Emergency Medicine MOC ABEM ConCert Exam Review

Educational Objective:

Diagnose thoracic outlet syndrome.

Key point:

In a hiker wandering through remote areas with a heavy backpack, the most likely mechanism is narrowing of the costoclavicular interval as the result of downward and backward pressure on the shoulders exerted by a heavy backpack.

Explanation:

This patient presents with typical complaints of what is known as thoracic outlet syndrome. The clinical spectrum of this syndrome varies depending on whether compression affects predominantly arterial, venous, or nervous components. Congenital cervical rib or fibrous extension of cervical rib and abnormal scalene muscle insertion both can cause thoracic outlet syndrome.

Reference:

Ferri FF, ed. Ferri’s Clinical Advisor. 2017.

Educational Objective:

List the contraindications to beta-blocker therapy in patients with ST-elevation myocardial infarction.

Key Point:

A risk factor for cardiogenic shock and contraindication to beta blockers is age older than 70 years.

Explanation:

The American Heart Association 2013 guidelines employ strict recommendations on beta-blocker therapy in patients with STEMI. The guidelines state that  oral beta-blockers should be initiated within the first 24 hours in patients with STEMI who do NOT have any of the following contraindications (Class I; level of evidence: B):

• Signs of heart failure

• Evidence of a low output state

• Increased risk for cardiogenic shock

• PR interval more than 0.24 seconds

• Second- or third-degree heart block

• Active asthma, or reactive airways disease

The patient criteria for "increased risk for cardiogenic shock" are very important, yet easily overlooked because they are only listed in a footnote. The footnote states that the following patients are at increased risk for developing cardiogenic shock in response to beta-blocker therapy:

• Age > 70 years

• Systolic blood pressure < 120 mm Hg

• Sinus tachycardia > 110 beats/minute

• Heart rate < 60 beats/minute

• Increased time since STEMI symptom onset (not specifically defined) 

This patient is 75 years of age, has a heart rate higher than 110 beats/minute, and his systolic blood pressure is below 120 mm Hg. All of these details preclude the use of a beta-blocker. As an additional note, this patient is highly likely to benefit from an angiotensin-converting enzyme inhibitor (ACE-I) because of his history of anterior MI, tachycardia, and prior MI. Each one of these criteria place him in a "most likely to benefit" subgroup for ACE-I .

Note: The American Heart Association (AHA) lists the same beta-blocker indications/contraindications in their 2013 STEMI guidelines and 2014 non-STEMI acute coronary syndrome (ACS) guidelines. In both guidelines, the beta-blocker recommendation receives a Class I classification. However, the 2013 STEMI guidelines cite a B level of evidence B  whereas the 2014 non-STEMI-ACS guidelines cite a level A of evidence for the same action (giving beta-blockers). This is not a contradiction; the evidence for/against the benefit of beta-blockers is somewhat stronger for patients with non-STEMI-ACS.

2022 editor’s note on STEMI guidelines: The 2013 AHA/ACC guidelines on STEMI remain the valid framework of national clinical STEMI recommendation (including the topic discussed in this question) as of March 2022. Several sections of the 2013 guidelines have been revised through various focused guidelines updates (mostly focused on the indications/contraindications of various revascularization strategies); however, the beta-blocker topic has remained unchanged.

References:

O'Gara PT, Kushner FG, Ascheim DD, et al; American College of Emergency Physicians; Society for Cardiovascular Angiography and Interventions. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;61(4):e78-e140.

Amsterdam EA, Wenger NK, Brindis RG, et al; ACC/AHA Task Force Members. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines [Erratum appears in Circulation. 2014;130(25):e433-e434]. Circulation. 2014;130(25):e344-e426.

 Lawton JS, e al. 2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Originally published 9 Dec 2021 Circulation. 2022;145:e18–e114

Tenofovir has been associated with renal impairment, including acute renal insufficiency and Fanconi syndrome. Fanconi syndrome should be suspected in the presence of proteinuria, hypokalemia, hyperchloremic nonanion gap metabolic acidosis, hypophosphatemia, and glucosuria. Disturbances in electrolyte may cause myalgia, muscle weakness, and dyspnea.

