Critical Care: Fellow Case Report Poster - Critical Care III |

What Happens in Vegas, Doesn't Always Stay in Vegas: A Case of Meningococcal Myopericarditis FREE TO VIEW

Dharmi Patel, MD; Antonio Beltran, MD
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UC Irvine, Cerritos, CA

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;150(4_S):253A. doi:10.1016/j.chest.2016.08.266
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SESSION TITLE: Fellow Case Report Poster - Critical Care III

SESSION TYPE: Affiliate Case Report Poster

PRESENTED ON: Tuesday, October 25, 2016 at 01:30 PM - 02:30 PM

INTRODUCTION: Acute meningococcemia is a clinical syndrome secondary to Neisseria meningitidis infection that can rapidly progress to shock, multi-organ failure, and death. We report a case of fulminant myopericarditis as the initial presentation of meningococcemia that recovered after early goal-directed therapy.

CASE PRESENTATION: A 25 year-old previously healthy male presented to the emergency room with one day of abdominal pain, nausea, fevers/chills, and pleuritic chest pain during a trip to Las Vegas with a “sick contact“. The patient was febrile and tachycardic with an otherwise normal physical exam. While in the ER, he became hypotensive to 63/43 despite 3 liters of normal saline. An electrocardiogram showed diffuse ST segment elevations. Initial labs were remarkable for a white blood cell count of 10.4 K/UL (92% neutrophils), lactic acid 1.8 mmol/L, and troponin <0.01. Echocardiogram showed an ejection fraction of 25% with diffuse hypokinesis. Chest radiograph was normal. He was started on norepinephrine, broad spectrum antibiotics and additional intravenous fluids with subsequent improvement in his blood pressure. While in the intensive care unit, his vasopressor requirement increased over the next 24 hours with lactate rising to 4.4 mmol/L and troponin to 75 ng/mL. By hospital day 2, his vasopressor requirements, lactate, and troponin decreased with additional fluids. Preliminary blood cultures were positive for gram negative diplococci, which speciated to Neisseria meningitidis. Lumbar puncture results were normal. Antibiotics were de-escalated to a 3rd generation cephalosporin. On HOD 4, the patient was weaned off the vasopressor and bedside echo showed improvement in his EF to 40%.

DISCUSSION: The exact mechanism of myocardial involvement in acute meningococcemia is unclear but is thought to be related to increased levels of interleukin 6. Dysfunction of the myocardium contributes to the high mortality from meningococcemia, with more than 50% of patients having some degree of myocarditis on post-mortem examination.

CONCLUSIONS: Due to the rapid progression and mortality of meningococcal myocarditis, it is important for the critical care physician to have a clinical suspicion for bacterial myocarditis in previously healthy patients who present with viral symptoms, sepsis, and acute cardiomyopathy. Early goal-directed therapy can result in rapid recovery and avoid fatal outcomes.

Reference #1: Razminia M, et al. Importance of early diagnosis and therapy of acute meningococcal myocarditis. Am J Ther. 2005;12:269-271

DISCLOSURE: The following authors have nothing to disclose: Dharmi Patel, Antonio Beltran

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