Potential Cardiac Tamponade Development Secondary to SARS-CoV-2 Infection

Upon initial discovery in late 2019, severe acute respiratory syndrome coronavirus 2, SARS-CoV-2, has managed to spread across the planet. A plethora of symptoms affecting multiple organ systems have been described, with the most common being nonspecific upper respiratory symptoms: cough, dyspnea, and wheezing. However, the cardiovascular system is also at risk following COVID-19 infection. Numerous cardiovascular complications have been reported by physicians globally, in particular cardiac tamponade Physicians must hold a high index of suspicion in identifying and treating patients with cardiac tamponade who may have contracted the novel coronavirus. This review will describe the current epidemiology and pathophysiology of SARS-CoV-2 and cardiac tamponade, highlighting their clinical course progression and the implications it may have for the severity of both illnesses. The paper will also review published case reports of cardiac tamponade, clinical presentation, and treatment of this complication, as well as the disease as a whole. © 2022 Elsevier Inc.

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.

Cardiac tamponade as the first presentation of thymoma: A case report during COVID-19 pandemic

We report a case of neoplastic cardiac tamponade, a life-threatening condition, as the initial presentation of an anterior mediastinal malignancy. A 69-year-old gentleman with no known history of malignancy presented to the emergency department with shortness of breath, reduced effort tolerance and chronic cough. Clinically, he was not in distress but tachycardic. He was subjected to echocardiography which revealed large pericardial effusion with tamponade effect. Pericardiocentesis drained 1.5 L of haemoserous fluid. CECT thorax, abdomen and pelvis revealed an anterior mediastinal mass with intrathoracic extension complicated with mass effect onto the right atrium and mediastinal vessels. Ultrasound-guided biopsy histopathology examination revealed thymoma. Due to locally advanced disease, tumour resection was not possible, and patient was referred to oncology team for chemoradiotherapy. We report this case study not only due to the rarity of the case but also to highlight its diagnostic challenge due to the COVID-19 pandemic. Copyright © The Author(s) 2022.

S P O N Ta N Eous R E S O Lut I O N O F Large Pericardial Effusion after Cardiopulmonary Resuscitation in a Chronic Kidney Disease Patient on Maintenance Haemodialysis

BACKGROUND: Here we discuss a chronic kidney disease (CKD) patient with large pericardial effusion who arrested secondary to tamponade and had an unintentional pericardial decompression secondary to cardiopulmonary resuscitation (CPR) that subsequently saved his life. AIM OF THE STUDY: To bring to light management difficulties in chronic kidney disease patients undergoing maintenance hemodialysis with large pericardial effusion METHODS: 67-year-old male a case of CKD on maintenance hemodialysis (for last two years) but inadequately dialyzed over last two months after recent Covid pneumonia was detected to have large pericardial effusion on echocardiography. He was planned for intensive heparin-free dialysis in view of absence of frank clinical and echocardiographic findings of tamponade with close surveillance for pericardial effusion. 60 minutes into hemodialysis patient developed dyspnea hypotension and cardiac arrest. Return of spontaneous circulation was achieved after three cycles of cardiopulmonary resuscitation. Echocardiography (echo) guided pericardiocentesis was planned based on clinical suspicion of tamponade. But echocardiography revealed only mild pericardial effusion. Chest X-ray showed new left pleural effusion. Pleurocentesis revealed hemorrhagic fluid. Subsequently done CT thorax showed multiple rib fractures. Patient was discharged on day eleven in stable condition with repeat chest X ray and echocardiography showing no further collection. RESULT(S): Though cardiac tamponade is largely a clinical diagnosis, various other features like echocardiography aid in its diagnosis. Diagnosis of tamponade in CKD patient with pericardial effusion is difficult because of several reasons. All classical clinical features of tamponade like hypotension or elevated systemic pressures may not be manifested all the time in cases of tamponade. Our patient developed clinical signs of tamponade 60 minutes into dialysis session indicating that precipitation of tamponade was likely due to reduction in preload due to ultrafiltration (UF) during hemodialysis. Though, daily dialysis is the initial preferred treatment of choice for uremic pericardial effusions in CKD patients without clinical or echocardiographic signs of tamponade, there are case reports which support early pericardiocentesis as treatment of choice in all large pericardial effusions in CKD patients on maintenance hemodialysis (MHD). In our case of large pericardial effusion, due to absence of frank clinical/ echocardiographic evidence of tamponade, we were prompted to go for aggressive dialysis treatment plan, but had tamponade during dialysis. CPR can cause inadvertent injury to surrounding structures, ribs, abdominal organs, and vascular injury. In our case, CPR-associated injury leads to unintentional pericardial decompression probably due to rib injury or due to high force generated during CPR coupled with high pericardial pressures which overcame the tensile strength of pericardium resulting in pericardial decompression. Findings of fractured ribs on CT scan post-resuscitation in our case supports that high force and pressure were generated during CPR. CONCLUSION(S): This case report supports early pericardiocentesis as treatment of choice for large pericardial effusion in CKD patients on MHD. Also, care should be taken while dialyzing these patient as rapid UF can precipitate tamponade.

