Modern Resident - The newsletter of AAEM/RSA
February/March 2016
Volume 8: Issue 3 | Facebook  Twitter  LinkedIn

Inside This Issue


Zika: An Emerging Infection
Danielle Goodrich, MD
Stanford/Kaiser Emergency Medicine

Zika virus is an important emerging mosquito-born infection. Zika virus is a member of the Flavivirus family, which is related to Dengue fever, Yellow fever, West Nile fever and Japanese Encephalitis. Recent outbreaks of Zika virus in different regions of the world underscore the importance for emergency physicians to be familiar with the disease and its possible sequelae.

The Zika virus is primarily transmitted through a bite from the Aedes mosquito. There is some evidence to suggest the Zika virus can also be transmitted through blood transfusions, perinatal transmission and sexual transmission. Symptoms of Zika are similar to other Arbovirus infections such as Chikungunya and Dengue.

Patients present with fever, myalgias, arthralgias, conjunctivitis and a maculopapular rash.2 Joint swelling, especially of the hands and feet, may also be present. Resembling Dengue fever, patients may complain of headache and retro-orbital pain. The infection is self-limiting and symptoms last two to seven days. Asymptomatic infection is common with only 20% of patients manifesting symptoms. Treatment is supportive.

There have been reports of an increase in Guillain-Barre Syndrome and other neurological symptoms in the context of Zika outbreaks.1 A link between Zika virus infection in pregnant women and subsequent birth defects is being investigated. Recently in Brazil, more than 1,000 cases of microcephaly were reported among newborns born to Brazilian mothers. In two cases, the Zika virus was isolated from the amniotic fluid of the mothers.

Prevention is key. There is no vaccine available. The Aedes mosquitoes are day-biting mosquitoes. Travellers to high-risk areas should use repellants, wear light colored and long sleeve shirts and pants, and ensure rooms are fitted with screens.2 Consider Zika fever in a returning traveller with a fever from an infected region.


  1. Kelser EA, Meet Dengue's cousin, Zika. Microbes and Infection (2015),
  2. Centers for Disease Control and Prevention. Zika Virus. 31 Dec. 2015. Web. 03 Jan. 2016.



Physician Advocacy: Disability Coverage for the EP
Linda Sanders, MD
Temple Unviersity Hospital

As a new generation of residents prepares to enter private and academic practice as attending emergency physicians, most intend to practice emergency medicine for the next 30 years, maybe more. But in an environment that demands that we have fine motor skills, quick decision making abilities, fast communication and the ability to practice at least eight hours a day, a physical or mental ailment can make one incapable of EM practice. The incidence of disability among practicing physicians is around 2-10%.2

As physicians, our greatest asset is our future earning potential. Thus it’s important to be informed about disability insurance, the minutia of the language within these policies, and what the options are for coverage from employers as compared to group or individual policies.

In terms of eligibility for these insurance policies, young, healthy, full-time physicians are most eligible. Policies place exclusions on pre-existing conditions and mental illness.3 Additionally they are priced based on age; so purchasing disability insurance earlier is better. There are also special offers only available to residents.

The most important aspect of any physician disability insurance policy is an Own-Occupation definition of disability, meaning that if you cannot practice emergency medicine you are considered disabled. Be aware that there are variations of this definition, which provide less coverage or change the definition after a certain number of years.

The ideal policy is non-cancelable and guaranteed renewable, meaning that they cannot cancel your policy or raise your premiums. Also take into account the waiting period before you are eligible to receive benefits, as this can be anywhere between 30 days to a year. Residual disability defines the length of coverage and the benefit amount, which are obviously important aspects, but a cost of living adjustment (COLA rider) is also important to ensure that your income increases every year to account for inflation. Be aware that employer provided benefits are not typically portable whereas individual policies will move with you to your new job.

Many physicians are quick to purchase life insurance, but often fail to consider the fact that one is much more likely to become disabled than die a premature death. Thus, seek coverage early when you are eligible for the most benefits and may avoid financial catastrophe in the future.


  1. Binder DS, Sklar DP. Disability issues in emergency physicians. Ann Emerg Med 2008 Jun; 51(6): 732-736.
  2. DeLisa JA, Thomas P. Physicians with disabilities and the physician workforce: a need to reassess out policies. Am J Phys Med Rehabil. 2005;84:5-11.
  3. Mcnamara RM, Ufberg JW. Emergency physician hiring practices: The effects of certain conditions on employability. J Emerg Med 2000; 18(1): 17-20.
  4. Ruffing MS. Disability insurance for emergency physicians: What you need to know, now!,-now!


Eyelid Lacerations
Kaitlin Fries, DO
Doctors Hospital

Eyelids are often one of the more complex locations for providers to perform laceration repairs. The eye has many important neighboring structures that can often be damaged by even minor trauma to the eye. As with any wound, it is important to start by doing a thorough exam of the tissue involved, being sure to assess for the possibility of a retained foreign body. Once the area has been evaluated it is time to ensure that a few critical nearby anatomical structures are still intact.

  1. Lacrimal canaliculus and nasolacrimal duct: Injuries to the tear ducts will present with a large amount of tears running down the patients face.2 Injury to these structures is typically seen with lacerations to the medial aspect of the lower lid.2 If missed the patient can experience chronic eye tearing.2
  2. Medial palpebral ligament: Patients who present with a “cross-eyed” appearance should be assessed for a laceration of the medial palpebral ligament.2
  3. Levator palpebrae muscle: Injuries to this muscle most commonly present as traumatic ptosis, as the function of the levator is to hold the eye in its normal position while open.2 Any laceration to the upper eyelid with periorbital fat extruding from it should raise suspicion for levator palpebrae injury.2

All of the injuries above, as well as those lacerations involving the inner surface of the eyelid, should be referred to an ophthalmologist for closure.1,2 For all uncomplicated eyelid lacerations, it is recommended to use a single layer closure with 6-0 nonabsorbable suture.1,2 Repairing lacerations that involve the lid margin requires very precise work to ensure the lid margins are properly aligned. Most texts recommend that this type of repair be referred to a consultant, such as plastic surgery.1,2 There is no need to apply a dressing, as this is likely to cause more discomfort to the patient.

