Questions, Board Review

Board Review Questions: December 2020

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. Which medication is most likely to be associated with constipation?
A. Amoxicillin-clavulanate
B. Benztropine
C. Bisacodyl
D. Colchicine


2. Which finding is a delayed sign or symptom of acute limb ischemia?
A. Blistering skin
B. Pale skin
C. Paresthesia
D. Reduced pulse


3. A 24-year-old woman presents via ambulance with headache, dizziness, and mild shortness of breath after a house fire. She has no burns on her skin and no soot in her mouth or nares, and she is not in respiratory distress. ABG analysis with co-oximetry reveals a carbon monoxide level of 30%. Her vital signs include BP 119/74, P 95, R 15, and T 36.9°C (98.4°F). Which additional finding, if present, makes hyperbaric oxygen therapy the correct intervention?
A. History of asthma
B. Pregnancy
C. Repeated nausea and vomiting
D. SpO2 of 94% on room air


4. A 52-year-old woman presents with fatigue and dyspnea on exertion. She has recently been taking chloroquine for malaria prophylaxis. Her SpO2 is 86% by pulse oximetry and does not improve with supplemental oxygen administration. Her skin appears cyanotic, and a chest x-ray is normal. Which antidote should be administered?
A. Amyl nitrite
B. Hydroxocobalamin
C. Methylene blue
D. Sodium thiosulfate


5. What is a potential complication of not repairing a galeal laceration?
A. Loss of frontalis muscle function
B. Profuse delayed hemorrhage
C. Scalp wound infection
D. Wound dehiscence

ANSWERS 

1. The correct answer is B, Benztropine.

Why is this the correct answer?
Benztropine is an anticholinergic medication used to treat Parkinson disease that is also known to cause constipation. Constipation has a wide range of causes, roughly divided into primary and secondary causes. Primary causes are intrinsic to the intestines and have no apparent source, such as irritable bowel or functional bowel disease. Secondary causes are local anatomic causes or systemic medical causes, including iatrogenic triggers from medication therapy. Almost every medication has been documented to be associated with constipation, but some drugs are more prone to inhibiting bowel motility. Chief among them are opioids, iron supplements, and anticholinergics (such as benztropine, diphenhydramine, and tricyclic antidepressants). Calcium channel blockers, antiepileptics, and most psychiatric medications are also commonly associated with constipation. Constipation should be a diagnosis of exclusion in the emergency department. Before assigning a patient’s abdominal pain to “just constipation,” the clinician should thoroughly consider other more life-threatening conditions. This is especially true for elderly patients in whom the chief complaint of abdominal pain carries a high mortality rate (up to 10%). 

Why are the other choices wrong?

  • Amoxicillin-clavulanate is more often associated with mild diarrhea. Severe diarrhea that develops several days after starting amoxicillin-clavulanate therapy should prompt investigation for a Clostridioides difficile
  • Bisacodyl, a laxative, is used as a therapy for constipation. However, long-term use of laxatives can result in atonic colon (also known as lazy bowel syndrome), a condition in which the colon no longer responds to normal stimuli to evacuate.
  • Colchicine, a therapy for gout, is more commonly associated with diarrhea. Patients are advised to titrate their use of colchicine, depending on the degree of diarrhea they develop.

REFERENCES
Schrank KS. Constipation. In: Adams JG, Barton ED, Collings JC, DeBlieux PMC, Gisondi MA, Nadel ES, eds. Emergency Medicine Clinical Essentials. 2nd ed. Elsevier Saunders; 2013:309-314.

Zuckerman MD, Church RJ. Gastrointestinal principles. In: Nelson LS, Howland MA, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS, eds. Goldfrank’s Toxicologic Emergencies. 11th ed. McGraw-Hill Education; 2019:287-296.

Shoenberger JM. Constipation. In: Walls RM, Hockberger RS, Gausche-Hill M, et al, eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. Vol 1. 9th ed. Elsevier; 2018:257-261.


2. The correct answer is A, blistering skin.

Why is this the correct answer?
Blistering skin is a sign of advanced limb ischemia, which occurs from a significant blockage in the arteries of the lower extremities and results in fluid buildup and blistering of the upper skin layers. Acute arterial occlusion produces a spasm in the distal arteries. At first, the limb appears pale. Over time, the spasm relaxes and causes the area to fill with deoxygenated blood, which leads to light blue or purple marbling of the skin. The limb can be salvaged at this stage. As the ischemia progresses, the stagnated blood coagulates, and the skin becomes darker in color and stops blanching. Large patches of fixed staining progress to blistering. At this stage, revascularization of the limb may lead to life-threatening reperfusion injuries.

