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TOXCARD: TOXIC ALCOHOL POISONING

Author: Kristin E. Fontes, MD (Emergency Physician, Santa Barbara Cottage Hospital and Goleta Valley Cottage Hospital) // Edited by: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital), and Brit Long, MD (@long_brit, EM Attending Physician, San Antonio Military Medical Center)

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Case presentation:

A 28-year-old female is brought to the emergency department by ambulance from home after her roommate found her disoriented and poorly responsive. The roommate reports finding a small container of antifreeze in the patient’s bedroom. Vital signs are as follows: T 37.0C, HR 65, BP 126/76, RR 32, and SpO2 98% on room air.  Venous blood gas shows pH 6.97, pCO2 21, pO2 38, HCO3 4.8, and lactate 6.75.

Question:

What are the laboratory abnormalities that can occur with toxic alcohol poisoning and how can it be treated?

Pearl:

Common features of toxic alcohol poisoning are elevated anion gap metabolic acidosis and elevated osmolar gap (the latter being a distinguishing feature from ethanol poisoning); osmolar gap usually elevated early after ingestion.(1,2)

Recall the toxic alcohol metabolites and their effects:

toxic alcohol metabolism

  • EG toxicity can cause significant renal failure due to oxalate crystal deposition in the kidneys and glycolic acid, which is directly nephrotoxic; hypocalcemia and tetany can also result due to oxalate binding to calcium.(1)
  • MeOH toxicity classically causes visual disturbances (“snowfield” vision) due to formic acid-induced optic neuropathy.(1)
  • Isopropanol toxicity causes ketosis without acidosis (no lactic acid formed!).  Usually benign clinical course but can occasionally cause hemorrhagic gastritis. Fomepizole and HD not usually indicated.(1)
  • Propylene glycol toxicity often due to intravenous medication preparations containing this alcohol (e.g., diazepam, lorazepam, esmolol, nitroglycerin, phenobarbital, phenytoin) can result in severe lactic acidosis.(1)
Treatment Approach:
  • Fomepizole competitively inhibits alcohol dehydrogenase, which is involved in the metabolism of all alcohols, including ethanol. It is given to prevent the buildup of toxic metabolites from ethylene glycol (glycolic acid, glyoxylic acid, and oxalic acid) and methanol (formic acid) whose deposition in tissues can cause irreparable damage.(1)
  • Fomepizole is indicated for MeOH or EG ingestion resulting in a metabolic acidosis with an elevated osmolar gap (not accounted for by ethanol) and a serum MeOH or EG level of at least 20 mg/dL.(1)
  • Fomepizole dosing: 1) Load: 15 mg/kg (max 1.5 g) IV, diluted in 100 mL of normal saline or 5% dextrose, infused over 30 minutes; 2) Maintenance: 10 mg/kg IV every 12 hours for 4 doses, then increase to 15 mg/kg until serum toxic alcohol level is less than 20 mg/dL.(1,3)
  • Hemodialysis is indicated for toxic alcohol poisoning with an elevated osmolar gap and/or severe metabolic acidosis refractory to standard therapy, refractory hypotension, or end organ damage (i.e. acute renal failure).(1,3)
  • Vitamin Supplementation: Give folic or folinic acid to patients with MeOH toxicity to divert metabolism away from formic acid to carbon dioxide and water. Give folic acid, pyridoxine, and thiamine to patients with EG toxicity to divert metabolism to nontoxic metabolites.(1,3)
Main points:

Consider toxic alcohol poisoning in a patient with an unexplained elevated anion gap metabolic acidosis and elevated osmolar gap. Consider fomepizole and/or HD in patients with severe toxic alcohol poisoning, especially if refractory to standard therapy.

 

References:
  1. Olson KR & California Poison Control System. (2012). Poisoning & drug overdose. New York: Lange Medical Books/McGraw-Hill.
  2. Emmett M and Palmer BF. Serum osmolal gap. In: UpToDate, Forman JP (Ed), UpToDate, Waltham, MA, 2016.
  3. LeBlanc C, Murphy N. Should I stay or should I go?: toxic alcohol case in the emergency department. Can Fam Physician 2009 Jan;55(1):46-9.

ToxCard: TCA Poisoning

Author: Tharwat El Zahran, MD (Medical Toxicology Fellow, Emory University School of Medicine) // Edited by: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital), and Brit Long, MD (@long_brit, EM Attending Physician, San Antonio Military Medical Center) screen-shot-2017-01-08-at-11-30-27-pm
Case Presentation:

2 yo male child presented to the ED with status epilepticus. His parents found an empty bottle of amitriptyline at home. He was intubated, given benzodiazepines and antiepileptic drugs. VS: BP 70/30, T 106 F, RR 24, HR 98, sat 98% RA, glucose 100 mg/dl. EKG is shown below.

EKG TCA PED

Question

What EKG findings occur in tricyclic antidepressant (TCA) poisoning? And how are they treated?

Pearl

TCAs alter the conformation of the sodium channel and slow the rate of rise of the action potential, which produces both negative dromotropic and inotropic effects. Sodium bicarb is the primary treatment for TCA poisoning.

  • All TCA are competitive antagonists of the muscarinic acetylcholine receptors and antagonize peripheral α1 adrenergic receptors.
  • Most prominent effects of TCA overdose result from binding to cardiac Na channels.
  • Acute ingestion 10-20 mg/kg of most TCAs cause cardiovascular and CNS toxicity. In children,  >5mg/kg results in toxicity.(1)
  • Signs of acute cardiovascular toxicity are refractory hypotension, acidosis, and arrhythmias. EKG indicators include intraventricular conduction delay (R shift of QRS axis and prolonged QRS), R in avR≥ 3mm, R/S>0.7 and arrhythmias. A QRS≥100 msec indicates increased incidence of serious toxicity, including coma, intubation, hypotension, seizures, and dysrhythmias. Sinus tachycardia is the most common EKG abnormality. (2)(3)
  • Acute neurological toxicity include AMS, delirium, agitation , seizures, and/or psychotic behavior with hallucinations, lethargy, coma.
Treatment approach
  • If the decision is made to intubate, avoid apnea, consider awake intubation, pretreat w benzos to raise seizure threshold and hyperventilate to promote alkalosis.(4)
  • If the EKG indicates signs of TCA poisoning as mentioned above,  give 1-2 meq/kg of sodium bicarb IV boluses at 3-5 min intervals.(4)
  • Continue bicarb drip until QRS duration <100, vitals stable, Na ~150, pH ~7.55. Watch for hypokalemia and hypocalcemia with bicarb drip.  Consider hypertonic saline (3%) if refractory or if serum pH>7.55.(4)
  • Hypotension unresponsive to sodium bicarb, or fluid boluses should be treated with vasopressors (norepi recommended).(4)
  • Treat dysrhythmias with lidocaine bolus of 1mg/kg IV followed by infusion of 20-50 mcg/kg/min.
  • Benzodiazepines, barbiturates, or propofol are recommended for seizures. Consider continuous EEG monitoring with neuromuscular blockade in refractory cases. Avoid phenytoin.(4)
  • For refractory cardiovascular poisoning consider intralipid or ECMO if available.(4)
Main point

TCAs are sodium channel blockers and primary treatment of TCA poisoning is sodium bicarb. The EKG abnormalities like QRS≥100,  R wave in avR ≥3mm, and R/S> 0.7 can predict significant toxicity.  Sodium bicarb displaces the TCA from the Na binding site by raising the Na+ gradient and increasing the pH.  Prolonged resuscitation might be necessary.

References
  1. Caksen et al. Acute amitriptyline intoxication: an analysis of 44 children. Human & Experimental Toxicology (2006) 25: 107-110
  2. Olgun et al. Clinical, Electrocardiographic, and Laboratory Findings in Children With Amitriptyline Intoxication. Pediatr Emer Care 2009;25: 170-173
  3. Paksu et al. Amitriptyline overdose in emergency department of university hospital: Evaluation of 250 patients. Human and Experimental Toxicology 2014;33:980–990
  4. Goldfrank’s Toxicologic Emergencies, 10th E, Chapter 71: Cyclic Antidepressants, p 972- 982.

 

 

Tox Cards: CO Poisoning

Author: Patrick C. Ng (Chief Resident, San Antonio Military Medical Center) // Edited by: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital), and Brit Long, MD (@long_brit, EM Attending Physician, San Antonio Military Medical Center)
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Case Presentation:
It is a cold day in the middle of December. A 56 yo female and her 29 yo daughter who is 8 months pregnant present to your ED with a chief complaint of generalized weakness and headache for 2 days. They mention that they think they both caught the flu due to the cold temperatures despite turning their heater on high and using oil lamps for extra heat in their apartment. Their vital signs are normal.
Question:
What are the most common signs/symptoms of carbon monoxide (CO) poisoning, and what are the general management plans?
Pearl:

CO poisoning presents with nonspecific symptoms that can be mistaken for other diagnosis such as the flu. Initial treatment includes high-flow supplemental O2. Hyperbaric oxygen therapy (HBOT) may or may not be the “standard of care” (controversial).

  • CO poisoning can be an elusive diagnosis, as non-specific symptoms such as headache, dizziness, nausea, fatigue, and chest pain are non-specific and can be consistent with many other disease processes.(1,2)
  • Key historical clues include people from the same household presenting with symptoms of headache and flu-like symptoms that improve throughout the course of the day (i.e. when patients leave their dwellings for work, school, etc.) and history of exposure to CO sources such as heaters and enclosed garages.(1,2)
  • A co-oximetry is a spectrophotometer that uses many different wavelengths to measure oxygenated hemoglobin (oxyHb), deoxygenated hemoglobin (deoxyHb), as well as carboxyhemoglobin (COHb) and methemoglobin (MetHb) concentrations.(3)
  • The use of greater number of wavelengths in a co-oximeter as compared to a standard pulse oximeter allows the co-oximeter to distinguish between other types of hemoglobin,  whereas a standard pulse oximetry can only distinguish between oxyHb and deoxyHb.(3)
  • Blood COHg levels commonly reaches a level of 10 % in smokers and may even exceed 15 %, as compared with 1 to 3 % in nonsmokers.(2)
  • Standard treatment includes  high-flow O2  via NRB mask (or intubation in severe cases) until symptoms resolve and CO levels return to baseline; pregnant patients should continue for at least 24 hours with fetal wellbeing assessment. Patients also require follow up at 1-2 months for neuropsychiatric assessment.(1,2)
  • Normal half life of Hb-CO is 4-6 hrs with room air oxygen, 40- min with high-flow O2, and 15-30 min with HBOT.(2)
  • Although the indications for HBO are controversial, some recommend HBO for any CO-poisoned patient with mental status change or history of syncope, signs of cardiac ischemia or arrhythmia, history of ischemic heart disease and CO level > 20%, symptoms that do not resolve with normobaric O2 therapy after 4-6 hours, or any pregnant patient with CO > 15%. Coma is generally an undisputed indication for hyperbaric-oxygen therapy.(2)
  • The use of HBO has been reported to reduce the risk of neurological/cognitive sequelae thought to be associated with carbon monoxide poisoning.(4,5)
Main Point:
Carbon monoxide poisoning can be a deadly diagnosis associated with significant morbidity and long-term permanent neurological damage. It can present with very non-specific symptoms. Specific historical clues as well as co-oximetry can help the emergency physician quickly make the diagnosis. High-flow O2 therapy is the initial standard therapy with some advocating HBOT for select severe or at risk cases.
References:
1. Piantadosi CA. Diagnosis and treatment of carbon monoxide poisoning. Respir Care Clin N Am. 1999;5:183-202.
2. Ernst A, Zibrak JD. Carbon Monoxide Poisoning. N Engl J Med 1998;339:1603-1608.
3. Hampson NB. Noninvasive pulse CO-oximetry expedites evaluation and management of patients with carbon monoxide poisoning. Am J Emerg Med. 2012 Nov;30(9):2021-4.