Eyebrow lacerations are typically simple and uncomplicated. It is not recommended to shave or trim the eyebrows.2 Using 5-0 nonabsorbable suture, start by placing a few sutures to align the superior and inferior margins of the brow hair.2 If necessary, next place a few deep sutures to approximate the superficial fascia.2 Then finish the repair with a simple interrupted closure. Once again, no dressing is necessary. For all eyelid and eyebrow lacerations, patients are recommended to perform daily wound care by cleaning and applying antibiotic ointment. Suture removal is generally scheduled in three to five days.1,2


  1. Tintinalli J. Emergency wound management In: Tintinalli's emergency medicine: Just the facts 2013: (3)54.
  2. Trott A. Special anatomical sites In: Wounds and lacerations: Emergency care and closure 1997: (2): 86-189.

Case Presentation: 80-Year-Old With a Bullous Rash
Avram Flamm, MS4
New York Institute of Technology - College of Osteopathic Medicine

An 87-year-old Hispanic male with a past medical history of diabetes mellitus type II, hyperlipidemia, hypertension, seizure disorder secondary to a neurocysticercosis infection, hypothyroidism and neuropathic pain presents with a persistent pruritic rash and blisters that started on his upper extremities and spread to his trunk and lower extremities in the past few days. The patient last visited his PCP four weeks ago and his medications include amlodipine, glipizide, thyroxine, finasteride, simvastatin, omeprazole, aspirin, enalapril, carbamazepine and gabapentin.

On physical exam, his initial vital signs include heart rate 80, BP 150/60 and temperature 97.3°F. The patient appears uncomfortable in bed due to excoriations. There are multiple excoriated erythematous plaques on his arms, legs and torso with multiple tense bullae and erosions ranging in size from 0.5-1.2cm. There was no involvement of face, oral mucosa or web spaces. Remainder of physical exam is unremarkable.

View larger image.

What is the best answer describing a diagnosis and plan?
A. Stevens-Johnson Syndrome, Fluids, Refer to burn center
B. Bullous Pemphigoid, Discontinue Medication
C. Cysticercosis, Ultrasound nodules to confirm, Albendazol
D. Pemphigus Vulgaris, Prednisone
E. Fixed Drug Eruption, Dermatology Consult

Answer: B

Bullous pemphigoid (BP) is the most common autoimmune blistering dermatosis caused by autoantibodies directed against the dermoepidermal junction, which leads to an inflammatory cascade causing separation of the epidermis from the dermis. This disease process is commonly seen in the elderly population and manifests with subepidermal vesicles and tense bullae.

BP has been noted to be medication-induced in some cases, and therefore potentially offensive medications should be discontinued. Most notably, in a case-control study comparing the drug history of consecutive patients with BP and control subjects, a statistically significant odds ratio was found in association of previous loop diuretics use and BP. However, the mechanism through which the disease is induced is not well understood. A few case control studies have found that patients with BP are more likely to have various neurological diseases, schizophrenia, psoriasis, cerebrovascular disease and dementia prior to the diagnosis of BP.

Treatment of BP includes oral and topical corticosteroids, steroid-sparing agents such as azathioprine, mycophenolate mofetil, tetracyclines with or without nicotinamide, dapsone, cyclophosphamide, intravenous immunoglobulin (IVIG), plasmapheresis and rituximab. The goal of treatment is to stop disease progression, reduce pruritus and stimulate blister healing.

This case is less consistent with Stevens-Johnson Syndrome, which would include flaccid bullae, positive Nikolsky sign, mucosal involvement and systemic symptoms (ie, fevers). Pemphigus Vulgaris differs from BP as the presentation commonly includes flaccid bullae, positive Nikolsky sign, mucosal involvement and positive Asboe-Hansen sign (bullae spreading).


  1. Daniel SB, Borradori L, Hall PR, Murrell DF, Evidence-based management of Bullous Pemphigoid, Dermatol Clin 29 (2011) 613–620.
  2. Zachariae COC. Gabapentin-induced Bullous Pemphigoid, ActaDermVenereol. 2002;82(5):396-7.
  3. Lloyd-Lavery, Chi, Wojnarowska. The associations between Bullous Pemphigoid and drug use, JAMA Dermatol. 2013;149(1):58-62.
  4. Gonzalez-Sicilia L, Cano A, Serrano M, Hernandez J. Stevens-Johnson syndrome associated with gabapentin. Am J Med 1998; 105: 455.
  5. Chen Y, Wu C, Lin M, et al. Comorbidity profiles among patients with bullous pemphigoid: A nationwide population-based study. Br J Dermatol. 2011;165(3):593-599.
  6. Taghipour K, Chi C, Vincent A, et al. The association of bullous pemphigoid wit hcerebrovascular disease and dementia: a case-control study. Arch Dermatol. 2010;146(11):1251-1254.
  7. Ruocco V, Sacerdoti G. Pemphigus and bullous pemphigoid due to drugs. Int J Dermatol 1991; 30: 307–312.

Button Batteries
Phillip Fry, MSIV
Midwestern University - Arizona College of Osteopathic Medicine

Patients presenting to the emergency department after ingesting a button or cylindrical battery typically warrant prompt foreign body removal. The majority of battery ingestion cases involves button batteries and occurs in children younger than six years of age.1 However, there is also a growing number of ingestions in the elderly with hearing aid batteries being mistaken for pills.

There are several mechanisms by which a battery can damage the esophagus, which is the most common site of injury after ingestion. The flow of electric current from the battery through the surrounding tissue occurs near the negative pole, and can cause local hydrolysis, hydroxide accumulation, and corrosive tissue injury.2 Even discharged or “dead” batteries still retain enough voltage to cause injury by producing an electric current.

A second method by which a battery ingestion can cause complications is the leakage of acidic contents. Once a battery makes it through the esophagus into the stomach, the acidity of the environment can erode the battery’s seal, releasing its contents. These contents cause liquefaction necrosis and saponification of lipid membranes.3 Another major complication is pressure necrosis from the battery lodging at a single site, causing irritation, inflammation and ischemia. These complications lead to serious sequelae such as esophageal burns, perforation or fistulas.

