Streptococcus Pneumoniae Purulent Pericarditis

Background Bacterial pericarditis represents < 1 % of all cases of pericarditis in the United States. Most cases of bacterial pericarditis are from contiguous spread from underlying pneumonia or mediastinitis. We present a case of pneumococcal pericarditis in a patient with untreated pneumonia. Case A 54-year-old male with a past medical history of recent COVID-19 pneumonia presented with worsening dyspnea for the past 3 weeks. Vitals were T 99.3, BP 122/93, HR 159 BPM, O2 sat 94% on 3 L NC. ECG demonstrated atrial flutter with 2:1 block. CT scan demonstrated a pericardial effusion and bilateral pleural effusions. Decision-making In the ED, he became hypotensive and bedside echo demonstrated large pericardial effusion with RV collapse. Emergent pericardiocentesis produced 750 cc of purulent fluid. Streptococcus pneumoniae was isolated from the initial fluid aspirate. Right thoracostomy tube was placed with pleural fluid gram stain and culture without bacterial growth. Due to continued purulent drainage from the pericardial drain, repeat CT scan demonstrated persistent pericardial effusion and loculated right sided pleural effusion. He underwent video-assisted thoracoscopic surgery with pericardial wash out and window. He improved and was discharged with 6 weeks of Ceftriaxone. Conclusion Purulent pericarditis is typically a fulminant disease associated with high mortality and rapid progression. Prompt identification and management is critical for patient survival. [Formula presented]Copyright © 2023 American College of Cardiology Foundation

Cardiac Angiosarcoma Presenting as Recurrent Pericardial Effusion and Constrictive Pericarditis

Background Malignancy accounts for 15-20% of moderate to large pericardial effusions. Among these, cardiac angiosarcomas are extremely rare. Case A 30-year-old male presented with dyspnea and fatigue, 9 months after COVID-19 infection. He had sinus tachycardia (117 beat/min). Chest X-ray showed cardiomegaly. Echocardiogram demonstrated a large circumferential pericardial effusion with right ventricular collapse. Decision-making Pericardiocentesis yielded 850 ml of bloody fluid, with symptomatic relief. He was discharged on colchicine and indomethacin with a presumptive diagnosis of post-viral pericarditis. A month later, he had recurrent symptoms and re-accumulation of large circumferential effusion. CT chest revealed multiple pulmonary nodules and bilateral pleural effusions. He underwent subxiphoid pericardial window and pleural biopsy. Fluid analysis and biopsy results were inconclusive. Over 3 weeks, he had worsening symptoms, despite a daily pericardial drain output of ~200 ml. Repeat echocardiogram showed loculation of the effusion with signs of constrictive pericarditis. He underwent pericardiectomy. Pathology revealed cardiac angiosarcoma. FDG PET scan showed thoracic metastasis. Anakinra was initiated. Conclusion Idiopathic and post-viral etiologies are the most common causes of pericardial effusion. Although rare, cardiac angiosarcoma should be on the differential diagnosis for recurrent pericardial effusion. [Formula presented]Copyright © 2023 American College of Cardiology Foundation

