomach can usually pass through the rest of the GI tract spontaneously without further complication. Foreign bodies that require immediate removal include objects that are very sharp, toxic (batteries) or magnetic. Safety pins, needles and other piercing objects must be removed immediately due to risk of bowel perforation.1-5 In the case of batteries, recent studies suggest that the real danger from batteries is not necessarily the leakage of alkaline material, but the development of a current through gastrointestinal tissues leading to hydrolysis of tissue fluids and production of hydroxide ions at the negative pole of the battery.6 Magnetic objects can be dangerous due to formation of magnetic fields that create pressure necrosis, fistulas and bowel perforation.4

Children under the age of four are the most common culprits of foreign body ingestion. Children may not present to the ED immediately if the event was unwitnessed since it may take time for complications to develop. Children with foreign body ingestion may appear asymptomatic or have vague symptoms such as dysphagia, weight loss, drooling, emesis, chest pain, sore throat, stridor, cough, altered mental status or fever.1-5 Typically, ingested foreign bodies include bones (fish, chicken) and common household items such as small toys, beads, button batteries and erasers. Coins are the most common ingested object by children (70% of reported cases), whereas peanuts are the most common objects to be aspirated.1-5

Unlike children, adults tend to present to the ED immediately after foreign body ingestion since the majority of events are accidental. Obstructive lesions or motility disorders of the esophagus such as GERD, hiatal hernia, abnormal rings/strictures and eosinophilic esophagitis have been identified as risk factors for acute food impaction.1,5 Individuals with these risk factors who develop obstruction have the predisposition to choke on poorly chewed meat, leading to the disorder known as “steakhouse syndrome.”7 Accidental ingestion may occur in “body packers” or “body stuffers” who have been known to ingest packaged illegal substances (heroin, cocaine) in order to avoid detection. If these packages rupture within the carrier, toxicity can occur rapidly.8

Diagnostic Testing and Treatment
Initial evaluation typically involves AP and lateral X-rays of the airway and chest. Radiopaque objects will readily appear, and radiolucent objects may be appreciated by looking for secondary signs of airway compression, atelectasis and hyperinflation. Ingestion of a small amount of contrast material may allow visualization of filling defects and confirm the presence of a radiolucent foreign body. However, this may increase the risk of aspiration and obscure endoscopy visualization and you should consult your GI specialist beforehand. Handheld metal detectors are sensitive and specific for identifying ingested metal objects.1-5,9

There are several techniques that are used to relieve obstructions. However, the most commonly used technique with the highest success rate is flexible endoscopy. The flexible endoscope has lower complication rates and higher patient comfort ratings compared to other instruments.1-5 If the obstruction does not require emergent removal and a less invasive approach is desired, glucagon can be administered to promote passage of a bolus by reducing the resting pressure of the smooth muscle at the lower esophageal sphincter.10


  1. Crockett SD et al. Emergency care of esophageal foreign body impactions: timing, treatment modalities, and resource utilization. Dis Esophagus. 2013 Feb-Mar;26(2):105-12.
  2. Alrazzak BA, Al-Subu A, Elitsur Y. Etiology and management of esophageal impaction in children: A review of 11 years. Avicenna J Med. 2013 Apr;3(2):33-6.
  3. Oncel M, Sunam GS, Ceran S. Tracheobronchial aspiration of foreign bodies and rigid bronchoscopy in children. Pediatr Int. 2012 Aug;54(4):532-5.
  4. Jayachandra S, Eslick GD. A systematic review of paediatric foreign body ingestion: presentation, complications, and management. Int J Pediatr Otorhinolaryngol. 2013 Mar;77(3):311-7.
  5. Sperry SL et al. Esophageal foreign-body impactions: epidemiology, time trends, and the impact of the increasing prevalence of eosinophilic esophagitis. Gastrointest Endosc. 2011 Nov;74(5):985-91.
  6. Marom T et al. Battery ingestion in children. Int J Pediatr Otorhinolaryngol. 2010 Aug;74(8):849-54.
  7. Stadler J et al. The "steakhouse syndrome." Primary and definitive diagnosis and therapy. Surg Endosc. 1989;3(4):195-8.
  8. Beckley I et al. Clinical management of cocaine body packers: the Hillingdon experience. Can J Surg. 2009 Oct;52(5):417-21.
  9. Brown JC et al. The utility of adding expiratory or decubitus chest radiographs to the radiographic evaluation of suspected pediatric airway foreign bodies. Ann Emerg Med. 2013 Jan;61(1):19-26.
  10. Thimmapuram J, Oosterveen S, Grim R. Use of glucagon in relieving esophageal food bolus impaction in the era of eosinophilic esophageal infiltration. Dysphagia. 2013 Jun;28(2):212-6.