It is important to determine both the type of battery ingested and the time of ingestion. Most large diameter (≥20mm) batteries are lithium cells and are associated with the most severe sequelae, including death.4 Damage to the esophagus may be seen as early as two hours after ingestion, with most severe injury occurring after eight to 12 hours. Localization of the battery through radiographs and prompt removal in symptomatic or asymptomatic individuals are the proper next steps. If left untreated, button batteries in the esophagus can lead to complications including perforation, stricture, fistula, massive hemorrhage and death.


  1. Litovitz T, Whitaker N, Clark L. Preventing battery ingestions: An analysis of 8,648 cases. Pediatrics. 2010;125(6):117.
  2. Litovitz TL. Button battery ingestions. A review of 56 cases. JAMA. 1983;249(18):2495.
  3. Kost KM, Shapiro RS. Button battery ingestion: A case report and review of the literature. J Otolaryngology. 1987;16(4):252.
  4. Litovitz T, Whitaker N, Clark L, White NC, Marsolek M. Emerging battery-ingestion hazard: Clinical implications. Pediatrics. 2010;125(6):1168.

Uremic Frost
Alexandra Murray, DO
Mercy St. Vincent Medical Center

Patients with chronic renal failure can present with a myriad of dermatological complaints. One of the most unique cutaneous disorders that can afflict severely uremic patients is uremic frost.1-3 Uremic frost appears as diffuse, white, friable deposits of crystalline material that is most commonly found on the face of patients with severe azotemia.1-3 Hirschsprung first described uremic frost in 1865, but this manifestation is rarely seen in first world countries secondary to the widespread availability of hemodialysis.1-2

The theory behind the pathophysiology is that when blood urea nitrogen levels are elevated, the concentration of urea and other nitrogenous waste products in sweat increases dramatically. These waste products then crystallize and deposit on the skin creating the white, frost-like appearance.1-3 One study estimated that uremic frost has an incidence of 3% for all cutaneous manifestations of renal failure.4 Considering how rare this condition is, it is important to differentiate uremic frost from more common dermatologic conditions in renal patients, such as retention keratosis, eczema and post-inflammatory desquamation.1

If there is a high suspicion of uremic frost based on history and presentation, the “frost” can be tested by diluting scrapings of the crystalline material in normal saline and testing for urea nitrogen levels that are comparable to serum urea levels.1-2 The frost will gradually disappear once the azotemia resolves. Images of uremic frost can be found at:


  1. Kuo CC, Hung JB, Tsai CW, Chen YM. Uremic Frost. CMAJ. 2010 Nov 23;182(17):E800.
  2. Mathur M, D'Souza AV, Malhotra V, Agarwal D, Beniwal P. Uremic Frost. Clin Kidney J. 2014 Aug;7(4):418-9.
  3. Bhattarai N, Panda M. Uremic Frost. Mayo Clin Proc. 2008 Dec;83(12):1309.
  4. Udayakumar P, Balasubramanian S, Ramalingam KS, Lakshmi CR, Srinivas CR, Mathew AC. Cutaneous manifestations in patients with chronic renal failure on hemodialysis. Indian J Dermatol Venereol Leprol. 2006 Mar-Apr;72(2):119-125.
  5. Walsh SR, Parada NA. Images in clinical medicine. Uremic frost. N Engl J Med. 2005 Mar 31;352(13):e13.

Acute Mountain Sickness Overview and Treatment
Joshua Nelson, MSIV
Loyola University Chicago Stritch School of Medicine

Scrapes, bruises, and blisters are commonplace in the backcountry, but no ailment more commonly interferes with activities at altitude than acute mountain sickness. Known colloquially as altitude sickness, acute mountain sickness (AMS) presents with a wide array of symptoms and intensity. Relative hypovolemia, fluid retention/redistribution, minor increases in intracranial pressure and endothelial cell dysfunction may result in headache, anorexia, insomnia, nausea, vomiting, fatigue, dizziness, paresthesias and dyspnea.

Hypobaric hypoxemia is the physiologic factor responsible for the above array of symptoms. As altitude increases, the partial pressure of oxygen (and all of the gases that comprise air) decreases. At an alveolar oxygen pressure of ~70mmHg, peripheral chemoreceptors in the carotid body activate the medullary respiratory centers and initiate hyperventilation. This compensation for hypoxemia results in a respiratory alkalosis, which causes a left shift on the oxygen-hemoglobin dissociation curve and exacerbates hypoxia by decreasing oxygen unloading in metabolically active tissues. In response to the alkalosis, the kidneys decrease the reabsorption of bicarbonate in the proximal convoluted tubules, which results in diuresis and hastens dehydration. Catecholamines are also released in response to rapid ascent, invoking an increase in heart rate, cardiac output, blood pressure, and systemic vascular resistance. Acclimatization through increases in 2,3 DPG (right shift on oxygen-hemoglobin dissociation curve) and EPO production by the kidneys (increased oxygen carrying capacity) does not occur until days to weeks after increases in altitude are achieved.

While individual susceptibility to AMS is variable, rate of ascent and altitude attained are the primary factors contributing to the development of hypobaric hypoxemia and symptoms. Prevention is the ideal course of action, and can be achieved through slow ascent (<2,000ft gain in sleeping altitude per day plus one additional night of acclimatization for every 4,000ft altitude gain), adequate hydration and avoidance of respiratory depressants (ethanol, opioids, etc). For those anticipating the development of AMS symptoms, the following prescription and alternative medications may be taken prophylactically:

  • Acetazolamide (Diamox) 125mg BID for one to two days prior to ascent (potentiates renal correction of respiratory alkalosis)
  • Ginkgo Biloba 120mg BID for five days prior to ascent (efficacy requires further investigation)

Onset of moderate to severe AMS symptoms should not be ignored, as the illness may rapidly progress to high altitude cerebral edema (HACE) or high altitude pulmonary edema (HAPE). Both of these are life threatening and require immediate medical attention. As such, discontinuation of ascent and serious consideration of descent are essential. Other treatment modalities include rehydration, supplemental oxygen and the following medications:

  • Acetazolamide 250mg BID until symptom free.
  • Dexamethasone (Decadron) 4mg PO q6hrs for severe symptoms or in sulfa allergic patients unable to take Acetazolamide.
  • Ibuprofen (unknown mechanism, other NSAIDs are less effective).