Traditional Cardiopulmonary Resuscitation In Cardiac Arrest For Patients On Venovenous Extracorporeal Membrane Oxygenation

Introduction: Mortality for patients on VV-ECMO remains high despite increased use during the COVID-19 pandemic. Unlike VA-ECMO which provides life support for cardiac failure and can be used as a bridge to definitive therapy during cardiac arrest (e-CPR), patients who arrest while on VV-ECMO currently may undergo traditional cardiopulmonary resuscitation (CPR). This poses many challenges such as potential cannula position disruption of the VV-ECMO system during compressions and it is unclear if patients on VV-ECMO will benefit from being offered traditional CPR. Hypothesis: Traditional CPR is effective in patients who arrest while on VV-ECMO. Method(s): A retrospective chart review of inpatient cardiac arrest data from a high-volume ECMO center was performed. Patients who arrested while on VV-ECMO were included. Data including demographics, etiology of arrest, return of spontaneous circulation (ROSC) and survival to discharge were reviewed. Survival data was compared with the ECLS International Summary of Statistics. Result(s): We identified 19 patients on VV-ECMO who underwent CPR for cardiac arrest between September 2012 and November 2021. The average age of the patients was 42.7 years and 89.5% (n=17) were men. Seven of the nineteen total patients (36.8%) were being treated for ARDS from COVID-19 pneumonia. The arrest occurred on average 35.6 days into hospitalization (range: 1-132 days). The initial rhythm was pulseless electrical activity in 13 patients (68.4%), and the etiologies of arrest included hypoxemia (n=10, 52.6%), ECMO machine failure or during oxygenator exchange (n=3, 15.8%), pneumothorax (n=2, 10.5%), and cardiac tamponade (n=1, 5.3%). ROSC occurred in all 19 patients (100%), however only 4 patients (21.1%) survived to discharge with good neurologic recovery. Survival to discharge for all-comers on VV-ECMO is 66%. Conclusion(s): While there is limited evidence for the effectiveness of traditional CPR for patients on VV-ECMO, in this sample, ROSC was universal and one-fifth of patients survived to discharge. Future studies should continue to study the utility of CPR on VV-ECMO and how to optimize technique to improve outcomes for these critically-ill patients.

Cardiovascular manifestation in multisystem inflammatory syndrome in children temporally associated with COVID-19-single center experience

Background and Aim: Cardiovascular manifestations are common (35-100%) in multisystem inflammatory syndrome in children (MIS-C), including ventricular dysfunction, shock, coronary artery dilation, pericardial effusion and conduction abnormalities. Our study aimed to analyse cardiovascular involvement in our patients with MIS-C treated in our hospital. Method(s): The retrospective cohort study included all patients with MIS-C treated from April 2020 to December 2021 in the Mother and Child Health Institute of Serbia. In every case, cardiovascular manifestations were analysed: ventricular dysfunction, coronary artery dilatation, pericardial effusion, shock and ECG changes. Result(s): The study included 77 patients, 45 boys and 32 girls, aver-age years of age 9.3 +/- 4.8. Elevated cardiac troponin I and pro-BNP were observed in 35.9% and 87.8% of patients, respectively. Myocardial dysfunction was observed in half of our patients (50.6%), with an average ejection fraction of 50.5 +/- 8.9%. Children older than 10 years had 4 times higher chances for myo-cardial dysfunction (OR 4.3, 95%CI 1.6-10.8;p = 0.003). Shock syndrome had 21.1% of children on admission, while 5.3% devel-oped shock during the in-hospital stay. Transient coronary artery (CA) dilatation was observed in 6.5% of patients;left CA in 3 pts (Z score +2,95 +/- 0.3), right CA in one patient (Z score +2), and in one LCA and RCA (RCA Z score 2.6). Transient CA dilatations were observed only in patients with KD-like clinical presentation (5/54 pts). Mild pericardial effusion with spontaneous resolution was detected in 28.6% of children, while one female adolescent had severe pericardial effusion with threatening cardiac tamponade. On the standard ECG, 53% of children had negative T wave in inferior or/and precordial leads averagely on day 2 (IQR 1-3 day);transient QTc prolongation was registered in 46% of patients, averagely on day 7 (IQR 5-9). Sinus bradycardia and coronary rhythm were registered in 42.1% of patients, while premature ven-tricular beats were observed in 2.7% of pts. left ventricle thrombus was detected in one patient with normal echocardiography find-ing. In this patient, increased activity of Factor VIII and XII was proven. Conclusion(s): Cardiac manifestations are common and potentially life-threatening in MIS-C and should be assessed for at presenta-tion and during the clinical course as indicated.