4. Tibbles PM, Perrotta PL. Treatment of carbon monoxide poisoning: a critical review of human outcome studies comparing normobaric oxygen with hyperbaric oxygen. Ann Emerg Med. 1994;24:269-276.
5. Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med 2002;347:1057–1067

Treatment for Salicylate Poisoning

Author: Sean Kolowich (Emory University School of Medicine) // Edited by: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

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Case presentation:

A 53 year-old previously healthy female is brought into the ED by family members 4 hours after ingesting 100 tablets of aspirin (325mg, unknown formulation). She has no complaints and denies any co-ingestions. VS: Temp 98.1 (oral), HR 93, BP 136/87, RR 20, pulse ox 98% on room air. CMP and ECG are unremarkable, ASA 47.1 mg/dL, ABG pH 7.48, pCO2 20, pO2 122.

Question:

What treatments should a salicylate poisoned patient receive?

Pearl/Pitfall: 

Patients with salicylate poisoning should receive IV bicarb to alkalinize the urine. Indications for hemodialysis include cerebral edema, pulmonary edema, renal failure, intractable acidosis, clinical deterioration, or ASA level > 100 mg/dL or > 70 mg/dL if chronic.

  • Support ABCs, prevent further organ toxicity by encouraging salicylate elimination
    • Alkalinize the serum/urine
      • 1-2 mEq/kg sodium bicarb. IV bolus followed by sodium bicarb. infusion (3 amps into 1L D5W) @ 1.5-2 X maintenance rate
        • goal serum pH ~7.5
        • goal urine pH >7.5
  • Salicylate overdose + IV sodium bicarbonate therapy = potential hypokalemia
    • Avoid hypokalemia because it prevents alkalization of the urine ® prolonged elimination of salicylate
      • goal K+ 4.0 to 4.5 mEq/L
    • Monitor calcium levels (ionized/total); IV NaHCO3 can cause hypocalcemia
  • Consider glucose supplementation if altered mental status
    • Serum glucose may be normal but CNS levels may be low 2/2 effects of salicylates
  • Indications for extracorporeal treatment (intermittent hemodialysis is ECTR of choice):
    • Salicylate level > 100 mg/dL (> 90 mg/dL if impaired kidney function) or > 70 md/dL if chronic.
    • Cerebral edema (altered mental status, seizures)
    • Renal failure
    • Pulmonary edema or new hypoxemia requiring supplemental O2
    • IF standard therapy fails AND:
      • Salicylate level > 90 mg/dL (> 80 mg/dL if impaired kidney function)
      • Systemic pH < 7.20
  • Continue IV sodium bicarb therapy b/w ECTR sessions
Main Point:

Patients presenting with acute salicylate toxicity should receive supportive care and alkalinization with IV sodium bicarbonate. Hemodialysis should be considered early in treatment and is indicated if there is evidence of end organ damage (AMS, ARDS), failure of standard therapy, or severely elevated salicylate levels.

 

References:

  1. Lugassy DM. Salicylates. In: Hoffman RS, Howland M, Lewin NA, Nelson LS, Goldfrank LR. Eds. Goldfrank’s Toxicologic Emergencies, 10e. New York, NY: McGraw-Hill; 2015.
  2. Levitan R, Lovecchio F. Salicylates. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e. New York, NY: McGraw-Hill; 2016.
  3. Juurlink DN, Gosselin S, Kielstein JT, et al. Extracorporeal Treatment for Salicylate Poisoning: Systematic Review and Recommendations From the EXTRIP Workgroup. Ann Emerg Med 2015; 66:165

Limitations of CIWA score

Author: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

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Case Presentation:

You are working a busy ED shift and are also managing a handful of boarded patients admitted to your ICU. Nursing resources are especially strained today. One of your intubated patients that you admitted for alcohol withdrawal starts having a seizure. His vitals are T 101F, HR 135, BP 175/100, RR 16, O2 sat 89% on 40% O2.

Question:

What are some of the limitations of using the CIWA score?

Pearl:

Although the CIWA score is a widely cited example of symptom-triggered therapy it has several important limitations and can be difficult to properly execute in the emergency department setting.

  • Symptom-triggered treatment for alcohol withdrawal using the CIWA score has many benefits including reduced progression to mechanical ventilation requirement, 4-fold decrease in benzodiazepine requirements, shorter duration of treatment, and shorter hospitalization stays by 2 days when compared to fixed-dosing scheduling.(1)
  • However, an important clinical limitation of CIWA as a tool to assess alcohol withdrawal is that it does not incorporate vital sign assessment, which can be an important and sometimes the only clue available in recognizing inappropriately treated DT patients.(2)
  • The CIWA score also does not address choice of benzodiazepines, frequency of administration, use of adjuvant medications and underlying medical conditions (renal failure, liver failure, respiratory failure, cardiac disease, age, etc.) in treating withdrawal.(2)
  • The CIWA score requires patients to be able to respond to questions and follow commands. This can be difficult in patients with language barriers, altered mental status or who are intubated.(2)
    • For example “Do you feel sick to your stomach, have you vomited?”; “Do you have any itching, pins-and-needles sensations, burnings, or numbness…?” and “Are you seeing anything that is disturbing you?” are some questions asked.
  • Many of the studies that have evaluated CIWA have excluded patients with seizures, which is an important sign of severe withdrawal and should be taken into consideration.(3)
  • Moreover, the CIWA score can be especially difficult to execute properly without adequate nursing staff. Many busy EDs are often understaffed and have limited nursing resources. Thorough staff training is required to appropriate use CIWA.(2) Studies have shown that the CIWA score tends to be administered irregularly by nursing staff, often used for patients who are not appropriate for symptom-guided treatment and can have a higher proportion of protocol errors.(4)
  • Scoring systems are important for symptom-triggered therapy and provide the ability for comparison analysis in clinical trials. However, many other scoring systems exist. An example is the Richmond Agitation Sedation Scale (RASS), which is observer based.(5) Many hospitals have their own scoring systems as well.
Main point:

Symptom triggered therapy has been shown to have better outcomes than fixed benzodiazepine scheduling in managing alcohol withdrawal. The CIWA score is a widely cited method of using symptom triggered therapy. However, physicians should not rely on just the CIWA score and other hospital and research protocols exist. The CIWA score has several important limitations including the exclusion of vital signs as an assessment, reliance of the patient’s ability to answer questions and follow commands, and can be time consuming in a busy ED environment.

References:
  1. Daeppen J, Gache P, Landry U, et al. Symptom-triggered vs fixed-schedule doses of benzodiazepines for alcohol withdrawal. JAMA. 2002;162(10):1117-1121.
  2. Sankoff J, Taub J, Mintzer D. American College of Medical Quality: Accomplishing much in a short time: use of a rapid improvement event to redesign the assessment and treatment of patients with alcohol withdrawal. Am J Med Qual. 2013; 28(2):95-102.
  3. Saitz R, Mayo-Smith MF, Roberts MS, Redmond HA, Bernard DR, Calkins DR. Individualized treatment for alcohol withdrawal: a randomized double-blind controlled trial. JAMA. 1994;272:519-523.
  4. Hecksel KA, Bostwick JM, Jaeger TM, Cha SS. Inappropriate use of symptom-triggered therapy for alcohol withdrawal in the general hospital. Mayo Clin Proc. 2008;83:274-279. 10.
  5. Sessler CN. The Richmond Agitation-Sedation Scale” validity and reliability in adult intensive care unit patients. Am J Respir Crit Care Med. 2002; 166:1338-1344.

Must Know Antimicrobial Regimens – Adults

Authors: Marina N. Boushra, MD (EM Resident Physician, Vidant Medical Center) and Cassandra Bradby, MD (EM Attending Physician, Vidant Medical Center) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

A 75-year-old man with a history of diabetes, hypertension, and dementia presents to the emergency department with a complaint of altered mental status. His nursing home caretaker endorses a dry cough for one week that has recently become productive and fevers with a Tmax of 38.9 ºC. She notes that he is not “acting like himself,” and elaborates that he is sleeping more, talking less, and has had multiple episodes of urinary incontinence, which is unusual for him. His vitals on arrival are T 38.5º C, HR 110, RR 30, BP 100/70. His exam is notable for somnolence, increased work of breathing with accessory muscle use, coarse rales at the base of the right lung, tachycardia, and dry mucus membranes.

Bacterial infections are a common diagnosis in the emergency department, and emergency physicians are often tasked with providing antibiotics for outpatient management or beginning antibiotics prior to admission. Antibiotic treatment is not without side effects, and treatment started in the emergency department is frequently empiric. Therefore, an understanding of the most likely causative organisms as well as local patterns of susceptibility and resistance is paramount to adequate treatment, appropriate antibiotic selection, and responsible antibiotic stewardship. Important historical details to elicit include allergies, recent antibiotic use, prior antibiotic failure, dialysis use, use of immunosuppressants or history of immunocompromise, culture results of prior infections, and contact with healthcare facilities, including recent hospitalization, living in a care facility, or recent invasive procedures such as ureteral catheterizations or intubation. These details offer vital information regarding possible bacterial resistance or the presence of opportunistic infection. Because multiple empiric regimens exist for infectious disease in the emergency department, contacting the hospital pharmacy about the local antibiogram may help tailor the empiric regimen to local microbial susceptibilities. Please keep this in mind with the recommendations discussed in each table. The following is a discussion of the most common or most emergent ED-diagnosed bacterial infections, their most likely causative organisms, and current recommendations for empiric treatment.

Pneumonia

Pneumonia is infection of the pleural parenchyma and can be broadly divided into community-acquired (CAP) and hospital-acquired pneumonia (HAP). A third category of pneumonia, healthcare-associated pneumonia, is discussed in more detail later in this paper. The majority of pneumonia is community-acquired but historical details such as recent hospitalization, intubation, or ventilator dependence should raise concern for HAP and multi-drug resistant organisms (MDROs). Travel history may be important for more rare causes of pneumonia. In patients with known or suspected HIV or AIDS, pneumocystis pneumonia should be strongly considered.

Community-Acquired Pneumonia (CAP)

CAP can be caused by a variety of pathogens, with the most common bacterial cause being Streptococcus pneumonia1–3. Other common organisms include respiratory viruses, Haemophilus influenza, and Mycoplasma pneumoniae1–3. In patients requiring ICU admission, S. pneumoniae is still common, but there is increased prevalence of Legionella pneumophila, Staphylococcus aureus, gram-negative bacilli, and influenza4. It is important to remember these differences in etiology and to cover adequately for these serious organisms in patients requiring ICU admission. Patients with risk factors for aspiration pneumonia should receive additional anaerobic coverage. Treatment for CAP has become increasingly more complicated due to rising resistance to antibiotics. Risk factors for drug resistance include age >65, alcoholism, medical comorbidities, immunosuppressive illness or medication use, and use of beta-lactam, macrolide, or fluoroquinolone antibiotics in the last 3-6 months5,6.