  1. Luks AM, McIntosh SE, Grissom CK, et al. Wilderness Medical Society consensus guidelines for the prevention and treatment of acute altitude illness. Wilderness Environ Med 2010.
  2. Hackett PH, Roach RC, Wood RA, et al. Dexamethasone for prevention and treatment of acute mountain sickness. Aviat Space Environ Med 1988.
  3. West JB, American College of Physicians, American Physiological Society. The physiologic basis of high-altitude diseases. Ann Intern Med 2004.
  4. West JB, Schoene RB, Milledge JS. High altitude medicine and physiology. Hodder Arnold, London 2007.
  5. Auerbach PS (Eds). Wilderness Medicine, 6th. Elsevier, Philadelphia 2012.

Salicylate Toxicity
Cynthia Gee, DO
Henry Ford Macomb

Salicylates are common compounds found in many over-the-counter medications, such as Aspirin, wart removers and Oil of Wintergreen. Their accessibilities can easily lead to overdosing and thus drug toxicity. Therapeutic serum salicylate concentrations are between 10 to 30mg/dL (0.7 to 2.2mmol/L) and toxicity is considered at a level above 40mg/dL (2.9mmol/L).

Salicylates inhibit cyclooxygenase, which decreases prostaglandin, prostacyclin and thromboxane production, leading to platelet dysfunction and gastric mucosal injury. These also stimulate the chemoreceptor zone (nausea and vomiting) and the respiratory zone in the medulla, leading to hyperventilation and ultimately respiratory alkalosis. Furthermore, this compound interrupts anaerobic cellular metabolism, causing metabolic acidosis.

Nonspecific symptoms, such as vomiting, diarrhea, altered mental status, non-cardiac pulmonary edema or hyperpyrexia are usually present. Thus, a thorough work-up, including but not limited to EKG, serum salicylate level, CBC, BMP, coagulation studies, UA, UDS and lactate is important. Imaging modalities to be ordered depend on the clinical picture.

Once a diagnosis is established, it is imperative to manage and control airway and breathing. Keep in mind that a patient’s respiratory alkalosis pattern keeps salicylate anions in the blood, preventing these anions from crossing from the serum into the CNS. Also, cerebral glucose may be lowered, even if serum glucose is at a normal level. Other treatments include volume resuscitation, activated charcoal, sodium bicarbonate (to alkalinize serum and urine), hemodialysis and consults to appropriate services such as nephrology and toxicology.


Tintinalli J, Levitan R, Lovecchio F. Salicylates. Tintinalli’s emergency medicine: A comprehensive study guide. 2016 (8th ed., pp. 1265-1268). New York: McGraw-Hill.

Schizophrenia in the ED
Heather Boynton, MD
UC San Diego Health System

The prevalence of schizophrenia is approximately one percent worldwide, but higher in urban and homeless populations, which are often populations that frequent emergency departments. Patients with schizophrenia tend to stay in the ED longer than patients without schizophrenia, with an average length of stay of 9.6 hours, the longest stay of any diagnosis according to one study. The CDC estimates almost half of ED visits relating to schizophrenia lead to either hospital admission or transfer to a psychiatric facility.

Long thought to be caused by a combination of genetic predisposition and environmental exposure, new research shows a clear link between overexpression of the C4A gene and increased risk of schizophrenia. This genetic activity leads to excessive synaptic pruning during a crucial developmental period that starts in late adolescence. The age of onset is typically from the late teens to the fourth decade, with an incidence in men roughly twice that of women.

Clinical manifestations of schizophrenia include positive, negative, cognitive and mood symptoms. Delusions, auditory hallucinations and disorganized speech are characteristic positive symptoms, and can often be controlled with medication. Negative symptoms include blunted affect, poverty of speech and lack of motivation. Cognitive symptoms (impaired working memory, attention and executive function) begin early in the premorbid phase of the disease. Mood symptoms (euphoria, depression) sometimes make schizophrenia and bipolar disorder difficult to distinguish. Disturbances predominantly in mood, even in the presence of psychosis, is more consistent with bipolar disorder.

Pearls for Practice:

1. Undifferentiated Psychosis
Ask family, friends or police about precedent symptoms. Gradual social withdrawal and deteriorating intellectual function warrant a full psychiatric and medical evaluation for schizophrenia or schizophreniform disorder. Be sure to adequately assess for organic causes of psychosis: hypoglycemia, electrolyte abnormalities, hypoxia, head trauma, brain mass, endocrine disorders. Rosen suggests that “in patients exhibiting abnormal behavior, an organic etiology is suggested by (1) new onset of symptoms in a patient older than 35 years, (2) rapid onset of symptoms in a previously normal person, (3) visual hallucinations, (4) abnormal vital signs, and (5) lethargy or disorientation.”

2. Off Medication
Rates of recidivism are high in schizophrenia. Decreased social function chips away at existing social support, and many schizophrenics are increasingly isolated over the course of their disease. While uncontrolled positive symptoms may bring patients to the ED, often a benign physical complaint is registered with triage: “my feet smell,” “arm numb,” “chest pain from being chased by police.” Listen carefully for flattened or unemotional speech in a patient whose presenting complaint seems a little odd. Additional history taking might include questions such as, “Do you feel like people are out to get you? Do you hear things that others don’t? Have you ever thought about hurting yourself or someone else?” Make sure your patient has a sitter for the length of their stay in the ED.

3. Medication Side Effect
Neuroleptic medication is the mainstay of schizophrenia treatment. Side effects include dystonia, akathisia, parkinsonism, tardive dyskinesia, orthostatic hypotension, esophageal dysmotility, hyperprolactinemia and neuroleptic malignant syndrome. Most antipsychotics also increase the QT interval and in high doses can predispose a patient to cardiac dysrhythmia. Ask whether the patient takes their medication orally or as an injection every two to four weeks. Assess patients for risk of non-adherence.


