ABSTRACT
Case Report: A 42-year-old male with no significant past medical history presented to the emergency department (ED) after a three-week history of myalgias, non-productive cough, and progressively worsening dyspnea accompanied by a two-week history of right-sided chest pain that all started four days after receiving his Pfizer COVID-19 booster vaccine. Chest pain was described as constant, non-radiating, and aggravated by positional changes. On ED arrival, the patient was febrile to 102.9degreeF and tachycardic with initial labs significant for leukocytosis of 13.6 Thou/uL, Creactive protein at 17.18 mg/dL, troponins negative x2, and a negative COVID-19 NAAT testing. EKG revealed diffuse T wave inversions and chest x-ray was noncontributory. Transthoracic echocardiogram (TTE) obtained showed a small fibrinous circumferential pericardial effusion with no evidence of cardiac tamponade;however, there was an interventricular septal bounce suggestive of effusive-constrictive pericarditis. This diastolic septal bounce was also seen on cardiac magnetic resonance imaging, along with a pericardial enhancement measuring up to 0.2 cm2 in thickness. With a negative infectious and autoimmune workup, along with low clinical suspicion for tuberculosis or malignancy, the leading differential was the temporal relationship between receiving the Pfizer COVID-19 mRNA booster vaccine and the development of effusive-constrictive pericarditis (ECP). The patient was started on Colchicine 0.6 mg twice daily, Ibuprofen 400 mg three times daily, and subsequently discharged after symptomatic improvement and being afebrile for 72 hours with plans for close cardiology follow-up. Discussion(s): ECP is a rare syndrome characterized by a concurrent decrease in pericardial compliance with pericardial effusion and is seen in 4.5% to 6.9% of patients who present with pericardial effusions. To date, less than five other case reports internationally have delineated a relationship between COVID-19 mRNA vaccines and the development of ECP, making recognition of this etiology challenging. In patients who have a mixed hemodynamic picture with subacute features of both cardiac tamponade and constrictive pericarditis, clinicians should have a high index of suspicion for ECP.
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SESSION TITLE: Pulmonary Involvement in Critical Care Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Hemophagocytic Lymphohistiocytosis (HLH) is a condition in which the body's natural ability to end an immune or inflammatory response is defective1. COVID-19 also presents with severe inflammation, and like HLH, leads to significantly elevated ferritin2. We present a case that was initially thought to be COVID-19, but the patient was diagnosed with HLH in the setting of S. aureus endocarditis. CASE PRESENTATION: A 62-year-old male with a history of atrial fibrillation, mechanical mitral valve on warfarin, type II diabetes, chronic obstructive pulmonary disease, and recently diagnosed COVID-19 presented to the hospital with progressive dyspnea. In the emergency department, he was found to be hypoxemic and in atrial fibrillation with rapid ventricular response. He had a fever of 39.3°C and his initial laboratory workup revealed hemoglobin of 11.9 g/dL, leukocytes of 5,700, platelets of 83,000, AST 35 U/L, ALT 34 U/L, CRP of 31.89 mg/dL, and ferritin of 1994 ug/L. The patient was admitted and started on dexamethasone 6 mg daily. The following day, the patient's blood work revealed a significant worsening of AST and ALT to 7280 U/L and 3319 U/L, respectively. D-dimer increased to 11861 ng/mL (DDU) and ferritin to 36,470 ug/L. On the third day of admission, his clinical status declined acutely as he became significantly bradycardic, progressing to a cardiac arrest after which he required cardiopulmonary resuscitation, intubation, and was transferred to the intensive care unit. A CT scan obtained revealed hepatomegaly of 22 cm and blood cultures were positive for S. aureus requiring vancomycin treatment. The patient was kept on dexamethasone due to concerns for HLH. Ferritin continued to worsen, reaching 50,749 ug/L. His sCD25 came back positive. Unfortunately, the patient expired on his fifth day of hospitalization after discussing with his family their goals for his care and switching his care to comfort only. DISCUSSION: HLH is a challenging condition since diagnosis is difficult and mortality is high. There are a few methods used to diagnose HLH. Usually, 5 of 8 criteria must be met, which was achieved with this patient. However, often the patient only fulfills 4 of 8 since many criteria are difficult to obtain such as bone marrow biopsy, sCD25, and CXCL9. A useful tool is the H-calculator3. Our patient scored a 180 indicating a 50-75% likelihood of HLH. Assessing the likelihood of disease is important since sCD25 and CXCL9 take time and if the patient is clinically deteriorating treatment should not be delayed. CONCLUSIONS: HLH is catastrophic and rare. Physicians should always have it as a differential diagnosis in patients with severe inflammatory states and elevated ferritins to avoid anchoring bias. If suspicion is high based on clinical evaluation and scores, treatment should not be delayed. Reference #1: Filipovich A, McClain K, Grom A. Histiocytic disorders: recent insights into pathophysiology and practical guidelines. Biol Blood Marrow Transplant. 2010;16(1 Suppl):S82-S89. doi:10.1016/j.bbmt.2009.11.014 Reference #2: Cheng L, Li H, Li L, et al. Ferritin in the coronavirus disease 2019 (COVID-19): A systematic review and meta-analysis. J Clin Lab Anal. 2020;34(10):e23618. doi:10.1002/jcla.23618 Reference #3: Fardet L, Galicier L, Lambotte O, et al. Development and validation of the HScore, a score for the diagnosis of reactive hemophagocytic syndrome. Arthritis Rheumatol. 2014;66(9):2613-2620. doi:10.1002/art.38690 DISCLOSURES: No relevant relationships by Areeka Memon No relevant relationships by Carissa Monterroso No relevant relationships by Carson Oprysko No relevant relationships by Eduardo Padrao No relevant relationships by Mouna Penmetsa