Pediatric Boric Acid Poisoning
Kaitlin Fries, MSIII
Ohio University College of Osteopathic Medicine

Boric acid is a common component of many household cleaning products and pesticides. It was formerly used in the medical community to irrigate body cavities, but was discontinued when its potential toxicity was discovered.2 Due to the decrease in medicinal use, it is very rare for emergency rooms to see cases of boric acid poisoning.2 Of those cases reported, it is typically an infant or child that has been affected due to the large amount of borate that would have to be ingested for an adult to experience toxicity.

Boric acid is an inorganic acid that is well-absorbed through mucus membranes and broken skin surfaces. There are no documented cases of toxic effects when absorbed through intact skin.2 Boric acid is water soluble allowing it to be distributed throughout the body especially in the brain, liver, and kidneys.2 On average, normal individuals have blood levels of approximately 1.4-2.5μg/ml of boron from ingesting common foods such as orange juice, vegetables, fruits, bread and cereal.1 Toxic symptoms are seen when blood levels reach 20-150μg/ml.1

Initial symptoms of toxicity tend to be nonspecific and may be mistaken for gastroenteritis. Typically, persistent blue green emesis is seen with or without similarly colored loose stools.1-3 The most characteristic symptom is the “boiled lobster” rash that is seen in 76% of cases.2 This exanthem starts out in a localized region and then spreads to the child’s entire body within a day. Two to three days later, desquamination occurs leading to the “boiled lobster” appearance.1-3 In severe cases, central nervous system symptoms such as convulsions may occur. Laboratory findings may include hypernatremia, hyperchloremia and metabolic acidosis.2

Not all cases require intervention. In a study of 784 cases of acute ingestions, 83% of patients were entirely asymptomatic and none developed severe symptoms.3 In symptomatic cases, treatment is focused on evacuation of the gastric contents. To date, no specific antidote has been identified to reverse boric acid poisoning and administration of activated charcoal has proven to be ineffective.1 The Maryland Poison Control Center recommends peritoneal dialysis be started if severe symptoms are present or when serum levels are >200μg/ml.1


  1. Baker MD, Bogema SC: Ingestion of boric acid by infants. Am J Emerg Med. 1986;4:358-361.
  2. Hamilton RA, Wolf BC. Accidental boric acid poisoning following the ingestion of household pesticide. JForensic Sci. 2007; 5.
  3. Livovitz TL, Klein-Schwartz W, Oderda GM, Schmitz BF. Clinical manifestations of toxicity in a series of 784 boric acid ingestions. Am J Emerg Med. 1988;6:209-13

The Impact of the Affordable Care Act on Emergency Medicine
Jenna Erickson, MSIII
Chicago Medical School

The Patient Protection and Affordable Care Act, commonly called Obamacare or the Affordable Care Act (ACA), represents the most significant regulatory overhaul of the country's health care system since the passage of Medicare and Medicaid in 1965. The ACA aims to increase the quality and affordability of health insurance by lowering the uninsured rate through expanded public and private insurance coverage.1 Ultimately, the ACA aims to lower health care costs for individuals, corporations, and the government. As new residents prepare to enter the practice of emergency medicine, they must be aware of the potential impact of the ACA.