ACUTE PERICARDITIS CAUSED BY COVID-19 INFECTION AND ITS MANAGEMENT

SESSION TITLE: Extraordinary Cardiovascular Reports SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 01:35 pm - 02:35 pm INTRODUCTION: The incidence of acute pericarditis is 3.32 per 100,000 person-years (11). Patone et. Al, found that 0.001% had acute pericarditis after a dose of the COVID-19 vaccine, while 11.9% were COVID-19 positive (11). 1.5% of patients with COVID- 19 developed new onset pericarditis and six-month all-cause mortality was 15.5% (2). CASE PRESENTATION: 48-year-old male with no known past medical history who presented with acute onset of sharp, left-sided chest pain and associated with dyspnea on exertion. He was not vaccinated for COVID-19 and denied being around any sick contacts. On physical examination he was afebrile, normotensive and saturating 99% on room air. EKG initially showed diffuse ST elevations in leads II,III, aVF, V2-V6. Initial high sensitivity trop was <6. He was incidentally found to be COVID positive. Initial echocardiogram was not suggestive of wall motion abnormalities or pericardial effusions. He was not initiated on management for COVID-19 pneumonia as he was asymptomatic and on room air. He was started on colchicine 0.6 mg BID and ibuprofen 400 TID for pericarditis treatment and symptoms resolved on follow up. DISCUSSION: COVID-19 causing pericarditis is relatively rare and our patient presented with pericarditis and no associated respiratory symptoms. The clinical signs of pericarditis include: a pleuritic or sharp chest pain relieved by leaning forwards, a pericardial friction rub auscultated near the left sternal border and EKG changes including diffuse ST elevations or PR depressions seen in the leads I,II,III, aVL, aVF and the precordial leads V2-V6 (3). The common complications seen with pericarditis are pericardial effusion, cardiac tamponade, and constrictive pericarditis (1). A common etiology for pericarditis is a viral illness which can be seen to precede the cardiac symptoms and be seen as flu-like symptoms or as gastrointestinal symptoms. Treatment is with colchicine and NSAIDs. Aspirin has been the drug of choice in patient's who present with pericarditis following a myocardial infarction, solely because the other NSAIDs have been studied and shown to interfere with myocardial healing (3)(4). NSAIDs were believed to be harmful in patient's diagnosed with COVID, due to upregulation of ACE2 receptors in multiple sites which is used by SARS-COV-2 as a point of entry into cells (9). Drake et. Al, looked at patients with COVID-19 pneumonia, and found use of NSAIDs did not play any significant role in mortality (10). First-line therapy for pericarditis is NSAIDs and colchicine. Second line therapy can be with corticosteroids and refractory therapy is generally with intravenous human immunoglobulins, Azathioprine or anti-IL1 agents such as Anakinra (12). CONCLUSIONS: COVID 19 continues to present with varying levels of comorbidities. Timely diagnosis and intervention of pericarditis precipitated by COVID-19 can lead to near complete recovery and prevent fatal outcomes. Reference #1: Dababneh E, Siddique MS. Pericarditis. [Updated 2021 Aug 11]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing;2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK431080/ Reference #2: Buckley BJR, Harrison SL, Fazio-Eynullayeva E, Underhill P, Lane DA, Lip GYH. Prevalence and clinical outcomes of myocarditis and pericarditis in 718,365 COVID-19 patients. Eur J Clin Invest. 2021 Nov;51(11):e13679. doi: 10.1111/eci.13679. Epub 2021 Sep 18. PMID: 34516657;PMCID: PMC8646627.1 Reference #3: Little WC, Freeman GL. Pericardial disease. Circulation. 2006 Mar 28;113(12):1622-32. doi: 10.1161/CIRCULATIONAHA.105.561514. Erratum in: Circulation. 2007 Apr 17;115(15):e406. Dosage error in article text. PMID: 16567581. DISCLOSURES: No relevant relationships by Atika Azhar No relevant relationships by Berty Baskaran No relevant relationships by Andres Cordova Sanchez No relevant relationships by Harvir Gambhir No relevant relationships by Hanish Jai