Acute limb ischemia, classified as ischemia of less than 14 days’ duration, is a true emergency. The symptoms can be summarized by the six Ps: pain, pallor, paralysis, pulse deficit, paresthesia, and poikilothermia. Tissue necrosis can occur within 6 hours of symptom onset. Patients with acute blood loss to the limb need immediate therapy, including antithrombosis and possibly revascularization. Patients with suspected acute limb ischemia require an immediate vascular consultation and likely need anticoagulation with heparin unless contraindicated. Causes of acute limb ischemia must be determined during the evaluation and can include thrombosis, embolism, vasculitis, vasospasm, compartment syndrome, and aortic dissection.

Why are the other choices wrong?

  • Pale skin is an early finding of acute limb ischemia rather than a delayed finding. As the thrombus occludes an artery, the arterial tree located distally to the occlusion will spasm and cause the skin to become “marble” pale or white in color.
  • Paresthesia, which can lead to anesthesia, is also one of the early signs of acute limb ischemia. It can be a sign of complete ischemia and typically requires acute surgical treatment.
  • A reduced or an absent pulse is another early sign of acute limb ischemia. An acute arterial occlusion by any mechanism and the distal arterial spasm to the occlusion can cause an absence of a palpable pulse.

REFERENCES
UpToDate article on acute lower extremity ischemia, available in full with a subscription

https://www.uptodate.com/contents/clinical-features-and-diagnosis-of-acute-lower-extremity-ischemia

Olinic DM, Stanek A, T─âtaru DA, Homorodean C, Olinic M. Acute limb ischemia: an update on diagnosis and management. J Clin Med. 2019 Aug 14;8(8):E1215.

Santistevan JR. Acute limb ischemia: an emergency medicine approach. Emerg Med Clin North Am. 2017 Nov;35(4):889-909.

Creager MA, Kaufman JA, Conte MS. Acute limb ischemia. N Engl J Med. 2012;366:2198-2206.


3. The correct answer is B, Pregnancy.

Why is this the correct answer?
Pregnancy is considered an indication for hyperbaric oxygen (HBO) therapy after carbon monoxide (CO) exposure if the mother has signs of ischemic injury, neurologic deficits, or a carboxyhemoglobin (COHb) level greater than 15%. High levels of maternal COHb can lead to significant fetal hypoxia and death or permanent neurologic or developmental injury if the CO is not displaced by oxygen. Other indications for HBO therapy include COHb levels over 40% (some institutions go as low as levels >25%) and signs of tissue ischemia, such as altered mental status, neurologic deficits, myocardial ischemia, cardiac dysrhythmias, and syncope. CO poisoning is known to cause delayed neurologic deficits, which is the primary reason for considering HBO therapy for patients with elevated COHb levels.

Why are the other choices wrong?

  • Underlying asthma does not increase the likelihood of delayed neurologic sequelae from CO exposure. Asthma can cause the patient to present with some bronchospasm from the inhaled irritant gas and smoke, but asthma is not an indication for HBO therapy.
  • Nausea and vomiting are common symptoms after smoke and CO exposure. However, HBO therapy or airway control is not indicated if the nausea and vomiting can be controlled or if they have resolved.
  • A low SpO2 level can be managed with supplemental oxygen and observation. A chest x-ray may be warranted to assess for other lung injury from smoke inhalation, but low SpO2 alone is not an indicator for HBO therapy. Supplemental oxygen at 100% can reduce the half-life of COHb to 1 hour from the normal 5 hours at room air; HBO therapy decreases that half-life even further, to 30 minutes.

REFERENCES
Nelson LS, Hoffman RS. Inhaled toxins. In: Walls RM, Hockberger RS, Gausche-Hill M, et al, eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. Vol 2. 9th ed. Elsevier; 2018:1926-1933.

Maloney GE. Carbon monoxide. In: Tintinalli JE, Ma OJ, Yealy DM, et al, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 9th ed. McGraw-Hill; 2020:1414-1417.