The next major implementation of the ACA is scheduled to take effect January 1, 2014. Under this policy, an estimated 25 million Americans who are currently uninsured will be required to carry health insurance.2 Whether this policy change will have a positive or negative effect on emergency medicine has been a topic of hot debate.

A potential positive outcome as a result of the ACA is the financial gain for hospitals due to insurance reimbursements. This effect has already been demonstrated with the recent ACA provision extending insurance coverage for patients aged 19-25 years. According to a study published in the May 2013 issue of the New England Journal of Medicine, increasing coverage for these patients led to roughly $147 million in emergency medical costs being billed to private insurance. Though increased insurance may yield less financial burden on emergency departments, the volume of patients may still prove problematic.

Emergency department overcrowding is one of the issues the government hopes the ACA will alleviate. Theoretically, requiring health insurance will increase access to primary care, therefore reducing the number of emergency department visits for non-emergent conditions. However, the proportion of uninsured patients does not account for the current crowding situation in most emergency department. According to the Department of Health and Human Services, patients receiving Medicaid account for nearly half of all emergency room visits. Many argue that this is due to a lack of primary care providers accepting Medicaid patients. With an estimated one-third of the uninsured projected to receive Medicaid, an increase in available primary care providers who accept Medicaid will be needed to prevent overcrowded emergency rooms.

What will the next phase of ACA bring to the emergency room? Will the volume of patients remain stable, but the financial burdens ease? Will more patients seek primary care as opposed to emergency care and ease overcrowding? Or will an increase of Medicaid patients cause emergency care overcrowding to become worse? Only time will tell.


  1. The Affordable Care Act, Section by Section. U.S. Department of Health and Human Services. 2013. Available at: Accessed September 19, 2013.
  2. Key Features of the Affordable Care Act by Year. U.S. Department of Health and Human Services. 2013. Available at: Accessed September 19, 2013.

Indications for CT in Pediatric Head Trauma
Ashley Grigsby, MSIV
Arizona College of Osteopathic Medicine

Between the years of 1995 and 2001, children with head injury ages 0 to 14 accounted for about 435,000 emergency department visits. Approximately 3,000 children die each year from head injuries. When evaluating children after head trauma, it is important to identify those that will require acute neurosurgical intervention (clinically important traumatic brain injury or ciTBI). Head CT is often used for evaluation of brain injuries in the emergency department. However, CTs may identify minor injuries that do not require intervention, and pediatric patients may be at increased risk for future malignancy from radiation exposure. For these reasons it is important to properly risk stratify pediatric patients to identify clinically important injuries while avoiding unnecessary radiation associated with CTs.

The PECARN (Pediatric Emergency Care Applied Research Network) rules for pediatric head CT were derived and validated by Kuppermann et al. Their rules can aid decision making to decrease the number of CTs performed, without missing those requiring intervention. The rules are divided by age and mechanism of injury.

Severe mechanism of injury is considered any of the following:
MVC with ejection, MVC with death of another passenger, roll over MVC, pedestrian without helmet struck by car, falls greater than 3 feet if age less than two years old, falls greater than 5 feet if age greater than two years old, or struck in head by high impact object.

The following are the recommendations on evaluation of children with blunt head trauma.

Less than two years old
First, assess the Glascow Coma Scale (GCS) and mental status of the patient and for skull fracture. If GCS <14 or signs of altered mental status, or palpable skull fracture, the risk of ciTBI is 4.4% and CT scan is recommended. If neither of these is present, you should assess for the following: occipital, parietal or temporal scalp hematoma, history of >5 seconds of loss of consciousness or severe mechanisms of injury. If the history is positive for any of those factures, risk of ciTBI is 0.9% and the physician can choose either CT or observation. If all of the factors are negative, then the risk of ciTBI is <0.05% and CT is not recommended.