Spotting the Needle Amongst the Haystack - When Asthma Isn't Asthma

Introduction/Background: Eosinophilic granulomatosis with polyangiitis (EGPA), previously known as Churg-Strauss Syndrome, is a rare, small to medium vessel ANCA associated vasculitis. Hallmarks of EGPA include asthma, chronic rhinosinusitis, and peripheral neuropathy. EGPA is characterized by a prodrome of asthma and allergic rhinitis, followed by peripheral blood hyper-eosinophilia and accumulation of extravascular eosinophils, and finally systemic vasculitis. Extrapulmonary involvement is common, sometimes with fatal outcomes. The onset of EPGA is typically between 25-50 years;however, EGPA also occurs during childhood and has a significant morbidity and mortality. Description/Method: Our patient presented to the emergency department with a 2-week history of lethargy, wheeze and left sided neck swelling. After testing COVID-19 positive eight months prior to this, she developed wheezy episodes and was subsequently diagnosed with asthma which was managed with bronchodilators as required. She was reviewed by an allergist who confirmed a dust mite allergy and prescribed Montelukast. She remained well during the summer months however during winter she had 3 distinctive episodes of wheeze and cough which were managed by antibiotics and prednisolone. In the emergency department, an echocardiogram was performed which showed a cardiac tamponade. She was transferred to CICU where she had a pericardial drain inserted. The fluid was abundant with inflammatory cells. Multiple investigations were performed as follows: Hb: 135g/L, wbc: 20.30 x 10 9/L, Eosinophils: 12.77 x 10 9/L, CRP: 51 mg/L, ESR: 75 mm/hr, LDH: 1188 IU/L, IgE: 8000 UI/ml, ANA, ANCA: negative. CT chest showed mediastinal lymphadenopathy and patchy bilateral infiltrate and cardiac MRI showed myopericarditis and LV fibrosis. BMA showed no malignant cells and sinusitis was confirmed by CT. On examination, she was underweight. Her nasal mucosa looked inflamed. Otherwise systemic examination was unremarkable. In the context of poor ejection fraction (20%) with LV fibrosis, urgent MDT was arranged and concluded that our working diagnosis was EGPA. The decision was made to start IV methylprednisolone 10mg/kg/day for 3 days and Ivermectin. That night our patient had a VF arrest which required a single shock conversion 4J/kg. There was 7-minute downtime. Treatment was escalated to include cyclophosphamide, rituximab and plasmapheresis. The patient made a remarkable recovery, extubated and transferred to a normal ward. Her eosinophils count and inflammatory markers improved dramatically following treatment. However, she developed severe neuropathic left leg pain and NCS confirmed peripheral neuropathy Discussion/Results: EGPA is a very rare disease and diagnosis can be challenging especially with the absence of histopathology diagnosis. Early empirical treatment especially in a very ill child in intensive care unit can save lives and divert the progress of the disease. This patient has fulfilled the American College of Rheumatology criteria to diagnose EGPA including asthma, eosinophil count > 10% of upper normal, peripheral neuropathy, pulmonary infiltrates on CT thorax and paranasal sinuses abnormalities. Cardiac biopsy of the fibrotic mass may be a useful tool for diagnosis;however, this invasive procedure may expose this patient with high risk of fatal arrhythmias. Since other causes of eosinophilia were ruled out including parasitic infections, lymphoproliferative disorders, and rare primary immunodeficiency syndromes (hyper-IgE syndrome due to STAT3 or DOCK8 deficiency and Omenn syndrome) and the patient responded well to treatment, the diagnosis of EGPA was supported. Key learning points/Conclusion: Asthma not responding to bronchodilator could be another diagnosis Eosinophilia should be interpreted with caution. Defer the need for histopathology diagnosis in critically ill children Cardiac involvement is a life-threatening marker Early diagnosis prevents life threatening complications.

RAPIDLY PROGRESSIVE PERIMYOCARDITIS IN SARS-COV-2 INFECTION

SESSION TITLE: Extraordinary Cardiovascular Reports SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 01:35 pm - 02:35 pm INTRODUCTION: The COVID-19 pandemic has resulted in millions of deaths worldwide. Many cases involved a primary pulmonary process, yet myocarditis associated with COVID-19 has been observed.1 We present a novel case of rapidly progressive fulminant peri-myocarditis with minimal lung involvement in acute COVID-19 infection. CASE PRESENTATION: A 39-year-old female with no medical history presented with chest pain and dyspnea with an acute COVID-19 infection. She had a brief cardiac arrest with rapid ROSC and no intubation. Chest CT angiogram showed essentially normal pulmonary parenchyma and moderate pericardial effusion. EKG showed sinus tachycardia with global ST segment elevation. An echocardiogram showed an ejection fraction (EF) of 25% with a moderate sized pericardial effusion and right ventricle collapse. She was transferred for emergent drainage of the effusion to our institution. Her circulatory shock initially improved following pericardial drainage, yet she declined warranting increasing vasopressor and inotropic support. An emergent echo showed an EF of less than 10% and no re-accumulation of pericardial fluid. It was clear that the patient required mechanical circulatory support (MCS) and was transferred to the catheterization lab. While in the lab, the patient suffered cardiac arrest and an Impella device was placed during prolonged ACLS without achieving ROSC. Venoarterial ECMO cannulation was then performed. She was transferred to a cardiac transplant center where she later developed multi-organ failure leading to death. DISCUSSION: While COVID-19 has been shown to affect multiple organs apart from the lungs, this case was notable due to minimal pulmonary involvement. The patient's manifestation of her infection was almost entirely cardiac in nature. MCS was discussed in the catheterization lab at the time of pericardial drain insertion. The decision was made to not pursue MCS as the patient's shock had improved. Additionally, the patient did not undergo pulmonary arterial catheter (PAC) placement. Prompt placement of a PAC has been associated with early access to MCS and reduced in-hospital mortality.2 Perhaps we would have obtained MCS earlier if PAC data supported this intervention before the patient deteriorated. It will be important to consider primary cardiac manifestations of COVID-19 infection and early consideration of invasive hemodynamic monitoring to identify a need for timely MCS. CONCLUSIONS: We present the first reported case of fulminant peri-myocarditis in the absence of acute hypoxemic respiratory failure or radiographic pulmonary parenchymal lung abnormality. Isolated rapidly progressive cardiogenic shock secondary to COVID-19 associated peri-myocarditis is a phenomenon important for critical care clinicians to be aware of during this pandemic. One should have a low threshold to establish invasive hemodynamic monitoring and consideration for early MCS in these cases. Reference #1: Siripanthong B, Nazarian S, Muser D, et al. Recognizing COVID-19-related myocarditis: The possible pathophysiology and proposed guideline for diagnosis and management. doi:10.1016/j.hrthm.2020.05.001 Reference #2: Osman M, Syed M, Patel B, et al. Invasive Hemodynamic Monitoring in Cardiogenic Shock Is Associated With Lower In-Hospital Mortality. Journal of the American Heart Association J Am Heart Assoc. 2021;10:21808. doi:10.1161/JAHA.121.021808 DISCLOSURES: No relevant relationships by Samuel Bullick No relevant relationships by Jonathan Greenberg No relevant relationships by Scott Slusarenko