TENSION PNEUMOMEDIASTINUM RESULTING IN OBSTRUCTIVE SHOCK IN COVID-19

SESSION TITLE: Bad bugs and Mediastinal Madness SESSION TYPE: Case Reports PRESENTED ON: 10/19/2022 09:15 am - 10:15 am INTRODUCTION: Pneumomediastinum is often witnessed in intensive care units secondary to mechanical ventilation, or blunt and penetrating trauma. However, it is rare for patients to develop tension pneumomediastinum. Tension pneumomediastinum within the context of Covid-19 pneumonia is even more rarely discussed. Here we discuss a patient with Covid-19 pneumonia who developed rapidly progressive tension pneumomediastinum. CASE PRESENTATION: 72-year-old male was admitted to the ICU for Covid-19 infection causing hypoxemic respiratory failure requiring mechanical ventilation. On ICU day 2 the patient developed sudden worsening of shock requiring multiple pressors. Clinical exam revealed extensive subcutaneous crepitus in the supraclavicular region extending to the neck. Chest XR showed extensive pneumomediastinum and pneumopericardium and no pneumothorax. There was concern for ongoing obstructive shock due to cardiac tamponade, cardiology was called to bedside to perform POC ultrasound. The heart could not be visualized due to subcutaneous air. CT scan showed extensive mediastinal air and subcutaneous emphysema. The significantly increasing air in the retrocardiac space and concavity of the atria were concerning for worsening tension physiology. Cardiothoracic surgery decided to place a mediastinal drain and create a pericardial window. In the hours that followed, the patient's hemodynamics improved, and his pressor requirement decreased to only low dose norepinephrine. On ICU day 3 he developed worsening severe mixed acidosis. On day 4, the patient was requiring over 100mcg per hour of norepinephrine and labs showed worsening renal and liver failure. In the afternoon of day 4, the patient experienced a cardiac arrest and expired. DISCUSSION: Most reported cases of pneumomediastinum with associated pneumopericardium are self-limited, however 38% of cases progress to create tension pneumomediastinum and life-threatening cardiac tamponade.1 There are few reports of tension pneumomediastinum complicated by pneumopericardium in patients with Covid-19,2 but there is concern that this condition occurs more frequently in critically ill patients with Covid-19.3 The management of cardiac tamponade as a result of tension pneumopericardium may include pericardiocentesis,2 placement of a pericardial window, or insertion of a mediastinal drain.3 While several reported patients who underwent these procedures survived to discharge successfully,1,3 there are also reports that suggest that the development of subcutaneous emphysema and pneumomediastinum may be indicative of worsening prognosis.3 CONCLUSIONS: The ideal management of tension pneumomediastinum in Covid-19 is not clear and prognosis of patients who develop tension pneumomediastinum is highly varied. Further study is needed to develop tools to identify pneumomediastinum with the potential to develop tension physiology and progress to obstructive shock. Reference #1: Hazariwala, V., Hadid, H., Kirsch, D. et al. Spontaneous pneumomediastinum, pneumopericardium, pneumothorax and subcutaneous emphysema in patients with COVID-19 pneumonia, a case report. J Cardiothorac Surg 15, 301 (2020). https://doi.org/10.1186/s13019-020-01308-7 Reference #2: Cummings RG, Wesly RL, Adams DH, Lowe JE. Pneumopericardium resulting in cardiac tamponade. Ann Thorac Surg. 1984;37(6):511-518. doi:10.1016/s0003-4975(10)61146-0 Reference #3: Al-Azzawi M, Douedi S, Alshami A, Al-Saoudi G, Mikhail J. Spontaneous Subcutaneous Emphysema and Pneumomediastinum in COVID-19 Patients: An Indicator of Poor Prognosis? Am J Case Rep. 2020;21:e925557-1-e925557-6. doi:10.12659/AJCR.925557 DISCLOSURES: No relevant relationships by Roger Alvarez, value=Travel Removed 03/30/2022 by Roger Alvarez No relevant relationships by Roger Alvarez, value=Consulting fee Removed 03/30/2022 by Roger Alvarez no disclosure on file for Michelle Hernandez;No relevant relationships by Rose Puthumana

