ABSTRACT
Audience: The targeted audience for this simulation are emergency medicine providers, including residents as well as advanced practice providers, to properly educate on recognizing, diagnosing, and managing methemoglobinemia. Introduction: Methemoglobinemia is a blood disorder characterized by the presence of ferric form of hemoglobin in the blood. This form of hemoglobin can carry oxygen but is unable to release it effectively causing a range of symptoms including headache, dizziness, nausea, and cyanosis. It is rarely congenital and mostly caused by the exposure to oxidizing agents, such as local anesthetics and quinolones.1 Normally, oxygen can bind to hemoglobin while it is in the ferrous state (Fe2+). In cases of methemoglobinemia, the heme iron configuration is converted from ferrous (Fe2+) to ferric (Fe3+), making it unable to bind to oxygen. As a result, normal ferrous hemes experience an increased affinity for oxygen causing a leftward shift in the oxygen dissociation curve. This in turn causes functional anemia due to reduced oxygen carrying capacity.1 Methemoglobinemia can result from exposure to different medications as well as environmental factors and presents like other disease processes including chronic obstructive pulmonary disease exacerbations. Congenital methemoglobinemia due to cytochrome b5 reductase deficiency is very rare, but the actual incidence is not known. Increased frequency of disease has been found in Siberian Yakuts, Athabaskans, Eskimos, and Navajo.2 Although it is also an unusual occurrence, acquired methemoglobinemia is much more frequently encountered than the congenital form.1In a 10-year retrospective study looking at the incidence rate of topical anesthetic-induced methemoglobinemia, it was found that the overall prevalence was 0.035%. A major risk factor was hospitalization at the time of a procedure being performed. An increased risk was also seen with benzocaine-based anesthetics.3. Educational Objectives: At the end of this simulation case, participants should be able to: 1) recognize shortness of breath, cyanosis and respiratory distress, and the difference between all of them based on the clinical presentation 2) identify the underlying cause of the condition by conducting a thorough history and physical 3) know how to identify and treat methemoglobinemia by ordering necessary labs and interventions and understand the pathophysiology leading to methemoglobinemia 4) recognize patient's response to treatment and continue to reassess. Educational Methods: This is a high-fidelity simulation case that allows participants to evaluate and treat methemoglobinemia in a safe environment. The case is followed by a debriefing and small group discussion to review patient care skills, medical knowledge, interpersonal communication, practice-based learning, and improvement. Research Methods: The educational content and efficacy were evaluated by oral feedback and a debriefing session immediately after completion of the simulation. A 5-point Likert scale was sent out to participants pre-simulation and post-simulation. Questions on the survey included whether they felt confident in their ability to recognize methemoglobinemia, understood the physiology and causes of methemoglobinemia, and felt confident in their ability to treat methemoglobinemia. Results: Sixteen learners responded to the survey, consisting of EM residents and medical students. Post simulation, approximately 92% of EM residents answered agree or strongly agree in their ability to recognize and treat methemoglobinemia compared to pre-sim survey of about 62.5%. Post-simulation feedback also resulted in positive reception, and learners found it useful to run through an uncommonly seen case in the hospital. Results showed overall improvement in recognition and treatment of methemoglobinemia among residents and medical students. Discussion: This simulation improved recognition of methemoglobinemia including signs and symptoms associated with it. Proper management and treatment options were included such as administration of methylene blue. Overall, this simulation was helpful in teaching EM residents how to recognize, manage, and treat methemoglobinemia. In addition, post-simulation debriefing allowed further discussion among residents, which they found valuable. Topics: Methemoglobinemia, shortness of breath, cyanosis, respiratory distress, anemia, methemoglobin, oxygen dissociation curve, emergency medicine simulation.
ABSTRACT
Audience: The goal of this simulation is to educate emergency medicine students, residents, attending physicians, and mid-level practitioners to recognize, diagnose, and manage acute cyanide toxicity. Introduction: Cyanide has an almond scent and is a naturally occurring compound. It is present within many different types of plants and fruits including apricots, apples, peaches, lima beans, and cassava plants but is harmless.1 The trace amounts of cyanide found within organic materials is of little concern because its high reactivity causes it to be metabolized rapidly and create other compounds. However, modern synthetic materials such as plastics, papers, textiles, and machinery can release a much greater concentration of hydrogen cyanide when exposed to high temperatures.1 As the use of contemporary nitrogen-containing synthetic polymers has expanded, the possibility of cyanide toxicity has become increasingly common and severe. Hydrogen cyanide is especially dangerous to humans because the gaseous form reacts quickly upon inhalation.2When cyanide enters the body via inhalation, it blocks the cells from utilizing oxygen by binding to the cytochrome oxidase in the mitochondria.2 The inability of the cell to use oxygen forces cells from aerobic metabolism into anaerobic metabolism. Anaerobic metabolism results in the production of lactic acid, which causes metabolic acidosis.3 The human body cannot sustain itself with the lack of oxygen and anaerobic metabolism for a prolonged period of time. Ultimately, the body will suffer cardiorespiratory arrest.1Symptoms of cyanide toxicity include headache, nausea, shortness of breath, and altered mental status.1 These are similar to those of carbon monoxide and carbon dioxide inhalation. However, symptoms of cyanide toxicity cannot be treated with supplemental oxygen as carbon monoxide and carbon dioxide are. Cyanide toxicity must be treated with an antidote - sodium thiosulfate, sodium nitrite, and hydroxocobalamin.4 Each of the antidotes works by binding with the highly reactive cyanide, neutralizing the compound, and converting it into a water-soluble product that will be cleared through renal excretion.4Fire victims often present to the emergency department critically