HYDROXYCHLOROQUINE CAN BREAK YOUR HEART

SESSION TITLE: The Cardiac Intensivist 2 SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: Hydroxychloroquine and chloroquine are medications derived from aminoquinoline. They are disease-modifying antirheumatic drugs used in the treatment of systemic lupus erythematosus (SLE). Although well tolerated, they do have side effects such as retinopathy, vacuolar myopathy, neuropathy, and as seen in our patient, cardiotoxicity. CASE PRESENTATION: Patient is a 48 year old female with a past medical history significant for chronic kidney disease secondary to autosomal dominant polycystic kidney disease, SLE on hydroxychloroquine who presented to the emergency department complaining of weakness. On arrival the patient was found to be in cardiogenic shock. Her transthoracic echocardiogram revealed a reduced ejection fraction of 37% and a large pericardial effusion concerning for tamponade physiology. Her COVID-19 PCR test was positive. She was taken for emergent pericardiocentesis which revealed 300cc of exudative fluid. Patient’s right heart catheterization revealed mean pulmonary capillary wedge pressure of 23 mmHg, pulmonary artery pressures of 44 mmHg/24 mmHg, mean 31mmHg, cardiac index 1.1L/min/m² by thermodilution, 1.7 L/min/m² by Fick. Following right heart catheterization and intra aortic balloon pump placement, the patient was admitted to the medical intensive care unit (MICU) and placed on intravenous inotropic and vasopressor support. Shortly after arrival to the MICU, patient had an increase in vasopressor requirements. Bedside ultrasound revealed cardiac tamponade. Patient had approximately 400cc of bloody pericardial fluid removed from her pericardial drain. The decision was made for emergent venoarterial extracorporeal membrane oxygenation (ECMO) to be initiated. Endomyocardial biopsy was performed which revealed vacuolization in the cytoplasm of several myocytes as well as lymphocytes in the interstitium of the endocardium. The vacuoles found in the cardiac myocytes were PAS positive. These biopsy results are consistent with hydroxychloroquine cardiotoxicity. The patient’s hydroxychloroquine was discontinued. In addition to hemodynamic support, she also received intravenous immunoglobuluin and systemic steroids. After a prolonged hospitalization she was successfully discharged. DISCUSSION: Cardiotoxicity is a rare adverse reaction seen with hydroxychloroquine. A 2018 systematic review revealed 127 cases of cardiac toxicity associated with the use of hydroxychloroquine or chloroquine. Most patients had been treated with the medication for a prolonged period of time and the toxicity is dose dependent. The mechanism behind hydroxychloroquine and chloroquine induced cardiomyopathy is believed to be secondary to lysosomal dysfunction as a result of toxic phospholipid accumulation in cardiomyocytes. CONCLUSIONS: In patients with new onset cardiomyopathy, a detailed medication reconciliation should be conducted to evaluate for toxins such as hydroxychloroquine and chloroquine. Reference #1: Della Porta, A., Bornstein, K., Coye, A., Montrief, T., Long, B., & Parris, M. A. (2020). Acute chloroquine and hydroxychloroquine toxicity: A review for emergency clinicians. The American Journal of Emergency Medicine. Reference #2: Abbi, B., Patel, S., Kumthekar, A., Schwartz, D., & Blanco, I. (2020). A Case of Cardiomyopathy With Long-term Hydroxychloroquine Use. JCR: Journal of Clinical Rheumatology, 26(8), e300. Reference #3: Chatre, C., Roubille, F., Vernhet, H., Jorgensen, C., & Pers, Y. M. (2018). Cardiac complications attributed to chloroquine and hydroxychloroquine: a systematic review of the literature. Drug safety, 41(10), 919-931. DISCLOSURES: no disclosure on file for Joseph Adams;no disclosure on file for Suliman Alradawi;No relevant relationships by George Kalapurakal No relevant relationships by Mohammed Siddiqui