  1. Marx JA, Walls RM, et al., eds. Rosen’s emergency medicine: Concepts and clinical practice. Philadelphia, PA: Mosby/Elsevier; 2010.
  2. Cheung A, Somers JM et al. Emergency department use and hospitalizations among homeless adults with substance dependence and mental disorders. Addict Sci Clin Pract. 2015 Aug 5;10:17.
  3. Moy E, Coffey R, et al. Length of stay in EDs: Variation across classifications of clinical condition and patient discharge disposition. Am J Emerg Med. 2016 Jan;34(1):83-7.
  4. Albert M, McCaig LF. Emergency department visits related to schizophrenia among adults aged 18-64: United States, 2009-2011. NCHS Data Brief. 2015 Sep;(215):1-8.
  5. LaCalle E, Rabin E. Frequent users of emergency departments: The myths, the data, and the policy implications. Ann Emerg Med. 2010; 56:42–48.



What Exactly is Activated Charcoal?
Erica Schramm, MS4
Cooper Medical School of Rowan University

Activated charcoal is commonly used for gastrointestinal decontamination following acute toxic ingestion of various medications and toxins, such as acetaminophen, benzodiazepines, antidepressants, antiepileptics and antipsychotics.1 Use of charcoal for gastric decontamination dates back to the early 19th century, when French pharmacist P.F. Touery reportedly demonstrated its efficacy dramatically after personally surviving an intentional ingestion of strychnine and charcoal.2 Modern activated charcoal is created from vegetable matter (such as wood pulp) heated at high temperatures and “activated” by an oxidizing gas. The resulting fine black particles of activated charcoal are porous with an extremely high surface area relative to weight, which allows absorption of a wide variety of particles with a molecular weight of 100 to 1,000 Daltons.3

Its mechanism of action is simple physical absorption of toxic particles from the luminal space of the GI tract. The porous activated charcoal forms a complex with toxin particles in the stomach and intestine. Because charcoal cannot be absorbed through the bowel wall, the toxin-charcoal complex is excreted in feces unchanged. It is recommended that activated charcoal be administered within one hour of toxic ingestion for maximal effect. The goal of therapy is to prevent GI absorption and facilitate excretion of orally ingested substances before they can be metabolized to exert their toxic systemic effects.1


  1. Hoegberg LG, Gude A. Techniques used to prevent gastrointestinal absorption. In: Hoffman RS, Howland M, Lewin NA, Nelson LS, Goldfrank LR. eds. Goldfrank's Toxicologic Emergencies, 10e. New York, NY: McGraw-Hill; 2015.
  2. Harchelroad F. High-surface-area charcoal-what’s next? Academic Emergency Medicine: Vol4. No3. 162-163.
  3. Haydock S. Poisoning, overdose, antidotes. In: Bennett PN, Brown MJ, Sharma M. eds. Clinical Pharmacology, 10e. New York, NY: Elsevier; 2012.


NSAID Toxicity
Sophia Johnson, DO and Shane Sergent, DO
Conemaugh Memorial Medical Center

Nonsteroidal anti-inflammatory drugs (NSAIDs) have a large therapeutic window making serious complications from acute overdose rare.1 The most common symptoms in overdose are related to CNS or GI toxicity.2 It is far more common to encounter complications from NSAID use at therapeutic doses. Ibuprofen is the most commonly implicated NSAID seen in overdose, with greater than 100mg/kg generally ingested to produce symptoms.1 Symptoms include nausea, vomiting and abdominal pain, with life-threatening gastrointestinal bleeding being rare.1 Severe toxicity is seen with ingestions of greater than 400mg/kg, which may cause metabolic acidosis, coma and apnea.1 Although kidney injury is rare, those patients who experience renal failure generally recover their kidney function.1

Most patients following an NSAID overdose will be asymptomatic, requiring supportive care.1 Patients should be screened for possible co-ingestants and a toxicologist should be consulted.1 Laboratory studies may be ordered, including CBC, BUN, creatinine, coagulation studies and electrolytes.2 Plasma drug level is not recommended as patient toxicity does not correlate well with the level.2 For large overdoses, monitor urine output.2 Activated charcoal can be used for GI decontamination within an hour of ingestion for large doses.1,2 Multi-dose activated charcoal is not recommended.2 Gastric lavage is typically not useful.1 If the patient has ingested an enterically coated preparation and the overdose is severe, whole-bowel irrigation may be used.1 Hemodialysis and alkalinization are not effective. Most overdoses do not cause long-term damage and treatment is symptomatic and supportive.1,2


  1. Rella JG, Carter WA. Nonsteroidal anti-inflammatory drugs. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. Tintinalli’s emergency medicine: A comprehensive study guide, 8e. New York, NY: McGraw-Hill; 2016. Accessed January 24, 2016.
  2. Lowry JA. Nonsteroidal anti-inflammatory drugs. In: Schafermeyer R, Tenenbein M, Macias CG, Sharieff GQ, Yamamoto LG. Strange and Schafermeyer's pediatric emergency medicine, 4e. New York, NY: McGraw-Hill; 2015. Accessed January 24, 2016.


Leptospirosis: A Unique Case Presentation
Samuel Bergin, MS4, Eric Sulava, MS4, and Daniel Lammers, MS4
F. Edward Hebert School of Medicine

A middle-age female, native to and living in Guam, was enjoying Thanksgiving evening with her family, rabbit and dog when she started to feel subjectively febrile with right lower quadrant abdominal pain. The following day she developed nausea, vomiting, anorexia and diarrhea and sought care in the ED.

In the ED, she was afebrile with a heart rate of 116, respiratory rate of 16 and blood pressure 92/48. She was unwell appearing with thready pulses, left-sided conjunctival suffusion and diffuse abdominal tenderness with rebound. Laboratory evaluation demonstrated multiple mild abnormalities: neutrophilia, thrombocytopenia, elevated INR, sterile pyuria, hyponatremia, hypokalemia, acute kidney injury and transaminitis. Lactate was notably 4.7. Her abdominal CT was indeterminate showing peri-uterine fat stranding with possible cholecystitis and appendicitis.