Treatment should be initiated as soon as a diagnosis of CAP is made to prevent decompensation. CAP can often be treated on an outpatient basis. Studies have shown that physicians often use inconsistent criteria when making the decision to admit patients for the treatment of CAP and overestimate short-term patient mortality, leading to an increased rate of unnecessary hospitalizations7. The 2007 guidelines for the Infectious Disease Society of America (IDSA) and the American Thoracic Society (ATS) recommend using the CURB-65 score or Pneumonia Severity Index (PSI), both well validated prediction rules and decision aids, to aid in the risk stratification of patients and making the decision to admit for inpatient treatment7–9. Interestingly, a recent article investigating oral vs. intravenous fluoroquinolones for non-critically ill patients with CAP showed no difference in mortality, ICU transfers, or need for vasopressors or intubation10. Studies have shown shorter time to treatment and shorter hospital stays for patients started on oral rather than intravenous antibiotics11. As such, it is important to consider oral therapy in non-critically ill patients with CAP who are being admitted for treatment but are able to tolerate oral medication.

Studies have shown similar efficacy in CAP for fluoroquinolones and macrolides plus a penicillin or cephalosporin12. Importantly, there is a high rate of macrolide resistance in S. pneumoniae in the United States; as such, macrolides should not be used as empiric monotherapy in areas where resistance to macrolides is >25%5,13–15. Recommended regimens are outlined in the Table 1 below. The IDSA is expected to publish new guidelines for the treatment of CAP that better reflect current trends in resistance in the summer of 2017.

Hospital-Acquired (nosocomial) Pneumonia (HAP)

Pneumonia patients with recent hospitalizations present a challenge in antibiotic selection. While the pneumonia may be caused by an MDRO picked up in the healthcare environment, it is also possible that the patient has a simple community-acquired organism. The multi-drug resistant (MDR) score assesses a particular patient’s risk for infection with an MDRO16,17. Patients with a high MDR score should be presumed to have a pneumonia due to a resistant organism and treated accordingly with broad-spectrum coverage as outlined in Table 1 below. Patients with low MDR scores can be treated with the more narrow-spectrum coverage used for CAP, with the possibility of widening the spectrum in the event of treatment failure. The Shorr score is a similar scoring tool to assess the risk of infection by an MDR and tailor empiric coverage appropriately18.  Antibiotic treatment for presumed HAP should cover for Staphylococcus aureus and Pseudomonas aeruginosa19. Local antimicrobial prevalence and susceptibility, especially within the hospital, is helpful to determining a regimen, but can often be deferred to the judgement of the admitting team. Empiric regimens as recommended in the 2016 IDSA/ATS guidelines for empiric management of HAP are outlined in Table 1 below.

Healthcare-Associated Pneumonia (HCAP)

Healthcare-associated pneumonia (HCAP) refers to pneumonia that may have been acquired in healthcare facilities such as nursing homes and dialysis centers. It was formerly grouped with HAP due to presumed increased susceptibility to MDROs. Several studies, however, have shown no increased susceptibility to MDROs in patient with HCAP, and it is conspicuously missing from the IDSA/ATS guidelines on the management of HAP19–24. As such, in the absences of other historical susceptibilities to MDROs such as comorbidities or severe illness, patients with HCAP may be treated as CAP19–24.

Table 1: Empiric Treatment of Pneumonia based on type, setting, and patient-specific factors8,19

Type Setting Patient Factors Regimen
CAP Outpatient No recent antibiotics, co-morbidities, high-rate of resistance -Doxycycline 100mg bid for five days

-Azithromycin 500mg on day 1 followed by 250mg for four days.*

-Clarithromycin 500mg bid for seven days*

Recent antibiotics, co-morbidities, high-rate of resistance -Levofloxacin 750mg daily for five days

-Moxifloxacin 400mg daily for five days

-Gemifloxacin 320mg daily for five days

-Combination therapy with a beta-lactam (amoxicillin 1g tid, amoxicillin-clavulanate 2g bid, cefpodoxime 200mg bid, or cefuroxime 500mg bid) PLUS either a macrolide (azithromycin 500mg on day 1, followed by 250mg for four days, or clarithromycin 500mg bid for five days) or doxycycline 100mg bid for five days.

Inpatient Mild-Moderate disease, managed on general floor -Levofloxacin 750mg IV or po

-Moxifloxacin 400mg IV or po

-Combination therapy with a beta-lactam (cefotaxime 1-2g, ampicillin-sulbactam 1.5-3g, ceftriaxone 1-2g) PLUS a macrolide (azithromycin 500mg IV, or clarithromycin 500mg orally)

Severe disease requiring ICU admission -Combination therapy with a beta-lactam (cefotaxime 1-2g, ampicillin-sulbactam 1.5-3g, ceftriaxone 1-2g) PLUS a respiratory fluoroquinolone (levofloxacin 750mg IV, or moxifloxacin 400mg IV) OR azithromycin 500mg IV.

-If penicillin allergic, a respiratory fluoroquinolone PLUS aztreonam 1g

-If MRSA suspected, add vancomycin 15-20mg/kg IV

HAP Inpatient Combination therapy is warranted, with one from each of the following 3 categories:

1) Piperacillin-tazobactam 4.5 g IV, Cefepime 2 g IV, Ceftazidime 2g IV, Imipenem/cilastatin 500mg IV

2) Azithromycin 500mg IV, Ciprofloxacin 400mg IV, Levofloxacin 750mg IV, or Gentamicin 5-7mg/kg IV

3) Vancomycin 15-20mg/kg IV, Linezolid 600mg IV

*Macrolide antibiotics should not be used as empiric monotherapy in areas of known S. pneumoniae resistance >25% to macrolides. If such resistance exists, pair with a beta-lactam as shown in the table above.

Urinary Tract Infection

Urinary tract infections can involve the lower urinary tract (cystitis) or the upper tract (pyelonephritis). Urinary tract infections are very common in women, with sexually active women being at higher risk. Risk factors for urinary tract infections include recent sexual intercourse, prior urinary tract infections, and recent spermicide use25. When present in men, urinary tract infections are typically associated with underlying anatomical anomalies, recent catheterization, or other risk factors. While not all urinary tract infections in males are necessarily complicated, a search for these risk factors should be conducted when a male is diagnosed with a urinary tract infection.

Uncomplicated Cystitis

Urinary tract infections in women begin by bacterial colonization of the vagina by fecal bacteria, which may ascend via the urethra to infect the bladder and kidneys. Uncomplicated cystitis and pyelonephritis in women is typically caused by Escherichia coli, though Proteus mirabilis, Klebsiella pneumoniae, and Streptococcus saprophyticus are occasionally found26,27. Empiric treatment for uncomplicated urinary tract infections is best tailored to the regional E. coli sensitivities and is outlined in Table 328. Of note, this table may be modified based on local resistance patterns. Sterile pyuria should raise concern for a possible sexually-transmitted infection (STI) and patients who fail to improve despite appropriate antibiotic treatment should be tested for STI.

Complicated Urinary Tract Infection

A complicated urinary tract infection is one which is associated with a condition that increases the risk for therapeutic failure, as outlined in Table 2. The microbial spectrum of complicated UTI is more broad, including not only the typical organisms associated with uncomplicated UTI but also more varied and resistant pseudomonal, staphylococcal, and Serratia species as well as fungi29,30. Complicated lower urinary tract infections may be managed as an outpatient, but indications for hospitalization include inability to tolerate oral therapy or suspected/ documented infection with a resistant organism such as extended-spectrum beta-lactamase producing organisms (ESBLs). Complicated pyelonephritis is the progression of infection resulting in emphysematous pyelonephritis, corticomedullary or perinephric abscess, or papillary necrosis. Complicated pyelonephritis is an indication for admission and intravenous antibiotic treatment.

Table 2: Conditions that increase the risk of treatment failure in UTI (complicated UTI)

Diabetes
Pregnancy
Renal failure
Hospital-acquired infection
Immunosuppression
Renal transplantation
Anatomic abnormality of the urinary tract
Symptoms >7 days prior to presentation
Presence of an indwelling foreign body (ureteral catheter, nephrostomy tube, ureteral stent)
Ureteral calculus

UTI and Asymptomatic Bacteriuria in the Pregnant Patient

Urinary tract infection and colonization in pregnant patients are worth special mention. While asymptomatic bacteriuria in a non-pregnant female does not warrant treatment, studies have shown a high rate of progression to symptomatic cystitis and pyelonephritis in pregnant patients31. As such, current recommendations suggest that any bacteriuria in a pregnant patient should be treated with antibiotics32. Additionally, although urinary tract infection in a pregnant woman is, by definition, complicated, fluoroquinolones, the first-line treatment for complicated cystitis, are a pregnancy class C medication and should be avoided33. Mild urinary tract infections in pregnant females are treated similarly to uncomplicated UTIs, as shown in Table 3 below. Follow-up cultures for resolution are important in this patient population34.

Table 3: Empiric treatment of uncomplicated and complicated urinary tract infections28,31,35.

Urinary Tract Infection Recommended regimen
Uncomplicated cystitis -Nitrofurantoin 100mg bid for five days*

-Trimethoprim-sulfamethoxazole 160/800mg bid for three days

-Cephalexin 500mg BID for 3-7 days

-Fosfomycin 3g in a single dose*

-Ciprofloxacin 250mg bid or Levofloxacin 250mg once per day for three days**

Complicated cystitis Outpatient:

-Ciprofloxacin 500mg bid or 1000mg daily for five to ten days

-Levofloxacin 750mg daily for five to ten days

Inpatient:

-Levofloxacin 500mg IV

-Ceftriaxone 1g IV

-Ertapenem 1g IV

-Gentamicin 3-5mg/kg IV +/- ampicillin 1-2g every 4-6 hours***

-Tobramycin 3-5mg/kg IV +/- ampicillin 1-2g every 4-6 hours***

Uncomplicated Pyelonephritis

 

 

Outpatient:

-Ciprofloxacin 500mg po bid for seven days or 1000mg daily for seven days

-Levofloxacin 750mg po daily for five to seven days

Inpatient:

-Levofloxacin 500mg IV

-Ceftriaxone 1g IV

-Ertapenem 1g IV

-Gentamicin 3-5mg/kg IV

-Tobramycin 3-5mg/kg IV

Complicated Pyelonephritis – Inpatient, mild-moderate disease:

-Ceftriaxone 1g IV

-Ciprofloxacin 400mg IV

-Levofloxacin 750 mg IV

-Aztreonam 1g IV

Inpatient, severe disease:

-Cefepime 2g IV

-Ampicillin 1g IV four times per day plus Gentamicin 5mg/kg IV daily

-Piperacillin-tazobactam 3.375g IV

-Meropenem 500mg IV

-Imipenem 500mg IV

-Doripenem 500mg IV

Asymptomatic bacteriuria and acute cystitis in the pregnant patient -Nitrofurantoin 100mg po bid for five to seven days (in second or third trimester)*

-Trimethoprim-sulfamethoxazole 160/800 mg po bid for three days****

-Fosfomycin 3g po in a single dose*

-Amoxicillin-clavulanate 500mg po tid for three to seven days

-Cephalexin 500mg po bid for three to seven days

-Cefpodoxime 100mg po bid for three to seven days

*Fosfomycin and nitrofurantoin should be avoided if there is concern for early pyelonephritis.

