Board Review Questions: December 2018

PEER (Physician’s Evaluation and Educational Review in Emergency Medicine) is ACEP’s gold standard in self-assessment and educational review. These questions are from PEER, updated continually on its digital platform. Order PEER to prepare!

1. A 52-year-old man is brought in by ambulance after 24 hours of right lower quadrant abdominal pain and fever. Vital signs include BP 85/45 (MAP 58), P 135, R 27, T 38.5°C (101.3°F); weight is 70 kg. While pursuing further diagnostic evaluation, treatment, and surgical evaluation for appendicitis, resuscitation is initiated. His blood pressure does not improve significantly with an additional 2 L of normal saline; lactate remains elevated at 4.6 mg/dL, and urine output is negligible. What is the best next step in management?
A. Administer stress-dose intravenous steroids and continue aggressive fluid resuscitation
B. Begin dopamine continuous infusion
C. Begin norepinephrine continuous infusion
D. Continue aggressive fluid resuscitation with repeat boluses

2. Which of the following findings is most consistent with a high likelihood of acute coronary ischemia?
A. Coronary artery disease risk factors
B. Presence of diaphoresis
C. Recent cocaine use
D. T-wave flattening on ECG

3. Which of the following factors predicts the highest risk for sudden death in an adult asthma patient?
A. History of smoking
B. Increased use of beta agonists
C. Inhaled corticosteroid use
D. Self-reported symptom severity

4. Which of the following findings is most consistent with cyanide poisoning?
A. Ketoacidosis
B. Lactic acidosis
C. Low venous oxygen saturation
D. Reddish plasma discoloration

5. A 21-year-old man presents with a painful, red, swollen ear 12 hours after being assaulted. What is the appropriate treatment?
A. Ice 20 minutes on and 20 minutes off and NSAIDs for pain
B. Incision and drainage and suturing of cotton pledgets to the pinna
C. Intravenous administration of broad-spectrum antibiotics
D. Placement of a cotton ear wick in the external auditory canal

Answers: 1. C; 2. B; 3. B; 4. B; 5. B

1. The correct answer is C, Begin norepinephrine continuous infusion.
Why is this the correct answer?
The patient in this case is presenting in septic shock; MAP is less than 65 mm Hg despite adequate (30 mL/kg) isotonic crystalloid resuscitation. He has evidence of organ hypoperfusion and dysfunction (elevated lactate and inadequate urine output [<0.5 mL/kg/hr]). (Alternative indicators of organ hypoperfusion include altered mental status and a mixed venous oxygen saturation of less than 70%.) At this point in his therapy, it is most reasonable to initiate vasopressor medications. Either norepinephrine or dopamine are listed in various guidelines, but evidence suggests norepinephrine is preferable because of a higher rate of all cause mortality and arrhythmias with dopamine. Early goal-directed therapy was based on the belief that a strict protocol-based treatment was the best approach to managing sepsis. However, the ProCESS trial in 2014 and other similar studies have since demonstrated three keys to the management of sepsis:

• Early recognition of sepsis

• Early antimicrobial therapy

• Adequate fluid hydration

Why are the other choices wrong?

  • The use of stress-dose intravenous steroids in septic shock is controversial, with conflicting study results. It is considered only in septic shock refractory to multiple vasopressors.
  • Initiating dopamine could be considered in this patient, but in septic shock, norepinephrine is the preferred agent.
  • Fluid resuscitation should continue in this patient to achieve ventricular filling, and more fluid might be indicated. However, he remains hypotensive with evidence of organ hypoperfusion, so vasopressors should be initiated.

Adams JG, Barton ED, Collings JL, et al, eds. Emergency Medicine: Clinical Essentials. 2nd ed. Philadelphia, PA: Elsevier; 2013:1454-1457.e1.

Marx JA, Hockberger RS, Walls RM, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 8th ed. St. Louis, MO: Elsevier; 2014:67-74.e1.