Greater than two years old
First, assess the GCS and look for signs of basilar skull fracture (battle sign, periorbital bruising, haemotympanum, CSF rhinorrhoea or CSF otorrhoea). If GCS <14 or there are signs of basilar skull fracture, the risk of ciTBI is 4.3% and CT is recommended. If neither is present, you should assess the following: history of loss of consciousness, history of vomiting, severe mechanism of injury or severe headache. If any of these are present, the risk of ciTBI is 0.9% and the physician can choose observation vs. CT scan. If none of the factors are present, the risk of ciTBI is <0.05% and CT is not recommended.

These rules give clinicians an objective way to evaluate the need for head CTs in children. It is important to remember that CTs are not without risk and should not be used in every patient.

The full publication with an evaluation algorithm is available for free from the PECARN website,


  1. Kuppermann N et al. Identifying children at very low risk of clinically-important traumatic brain injuries after blunt head trauma. Lancet. 2009:374 1160-70.
  2. Schutzman S. Minor head trauma in infants and children. Up to Date. [Internet] 2013 [cited 2013 September 13].

Indications for Thrombolysis in Submassive PE
Thomas Doran, OMSIV
Lake Erie College of Osteopathic Medicine

The use of alteplase in patients with sub-massive PE is controversial. Sub-massive PE is defined as a patient who is hemodynamically stable but with evidence of right heart strain.1 Although patients may benefit from clot lysis, this must be balanced with the risk of bleeding complications. The 2011 guidelines for the use of fibrinolysis in PE attempt to address this issue. The guideline definitions of sub-massive PE includes PE with EKG changes indicating right heart strain (such as S1Q3T3 changes or changes suggesting anteroseptal ischemia), but require demonstrated RV enlargement on CT, or Echo, or an elevation in troponin or BNP prior to considering initiation of fibrinolysis.

Per the guidelines, the primary treatment goal with thrombolysis in sub-massive PE is not reduction in mortality, but rather, improved quality of life and long-term pulmonary function. The short-term mortality of sub-massive PE treated solely with anticoagulation (e.g., heparin and warfarin) is already excellent at <3.0%. Rather, secondary adverse outcomes such as persistent RV dysfunction, CTEPH (chronic thromboembolic pulmonary hypertension) and impaired quality of life represent primary goals of treatment. Particularly in the young person, whose risk of hemorrhage is low, there is an opportunity to intervene to prevent adverse long-term outcomes of PE.1 With alteplase, some argue that we can improve outcomes by preventing sub-massive PE patients from becoming “pulmonary cripples.”3

Use of thrombolytics for sub-massive PE is supported by the AHA guidelines if the aforementioned conditions are met; however, many practitioners have been hesitant to pursue this route until larger scale trials have demonstrated the benefits. With this in mind the MOPPET (Moderate Pulmonary Embolism Treated with Thrombolysis) and the PEITHO (Pulmonary Embolism Thrombolysis) studies are two large scale randomized controlled trials, which were designed to demonstrate the safety and efficacy of alteplase treatment in less than massive PE — both showed positive outcomes.3,4


  1. AHA Scientific Statement. Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension. Circulation. 2011; 123: 1788-1830
  2. Weingart, Scott. EMCrit Wee – The MOPPET Trial. December 2012.
  3. Nainggolan, Lisa. PEITHO: Persuasive for Thrombolysis in PE? Mar 12, 2013.
  4. Nainggolan, Lisa. MOPETT: Is Half-Dose Thrombolysis Feasible for Moderate PE? Heartwire Conference News. Mar 27, 2012.

Risk Stratification for Pulmonary Embolism
Geoff Jara-Almonte, MD
Hennepin County Medical Center

How do you decide who needs a workup for PE? Who needs a D-dimer? Who needs a CT? You need to decide on the pre-test probability — the risk — that your patient has a PE.