**Fluoroquinolones, if possible, should be reserved for other important uses to avoid resistance against this class of antibiotics.

***Adding ampicillin provides Enterococcus coverage

****Should be avoided in first trimester and at term

Cellulitis and Soft-Tissue Infection

Cellulitis and Erysipelas

Cellulitis and erysipelas are bacterial skin infections that differ in that erysipelas involves the upper dermis and superficial lymphatics while cellulitis involves the deeper dermis and subcutaneous fat tissue. Both manifest with localized skin erythema, edema, warmth, and pain. Because of the more superficial nature of erysipelas, these lesions are typically more raised and better demarcated than cellulitis. Erysipelas also presents more acutely and with more systemic symptoms such as fevers and chills. The most common pathogens in cellulitis are beta-hemolytic streptococci and S. aureus, including methicillin-resistant S. aureus (MRSA)36–38. Beta-hemolytic streptococci are the most common cause of erysipelas36,39.

Lesions consistent with cellulitis should be examined closely for the presence of a drainable abscess. History is particularly important in the patient with possible cellulitis as cellulitis associated with human or animal bites or with water exposure needs different coverage than uncomplicated cellulitis. The presence of an indwelling device near the region of cellulitis is also important, as it is an indication of device infection.

The treatment of uncomplicated cellulitis is based on whether or not there is associated purulence. Current guidelines group erysipelas with non-purulent cellulitis in terms of treatment, as the lesions are often difficult to distinguish from each other and are caused by a similar spectrum of organisms. Patients with purulent cellulitis should receive empiric coverage for MRSA pending culture results40. Patients with non-purulent cellulitis or erysipelas should receive empiric coverage for beta-hemolytic streptococcus and MSSA, although patients with systemic symptoms, recurrent infection, or prior infection with MRSA should receive additional MRSA coverage36. Cellulitis can typically be managed as an outpatient; patients with signs of systemic toxicity, rapid progression, indwelling devices, or failure of outpatient management should be admitted for parenteral antibiotics. In addition to antibiotics, elevation of the affected area is an important aspect of treatment as it helps promotes drainage of edema and inflammatory substances, speeding symptomatic improvement36.

Table 4: Empiric treatment of cellulitis and erysipelas36

Infection Recommended regimen
Uncomplicated nonpurulent cellulitis without MRSA risk factors or erysipelas Outpatient -Dicloxacillin 500mg po qid for 5-10 days

-Cephalexin 500mg po qid for 5-10 days

-Clindamycin 450mg po tid for 5-10 days

Inpatient -Cefazolin 1-2g IV tid

-Ceftriaxone 1g IV every 24 hours

-Oxacillin or nafcillin IV every 4 hours

-Clindamycin 600-900mg IV tid

Uncomplicated purulent cellulitis or nonpurulent cellulitis with MRSA risk factors

 

Outpatient -Clindamycin 300-450mg po 3-4 times per day for 5-7 days

-Trimethoprim/sulfamethoxazole 1-2 DS tablets po bid for 5-7 days

-Doxycycline 100mg bid for 5-7 days

Inpatient -Vancomycin 15-20mg/kg/dose IV bid

-Clindamycin 600mg IV tid 

-Linezolid 600mg IV two times per day

-Daptomycin 4mg/kg/dose IV once daily

Skin abscesses

Skin abscesses are most commonly due to S. aureus (MRSA or MSSA), although polymicrobial infection with flora from the skin or adjacent mucosal tissues is also common36,40–42. Risk factors for MRSA infection include recent hospitalization or antibiotic use, contact with healthcare environments, institutionalization, HIV infection, intravenous drug use, and diabetes. Source control, in the form of warm compresses to promote drainage or incision and drainage, is important. The role of antibiotics following source control is debated. Studies have shown a slightly increased cure rate with the use of antibiotics following incision and drainage of uncomplicated abscesses, but also a higher rate of diarrhea and adverse effects43,44. Antibiotics should be started for large (>2cm) or multiple abscesses, extensive surrounding cellulitis, systemic symptoms, immunocompromise or co-morbidities, the presence of an indwelling device, or in cases where incision and drainage alone fails to achieve adequate clinical response36. Hospitalization and parenteral antibiotics should be considered for patients with extensive skin involvement or signs of systemic toxicity.

Table 5: Empiric antibiotic treatment of abscesses following source control36

Outpatient If suspicion for MRSA:

-Clindamycin 300-450mg po 3-4 times per day for 5-7 days

-Trimethoprim/sulfamethoxazole 1-2 DS tablets po bid for 5-7 days

-Doxycycline 100mg po bid for 5-7 days

If no suspicion for MRSA:

-Dicloxacillin 500mg po bid for 5-7 days

-Cephalexin 500mg po bid for 5-7 days

Inpatient -Vancomycin 15-20mg/kg/dose IV bid

-Clindamycin 600mg IV tid 

-Linezolid 600mg IV two times per day

-Daptomycin 4mg/kg/dose IV once daily

Sexually-Transmitted and Vulvovaginal Infections

Sexually transmitted infections (STI) are a diagnosis of immense public health importance. While the results of lab testing are often not available in the emergency department, physicians should have a low threshold for the initiation of treatment in patients with presentations consistent with STI. Treatment for common STIs is outlined in Table 6 below45. Counseling patients about safe sex practices and urging them to inform their partners is paramount to infection control.

Pelvic Inflammatory Disease

Pelvic inflammatory disease (PID) is infection of the upper genital tract (uterus, endometrium, fallopian tubes, ovaries) in women. PID may extend to involve adjacent structures, causing periappendicitis, pelvic peritonitis, and perihepatitis (Fitz-Hugh-Curtis syndrome). The majority of PID is caused by ascending sexually-transmitted infections (STI), with Neisseria gonorrhea and Chlamydia trachomatis being the most commonly implicated pathogens in PID45. The diagnosis of PID is often a presumptive one based on presentation. Due to the risk for tubal scarring leading to infertility or risk of ectopic pregnancy, even minimal symptoms without an alternative diagnosis warrant the start of antibiotic therapy to reduce the risk of serious complications due to delay of therapy. Mild to moderate disease can be treated as an outpatient. Indications for hospitalization and intravenous antibiotics include pregnancy, clinically severe disease, complicated PID (pelvic abscess), and intolerance to, noncompliance with, or failure of oral antibiotics. Empiric coverage for inpatient and outpatient management of pelvic inflammatory disease are outlined in Table 646,47.

Table 6: Recommended treatment regimens for select genitourinary infections45–47

Chlamydia -Azithromycin (1g po in one dose)

-Doxycycline (100mg bid for 7 day)

Gonorrhea* -Ceftriaxone (250mg IM or IV in one dose) plus azithromycin (1g po in one dose) or doxycycline (100mg bid for 7 days)
Trichomonas -Metronidazole (2g po in a single dose or 500mg bid for seven days)

-Tinidazole (2g po in a single dose)

Bacterial Vaginosis -Metronidazole (500mg  po bid for seven days)

-Metronidazole vaginal gel 0.75% (5g intravaginally for five days)

-Clindamycin vaginal gel 2% (5g intravaginally for seven days)

Candida Vulvovaginitis Fluconazole (150mg po in one dose)
Pelvic Inflammatory

Disease

Outpatient management -Ceftriaxone (250mg IM in one dose) plus doxycycline (100mg po bid for 14 days)

-Cefoxitin (2g IM) with probenecid (1g orally) plus doxycycline (100mg po bid for 14 days)

Inpatient management -Ceftriaxone (250mg IM in one dose) plus doxycycline (100mg po bid for 14 days)

-Cefoxitin (2g IM) with probenecid (1g orally) plus doxycycline (100mg po bid for 14 days)

*Patients with gonorrhea should also be treated for chlamydia due to high rates of concomitant infection.

Bacterial meningitis

While meningitis is not as common an emergency department diagnosis as the bacterial infections discussed above, patients with meningitis are often quite ill, and knowledge of appropriate antibiotic coverage can speed time to therapy. The most common causes of community-acquired meningitis in adults in developed countries are Streptococcus pneumoniae, Neisseria meningitidis, and, in older adults, Listeria monocytogenes48,49. Empiric treatment should be initiated as soon as meningitis is suspected. Empiric regimens should include ceftriaxone (2g every 12 hours) or cefotaxime (2g every 4-6 hours) for coverage of N. meningitidis and S. pneumoniae as well as vancomycin due to increasing rates of S. pneumoniae resistance to third-generation cephalosporins50,51. In patients >50 years of age or with immunocompromise, ampicillin (2g every 4 hours) should be added to provide coverage for L. monocytogenes49.

Adverse Effects of Antibiotic Use

A discussion of antibiotic use in the emergency department would be remiss without mention of the adverse effects of antibiotics commonly used in the ED. While the use of certain antibiotics may be unavoidable due to patient allergies or susceptibility patters, knowledge of the adverse effects of antibiotics may help guide therapeutic choices and inform or temper patient expectations.

Clostridium difficile infection should always be a consideration when starting antibiotics. Clindamycin is the most common culprit in antibiotic-associated C. difficile infection, but cephalosporins, penicillins, and fluoroquinolones are also common causes52–56. Aminoglycosides, tetracyclines, metronidazole, and vancomycin are rarely associated with C. difficile infection, though any antibiotic use increases the risk for C. difficile infection57. Other important adverse effects include QT prolongation with arrhythmia associated with macrolide and fluoroquinolone use and the risk of peripheral neuropathy and (the uncommon, but oft-cited) tendon rupture with fluoroquinolone use. Common or serious side effects of antibiotics used in the emergency department are summarized in Table 7 below.