4. The correct answer is C, Methylene blue.

Why is this the correct answer?
This patient is experiencing methemoglobinemia as a result of chloroquine exposure, the antidote for which is methylene blue. Methylene blue is converted (via a G6PD pathway) to leucomethylene blue, a reducing agent that converts methemoglobin back to hemoglobin. Methemoglobinemia occurs when the ferrous (Fe2+) form of iron in hemoglobin is oxidized to the ferric (Fe3+) form. The ferric form of iron cannot transport oxygen and is associated with a shift in the oxygen dissociation curve, resulting in an increased affinity of bound oxygen to hemoglobin. Many oxidizing medications have been implicated in methemoglobinemia, including benzocaine, chloroquine, dapsone, phenazopyridine, prilocaine, and primaquine.

Symptoms of significant methemoglobinemia reflect those of hypoxia. The associated cyanosis is due to the color of methemoglobin, not deoxygenated hemoglobin, so oxygen administration does not resolve it. Peripheral pulse oximetry is prone to report a false value of SpO2 in patients with significant methemoglobinemia due to inference of light transmission used to detect hemoglobin SpO2. The pulse oximeter reading in patients with methemoglobin concentrations greater than 30% is often near 85%. The diagnosis of methemoglobinemia is confirmed with co-oximetry to measure the methemoglobin percentage. 

Why are the other choices wrong?

  • Amyl nitrite is an oxidizing agent that induces methemoglobinemia as part of the treatment for cyanide poisoning. Amyl nitrite can be used via the inhaled route when intravenous access is unavailable. Methemoglobin has an affinity for cyanide, and binding to it forms nontoxic cyanomethemoglobin.
  • Hydroxocobalamin is a vitamin B12 precursor that is an effective antidote for cyanide poisoning. Hydroxocobalamin binds to cyanide, forming active and nontoxic vitamin B12 (cyanocobalamin). However, hydroxocobalamin does not have a role in treating methemoglobinemia.
  • Sodium thiosulfate is typically administered in conjunction with amyl nitrite or sodium nitrite in the treatment of cyanide poisoning. Sodium thiosulfate helps detoxify cyanide to thiocyanate, but it does not have a role in treating methemoglobinemia.

REFERENCES
Howland MA. Methylene blue. In: Nelson LS, Howland MA, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS, eds. Goldfrank’s Toxicologic Emergencies. 11th ed. McGraw-Hill Education; 2019:1713-1717.

Farmer BM, Nelson LS. Dyshemoglobinemias. In: Tintinalli JE, Ma OJ, Yealy DM, et al, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 9th ed. McGraw-Hill; 2020:1329-1332.  


5. The correct answer is A, Loss of frontalis muscle function.

Why is this the correct answer?
The galea aponeurosis is a fibrous tissue that acts as the fascia of the scalp and inserts into the frontalis muscle, which contributes to facial expression. Failure to repair a galeal laceration can lead to loss of frontalis muscle function, which can have a significant cosmetic impact. Standard of care does not absolutely dictate galeal closure, but not doing so is associated with increased risk of subgaleal hematoma, poorer cosmetic outcomes, and loss of frontalis muscle function.

Why are the other choices wrong?

  • Galeal closure does not affect the risk of delayed hemorrhage in scalp lacerations. Adequate irrigation and exploration of scalp wounds are essential to evaluate for foreign bodies. Hemorrhage is most likely to occur at the time of injury and repair.
  • Scalp lacerations can become infected regardless of whether the galea is repaired. There is no clear consensus as to whether galeal repair decreases the risk of subgaleal infection, but it does not decrease the risk of skull osteomyelitis, a rare complication.
  • There is no increased risk of wound dehiscence if the galea is not repaired as long as the wound is closed appropriately. However, the resulting scar may be wider or more depressed than if the galea had been repaired.

REFERENCES
Papa L, Goldberg SA. Head trauma. In: Walls RM, Hockberger RS, Gausche-Hill M, et al, eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. Vol 1. 9th ed. Elsevier; 2018:301-329.

Simon BC, Hern HG. Wound management principles. In: Walls RM, Hockberger RS, Gausche-Hill M, et al, eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. Vol 1. 9th ed. Elsevier; 2018:659-673.

Wright DW, Merck LH. Head trauma. In: Tintinalli JE, Ma OJ, Yealy DM, et al, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 9th ed. McGraw-Hill; 2020:1683-1695.

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