Emergency Medicine MOC ConCert Exam Review

Educational Objective:

Describe the treatment of monkey B virus infection.

Key Point:

Monkey B virus is a herpes viral infection transmitted by macaque monkeys; it has a high mortality rate when left untreated. Treatment is prompt admission for intravenous acyclovir.

Explanation:

The greatest concern with monkey bites is exposure to herpes B virus, for which up to 70% to 100% of macaque monkeys used in research are seropositive. The most important step in post-exposure prevention is to scrub the bitten area with soap and a concentrated solution of detergent, povidone iodine, or chlorhexidine, and then to irrigate the area for 15 to 20 minutes. Prophylaxis with valacyclovir is often recommended.

In cases of herpes B virus infection, patients typically present 2 to 5 weeks after exposure with vesicles overlying the affected area, as well as flu-like symptoms and localized lymphadenopathy. If the infection is not treated, then the illness progresses to central nervous system (CNS)–related symptoms that can continue to progress to seizures, paralysis, and coma. If the infection is left untreated, the mortality rate of 80%; however, this risk is markedly reduced with viral therapy.

Antiviral prophylaxis for herpes B virus includes 5 days of valacyclovir. For patients who already present with symptoms, but not CNS-related sequela, treatment is inpatient admission for 2 to 3 weeks of intravenous acyclovir. Ganciclovir is indicated for CNS manifestations.

Reference:

Eilbert WP. Mammalian bites (chapter 54). In: Wall R, et al. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 9th ed., 2018:690-697.

Educational Objective:

Describe the management of non–ST elevation acute coronary syndrome in a patient after undergoing coronary artery bypass grafting.

Key Point:

An early, invasive strategy should be strongly considered in patients with non–ST elevation acute coronary syndrome (e.g. cardiac ischemia without infarction) whenever they have a surgical history of coronary artery bypass grafting.

Explanation:

A patient such as this one with a previous history of CABG remains at high risk for acute coronary syndrome via disease progression of ungrafted, native vessels, or significant atherothrombotic disease in grafted vessels. These patients also typically have more extensive coronary artery disease and have more comorbidities than their counterparts.

The 2014 practice guidelines on non–ST elevation acute coronary syndrome (NSTE-ACS) recommend that patients with prior CABG and NSTE-ACS should be strongly considered for an early, invasive strategy because of their increased risk (class I recommendation). In addition, these patients should receive guideline-directed antiplatelet and anticoagulation therapy.

Reference:

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.

Educational Objective:

Explain the relationship between the dual vascular system of the lung and mild, moderate, and massive hemoptysis

Key Points:

• The pulmonary vessels branch off the pulmonary artery and are a low-pressure system that forms a functional unit with the alveoli for the purpose of gas exchange. They are less likely to cause massive hemoptysis and are probably the cause of this patient’s moderate hemoptysis from diseased alveoli/pulmonary vessel units. 

• Vascular disruption of either vascular system of the lung may occur from infection, trauma, cancer (with malignant invasion of the vessel), infarction, fistula formation, coagulopathy, or invasive pulmonary procedures.

Explanation:

The lung is supplied by the dual circulatory systems of (1) systemic (high-pressure) bronchial arteries that branch off the aorta and (2) the (low-pressure) pulmonary arteries that branch off the main pulmonary artery from the right cardiac ventricle. The bronchial vessels are part of the regular systemic vascular system; they assure the survival of the lung tissues. The pulmonary vessels are responsible for gas exchange and therefore form a tight unit with the alveoli.

Moderate hemoptysis typically is the result of alveolar disease leading to disruption of pulmonary vessel/alveolar units. Disruption of these low-pressure vessels resembles venous bleeding.

All other hemoptyses (both mild and massive) stems from vascular disruption of the high-pressure bronchial vessels: 

• Trace hemoptysis typically originates from the disruption of tiny tracheobronchial capillaries after vigorous coughing or in the context of bronchitis.

• All massive hemoptysis is secondary to some type of non-capillary vascular disruption of a high-pressure bronchial vessel within the trachea, bronchi, small caliber airways, or lung parenchyma. This may be due to trauma, coagulopathy, cancer, invasive pulmonary procedures, or fistula formation (often a delayed effect of trauma). 