In the first 48 hours after admission, she developed a fever, tachypnea and worsening tachycardia. Labs showed a progressively elevating leukocytosis and a cholestatic pattern of transaminitis. She received nine liters of fluid, vasopressors and courses of piperacillin/tazobactam, doxycycline and vancomycin. She underwent an exploratory laparoscopy where gross purulent fluid was found in the pouch of Douglas, without identifiable source. On hospital day four, her rapid leptospirosis test came back positive. Her antibiotics were switched to moxifloxacin to cover both leptospirosis and possible pelvic inflammatory disease. She was discharged on hospital day nine.

Leptospirosis is a zoonotic spirochete that is endemic to many tropical areas of the world. It is spread typically through exposure to rodent urine or contaminated fresh-water.5 Outbreaks are associated with increased rainfall and flooding. Mortality rate ranges from approximately 5-10% of general admissions to upwards of 50% of ICU admissions.1-2

Typically the illness, with an incubation period of up to three weeks, presents as a self-limiting flu-like illness with a classic finding of conjunctival suffusion. The vasculitic nature of the disease can cause multi-organ dysfunction, with common laboratory findings of sterile pyuria, hypokalemia, thrombocytopenia and hypocoagulability.6 When leptospirosis involves jaundice, kidney failure and coagulopathy it is known as Weil’s disease.

Diagnosis is most typically made via serology (agglutination tests and IgM ELISA) or PCR, though culture is also feasible. The Leptorapide test, used to diagnosis the patient in this case, has a sensitivity of 90.91% and a specificity of 95.24%.

Most cases are self-limiting, but when intervention is needed the mainstay of treatment is doxycycline. In pediatric or pregnant patients, alternative options include azithromycin or amoxicillin. For severe disease, antibiotic coverage includes intravenous doxycycline, ceftriaxone or cefotaxime. There is a potential role for doxycycline chemoprophylaxis when entering an endemic area.4 Of note, Jarisch-Herxheimer reactions may occur after the start of antibiotics.3


  1. Amilasan AS, Ujiie M, Suzuki M, et al. Outbreak of leptospirosis after flood, the Philippines, 2009. Emerg Infect Dis 2012; 18:91.
  2. Chawla V, Trivedi TH, Yeolekar ME. Epidemic of leptospirosis: An ICU experience. J Assoc Physicians India 2004; 52:619.
  3. Guerrier G, D'Ortenzio E. The Jarisch-Herxheimer reaction in leptospirosis: A systematic review. PLoS One 2013; 8:e59266.
  4. Takafuji ET, Kirkpatrick JW, Miller RN, et al. An efficacy trial of doxycycline chemoprophylaxis against leptospirosis. N Engl J Med 1984; 310:497.
  5. World Health Organization. Global burden of human leptospirosis and cross-sectoral interventions for its prevention and control. (Accessed on December 8, 2015).
  6. Yang HY, Hsu PY, Pan MJ, et al. Clinical distinction and evaluation of leptospirosis in Taiwan--a case-control study. J Nephrol 2005; 18:45.


Wilderness Medicine: 
Special Considerations for Submersion Injuries

Mike Wilk, MS4
Loyola University Chicago Stritch School of Medicine

Drowning still remains a leading cause of accidental death in the United States, particularly for young children.1 In the past, many terms were developed in reference to subtypes of drowning such as near drowning, dry and wet drowning and shallow water blackout. However, recent guidelines have been simplified and now only categorize a drowning as fatal or non-fatal.2 Drowning occurs after an initial period of panic and breath holding, which eventually leads to reflex inspiration as water enters the respiratory tract causing widespread hypoxia.

Based on previous animal model studies, it was once thought that there were physiological differences in saltwater versus freshwater submersion injuries that could thus require differing treatments. For example, it was thought that since freshwater submersion aspiration contents are hypotonic, it would result in intravascular fluid overload leading to hypotonic serum levels. Contrasting saltwater submersions, aspiration was thought to be hypertonic in nature, thus leading to massive pulmonary edema and hypertonic serum levels. In reality, nearly all survivors simply do not aspirate enough fluid that lead to clinically relevant changes.3

One caveat to note involves submersion injuries sustained in the Dead Sea, given its high salt content.4 One paper reviewed 69 cases of “near drowning” which found these patients to have hypercalcemia, hypermagnesia and hyperphosphatemia. No significant difference in potassium, sodium or chloride levels were found. For these patients, treatment should focus on aggressive diuresis.

In regards to initial management, resuscitation efforts should emphasize rescue breathing (versus an emphasis on uninterrupted chest compressions in typical cardiac arrest patients). If the patient does not respond and an absence of pulse has been confirmed, the rescuer can continue down the traditional BLS/ACLS algorithm. Despite common portrayal in media outlets, the Heimlich maneuver has not been proven to add any benefit in this patient population.5

The final unique consideration for these patients are those in cold-water immersions. As hypothermia has been found to have protective effects, resuscitation should continue until the patient’s core body temperature is warmed to approximately 90°F to 95°F, unless the patient has obviously expired.6


  1. Centers for Disease Control and Prevention (CDC). Drowning--United States, 2005-2009. MMWR Morb Mortal Wkly Rep. 2012 May 18;61(19):344-7.
  2. Truhlář A, Deakin CD, Soar J, Khalifa GE, Alfonzo A, Bierens JJ. Cardiac arrest in special circumstances section Collaborators. European Resuscitation Council Guidelines for Resuscitation 2015: Section 4. Cardiac arrest in special circumstances. Resuscitation. 2015 Oct;95:148-201.
  3. Modell, J.H. Serum electrolyte changes in near-drowning victims. JAMA. 1985; 253: 557.
  4. Saidel-Odes LR, Almog Y. Near-drowning in the Dead Sea: A retrospective observational analysis of 69 patients. Isr Med Assoc J. 2003 Dec;5(12):856-8.
  5. Rosen P, Stoto M, Harley J. The use of the Heimlich maneuver in near drowning: Institute of Medicine report. J Emerg Med 1995; 13:397.
  6. Jolly BT, Ghezzi KT. Accidental hypothermia. Emerg Med Clin North Am 1992; 10:311.