2. The correct answer is B, Presence of diaphoresis.
Why is this the correct answer?
The presence of diaphoresis, while not diagnostic of ACS, is strongly suggestive of ACS and presents a high likelihood for it. Of course, when taking a history and performing a physical examination, the emergency physician should investigate other explanations for diaphoresis, including hypoglycemia, high environmental temperature, anxiety, medications, and so on. In the approach to a patient with suspected acute coronary ischemia, the emergency physician has to consider many factors of the history and examination — how the patient describes his or her symptoms, what the patient’s medical history is, whether there is a family history of cardiovascular disease, what clues the ECG provides, what abnormalities are noted in cardiac markers, and often more. The high likelihood features of ACS, in addition to diaphoresis, include chest pain that is similar to the patient’s prior anginal chest pain, known coronary artery disease, a history of MI, mitral regurgitation, hypotension, pulmonary edema, new ST-segment elevation greater than or equal to 1 mm or T-wave inversion in multiple anatomically oriented leads, and elevated cardiac serum markers.

Why are the other choices wrong?

  • If a patient presents with classic risk factors for coronary artery disease such as a medical history of hypertension, diabetes mellitus, or hyperlipidemia; a family history of MI before age 50 years; and smoking, the emergency physician should, of course, consider ACS. But these features are not the most suggestive of acute coronary ischemia, and are not even high likelihood features for ACS. They represent, at most, intermediate likelihood features.
  • Recent cocaine use is a low likelihood finding for acute MI.
  • Although T-wave flattening is an abnormal ECG finding, it has a low likelihood for ACS.

Marx JA, Hockberger RS, Walls RM, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 8th ed. St. Louis, MO: Elsevier; 2014:997-1033.

Mattu A, Brady WJ, et al, eds. Cardiovascular Emergencies. Dallas, TX: American College of Emergency Physicians Publishing; 2014:11-35.

O’Connor RE, Al Ali AS, Brady WJ, et al. Part 9: Acute Coronary Syndromes—2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2015;132:S483-500.

3. The correct answer is B, Increased use of beta agonists.
Why is this the correct answer?
Numerous factors forecast an increased risk of sudden death due to asthma. One of the most-studied risk factors is increased use of beta agonists via metered-dose inhaler or nebulizer. The increase is likely secondary to delayed formal evaluation of asthma exacerbation in patients using beta agonists. Researchers recently have found that frequent use of short-acting, beta agonists results in tolerance to the medication as well as increased lung reactivity to stimuli. Poor self-perception or physician perception of a patient’s asthma and a lack of having or following a formal care plan are also risk factors for asthma-related death. Use of illicit drugs, including heroin and cocaine, has been found to increase the risk for hospitalization, intubation, and fatal asthma. More severe asthma (as indicated by current or recent use of steroids, hospitalization, and intubation within the past year) is also a risk factor for asthma-related death. Finally, recent studies indicate that sensitization to mold is a risk factor for increased asthma severity and death. It is important for emergency physicians to ask patients about these risk factors to educate them and improve treatment plans when needed.

Why are the other choices wrong?

  • In several studies, smoking was not found to have increased the risk of death in fatal asthma, possibly because the patients were more likely to have the diagnosis of COPD as a cause of death than asthma. One small study in 1996 reported a risk in adult male athletes who were smokers, but this has not been found in more recent studies with larger cohorts.
  • The use of inhaled corticosteroids has been shown to control patients’ asthma symptoms. One study revealed that the use of an average of one or more canisters of inhaled corticosteroids over the prior 3 months decreased the incidence of fatal asthma. Another showed that premature cessation of inhaled corticosteroids increased the risk of fatal asthma.
  • Patients’ reports of the severity of their asthma are highly unreliable. Those who report severe asthma are not more likely to die from asthma, and those who do not accurately perceive the severity of their disease are more likely to die from asthma.

D’Amato G, Vitale C, Molino A, et al. Asthma-related deaths. Multidiscip Respir Med. 2016;11:37.

Marx JA, Hockberger RS, Walls RM, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 8th ed. St. Louis, MO: Elsevier; 2014:941-955.