Table 7: Common and serious adverse effects of commonly used antibiotics

Antibiotic Common Adverse Effects Serious Adverse Effects Comments
Beta-lactams C. diff infection, diarrhea Hypersensitivity reactions High risk of C. diff, especially with broader coverage and with ampicillin
Macrolides Diarrhea, nausea, vomiting, abdominal pain QT prolongation (especially with erythromycin)
Clindamycin C. diff infection, diarrhea Serious hypersensitivity reactions Most common cause of C. diff
Fluoroquinolones Anorexia, nausea, vomiting, abdominal pain Tendon rupture, peripheral neuropathy, QT prolongation High C. diff risk
Tetracyclines Nausea, diarrhea, photosensitivity Inhibition of bone growth and tooth discoloration (a concern in children) Low C. diff risk
Vancomycin Abdominal pain, nausea Nephrotoxicity, ototoxicity, Red man syndrome, hypotension Red man syndrome can be prevented with pretreatment with antihistamines
Aminoglycosides Nephrotoxicity, ototoxicity Need frequent monitoring of drug levels
Metronidazole Headache, dizziness, metallic taste Disulfiram-like reaction Low C. diff risk
  • Summary

Table 8: Common and serious bacterial infections and recommended empiric treatment

Infection Important organisms to cover Recommended Regimens
Community-acquired pneumonia S. pneumoniae CAP outpatient: doxycycline, macrolide +/- penicillin or cephalosporin

CAP inpatient, mild: respiratory fluoroquinolone, macrolide + penicillin or cephalosporin

S. pneumoniae, L. pneumophila, S. aureus CAP inpatient, severe: penicillin or cephalosporin+ fluoroquinolone OR azithromycin
Hospital-acquired pneumonia S. pneumoniae, MRSA, P. aeruginosa HAP inpatient: anti-pseudomonal penicillin or cephalosporin, or fluoroquinolone, or carbapenem + vancomycin/linezolid
Uncomplicated cystitis E. coli Nitrofurantoin or fosfomycin or TMP/SMX or ciprofloxacin

 

Complicated cystitis or uncomplicated pyelonephritis E. coli, Pseudomonas sp., Staphylococcus sp. Outpatient: Fluoroquinolone

Inpatient: Fluoroquinolone or aminoglycoside or third-generation cephalosporin or carbapenem

Complicated pyelonephritis E. coli, Pseudomonas sp., Staphylococcus sp. Inpatient, mild-moderate: third-generation cephalosporin or monobactam

Inpatient, severe: anti-pseudomonal penicillin or cephalosporin, carbapenem

Asymptomatic bacteriuria or simple cystitis in the pregnant patient E. coli Nitrofurantoin or TMP/SMX or fosfomycin, or penicillin or cephalosporin with gram-negative coverage
Nonpurulent cellulitis or abscess without MRSA risk factors, erysipelas Beta-hemolytic streptococcal species, MSSA Outpatient and inpatient: staphylococcal penicillin or cephalosporin
Purulent cellulitis, nonpurulent cellulitis or abscess with MRSA risk factors Beta-hemolytic streptococcal species, MSSA, MRSA Outpatient: Clindamycin or TMP/SMX or doxycycline

Inpatient: Vancomycin or clindamycin

Chlamydia C. trachomatis Azithromycin or doxycycline
Gonorrhea N. gonorrhea AND C. trachomatis Ceftriaxone plus azithromycin or doxycycline
Trichomonas Trichomonas vaginalis Metronidazole or tinidazole
Bacterial vaginosis Polymicrobial, anaerobic gram-negative rods Metronidazole oral or intravaginal gel or clindamycin
Candida Vulvovaginitis C. albicans, C. glabrata Fluconazole
Pelvic Inflammatory Disease N. gonorrhea, C. trachomatis Inpatient and outpatient: third generation cephalosporin plus doxycycline
Bacterial meningitis S. pneumoniae, N. meningitidis, L. monocytogenes (if >50 years or immunocompromised) Vancomycin plus third generation cephalosporin +/- ampicillin if age >50 or immunocompromised

 

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Seizure Mimics: Pearls & Pitfalls

Authors: James L Webb, MD (Internal Medicine, SAUSHEC, USAF) and Brit Long, MD (@long_brit) // Edited by: Erica Simon, DO, MHA (@E_M_Simon) & Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

A 20 year-old female presents to the ED after a witnessed fall. According to bystanders, the young woman was walking towards a gym treadmill when she collapsed to the floor below, convulsing for approximately1-2 minutes. Upon EMS arrival VS were within normal limits, GCS was noted as 14 (confusion, orientation only to self), EKG revealed NSR, and accucheck demonstrated a blood glucose of 134. Intravenous access was obtained en route to your facility.

As you interview and examine the patient, you note ABCs intact, a GCS of 15, an ample history remarkable only for report of a “rising feeling in the abdomen” prior to the event, and a secondary survey without obvious signs of trauma. ED evaluation, to include a CBC, CMP, EKG, and non-contrasted head CT are all within normal limits. Urine Hcg is negative.

Was this a seizure? What’s the appropriate patient disposition? If you’ve got questions, we’ve got important details on seizures and their mimics.

 

Background

Current data indicate that nearly 2 million U.S. residents are affected by Epilepsy.1-2 In addition to this population, approximately 150,000 Americans (age >18 years) present to healthcare providers annually following an apparent first seizure.1-2 As assigning a diagnosis a seizure or seizure disorder is not without significant health and quality of life implications (employment repercussions, driving restrictions, etc.1-5), emergency physicians must be aware of conditions that may mimic seizure activity: syncope, psychogenic non-epileptic seizures, metabolic derangements, stroke or TIA, sleep disorders, and migraines.

 

Seizures – A Review

Seizures result from abnormal neurologic electrical activity. This abnormal activity can occur in both hemispheres (generalized seizure) or within one hemisphere (focal seizure), which may spread to the entire brain. Generalized seizures are more common than focal seizures, and often have a genetic association.6 Generalized tonic-clonic seizures most frequently occur in adults – the motions of which consist of a tonic phase with muscle stiffening, followed by a clonic phase with rhythmic muscle contractions.6-7 Focal seizures often occur in the setting of cerebral insult.7 Unlike generalized seizures, symptoms of focal seizures vary according to the anatomic location of the abnormal electrical activity.6,8

Seizures can be classified as provoked or unprovoked. Provoked seizures are those with identifiable causes, which can be isolated to the brain, or are thought to occur secondary to a systemic disorder or illness. Such causes include: brain trauma, CNS infection (i.e. meningitis, encephalitis, brain abscess), anoxic brain injury, intracranial hemorrhage or surgery, metabolic disorders, illicit drug abuse or intoxication (most commonly tricyclic antidepressants and isoniazid), or alcohol withdrawal.9,10  Seizures may also occur in the setting of metabolic derangements (hypoglycemia or hyponatremia).9-12

 Unprovoked seizures are those with no discernible cause, or those occurring greater than seven days following precipitating factors or events. What factors or events might the emergency physician identify through the H&P?

  • Pregnant patient with a seizure –>evaluate for eclampsia
  • Child with an recent illness –>evaluate for personal and familial history of febrile seizures
  • In all patients –>inquire regarding a history of recent head trauma (occurring within 1 week prior to presentation)

It is particularly important to perform a thorough H&P in this patient population, as 50% of individuals experiencing an unprovoked seizure will experience a recurrence.11

 

Approach

Patients presenting with altered mental status (AMS)/seizure concern should be quickly assessed10,13-15,17:

  • ABCs
  • Consider obtaining a POC glucose level
  • First line treatment for seizure activity: benzodiazepines (lorazepam 0.1 mg/kg IV)
    • Second line agents: phenytoin, fosphenytoin, levetiracetam, or valproic acid
      • Intubation with propofol or ketamine with contiguous EEG (in consultation with neurology) may be required.14-17
    • After addressing ABCs, perform an H&P, complete a physical examination (PE), and obtain IV access. Consider: CBC, CMP, EKG, serum Hcg, anticonvulsant level if applicable, imaging as appropriate (CT recommended in the setting of new focal deficits, head trauma, continued AMS, immunocompromised state, history of cancer, persistent fever, focal seizures, history of stroke, or anticoagulation), +/- an LP.13,15-19
      • Note: neuroimaging should be performed in patients with suspected new-onset seizures, but may occur in the outpatient setting for those with a first time generalized tonic-clonic seizure with a normal neurologic exam. MRI is preferable with a higher yield of identifying abnormalities in the non-emergent setting.13,15-19
    • Disposition is often determined in conjunction with specialty consultation. Admission may be required in the setting of persistent neurologic deficit, persistent AMS, or poor social situation.13,15-19 Patients who return to mental status baseline, possess a normal neurologic exam, and whose labs and imaging are without pathology, may be discharged with outpatient follow-up.13,19

 For an in-depth discussion of seizure evaluation and management, see:  http://www.emdocs.net/treatment-of-seizures-in-the-emergency-department-pearls-and-pitfalls/

 

Evaluating Seizure Activity in Patients with Return to Mental Status Baseline

 A definitive diagnosis of seizure is made by EEG interpretation during seizure activity. As this is often times impossible in the ED setting, the emergency physician must seek out signs and symptoms commonly associated with seizure activity9,13,20:

  • HPI significant for aura: déjà vu, a rising sensation in the abdomen, abnormal taste or smell, or autonomic changes.
    • Activity commonly associated with a true seizure: witnessed tonic/clonic movements or observed head turning in the setting of a generalized seizure, or the abrupt onset of limb movements, abnormal sensations, or hallucinations in the setting of a focal seizure. 6,7,20
    • A postictal period occurring for minutes to hours with confusion, disorientation, and drowsiness.
  • Physical exam remarkable for tongue biting.

See Table 1 for signs and symptoms related to seizure activity in studies comparing seizures versus syncope. *Urinary incontinence was demonstrated to lack clinical significance.

screen-shot-2017-01-01-at-3-57-34-pm

What about laboratory studies?

 A lactate level may be useful in differentiating seizures from psychogenic non-epileptic seizures and syncope (sensitivity of 88%, specificity 87% for true seizure activity), 24 while an elevated CK is suggestive of epileptic seizures (specificity 85-100%), but demonstrates variable sensitivity (15-88%).25

 

Seizure Mimics

Studies indicate that approximately 20% of patients presenting for evaluation of seizure are misdiagnosed as having epilepsy.26  Conditions most commonly mistaken for epitileptiform seizure activity include syncope and psychogenic non-epileptic seizures.5 Detailed below is a review of seizure mimics with tips and tricks for ED evaluation and disposition.

Syncope

Syncope is a sudden loss of consciousness (LOC) due to decreased cerebral perfusion, resulting in loss of postural tone, with rapid return to mental status baseline. Syncope may be cardiac, orthostatic, or neurocardiogenic (vasovagal) in origin.

Historical evidence favoring a syncopal episode versus a seizure27-34:

  • Presentation –>LOC with rapid return to mental status baseline.
  • History –>Remarkable for precipitating factors: recent illness (emesis/diarrhea – hypovolemia), recent medication changes (i.e. B-blockers and bradycardia, diuretics causing hypovolemia, etc.), LOC following increased vagal tone (coughing, defecation, shaving).  LOC during physical exertion. In obtaining the HPI, it is important to note that myoclonic jerking occurs in up to 90% of patients experiencing syncope.27

Management and Disposition Pearls:

  • Evaluation –> EKG for dysrhythmias, consider a CBC and CMP to assess for anemia and electrolyte derangement, consider cardiac markers as indicated.
  • Disposition–>As appropriate. Referral for tilt-table testing in the setting of neurocardiogenic syncope may be considered after ruling out life-threatening conditions.

Notes on Syncope of Cardiac Origin

Syncope secondary to cardiac dysrhythmias or structural heart disease may present similarly to a seizure, however, the following suggest cardiac origin27-29, 33,34:

  • Presentation –>Most commonly an elderly patient.
  • History –>The absence of a prodrome; ROS positive for palpitations prior to LOC; CP or LOC during exertion.

Management and Disposition Pearls:

  • Evaluation –>PE for murmurs, rubs, gallops and s/s of heart failure (JVD, peripheral edema, hepatojugular reflex, etc.); EKG for dysrhythmias: SVT, VT, Mobitz type II second-degree, or third-degree AV block, bundle branch blocks, Long QT Syndrome, Brugada Syndrome, WPW Syndrome, Right Ventricular Dysplasia, and pacemaker malfunction have all been associated with syncopal episodes.33 Consider bedside POCUS or formal echocardiogram to evaluate for cardiac structural anomalies.
  • Disposition –>As appropriate. In the large majority of cases admission is required for adjunct testing.