North American Snake Bites
Andy Pittner, MSIV
Loyola University Chicago Stritch School of Medicine

The Center for Disease Control and Prevention (CDC) estimates that 7,000-8,000 people are bitten per year by a venomous snake and approximately five of those people die each year.1 The most common family of venomous snakes in the U.S. are the viperidae, subfamily crotalinae, common name “pit viper,” species: rattlesnakes, cottonmouth, copperhead and water moccasins. Pit Vipers are found in all states except for Maine.2

Snakebites from venomous snakes do not always result in envenomation and may be a “dry bite,” but all snakebites must be treated as presumed envenomation. Crotalids harbor a hemotoxin, which causes defibrinization, with or without thrombocytopenia and can cause anaphylaxis, compartment syndrome and rhabdomyolysis.4 The following are initial management steps of envenomation as outlined by Advanced Wilderness Life Support (AWLS) and CDC Initial Management:1,3

  1. Do not attempt to handle or kill the snake. Remember what it looks like or take a picture. Ensure scene safety, and avoid additional envenomations.
  2. Keep the patient calm and still. Do not take anything to accelerate heart rate such as caffeine.
  3. Do not apply any pressure dressings, tourniquets or ice. Do not slash the wound and do not suck the venom out. Keep bite below the level of the heart.
  4. Mark the leading edge of swelling/tenderness if present and continue to reassess every 15 minutes.
  5. Cover bite wound with a clean dry dressing.
  6. Evacuate. All snakebites receive medical care immediately. There is no way to tell if it was a dry bite.

The antivenom CroFab® is a polyvalent Immunoglobulin Fab used for North American Pit Viper envenomation. It is most effective in the first six hours post envenomation. Indications include rapidly spreading swelling, life threatening airway compromise, elevated prothrombin time or decreased fibrinogen and platelets. Poison Control should be contacted in all cases in which CroFab® is considered.5

Outcomes following envenomations are variable. One large study in Texas reviewed 90 snakebites, of which 88 patients received antivenom with an average dose of 10 vials. No patients died, but complications included suspected compartment syndrome in 10 patients, secondary skin and soft tissue infection in eight patients, anaphylactic reaction in four patients, DIC in three patients, bite site skin necrosis in two patients, bite site hematoma in three patients and acute kidney injury and rhabdomyolysis in one patient each. Twenty patients (22.2%) required surgical intervention; debridement in 10 patients and fasciotomy in the other 10 patients.6


  1. CDC: Venomous snakes. Page last updated: July 24, 2015
  2. McDiarmid RW, Campbell JA, Touré T. Snake species of the world: A taxonomic and geographic reference, vol. 1. Herpetologists' League. 1999 511 pp. ISBN 1-893777-00-6 (series). ISBN 1-893777-01-4 (volume).
  3. AWLS book.
  4. Bush SP. Rattlesnake Envenomation. Updated June 25, 2015.
  6. CroFab.
  7. Abbey JM, Jaffar NA, Abugrara HL, Nazim M, Smalligan RD and Khasawneh FA. Epidemiological characteristics, hospital course and outcome of snakebite victims in West Texas. Hospital Practice. 2015 43:4, 217-220, DOI: 10.1080/21548331.2015.1071637.


International Corner: Typhoid and Paratyphoid Fevers
Aaron Tyagi, MD
EW Sparrow Hospital - Michigan State University

The story of “Typhoid Mary” is one that is part of medical school lore. For many of us, that is the extent of it: an “ancient” story. However, this enteric bug is still relevant and is a potentially severe consequence of traveling abroad. According to the CDC, each year as many as 300 cases of typhoid fever and 100 cases of paratyphoid fever are documented in the U.S. With that in mind, it is still a worthwhile differential to maintain in a patient with unexplained fever and enteric illness.

Typhoid and paratyphoid fevers are caused by the gram-negative bacillus (rod) Salmonella enterica Typhi and Paratyphi, respectively. Further, paratyphoid fever may be caused by any of the serotypes Paratyphi A, B or C.

The CDC reports approximately 220 million cases of typhoid fever and 6 million cases of paratyphoid fever worldwide each year. Endemic areas include Eastern and Southeastern Asia, the Caribbean, Central and South America. Of these cases, most are caused by Salmonella enterica Paratyphi serotype A. However, this does not exclude other serotypes. For example, as recently as May 8th, 2012, the North Carolina Health Department reported 55 cases of Salmonella Paratyphi serotype B. The source was traced back to tempeh from a local restaurant.

Human-to-human transmission is the only mode of transmission of the bacteria, typically in contaminated food or water. Transmission may be from either acute or chronic carriers. Chronic carriage of Salmonella is defined by presence of the urine antigen >12 months after an acute infection and occurs in up to 6% of cases.

The incubation time for the bacteria ranges from one to four weeks. After incubation, non-specific symptoms such as headache, malaise, fevers of 102-104°F, nausea, vomiting, constipation and diarrhea are observed. Hepatosplenomegaly and a “rose spot” rash (salmon-colored macules on the trunk and abdomen) may also present.

It may be easy to misdiagnose this illness as heat exhaustion or heat stroke, or one of a number of other disease processes. Keeping that in mind, patient history of travel abroad as well as dietary habits may be crucial in making the proper diagnosis.

Since there is no definitive test to confirm Salmonella infection, the diagnosis is typically one made clinically. Blood and stool cultures may be sent, but may not provide conclusive evidence of infection. Bone marrow culture is another diagnostic modality that is an option that may be used in conjunction with blood cultures. Finally, the Widal test is a serum Ig test for Typhi antigens but is not very specific.

