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• W2895075492 abstract "SESSION TITLE: Critical Care 1 SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Stress cardiomyopathy or Takotsubo syndrome, is characterized by severe but transient left ventricular dysfunction (1,2). Plasma catecholamines have been found to be elevated in patients suffering from this condition, usually derived from severe emotional or physical stress (2). Takotsubo syndrome has also been reported in the setting of exogenous catecholamine administration.1,2 CASE PRESENTATION: Our patient is a 36 year old woman admitted to our facility for incision and drainage of hand abscess due to a dog bite. She was placed on intravenous (IV) levofloxacin and oxycodone for pain control. On postoperative day 1 and while IV levofloxacin was infusing, patient developed a new papular rash on neck and arms. At this time all patient’s vital signs were within normal range and she was asymptomatic. On call physician administered 50 mg of diphenhydramine but continued IV infusion. About 15 minutes later, patient became anxious, diaphoretic and complained of chest pressure. Her heart rate increased from 80 to 115, without any other change in vital signs or physical exam. Rapid response team was called for concern of anaphylactic reaction, and team leader administered epinephrine 1mg (1:10,000) IV push. Shortly after, patient became extremely tachycardic, hypertensive and diaphoretic. Another 1 mg (1:10,000) of epinephrine was administered intravenously. Immediately after, patient’s condition deteriorated significantly. She became severely hypotensive (60/palp) and tachycardic (160). At this time a bedside echocardiogram was performed demonstrating an ejection fraction of 10% with akinesis in the entire apex and basal segments preserved. An EKG demonstrated ST elevation on lateral leads. Patient required intubation and hemodynamic support with multiple vasopressors and an intra-aortic balloon pump. After 8 days, patient’s echocardiogram revealed an ejection fraction of 35% and she was extubated, on room air and requiring no vasopressor support. DISCUSSION: Stress cardiomyopathy secondary to epinephrine in the treatment of anaphylaxis has been reported in the literature (1,2). Risk is increases with intravenous administration and higher doses (3). In our case, patient’s hypotension presented immediately after second dose of IV epinephrine, suggesting this was the triggering factor. This presentation supports the theory that catecholamine induced myocardial stunning gives rise to left ventricular dysfunction in Takotsubo Syndrome (3). CONCLUSIONS: This case highlights the importance of adequate dosing of epinephrine in the setting of anaphylaxis. The majority of cases in the literature are associated with intravenous administration and higher doses of epinephrine (3). Prompt recognition of stress induced cardiomyopathy is of utmost importance, as most patients recover cardiac function almost entirely and have a favorable prognosis (1,2). Reference #1: Y-Hassan S, Clinical features and outcome of epinephrine-induced takotsubo syndrome: Analysis of 33 published cases. Cardiovasc Revasc Med. 2016 Oct - Nov;17(7):450-455. Reference #2: Nazir S, Lohani S, Tachamo N, et al., Takotsubo cardiomyopathy associated with epinephrine use: A systematic review and meta-analysis. Int J Cardiol. 2017 Feb 15;229:67-70. Reference #3: Ghanim D, Adler Z, Qarawani D, et al., Takotsubo cardiomyopathy caused by epinephrine-treated bee sting anaphylaxis: a case report. J Med Case Rep. 2015; 9: 247. DISCLOSURES: No relevant relationships by Carolina Landeen, source=Web Response" @default.
• W2895075492 created "2018-10-12" @default.
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• W2895075492 date "2018-10-01" @default.
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• W2895075492 title "EPINEPHRINE HEART, MY ACHY BREAKY HEART: A CASE OF EPINEPHRINE-INDUCED STRESS CARDIOMYOPATHY IN ANAPHYLAXIS TREATMENT" @default.
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