 

Psychogenic Non-Epileptic Seizure (PNES) Disorder

PNES, a condition characterized by the presence of seizure-like activity occurring in the absence of EEG changes, is difficult to differentiate from a true seizure in the emergency setting; even more so as nearly 40% of patients with epilepsy suffer from the disorder.35 Characteristics that make PNES more likely include35-39:

  • Presentation –>Patient in their 20s-30s,35 experiencing an event characterized by asynchronous extremity movements, rapid head turning, pelvic thrusting, eye closing, or geotropic eye movements. Clinical clues useful for the provider: the absence of tongue biting, a prolonged duration (>2 mins), a patient who can recall the event, or a patient who was witnessed to have been crying during the seizure-like activity.
  • History –>Approximately 70% have a PMHx of a psychiatric disorder (depression, PTSD, personality disorder).36,37

Management and Disposition Pearls:

  • Evaluation –>When in doubt: treatment as appropriate (ABCs +/- benzodiazepines). Video EEG is the gold standard for diagnosis, therefore specialty consultation is required.
  • Disposition –>In consultation with neurology/neuropsychiatry. Treatment is often targeted to the underlying psychiatric disorder.39

 

Metabolic Derangements

Metabolic disorders are identified in 2.4-8% of patients presenting with first generalized seizure.9,10,13 Hypoglycemia and hyponatremia are the most common, but other disorders may include hypernatremia, hyperglycemia, hypercalcemia, and uremia.9,10,13

 Management and Disposition Pearls:

  • Evaluation –>Accucheck for all patients with AMS/seizure activity. CMP as appropriate.
  • Disposition –>Treatment and admission requirements based upon laboratory findings.

 

Stroke and TIA 

Stroke/TIA can be confused with a seizure when there is resolution of the neurologic deficit previously caused by cerebral ischemia. Characteristics of Stroke/TIA18,40,41:

  • Presentation –>Most commonly a middle-aged or elderly patient. HPI remarkable for negative symptoms: numbness, weakness, or blindness.
  • History –>PMHx significant for HTN, HLD, cardiac arrhythmia, family history of CVA

Management and Disposition Pearls:

  • Evaluation –>PE: focused neurological examination, accucheck, EKG for dysrhythmias, performance of risk stratification to determine the requirement for cerebral vasculature imaging.
  • Disposition –>As appropriate. Inpatient admission may be required for MRI, carotid ultrasonography, echocardiography, and medication optimization.

 

Sleep Disorders

Narcolepsy with cataplexy may present similarly to seizures. Narcolepsy is defined by excessive daytime sleepiness, lapses into sleep, or multiple naps during the same day at least 3 times per week for a duration of 3 months time. Cataplexy is the sudden loss of tone in response to emotion. 42-45

  • Presentation –>Patient suddenly collapses, but rapidly recovers to mental status baseline with complete recollection of the  event. 42-45

Management and Disposition Pearls:

  • Evaluation –>Thorough history-taking often allows differentiation from seizure activity.
  • Disposition –>Specialty referral for overnight polysomnography and sleep latency testing. Driving restriction is often state-mandated if the condition is suspected. 42-45

 

Migraines

 Migraines are recurrent headaches with or without aura (visual or sensory symptoms). Symptoms include throbbing headache, nausea, vomiting, and sensitivity to light and sound. Auras are often positive visual symptoms. Migraines with aura are similar to certain focal seizures with visual symptoms (hallucinations) or generalized seizure prodrome (aura). Signs and symptoms making a diagnosis of migraine more likely19, 50-52:

  • Presentation –>headache characterized by unilateral pain, throbbing pain, moderate-severe pain, and aggravated by physical activity, +/- nausea/vomiting or photo-/phonophobia
  • History –>PMHx significant for migraines.

Keep in mind, complex migraines may present with neurologic symptoms causing weakness, alteration in consciousness, or LOC.

Management and Disposition Pearls:

  • Evaluation –>PE: focused neurological examination. Rule out intracranial pathology as appropriate (CVA/SAH/meningitis/encephalitis – CT, LP, etc.)
  • Disposition –>As appropriate. In the setting of negative imaging (+/- negative LP), neurology consultation is appropriate as prophylactic medications (TCAs, B-blockers, anti-epileptics) may be considered for outpatient therapy.

 

Summary

– Seizures are caused by abnormal neurologic electrical activity resulting in motor, sensory, and behavioral symptoms.
In all patients presenting with AMS or actively seizing: ABCs, accucheck, initiate therapy as appropriate (benzodiazepines first line).
– For patients presenting after return to baseline mental status: a thorough history and physical examination are key to differentiating between a true seizure and its mimic.
– If a seizure is not suspected, consider syncope, psychogenic non-epileptic seizures, stroke or TIA, sleep disorders, and migraines.

 

References/Further Reading

  1. Hauser WA, Beghi E. First seizure definitions and worldwide incidence and mortality. Epilepsia. 2008;49 Suppl 1:8-12.
  2. Krumholz A, Wiebe S, Gronseth GS, et al. Evidence-Based Guideline: Management of an Unprovoked First Seizure in Adults: Report of the Guideline Development Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Epilepsy Curr. 2015 May-Jun;15(3):144-52.
  3. Lowenstein DH, Alldredge BK. Status epilepticus. N Engl J Med. 1998 Apr 2;338(14):970-6.
  4. England MJ, Livermari CT, Schultz AM, Strawbridge LM Institute of Medicine (US) Committee on the Public Health Dimensions of the Epilepsies; England MJ, Livermari CT, Schultz AM, Strawbridge LM, editors. Epilepsy Across the Spectrum: Promoting Health and Understanding. Washington, DC: The National Academies Press; 2012.
  5. Xu Y, Nguyen D, Mohamed A, et al. Frequency of a false positive diagnosis of epilepsy: A systematic review of observational studies. 2016 Aug 23;41:167-174.
  6. Berg AT, Berkovic SF, Brodie MJ, et al. Revised terminology and concepts for organization of seizures and epilepsies: report of the ILAE Commission on Classification and Terminology, 2005-2009. Epilepsia. 2010 Apr;51(4):676-85.
  7. Chang BS, Lowenstein DH. Epilepsy. N Engl J Med. 2003 Sep 25;349(13):1257-66.
  8. Fisher RS, Acevedo C, Arzimanoglou A, et al. ILAE official report: a practical clinical definition of epilepsy. Epilepsia. 2014;55(4):475.
  9. Beghi E, Carpio A, Forsgren L, et al. Recommendation for a definition of acute symptomatic seizure. Epilepsia. 2010;51(4):671.
  10. Fields MC, Labovitz DL, French JA. Hospital-onset seizures: an inpatient study. JAMA Neurol. 2013 Mar;70(3):360-4.
  11. Riggs JE. Neurologic manifestations of electrolyte disturbances. Neurol Clin. 2002 Feb;20(1):227-39.
  12. D’Onofrio G, Rathlev NK, Ulrich AS, et al. Lorazepam for the prevention of recurrent seizures related to alcohol. N Engl J Med. 1999 Mar 25;340(12):915-9.
  13. Dunn MJ, Breen DP, Davenport RJ, Gray AJ. Early management of adults with an uncomplicated first generalised seizure. Emerg Med J. 2005 Apr;22(4):237-42.
  14. Pillow MT. Seizure Assessment in the Emergency Department. Emedicine: Medscape. http://emedicine.medscape.com/article/1609294-overview. Accessed 11 August 2016.
  15. American College of Emergency Physicians. Clinical policy: Critical issues in the evaluation and management of adult patients presenting to the emergency department with seizures. Ann Emerg Med. 2014 Apr;63(4):437-47.e15.
  16. Shorvon S, Ferlisi M. The treatment of super-refractory status epilepticus: a critical review of available therapies and a clinical treatment protocol. Brain. 2011 Oct;134(Pt 10):2802-18.
  17. Brophy, Gretchen M., Claassen J, et al. Guidelines for the evaluation and management of status epilepticus. Neurocrit Care 2012 Aug;17(1):3-23.
  18. Harden CL, Huff JS, Schwartz TH, et al. Reassessment: neuroimaging in the emergency patient presenting with seizure (an evidence-based review): report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2007 Oct 30;69(18):1772-80.
  19. French JA, Pedley TA. Clinical practice. Initial management of epilepsy. N Engl J Med. 2008 Jul 10;359(2):166-76.
  20. Manford M. Assessment and investigation of possible epileptic seizures. J Neurol Neurosurg Psychiatry. 2001;70(Suppl 2):ii3–ii8.
  21. Brigo F, Nardone R, Bongiovanni LG. Value of tongue biting in the differential diagnosis between epileptic seizures and syncope. Seizure. 2012 Oct;21(8):568-72.
  22. Brigo F, Nardone R, Ausserer H, et al. The diagnostic value of urinary incontinence in the differential diagnosis of seizures. Seizure. 2013 Mar;22(2):85-90.
  23. Sheldon R, Rose S, Ritchie D, et al. Historical criteria that distinguish syncope from seizures. J Am Coll Cardiol. 2002 Jul 3;40(1):142-8.
  24. Matz O, Zdebik C, Zechbauer S, et al. Lactate as a diagnostic marker in transient loss of consciousness. Seizure. 2016 Aug;40:71-5.
  25. Brigo F, Igwe SC, Erro R, Bongiovanni LG, et al. Postictal serum creatine kinase for the differential diagnosis of epileptic seizures and psychogenic non-epileptic seizures: a systematic review. J Neurol. 2015 Feb;262(2):251-7.
  26. Smith PE. Epilepsy: mimics, borderland and chameleons. Pract Neurol. 2012 Oct;12(5):299-307.
  27. Chen LY, Benditt DG, Shen WK. Management of syncope in adults: an update. Mayo Clin Proc. 2008 Nov;83(11):1280-93.
  28. Walsh K, Hoffmayer K, Hamdan MH. Syncope: diagnosis and management. Curr Probl Cardiol. 2015 Feb;40(2):51-86.
  29. Huff JS, Decker WW, Quinn JV, et al.; American College of Emergency Physicians. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with syncope. Ann Emerg Med. 2007 Apr;49(4):431-44.
  30. Grubb BP. Clinical practice. Neurocardiogenic syncope. N Engl J Med. 2005 Mar 10;352(10):1004-10.
  31. Lempert T, Bauer M, Schmidt D. Syncope: a videometric analysis of 56 episodes of transient cerebral hypoxia. Ann Neurol 1994 Aug;36(2):233–7.
  32. McKeon A, Vaughan C, Delanty N. Seizure versus syncope. Lancet Neurol. 2006 Feb;5(2):171-80.
  33. Morag R. Syncope. Emedicine: Medscape. http://emedicine.medscape.com/article/811669-overview. Accessed 15 August 2016.
  34. Moya A, Sutton R, Ammirati F, et al. Guidelines for the diagnosis and management of syncope (version 2009). the task force for the diagnosis and management of syncope of the European Society of Cardiology (ESC). Eur Heart J. 2009 Nov;30(21):2631-71.
  35. Alsaadi TM, Marquez AV. Psychogenic nonepileptic seizures. Am Fam Physician. 2005 Sep 1;72(5):849-56.
  36. Panagos PD, Merchant RC, Alunday RL. Psychogenic seizures: a focused clinical review for the emergency medicine practitioner. Postgrad Med. 2010 Jan;122(1):34-8.
  37. Shaibani A, Sabbagh MN. Pseudoneurologic syndromes: recognition and diagnosis. Am Fam Physician. 1998 May 15;57(10):2485-94.
  38. LaFrance WC Jr, Baker GA, Duncan R, et al. Minimum requirements for the diagnosis of psychogenic nonepileptic seizures: a staged approach: a report from the International League Against Epilepsy Nonepileptic Seizures Task Force. 2013 Nov;54(11):2005-18.
  39. Siket MS, Merchant RC. Psychogenic seizures: A review and description of pitfalls in their acute diagnosis and management in the emergency department. Emerg Med Clin North Am. 2011 Feb;29(1):73-81.
  40. Johnston SC. Clinical practice. Transient ischemic attack. N Engl J Med 2002 Nov 21; 347(21):1687-92.
  41. Nanda A. Transient Ischemic Attack. Emedicine: Medscape. http://emedicine.medscape.com/article/1910519-overview. Accessed 22 August 2016.
  42. American Academy of Sleep Medicine. The International Classification of Sleep Disorders-Revised: Diagnostic and Coding Manual. 3rd ed. Rochester, MN: American Academy of Sleep Medicine; 2014.
  43. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. Arlington, VA: American Psychiatric Association; 2013. 372-78.
  44. Bozorg, A. Narcolepsy. Emedicine: Medscape. http://emedicine.medscape.com/article/1188433-overview. Accessed 22 August 2016.
  45. Scammell TE. Narcolepsy. N Engl J Med. 2015 Dec 31;373(27):2654-62.
  46. Tarsy D, Simon D. Dystonia. N Engl J Med. 2006 Aug 24;355(8):818-29.
  47. Smith PE. If it’s not Epilepsy. J Neurol Neurosurg Psychiatry 2001;70:9-14.
  48. Moberg-Wolff EA. Dystonias. Emedicine: Medscape. http://emedicine.medscape.com/article/312648-overview. Accessed 22 August 2016.
  49. Albanese A, Barnes MP, Bhatia KP, et al. A systematic review on the diagnosis and treatment of primary (idiopathic) dystonia and dystonia plus syndromes: report of an EFNS/MDS-ES Task Force. Eur J Neurol. 2006 May;13(5):433-44.
  50. Sances G, Guaschino E, Perucca P, et al. Migralepsy: a call for a revision of the definition. Epilepsia 2009;50:2487–96.
  51. Goadsby PJ, Lipton RB, Ferrari MD. Migraine–current understanding and treatment. N Engl J Med. 2002 Jan 24;346(4):257-70.
  52. Chawla J. Migraine. Emedicine: Medscape. http://emedicine.medscape.com/article/1142556-overv