CARDIAC TAMPONADE AS A DEADLY COMPLICATION OF TENSION PNEUMOPERICARDIUM: A CASE REPORT

SESSION TITLE: Cardiovascular Complications in Patients with COVID-19 SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Pneumopericardium is the presence of air or gas in the pericardial space, usually secondary to blunt or penetrating trauma. Most pneumopericardium are non-tension. The use of positive pressure ventilation (PPV) increases the chances of developing a tension pneumopericardium. We report the case of a 22-year-old male patient admitted for COVID-19 pneumonia who developed pneumopericardium with cardiac tamponade features. CASE PRESENTATION: A 22-year-old male was admitted for acute respiratory distress syndrome due to COVID-19 pneumonia and required intubation on hospital day 10. The next day, he became febrile with new leukocytosis. A chest x-ray showed new extensive pneumomediastinum and pneumopericardium. Vasopressor support and broad-spectrum antibiotics were started for septic shock, however he continued to decompensate rapidly, requiring maximal medical support. His arterial line waveform showed pulsus paradoxus, leading to concern for underlying tension pneumopericardium. Bedside echo was unrevealing as imaging was obstructed by the air in pericardial sac. The patient was too unstable for a CT scan of the chest. After extensive discussion with his family, he was placed on palliative measures only and expired. DISCUSSION: Pneumopericardium is due to an abnormal connection between the pericardial space and a source of air or gas. Levin and Macklin describe three main mechanisms by which this connection can be made. The first: acute rises in alveolar pressure and volume or ventilator associated lung injury leading to rupture of alveoli with gas tracking along perivascular and peri bronchial sheaths to the mediastinum. The second: macro-perforation of the pericardial space leading to communication with respiratory or gastrointestinal tracts. Third: existence of a pneumothorax in the presence of traumatic pericardial tear or congenital pleuro-pericardial connection. Spontaneous pneumopericardium without any anatomic connection is rare and is due to a direct extension of infectious etiologies of the lungs or by an infection of the pericardial space with gas forming bacteria. A tension pneumopericardium causing cardiac tamponade can develop from pneumopericardium with PPV where the pericardial sac acts as a shutter valve letting air in but not out as has been reported sparingly in the literature. Cummings et al described 93 patients who developed tamponade out of 252 patients with pneumopericardium. Our patient possibly developed a pleuro-pericardial tract secondary to his pneumonia. With continued PPV his simple pneumopericardium likely developed into a tension pneumopericardium evidenced by arterial waveforms consistent with pulsus paradoxus, worsening hypotension despite maximal vasopressor support and development of ventricular tachycardia. CONCLUSIONS: Our case highlights the importance of considering pneumopericardium causing cardiac tamponade in the setting of mechanical ventilation. Reference #1: Mindaye ET, Arayia A, Tufa TH, Bekele M. Iatrogenic pneumopericardium after tube thoracostomy: A case report. Vol. 76, International journal of surgery case reports. 2020. p. 259–62. Reference #2: Cummings RG, Wesly RL, Adams DH, Lowe JE. Pneumopericardium resulting in cardiac tamponade. Ann Thorac Surg. 1984 Jun;37(6):511–8. Reference #3: Levin AI, Visser F, Mattheyse F, Coetzee A. Tension pneumopericardium during positive-pressure ventilation leading to cardiac arrest. J Cardiothorac Vasc Anesth. 2008 Dec;22(6):879–82. MACKLIN CC. TRANSPORT OF AIR ALONG SHEATHS OF PULMONIC BLOOD VESSELS FROM ALVEOLI TO MEDIASTINUM: CLINICAL IMPLICATIONS. Arch Intern Med [Internet]. 1939 Nov 1;64(5):913–26. Available from: https://doi.org/10.1001/archinte.1939.00190050019003 DISCLOSURES: No relevant relationships by Aarti Mittal No relevant relationships by Beenish Naqvi