ill. They will likely have obvious external thermal burns and traumatic injuries; however, it is important for emergency personnel to recognize the respiratory distress and metabolic derangements that are most likely occurring due to toxic gas inhalation. People who are trapped within a burning structure are exposed to carbon monoxide, carbon dioxide, and cyanide from the combustion of contents within the building. These toxic gasses will cause severe tissue hypoxia without significant vital sign changes.5 The respiratory distress and metabolic compromise will be acutely more fatal than the obvious external injuries and burns. The challenge in treating these patients is for the healthcare team to know the differential diagnoses, prioritize airway, breathing and circulation, and to empirically treat the patient as if they have a confirmed exposure.It is estimated that 35% of all fire victims have toxic levels of cyanide upon arrival to the emergency room.2 Acute cyanide toxicity can become fatal within minutes; however, a prompt diagnosis and treatment can be lifesaving. Unfortunately, due to the limited amount of time the human body can sustain anaerobic metabolism and tissue hypoxia, blood test results are not available in time to be clinically applicable.2 Rather, the emergency room personnel must begin treatment immediately upon recognizing that toxic smoke inhalation may have occurred.We understand the importance of knowing how to treat fire victims. Therefore, the goal of this simulation case is to expose the emergency providers to cyanide poisoning and educate emergency providers about the critical steps of how to approach, diagnose, and treat cyanide toxicity. Educational Objectives: After the completion of this simulation, participants will have learned how to: 1) identify clues of smoke inhalation based on a physical examination; 2) identify smoke inhalation-induced airway compromise and perform definitive management; 3) create a differential diagnosis for victims of fire cyanide poisoning, carbon monoxide, and carbon dioxide; 4) appropriately treat cyanide poisoning; 5) demonstrate the importance of preemptively treating for cyanide poisoning; 6) perform an initial physical examination and identify physical marks suggesting the patient is a fire and smoke inhalation victim; and 7) familiarize themselves with the Cyanokit and treatment with hydroxocobalamin. Educational Methods: This is a high-fidelity simulation case in which participants work through a case of a patient who has been exposed to fire. The participants will be able to work hands-on to evaluate, diagnose, and treat cyanide poisoning in an emergency event. Afterwards, there will be a small group discussion and debriefing of the case in order to review patient care skills, interpersonal and communication skills, medical knowledge, and system-based practice. Research Methods: The participants were instructed to complete a survey before and after the simulation case. A quality Likert Scale was used to assess the participants' comfort level of diagnosing, treating, and managing a patient with toxic smoke inhalation. A score of 1 represented a negative experience and 5 represented a very positive experience. The surveys were then reviewed by the research team to determine if the simulation case improved the participants' comfort level. The survey answers were compared collectively, as well as individually, and were analyzed between the pre-simulation and post-simulation results. Results: Our simulation involved 25 participants: 20 participants were emergency medicine resident physicians and 5 were 4th-year medical students. In the pre-simulation survey, participants reported a mean of 2.7 out of 5 when asked to rate their confidence in their ability to treat a smoke inhalation victim. The post-simulation survey showed a significant increase to a mean of 3.5 out of 5. Participants were also asked to evaluate the usefulness of the simulation: 15 participants rated the case as a 5, which represented "very useful," and the other 10 participants rated the case as a 4, which represented "useful." The mean value when asked to assess the simulation case's usefulness and applicability in emergency medicine was 4.6 out of 5. Discussion: This simulation allows providers to focus on victims of fire. Fire victims are often critically ill and require time sensitive treatment. This simulation gives providers a chance to review their knowledge and prepare them for real life cases. Based on the survey results, the simulation improved awareness and understanding of the symptoms of acute cyanide toxicity and improved the participant's ability to recognize, diagnose, and treat cyanide poisoning. Topics: Cyanide toxicity, carbon monoxide toxicity, cyanide antidote, fire victim, intubation, airway intervention, oxygen treatment, history taking, lab testing ordering, symptom identification, interpretation of lab results, emergency medicine simulation.
ABSTRACT
INTRODUCTION: The imaging standard for evaluation of acute pulmonary embolism (PE) includes a computed tomography pulmonary angiogram. Ultrasonography has shown promise in obtaining the tricuspid annular plane systolic excursion (TAPSE) measurements, which may be of clinical importance in patients with acute PE. The objective of this study is to evaluate the diagnostic capability of TAPSE measurements for patients with suspicion for acute PE. METHODS: We prospectively enrolled patients who came to the emergency department with suspicion of acute PE. Each patient underwent a point-of-care sonogram where a TAPSE measurement was obtained, followed by computed tomography pulmonary angiogram. Based on the computed tomography pulmonary angiogram findings, patients were grouped into 3 categories: no acute PE, clinically insignificant acute PE, or clinically significant acute PE. RESULTS: We enrolled 87 patients in this study. Twenty-three (26.4%) of these patients were diagnosed with PE. Of patients with PE, 15 (65%) were found to have a clinically significant acute PE. Analysis of mean TAPSE measurements between patients with clinically significant acute PE and those with insignificant or no PE was 15.2 mm and 22.7 mm, respectively (P ≤ .0001). Following receiver operating characteristic curve analysis, optimum TAPSE measurement to identify clinically significant acute PE is 18.2 mm. A cutoff TAPSE measurement of 15.2 mm shows a sensitivity of 53.3% (95% confidence interval, 26.7%-80%) and a specificity of 100% (95% confidence interval, 100%-100%) for the diagnosis of a clinically significant PE. CONCLUSIONS: Our data suggest that TAPSE measurements less than 15.2 mm have a high specificity for identifying clinically significant acute PE.