 

 

The Road to Academic Emergency Medicine

Authors: Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital), and Jennifer Robertson, MD, MSEd (Assistant Professor, Emory University, Atlanta GA)

Emergency physicians train to be highly proficient in the resuscitation and management of acutely ill patients.  In addition, all emergency medicine (EM) training programs focus on preparing physicians to care for these patients in community practice settings. While most EM graduates go on to practice in community settings, academic EM is an option for interested physicians.

In general, academic EM was established to provide the teaching, research, and leadership goals of the specialty. For current residents and community doctors, specific pathways for practicing academic EM are now available, which allow new graduates to directly enter academic EM from residency or transition from community to academic EM.

The decision to practice academic or community practice can be a difficult one to make, as there are perks and drawbacks in both settings. This post will evaluate the road to academic emergency medicine, the positives and negatives, and provide tips for success. However, before we start, we need to understand the difference between academic and community EM.

What is academic emergency medicine?

An academic emergency medicine practice is defined by its providers spending the majority of their time in resident education/supervision, along with scholarly activity (academic writing, teaching, or research).1-5 This focus came into existence in order to meet the teaching, research, administrative, and educational aspects of emergency medicine. The majority of academic providers are associated with a teaching hospital, and many have time protected for academic pursuits. Over 40% of current residents are interested in pursuing an academic career, but the road to determining whether an academic or community practice is right for you can be difficult.1

Unfortunately, many graduating residents feel ill prepared to begin a career in academics, and program directors agree. A survey of EM residency directors found that only 29% feel their program graduates are prepared for an academic career involving original research.2 Obstacles include insufficient research training and resident difficulty in finding knowledgeable collaborators and mentors.

What is community practice?

Community EM refers to practices based mostly on clinical medicine. In community EM, providers spend the majority of their time on clinical duties (usually shifts), rather than supervising and educating residents. Providers may have other obligations such as administrative tasks, but their primary focus is direct patient care. However, the actual amount of patient care duties will vary within individual departments, hospitals, and even parts of the country. Pay is often based on the number of shifts and relative value units (RVUs) per shift. However, overall pay can be also be affected by partnerships, bonuses based on productivity, patient satisfaction, and quality measures.

 Why academic EM?

Academic medicine seeks to pursue scholarship, expand knowledge, and pass on that knowledge. This is most commonly done through resident education and supervision. Education and scholarly activity are ultimately the goals, though these can take several forms. Academics provides career diversity, expertise development, formation of educational philosophy and techniques, specialty advancement, networking and formation of relationships, and research development. It can allow physicians to influence hospital and institution practices, and provide a bit of control in his or her schedule. Best of all, academic EM gives physicians the chance to affect and improve the care of many patients through resident education and scholarly activity.

There are several negative factors associated with academic EM. You will likely work more hours combined, make less money, work fewer clinical hours, and experience more pressure to be scholarly productive (we will cover this later), as compared to community practice.

We know the decision is difficult.

Residency rotations in both settings can provide glimpses of both types of practice. Hybrid programs are also in existence, and it is never too late to switch from one to the other.

In the meantime, how should a resident prepare for academic EM? Residency is the time to obtain several important skills.

1) The first is the most fundamental and important: clinical competency. Excellence in patient care is fine-tuned during residency. Every patient encounter, lecture, and time spent studying should focus on learning and enhancing clinical evaluation and management.

2) The next skill is teaching and knowledge dissemination. This is primarily learned via supervising junior residents or medical students at the bedside or by mentorship. In addition, lecture-based learning and teaching are also paramount.

3) Research skills are essential, no matter what environment you will practice in. Experience in reviewing the literature, establishing research questions and study designs, data collection/analysis, and presentation of data is important.  This can be difficult to obtain through journal clubs only, and some form of higher education is often beneficial for developing key research skills.

4) Expressing ideas and disseminating your knowledge are important, not only for abstracts, papers, and grants, but for hospital protocols and committees.

5) Administrative skills are helpful for both community and academic settings.

6) As most physicians (especially in EM) know, “people” skills are essential, not only to your clinical practice but also in forming long-lasting relationships and collaborations. Whether you go into academic or community EM, these skills are critical.

7) Finally, developing a personal learning strategy is important for continued clinical development.

Ok, so academic EM sounds like your thing… Now what?

There are several aspects of career planning that will help you find the best fit and succeed in academic EM. Each of the following components summarize key information for not only academic survival, but also for long term success.

Preparing for Academics

  1. The importance of a mentor – Mentorship is a key component of a healthy career. Forming a healthy mentoring relationship leads to academic success and career satisfaction, especially when formal postgraduate training is not completed.15-19 Look for mentors within the department, your institution, other institutions, prior training places, and from regional/national meetings. Mentors assist in setting and achieving goals, providing feedback on performance, building confidence and moral support, helping you get involved in committee work, introducing mentees to leaders in your field, protecting you and your interests, and keeping you on track. Your mentor is your advocate.   When choosing a mentor, there are several considerations. These include ensuring the mentor has a track record in the area of your interest, has available time and interest, possesses a personality that fits, and does not possess conflicts of interest. More than one mentor can be helpful, and mentors outside of EM can provide a different viewpoint for you.
  1. Setting time goals: 1, 3, 5, 10 years – Short and long term goals are necessary for a successful career, as a resident and faculty member. You have probably been setting goals all of your life, and just like before, it is important to possess concrete and obtainable goals. A career plan should be established, with each year broken down into separate goals that work toward achieving the long term goal. Keep in mind these may need to be revised, and these goals should be used as a guide for feedback/evaluation sessions. These goals should be discussed with your mentor, with regular meetings and feedback sessions to keep you on track.
  1. Finding your niche – Even though EM is a broad specialty, the majority of academic leaders are known for expertise in one or several areas of knowledge. This is essential for those forming a career: determine what interests or excites you and what opportunities are available to focus on these interests. Ask yourself what your passion is and what excites you. Another key is to consider what you do not enjoy. When you recognize what you like and dislike, then seek to get involved in your area of interest, with a goal of academic productivity (through research, lectures, or publishing). Research projects should also focus on this. Because of EM’s broad spectrum, some may want to target what’s currently available at their institution. Others may take too much on, spreading themselves too thin. It can be difficult to focus on one or two areas, but do your best to choose what interests you the most.
  1. Keep an academic portfolio and curriculum vitae – As most know, a curriculum vitae (CV) is a necessity. Even though different formats may be used, all contain the same information. Your mentor and senior department leadership can provide valuable assistance in forming and fine-tuning your CV. A personal academic profile or portfolio should also be maintained, as this summarizes your teaching, compiles your awards and evaluations, and should also contain examples of lectures and other academic achievements. Both are vital for academic success and promotion.
  1. Join an EM organization – Several emergency medicine societies are available, and each can provide significant benefits. Organizations include AAEM, ACEP, SAEM, CORD, NAEMSP, and several others. These organizations provide valuable networking and socializing opportunities for residents and faculty of all levels. Many of these organizations also have committees, which provide opportunities to improve nonclinical educational skills, form relationships with physicians with similar interests, and contribute to EM. If you can, attend meetings that allow open attendance. You will gain valuable skills in learning how to manage meetings and conferences by watching those in charge.
  1. Networking – There are several aspects to networking. Joining a committee or task force can be helpful and provide links to other departments and senior leaders. Speaking with everyone in the department, from interns to department chair, can form relationships that last. Everyone in EM has lessons learned or advice they can offer. Ask senior department members for connections or to introduce you to other leaders.
  1. Remember your colleagues and provide assistance to others – An academic physician with goals will develop and advance. As you begin to grow in your career, seek to help and mentor others. You obtained your success with the assistance of others, including your mentor and family, and you need to extend this same courtesy to others around you. Involve others in your projects and educational goals. By seeking the advancement of other EM colleagues, you form friendships and long-lasting relationships. If you switched programs, remember those back home and acknowledge them in your success.

What about postgraduate training?

Postgraduate training can help through providing focus on future work, as well as training in teaching, writing, research, and funding. Unfortunately, medical school and residency often do not prepare physicians for an academic career. Though not mandatory for an academic position, postgraduate training can facilitate academic training, enhance career satisfaction, and increase chances of academic success. This training also assists mentoring relationships and collaborative relationships. Dedicated postgraduate training may be the only means of obtaining truly protected time to develop academic skills. Interestingly, fellowship or postgraduate-trained physicians are more likely to obtain success and career satisfaction if involved in an academic program. This training provides increased job mastery, leading to less stress, greater certainty, and improved vision of career goals. Fellowships include pediatric EM, toxicology, undersea and hyperbaric medicine, sports medicine, ultrasound, palliative care, EMS, critical care, and several others. However, further training does delay maximum salary potential.