Clinical Gestalt
In one meta-analysis, experienced physician judgment was comparable with clinical decision rules.1 A more recent retrospective analysis found unstructured judgment performed better than either the Wells or Geneva scores in stratifying patient to low and high risk.2 However, this study was limited by being a retrospective analysis of a prospective cohort, and by the high prevalence of PE (30%) in their patient population, and thus, the results may not be as applicable to American populations where prevalence is generally much lower.3

Wells Score
The Wells Score is a validated clinical decision rule that takes into account six variables, each assigned a weighted point value to come up with a final score. Patients are stratified into low, intermediate and high risk categories. It relies heavily on clinician gestalt — the two most important variables are “signs and symptoms of DVT” and “PE is the most likely diagnosis.” In the original protocol a score of less than two was low risk and those patients could be ruled out with a negative D-dimer. All others were imaged. Subsequent validation studies have used a dichotomized yes/no approach. They called a score less than four “PE unlikely” and showed that those patients could be safely ruled out with a negative D-dimer.4

A recent meta analysis, again, demonstrated the safety of both the original and dichotomized Wells score at ruling out PE. It also suggested that intermediate probability patients (Wells <7) could be safely ruled out with a negative highly sensitive D-dimer in populations with a low prevalence of PE, though this is not standard of practice.5

Some authors have suggested that in low risk (Wells <4) or elderly patients, a modified D-dimer cutoff of twice normal could be used with significant reduction in imaging and only a small sacrifice in sensitivity. This was prospectively evaluated by Kline in a recent study, but has yet to be replicated.6

The PERC Rule was developed to identify those patients at extremely low risk of PE in which the benefit of further testing would be outweighed by the risks.7 The rule takes into account eight variables; absence of all eight in a low risk patient can safely exclude PE. A recent meta-analysis of 12 studies found a sensitivity of 97% and negative predictive value of 0.17.8

The rule has limitations: it was derived from a population with a low prevalence of PE, 11%, and has not performed well in higher-prevalence populations.9 The prospective validation population was comprised of patients in which clinicians thought a negative D-dimer would exclude PE, or patients who by the Wells score would stratify as low-risk or PE-unlikely. Its applicability is restricted to only these populations.


  1. Sanjeev D et al. Does This Patient Have Pulmonary Embolism? JAMA. 2003;290(21):2849-2858.
  2. Penaloza A et al. Comparison of the unstructured clinician gestalt, the wells score, and the revised Geneva score to estimate pretest probability for suspected pulmonary embolism. Ann Emerg Med. 2013 Aug;62(2):117-124.
  3. Ceriani E. Clinical prediction rules for pulmonary embolism: a systematic review and meta-analysis. J Thromb Haemost. 2010 May;8(5):957-970.
  4. Wolf SJ et al. Prospective validation of Wells Criteria in the evaluation of patients with suspected pulmonary embolism. Ann Emerg Med. 2004 Nov;44(5):503-510.
  5. Ceriani E. Clinical prediction rules for pulmonary embolism: a systematic review and meta-analysis. J Thromb Haemost. 2010 May;8(5):957-970.
  6. Kline, JA et al. D-dimer Threshold Increase with Pretest Pobability Unlikely for Pulmonary Embolism to Decrease Unnecessary Computerized Tomographic Pulmonary Angiograpy. J Thromb Hemost. 2012 10:527-81.
  7. Kline, JA et al. Clinical Criteria to Prevent Unnecessary Diagnostic Testing in Emergency Department Patients with Suspected Pulmonary Embolism; J Thromb Hemost; 2004;12:1247-1255.
  8. Singh, B et al. Diagnostic Accuracy of Pulmonary Embolism Rule-Out Criteria: A systematic Review and Meta-analysis. Ann Emerg Med. 2012;59(6);517-520.
  9. Huli, O et al. The Pulmonary Embolism Rule-Out Criteria (PERC) Rule Does Not Safely Exclude Pulmonary Embolism. J Thromb Hemost. 2010;9:300-304.