CARDIAC TAMPONADE SECONDARY TO COVID-19 INFECTION

SESSION TITLE: Infections In and Around the Heart Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Due to the novelty of COVID-19 virus, complications of this severe respiratory infection are continually emerging. The inflammatory response to the virus carries a high mortality rate and can lead to a variety of cardiothoracic complications such as acute coronary syndrome, thromboembolism, and heart failure [1]. Here, we present a case of a young female who suffered cardiac tamponade (CT) from a pericardial effusion (PEEF) attributed to COVID-19 infection, which has only been described a handful of times in the literature. CASE PRESENTATION: A 33-year-old female with a history of Down syndrome and morbid obesity presented with worsening dyspnea and fever for one week. Her initial oxygen saturation was 50% on room air, and bilevel noninvasive ventilatory support was initiated. Her viral PCR was positive for COVID-19. A computed tomography angiogram of the chest revealed small bilateral pulmonary emboli, diffuse ground-glass consolidations, and small bilateral pleural effusions. Her respiratory status continued to decompensate and she was placed on mechanical ventilation. She became hypotensive requiring vasopressor support. The following morning, an echocardiogram (TTE) revealed an ejection fraction of 40-45% and a new PEEF with early right ventricular diastolic collapse consistent with CT physiology. She underwent emergent pericardiocentesis, and 220 mL of bloody fluid was drained. PEEF studies revealed a glucose level of 186 mg/dL, LDH of 1380 U/L, and protein of 3.0 g/dL. Total nucleated count was 16,545/uL with 68% neutrophils. Gram stain showed a few white blood cells without organisms, and final bacterial, fungal, and acid-fast cultures were negative. A pericardial drain was left in place, but the procedure was complicated by a pneumothorax and a chest tube was placed. A follow-up TTE the next day revealed improvement of the PEEF without signs of CT. A repeat chest x-ray showed resolution of the pneumothorax. Unfortunately, the patient’s oxygenation and hemodynamic status continued to worsen. She eventually suffered cardiac arrest with pulseless electrical activity and succumbed to her illness. DISCUSSION: New knowledge regarding complications of COVID-19 infection is continually emerging. According to a February 2022 systematic review, only 30 cases of severe PEEFs with CT secondary to COVID-19 have been recorded. The mechanism by which PEEFs form is unclear. It is proposed that the entry of the virus into inflammatory cells causes a release of cytokines such as TNF-alpha, IL-1, IL-6, and IL-8. This resulting cytokine storm allows rapid inflammation and infiltration of fluid into the pericardial sac [1]. CONCLUSIONS: In a decompensated patient with COVID-19, a stat TTE should be obtained to rule out PEEF. Physicians must be cognizant of this uncommon yet highly fatal complication in unstable COVID-19 patients, as cardiac tamponade is a potentially reversible cause of cardiac arrest. Reference #1: Kermani-Alghoraishi, M., Pouramini, A., Kafi, F., & Khosravi, A. (2022). Coronavirus Disease 2019 (COVID-19) and Severe Pericardial Effusion: From Pathogenesis to Management: A Case Report Based Systematic Review. Current problems in cardiology, 47(2), 100933. https://doi.org/10.1016/j.cpcardiol.2021.100933 DISCLOSURES: No relevant relationships by Amanda Cecchini No relevant relationships by Arthur Cecchini No relevant relationships by Kevin Cornwell No relevant relationships by Krupa Solanki