4. The correct answer is B, Lactic acidosis.
Why is this the correct answer?
Cyanide inhibits oxidative phosphorylation and can rapidly lead to apnea, loss of consciousness, convulsions, hemodynamic instability, and death. By inhibiting aerobic metabolism, anaerobic metabolism ensues, and a lactic acidosis (not ketoacidosis) develops. Cells are unable to extract oxygen; therefore, a high (not low) venous oxygen saturation is expected. This disruption in oxygen use can lead to “arterialization” of venous blood. Confirmatory cyanide levels are not rapidly available, and antidote administration is required quickly, so a high level of suspicion based on history (smoke exposure, suicide attempt in chemist or jeweler) in combination with clinical manifestations and rapidly available laboratory test results (metabolic acidosis, elevated lactate, elevated venous oxygen saturation) is necessary.

Why are the other choices wrong?

  • Ketoacids (acetoacetate, beta-hydroxybutyrate) are released in the blood from lipid metabolism. Excess accumulation is responsible for the anion gap acidoses found in diabetic ketoacidosis and alcoholic ketoacidosis. Ketoacids do not accumulate significantly in cyanide poisoning, which is characterized by the accumulation of lactate (lactic acidosis).
  • By inhibiting oxidative phosphorylation, cyanide prevents cells from using oxygen. In significant cyanide toxicity, venous blood can return “arterialized” with a high (not low) oxygen saturation.
  • Hydroxocobalamin, an effective antidote for cyanide poisoning, is bright red, and administration causes reddish discoloration of skin, urine, and plasma. Cyanide poisoning itself can cause venous blood to appear arterial but does not cause plasma discoloration.

Hoffman RS, Howland MA, Lewin NA, et al, eds. Goldfrank’s Toxicologic Emergencies. 10th ed. New York, NY: McGraw-Hill; 2015:1602-1606.

Wolfson AB, Hendey GW, Ling LJ, et al, eds. Harwood-Nuss’ Clinical Practice of Emergency Medicine. 6th ed. Philadelphia, PA: Lippincott, Williams & Wilkins; 2014:1419-1420.

5. The correct answer is B, Incision and drainage and suturing of cotton pledgets to the pinna.
Why is this the correct answer?
This patient has an auricular hematoma, and the time frame indicates that the redness and swelling are likely caused by a hematoma and not profound infection or abscess. Incision and drainage of the hematoma, followed by the placement of sutured cotton pledgets, is indicated to prevent pressure necrosis of the underlying cartilage, which can result in a chronic deformity commonly known as cauliflower ear. If the skin is prepared with an antiseptic prior to incision and drainage, the risk of infection is outweighed by the benefit of reduction in long-term deformity. Preparing the skin with alcohol, chlorhexidine, or Betadine reduces the risk of infection. Once proper bolsters have been placed, the ear is relatively protected from further trauma until the follow-up appointment.

Why are the other choices wrong?

  • The use of ice and NSAID pain medications is helpful if a hematoma is not present, but in the case of an auricular hematoma, it is not sufficient. Incision and drainage are performed to reduce the incidence of cartilaginous deformity later on.
  • Broad-spectrum antibiotics are not indicated unless the skin has been violated. In the case of an auricular hematoma, antibiotics may be prescribed after incision and drainage to protect the exposed cartilage from infection. But there is no indication to prescribe them when there is no significant hematoma and when the skin has not been violated. Intravenous antibiotics should be reserved for treating significant infection.
  • The patient in this case is suffering from trauma and an auricular hematoma, not otitis externa. The reason to place a cotton wick is to facilitate drainage of the external auditory canal and to administer topical antibiotics in the case of otitis externa, an infectious process.

Marx JA, Hockberger RS, Walls RM, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 8th ed. St. Louis, MO: Elsevier; 2014:378.

Roberts JR, Hedges JR, eds. Clinical Procedures in Emergency Medicine. 6th ed. St. Louis, MO: WB Saunders; 2013:1317-1320.

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