Pearls: The bronchial vascular system is divided into a deep and superficial subsystem. The deep bronchial arteries drain into deep bronchial veins, which in turn drain into the main pulmonary vein or directly into the left atrium. In other words, the deep bronchial vascular subsystem drains into the same veins as the pulmonary vascular system! The superficial bronchial veins, on the other hand, either drain into the azygos vein (right side of the body) or the accessory hemiazygos vein or the left superior intercostal vein (left side of the body).

Figure. Notice that both the pulmonary and bronchial arterioles drain into the pulmonary venule.

References:

Brown III CA.Hemoptysis. (Chapter 21) In: Walls R, et al. Rosen’s Emergency Medicine: Concepts and Clinical Practiceth ed., 2018: 190-194.e1.

https://www.kenhub.com/en/library/anatomy/bronchial-veins   (Accessed April 22, 2021)

Educational Objective:

Discuss the cardiopulmonary resuscitation of a patient with severe accidental hypothermia.

Key Point:

Given the lack of human data, the following is considered reasonable in patients with ventricular fibrillation: single attempt at defibrillation regardless of core temperature, followed by active core rewarming (e.g., with cardiopulmonary bypass or extracorporeal membrane oxygenation [ECMO]). During rewarming, clinical judgment must be used to deliver/not deliver further shocks and/or advanced cardiovascular life support (ACLS) medications.

Explanation:

The ECG shows ventricular fibrillation, which may occur as a result of the irritable and sensitive myocardium in patients with severe hypothermia.

For the sake of cardiac arrest, severe hypothermia is often defined as ≤ 30°C (86°F) rather than the customary ≤ 28°C (82.4°F). The top priority is rapid active core rewarming.

Neither the core temperature at which defibrillation should first be attempted nor the ideal number of shocks or pharmacological approach has been established or studied in humans, leading to a lack of specific guidelines. The recent American Heart Association (AHA) recommendations (2010 AHA hypothermia guidelines, unchanged in 2015 and 2017) have relaxed earlier statements about withholding defibrillation and/or drugs until the patient has been rewarmed to ≥ 30°C (86°F). The 2010 ACLS guidelines (still valid in 2018) state:

“If ventricular tachycardia (VT) or ventricular fibrillation (VF) is present, defibrillation should be attempted. If VT or VF persists after a single shock, the value of deferring subsequent defibrillations until a target temperature is achieved is uncertain. It may be reasonable to perform further defibrillation attempts according to the standard basic life support (BLS) algorithm concurrent with rewarming strategies (Class IIb, Level of Evidence C). The recommendation for administration or withholding of medications is not clear. It may be reasonable to consider administration of a vasopressor during cardiac arrest according to the standard ACLS algorithm concurrent with rewarming strategies (Class IIb, Level of Evidence C).”

The AHA guidelines do not state a core temperature at which regular ACLS protocols begin to apply.

Inotropes and antiarrhythmic medications are a complex topic in the severely hypothermic patient until after rewarming to 30°C (86°F; or low end of moderate hypothermia range). Again data are lacking.

The Auerbach chapter on hypothermia has an excellent discussion on resuscitation pharmacology in severely hypothermic patients. The author recommends that pharmacologic manipulation of the pulse and blood pressure (including manipulation with epinephrine) should be avoided in patients with core temperatures < 30°C (86°F), though they elude to controversy in this area and cite an animal study that showed vasopressors to be beneficial at core temperatures < 30°C (86°F).

The ACLS vasopressor statement is indeed based on this single animal study, in which administration of vasopressors after induced ventricular fibrillation below 30°C (86°F) resulted in a higher return of spontaneous circulation.

References:

Field JM, et al. Part 12: Cardiac Arrest in Special Situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(suppl 3): S640 –S656. (Editor’s Note: the hypothermia section was not updated for the 2015 ACLS guidelines or 2017 focused updates, so the 2010 hypothermia section of ACLS is still valid)

Danzl DF, Huecker MR. Accidental Hypothermia. In: Auerbach PS, et al. Auerbach's Wilderness Medicine. 7th ed. Philadelphia, PA: Elsevier; 2017:135-162.

Neumar RW, Shuster M, Callaway CW, et al. Part 1: executive summary: 2015 American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2015;132(18 suppl 2):S315-S367.

Zafren K, Danzel DF. Accidental Hypothermia (Chapter 132). In: Walls RM, et al. Rosen's Emergency Medicine: Concepts and Clinical Practice. 9th ed. Philadelphia, PA: Elsevier; 2018:1743-1754.e3.

Stages of Hypothermia