If you are considering a fellowship, look at each program’s expected clinical time, training value, access to mentors, research opportunities, and total experience. The vast majority of EM fellowship programs offer complete, valuable experiences. If interested in education, fellowship training necessity is less defined. This fellowship is growing, but many departments offer formal, structured, multiyear educational training opportunities. For more information on fellowships, please see EMRA’s complete guide at: https://www.emra.org/uploadedfiles/emra/emra_publications/emra_fellowshipguide_v1_0816.pdf

The nuts and bolts for success in academic EM

What roles are there? Academic EM is comprised of many positions, and each institution and program will vary. Research roles include director, clinical trial director, research advisor, and research assistants’ program director. Educational roles can be residency director, associate residency director, medical student director, medical school leadership (dean), rotating resident director, fellowship director, CME director, hospital committee director, and others. There are also specialty roles such as ultrasound, hyperbaric chamber, chest pain, etc. Administrative roles include chief/chair, EMS director, operations director, pediatric ED director, CQI/Risk management director, and others.

Finding the right program – A program that will provide the environment and tools to help you flourish is important. First, characterize the institution, and evaluate what the program rewards (publications, lectures, clinical throughput). Are you just another cog in a vast machine? What would happen if you leave the program? You should ensure true opportunities to advance clinically and professionally exist in the program. Ultimately, look at what the institution and the program can do for you, rather than what you can do for the institution/program.  

Several program types or models possess different attributes. The egalitarian model treats everyone the same, regardless of specific talents or interests. Faculty work similar numbers of shifts, teach a similar number of lectures, carry similar administrate duties, and are expected to have similar productivity. The specialization model demonstrates a more team-based approach. All faculty work clinically, but the department can modify career development to better match faculty member strengths, weaknesses, interests, and dislikes. Shift numbers can vary based on faculty member roles and productivity.

Promotion and tenure – There are progressive ranks with timelines for academic physicians including assistant professor, associate professor, and full professor. Many are based on specific criteria such as publications, grants, regional/national recognition, teaching portfolios, and clinical productivity. An area of focus or niche can be helpful. This should be discussed with your department/program leadership and mentor. A mark of a strong program is a definitive track for career advancement, so you must inquire about this component of the academic program. Many offer workshops or provide further faculty development, which can significantly improve your advancement.

Research – Research is one of the fundamental means of growth for EM. The research environment physicians experience during residency often shapes future interest in research.1,4  At its core, research involves formulating a question, addressing the question with appropriate study design, collection and interpretation of data, and presenting the results in a peer-reviewed journal. This is often a long process, requiring time, effort, and mentorship for residents. Faculty have several goals when it comes to research: conducting research themselves, educating residents on scientific study, and/or how to conduct a study.

A large number of relevant areas of study are in existence. The majority of academic centers will desire their physicians to be “academically productive,” or obtain clinically relevant publications or grants. Research topics can be clinical, basic science, education, policy, or clinical operations. Mentorship and senior physician assistance to residents and new faculty seeking a research track are essential. Properly forming a research question and designing a protocol can be challenging, and thus, the more experience you can obtain, the better.

Teaching – Education is one of the key factors in an academic position. All physicians teach, whether the audience is nurses, technicians, or other physicians. One major component of an academic program is working with residents. Most programs expect academic clinicians to teach on shift as well as present lectures at conferences several times per year. This aspect is often one of the most fulfilling aspects of academic medicine, as you have the opportunity to affect the growth of future EM physicians. You may also work with students and off-service residents, and your relationship with these learners can have significant impact on their education, patient care, and relationships with the emergency department in their future careers.

Residency provides valuable time for honing educational skills. Some programs have dedicated programs for teaching, while others expect those interested in teaching to pick up the skills on their own. Focusing on shift teaching, presentation skills, and creation of lectures are great places to start for residents and new faculty. In emergency medicine, it can be difficult to work on your teaching skills, as there are so many options for teaching and so many different learners. Many adult learners seek information that will directly and positively impact their future careers. Thus, it is important to focus on how individuals learn and how you can make a difference in their learning experiences.

Teaching involves the ability to observe, question, and review trainee performance in actual patient care settings. When developing your own education techniques, look at the educators around you. New faculty and senior residents should pay close attention to those teachers who demonstrate master education skills. At the same time, strongly consider providers who are working on their own deficiencies. You should seek to recognize and understand these deficiencies so you can avoid them. Recognizing these skills and one’s own shortcomings will allow you to grow as an educator.

Scholarly Activity – One major aspect of an academic career is scholarly activity. In the past this included writing, either book chapters, original research, or review articles. The majority of academic programs still rely on clinical research and formal publication in medical journals. The academic environment is evolving, with several other opportunities. Free Open Access Medical Education (FOAMed) is one of these, with a growth of blogs and podcasts. Many academic physicians have now based their career on this avenue. Other options include ACEP’s Critical Decisions in Emergency Medicine, case reports, images, and specialty organization newsletters. Most programs will ask for at least one lecture per academic year, often grand rounds. However, speaking at regional, national, or international meetings is another means of scholarly productivity.

Once you have a project, seek to present the results in multiple settings and formats. Start with presenting an abstract at a conference, then seek publishing in a peer-reviewed journal. A FOAMed blog publication is also an option. Presenting this further at other functions, such as a grand rounds lecture, offers another avenue.  Publication in this format develops writing skills, develops an area of expertise, and advances your career. Remember, most programs still focus productivity on peer-reviewed publications.

The Literature – Residency programs usually promote some form of literature understanding through several formats: journal clubs, evidence-based medicine projects, and education on clinical shifts. Faculty may lead discussions or projects for literature awareness, aimed at promoting a deeper understanding of EM studies. For faculty, a key component of academics is staying abreast of the current literature, as well as “classic” studies. This can be difficult with all of your other duties and clinical shifts, but this is vital to your own education. There are multiple means of remaining current, from subscriptions to journals (Annals of EM, American Journal of EM, Journal of EM, etc.), podcasts (EM:RAP, EMA, EMCrit), and blogs (ALiEM, emDocs, Core EM, EM Updates, REBEL EM). FOAMed has revolutionized medical learning, and residents and faculty can use FOAMed to remain abreast of new, exciting medical updates.

Goals and Persistence – Specific goals with a timeline are a necessity for success in academic medicine, and they must be written down to solidify their importance. The act of setting the goal with timeline, verbalizing it, and writing it creates a commitment. Remember, academic medicine can be and will be difficult. There will be setbacks, but do not be discouraged. You will have papers and grants rejected. Make changes and keep going.

Collaboration – Finding others interested in your niche or topic can benefit. With our schedules, it can be difficult to frequently meet with your mentor to discuss areas of interest. This is where collaboration can help. Team members can provide skills and perspectives that will improve the quality of projects. Just make sure you set specific goals for the project, with a timeline.

Other Specifics – Determine what percentage of your work week should be clinical and what should be given to the rest of your academic pursuits. You should consider what you want to be doing in 5-10 years. Where do you see yourself? Saying “no” is ok if you have too much on your plate.

I think I know how to succeed, but what can I mess up?

There are many pitfalls in academics. These include not enough protection from other duties (working too many clinical shifts with the expectation for academic productivity), not enough training for an academic career (research focus without training on research question and protocol formation), failure to have a mentor (one of the cornerstones of academic success), failure to form a plan/timeline of goals, lack of balance (which leads to burnout), biting off too much, and not listening to feedback.

Importance of Balance – Maintain balance and block off time for your family and hobbies. Success takes time, and it will not occur overnight. Recent years have seen an emphasis on physician health. This really comes down to balancing many aspects of life including your shifts, academics, community activities, exercise, hobbies, family, religious/spiritual concerns, friends, and future plans. Pushing too hard and too fast with too much will lead to burnout.

The Decision – Residency is a great time to explore academics and community practice. Rotations in both settings can help you determine which practice is the best fit for you. You can always switch settings, or in other words, it is never too late to go from community to academic practice. Work on perfecting your clinical skills and management early, as this is essential to both academic and community medicine.

Thanks for reading. For more, please see the resident section of the CORD website at http://www.cordem.org/i4a/pages/index.cfm?pageID=4077

Please comment below with other tips or questions!

References/Further Reading

  1. Stern SA, Kim HM, Neacy K, Dronen SC, Mertz M. The impact of environmental factors on emergency medicine resident career choice. Acad Emerg Med. 1999 Apr;6(4):262-70.
  2. Neacy K, Stern SA, Kim HM, Dronen SC. Resident perception of academic skills training and impact on academic career choice. Acad Emerg Med. 2000; 7:1408–15.
  3. Aycock RD, Weizberg M, Hahn B, Weiserbs KF, Ardolic B. A survey of academic emergency medicine department chairs on hiring new attending physicians. J Emerg Med. 2014 Jul;47(1):92-8.
  4. Sanders AB, Fulginiti JV, Witzke DB, Bangs KA. Characteristics influencing career decisions of academic and nonacademic emergency physicians. Ann Emerg Med. 1994;23:81–7
  5. Clinton JE. Educating academic emergency physicians. Acad Emerg Med. 1999;6:260–1.
  6. Stead LG, Sadosty AT, Decker WW. Academic career development for emergency medicine residents: a road map. Acad Emerg Med 2005 May;12(5):412-16.
  7. Hobgood C, Zink B (eds). Emergency Medicine: An Academic Career Guide, ed 2. Lansing, MI: Society for Academic Emergency Medicine; 2000.
  8. Faculty Development Web site. Available at: www.saem.org/ facdev/fac_dev_handbook/. Accessed Nov 10, 2016.
  9. Cydulka C. Preparing for a career in academics. Emergency Medicine: An Academic Career Guide. Available at: http:// www.saem.org. Accessed Sep 18, 2001.
  10. Hall KN, Wakeman MA. Residency-trained emergency physicians: their demographics, practice evolution and attrition from emergency medicine. J Emerg Med. 1999;17(1):7-15.
  11. Reinhart MA, Munger BS, Rund DA. American Board of Emergency Medicine Longitudinal Study of Emergency Physicians. Ann Emerg Med 1999;33(1):22-32.
  12. Kellerman AL. Are you considering an academic career? EMRA. Available at https://www.emra.org/resources/career-planning/practice-spaces/are-you-considering-an-academic-career-/. Accessed 04 November 2016.
  13. Pines JM. The young physician in academic emergency medicine: tips for success. AAEM. Available at http://www.ypsaaem.org/yps-articles/past-yps-articles/2006/the-young-physician-in-academic-emergency-medicine-tips-for-success. Accessed 04 November 2016.
  14. Sokolove P, Stern S, Baren J. An academic career: is it right for you? 2008 SAEM Annual Meeting, May 2008. Available at http://www.slideshare.net/changezkn/life-after-residency-academic-emergency-medicine. Accessed 04 November 2016.
  15. Taylor JS. Academic Medicine 2001;76:366-372.
  16. Stack SJ, Watson MJ. Enriching the resident-faculty relationship. Ann Emerg Med. 2001; 38:336–8.
  17. Osborn TM, Waeckerle JF, Perina D, Keyes LE. Mentorship: through the looking glass into our future. Ann Emerg Med. 1999; 34:285–9.
  18. Hazzard WR. Mentoring across the professional lifespan in academic geriatrics. J Am Geriatr Soc. 1999; 47:1466–70.
  19. Peluchette JV, Jeanquart S. Professionals’ use of different mentor sources at various career stages: implications for career success. J Soc Psychol. 2000; 140:549–64.
  20. Holmboe ES, Ward DS, Reznick RK, Katsufrakis PJ, Leslie KM, Patel VL, Ray DD, Nelson EA. Faculty development in assessment: the missing link in competency-based medical education. Acad Med. 2011; 86(4):460-7.