The advent of the antibiotic age has largely decreased the lethality of Typhoid and Paratyphoid fevers, when promptly diagnosed. The mortality has dropped to <1% with proper antibiotic coverage. Flouroquinolones are a drug of choice, such as ciprofloxacin 500mg BID or ofloxacin 400mg BID, either orally or parenterally for 7-10 days. However, in endemic areas with drug-resistant bacteria, third-generation cephalosporins may be a more effective treatment option, such as ceftriaxone 2-3g once daily parenterally or cefixime 20mg/kg/day orally in two separate doses for 7-14 days. In children, consider ciprofloxacin 30mg/kg/day, maximum 1000mg either orally or parenterally for 7-10 days; or ceftriaxone 100mg/kg/day intravenously once daily, maximum 4g/day for 10-14 days.

Mainstays of prevention include hand washing, good overall hygiene and vaccination. The CDC currently has two vaccine options for the Typhoid bacteria: oral live attenuated vaccine (Vivotif, manufactured from the Ty21a strain of Salmonella Typhi by PaxVax), and Vi capsular polysaccharide vaccine (ViCPS) (Typhim Vi, manufactured by Sanofi Pasteur) for intramuscular use.

Low-grade fever may remain for up to five days in patients treated for Typhoid/ Paratyphoid fever. In fact, patients may often feel symptomatically worse in the first five days post-treatment. Close follow up should be assured for all discharged patients with suspected Typhoid/ Paratyphoid fever.


  1. Lynch MF, Blanton EM, Bulens S, et al. Typhoid fever in the United States, 1999-2006. JAMA 2009; 302:859.
  2. Edelman R, Levine MM. Summary of an international workshop on typhoid fever. Rev Infect Dis 1986; 8:329.
  3. Parry CM, Hien TT, Dougan G, et al. Typhoid fever. N Engl J Med 2002; 347:1770.
  4. Gupta SK, Medalla F, Omondi MW, Whichard JM, Fields PI, Gerner-Smidt P, et al. Laboratory-based surveillance of paratyphoid fever in the United States: travel and antimicrobial resistance. Clin Infect Dis. 2008 Jun 1;46(11):1656–63.
  5. Gilman RH, Terminel M, Levine MM, et al. Relative efficacy of blood, urine, rectal swab, bone-marrow, and rose-spot cultures for recovery of Salmonella typhi in typhoid fever. Lancet 1975; 1:1211.
  6. Typhoid and Paratyphoid Fever. Yellow Book. Chapter 3(81).


Board Review: Acute Chest Syndrome
Sophia Johnson, DO and Shane Sergent, DO
Conemaugh Memorial Medical Center

Acute chest syndrome is the leading cause of death in patients with sickle cell anemia (SCA) and results from pulmonary ischemia and infarction.1,2 It is more common in children, especially between the ages of two and four.2,3 It should remain high on the differential in patients with SCA presenting with chest pain, as these patients can deteriorate rapidly.1 There are multiple possible etiologies, including lung infection, fat embolism and rib infarction.3 One study showed that about half of patients admitted had infectious pathogens isolated, the most common being Chlamydia pneumoniae and Mycoplasma pneumoniae.3 It can also be caused by over-aggressive hydration in patients with pain crises from sickle cell anemia.3 Presenting signs and symptoms characteristic of acute chest syndrome include respiratory symptoms, chest pain, cough, hypoxia, fever and new infiltrate on chest X-ray.1-3

Chest X-ray should be obtained, but may be normal in the first few days and clinical severity may be discordant with the radiograph.1,3 Treatment should begin immediately and involves oxygen, hydration, pain control, antibiotics, bronchodilators and exchange transfusion.1,3 Many recommend a full course of broad-spectrum antibiotics to cover for community-acquired pneumonia pathogens.3 No clear guidelines exist for exchange transfusion, and practice patterns may vary.3 Hydroxyurea reduces the occurrence and inhaled nitric oxide can also be helpful in management.3 Patients should be admitted to the hospital, typically to the intensive care unit.2


  1. Claudius I. Chapter 84. Sickle Cell Anemia in children. In: Cline DM, Ma O, Cydulka RK, Meckler GD, Handel DA, Thomas SH. Tintinalli's Emergency Medicine Manual, 7e. New York, NY: McGraw-Hill; 2012. Accessed November 17, 2015.
  2. Seller BR, Kontrick AV. Sickle Cell emergencies. In: Sherman SC, Weber JM, Schindlbeck MA, Rahul G. P. Clinical Emergency Medicine, 1e. New York, NY: McGraw-Hill; 2014. Accessed November 18, 2015.
  3. Williams-Johnson J, Williams E. Sickle Cell Disease and other hereditary hemolytic anemias. In: Tintinalli JE, Stapczynski J, Ma O, Cline DM, Cydulka RK, Meckler GD. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. New York, NY: McGraw-Hill; 2011. Accessed November 18, 2015.
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 Montony,

Modern Resident Contributors

Special thanks to this issue's contributors:

Samuel Bergin; Heather Boynton, MD; Thomas Doran, DO; Avram Flamm; Kaitlin Fries, DO; Phillip Fry; Cynthia Gee, DO; Danielle Goodrich, MD; Sophia Johnson, DO; Daniel Lammers; Alexandra Murray, DO; Joshua Nelson; Andy Pittner; Linda Sanders, MD; Erica Schramm; Shane Sergent, DO; Eric Sulava, Aaron Tyagi, MD; and Michael Wilk.

Interested in writing?
Email submissions to:

Please submit articles by March 15th for the April/May edition.

Articles appearing in Modern Resident are intended for the individual use of AAEM members. Opinions expressed are those of the authors and do not necessarily represent the official views of AAEM/RSA. Articles may not be duplicated or distributed without the explicit permission of AAEM/RSA.

Permission is granted in some instances in the interest of public education. Requests for reprints should be directed to AAEM/RSA, 555 East Wells Street, Suite 1100, Milwaukee, WI 53202, Tel (800) 884-2236; Fax: (414) 276-3349, Email:


AAEM/RSA  |  555 East Wells Street, Suite 1100  |  Milwaukee, WI 53202
Tel: (800) 884-2236  |  Fax: (414) 276-3349  |  Email:

If you do not wish to be included in our mailing list, please forward this message to