HIV and heroin abuse can cause focal segmental sclerosis, which usually presents with rapidly progressive renal failure and proteinuria. Hepatitis B virus can also cause nephrotic syndrome from membranous glomerulopathy. Efavirenz is not associated with kidney dysfunction and it does not require dose adjustments for renal insufficiency.

References:

Mathew G, Knaus SJ. Acquired Fanconi’s syndrome associated with tenofovir therapy. J Gen Intern Med. 2006;21:C3-C5.

Panel on Antiretroviral Guidelines for Adults and Adolescents; U.S. Department of Health and Human Services. Guidelines for the use of antiretroviral agents in HIV-1-infected adults and adolescents. Accessed December 14, 2012.

The zygoma usually fractures in multiple places, as was the case in this patient; all fractures usually occur at or near the bone’s three junctions (see illustration). Fractures through the mid-part of the zygoma are unlikely due to the robust thickness of that part of the bone. The following three sutures are disrupted in the classic "tripod" fracture of the zygoma:

1. zygomatic arch (zygomaticotemporal suture)
2. frontozygomatic suture
3. zygomaticomaxillary suture

Fracture through the zygomatico-maxillary suture in particular leads to a long list of symptoms, due to the fact that this suture travels through the inferior orbital rim and the lateral wall of the maxillary sinus. A classic zygomatic tripod fracture can be expected to present with the following signs:

flattening of the zygomatic protuberance (often obscured by edema)
step deformity of the orbital rim
anesthesia in the distribution of the inferior orbital nerve
diplopia or decreased elevation of upward gaze
subcutaneous emphysema if the maxillary sinus is involved
Epistaxis due to bleeding into the maxillary sinus, which then overflows into the nose
Painful, restricted jaw motion, due to the displaced zygoma impinging in the mandibular coronoid process.

A septal hematoma would not be an expected finding in a zygomatic tripod fracture and should lead to a search for other, unrelated injuries (nasal fractures, Le Fort fractures or a naso-ethmoidal-orbital fractures).

Zygomatic fractures can be visualized on a jug handle (submento vertex) or Water’s x-ray view, but, as with other maxillofacial fractures, CT-scan has become the standard in most institutions.

Typically, a delayed elevation of the fractured bone is performed if the patient has a persistent deformity or restriction of mandibular motion (the pictured patient might require a more urgent repair of her significant deformity).

Reference:
Marx: Rosen's Emergency Medicine, 7th ed.: Mosby; 2009. CHAPTER 39 - Facial TraumaReferences
Townsend: Sabiston Textbook of Surgery, 18th ed. 2007, HEAD AND NECK

Educational Objective:

Characterize the clinical features of amyotrophic lateral sclerosis.

Key Point:

Patients with ALS typically demonstrate asymmetrical distal weakness without sensory findings. Nearly all cases eventually develop fasciculations.

Explanation:

ALS, which is the most common form of motor neuron disease, includes both upper motor neuron (Betz cell) disease (manifesting as hyperreflexia, clonus, and a positive Babinski sign) and lower motor neuron (anterior horn cell) disease (manifesting as atrophy and fasciculations). Referral for electrophysiologic testing is critical to distinguish it from multifocal motor neuropathy. Traditionally, treatment for ALS was supportive only; however, riluzole was recently approved by the US Food and Drug Administration for the treatment of ALS and has been found to improve survival and slow disease progression. Anterior horn cells are proximal to where motor and sensory fibers merge, so manifestations of the disease are purely motor. Although there is electrophysiologic evidence of autonomic involvement, it is generally subclinical.

References: 

Moujalled D, White AR. Advances in the development of disease-modifying treatments for amyotrophic lateral sclerosis. CNS Drugs. 2016;30:227-243.

Snow DC, Bunney EB. Peripheral nerve disorders (chapter 97). In: Walls, R, et al. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 9th ed., 2018:1307-1320.