COVID-19 CARDIAC TAMPONADE WITH CARDIOGENIC SHOCK IN A PREVIOUSLY VACCINATED YOUNG ADULT: A CASE REPORT

SESSION TITLE: Cardiovascular Complications in Patients with COVID-19 SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Previous case reports have shown a number of cardiac complications associated with, and attributed to COVID-19 infection including acute myocardial injury and infarction, dysrhythmias, acute heart failure, pericarditis, and venous thromboembolic events, among others. Up until this point, these cases have all been documented in unvaccinated individuals 1. CASE PRESENTATION: Here we report a unique case of a 40-year-old previously vaccinated woman who presented with generalized weakness, chest pain, dyspnea, and vomiting. She was found to be septic and positive for COVID-19. Transthoracic echocardiogram showed a small pericardial effusion on admission and the patient was diagnosed with acute myopericarditis secondary to COVID-19. Within the first 24 hours following admission, the patient's condition rapidly deteriorated and she developed worsening pericardial effusion, with subsequent cardiac tamponade, and cardiogenic shock. Following attempted pericardiocentesis and surgical drainage, cardiac function did not improve and she expired soon after. DISCUSSION: Despite most of the clinical attention being focused on the effects of SARS-CoV-2 on the respiratory system and the pneumonia it causes, there have been more reported complications involving other organ systems, particularly the heart and kidneys. Studies have shown three main categories of cardiac involvement and complications related to COVID-19: myocardial injury, acute heart failure, and arrhythmia. Focusing on myocardial injuries, there have been some reports attempting to elucidate the frequency of myo- and pericarditis as complications of COVID-19. Yet still to this date, little is known about pericarditis as a COVID-19 complication. Of the case reports published thus far regarding COVID-19 pericarditis, the majority of them do not exhibit cardiac tamponade. In one systematic review published in September, 2021, a total of 33 studies including 32 case reports and one case series were included and pericardial effusion and cardiac tamponade were reported in 76% and 35% of the cases, respectively 2. To our knowledge, our case is the first of its kind, illustrating cardiac tamponade in a fully vaccinated individual. Although, there have been no clear mechanisms explaining the pathogenesis of cardiac involvement in patients suffering from COVID-19, multiple possibilities have been hypothesized. Similar to other cardiotoxic viruses, an inflammatory response is likely triggered resulting in pericarditis and pericardial effusion 3. When left unabated, cardiac tamponade can occur. CONCLUSIONS: Our case documents a reminder of the critical nature of SARS-CoV-2, even in vaccinated patients. To our knowledge, this is the first reported case of cardiac tamponade in a previously vaccinated individual. This case highlights the importance of quick diagnosis and treatment in patients suffering from potential lethal complications of COVID-19. Reference #1: Long B, Brady WJ, Koyfman A, Gottlieb M. Cardiovascular complications in COVID-19. Am J Emerg Med. 2020;38(7):1504-1507 Reference #2: Diaz-Arocutipa C, Saucedo-Chinchay J, Imazio M. Pericarditis in patients with COVID-19: a systematic review. J Cardiovasc Med (Hagerstown). 2021 Sep 1;22(9):693-700 Reference #3: Inciardi RM, Lupi L, Zaccone G, et al. Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19). JAMA Cardiol. 2020;5(7):819–24 DISCLOSURES: no disclosure on file for Thomas Bumbalo;no disclosure on file for Thaddeus Golden;No relevant relationships by Omar Kandah

SARS-COV-2-INDUCED COAGULOPATHY DEMONSTRATING HEMORRHAGIC CARDIAC TAMPONADE: A TIGHT SQUEEZE

SESSION TITLE: COVID-19 Case Report Posters 3 SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: There is a growing volume of evidence of extrapulmonary manifestations of Coronavirus disease 2019 (COVID-19), particularly within the cardiovascular and hematological systems. In this case, we describe a unique manifestation of a COVID-19 presenting with a hemorrhagic pericardial effusion and cardiac tamponade physiology with a supratherapeutic international normalized ratio (INR). CASE PRESENTATION: A 68-year-old male with coronary artery disease and atrial fibrillation on warfarin presented to the emergency department with acutely worsening shortness of breath. Upon arrival, he was hypotensive, tachypneic, and hypoxic. Physical exam findings included jugular venous distention and muffled heart sounds. A transthoracic echocardiogram demonstrated a large concentric pericardial effusion with tamponade physiology (Figure 1). Pertinent initial laboratory values included an elevated INR of 6.1, a prolonged prothrombin time of 61.2 seconds, and an elevated D-dimer level of 5.34 mg/L (Table 1). The prolonged INR was reversed with prothrombin complex concentrate (PCC). Emergent pericardiocentesis yielded 1.7L of dark-bloody appearing fluid. Pericardial fluid analysis (Table 1) demonstrated over 2.4 million red blood cells and 3,650 total nucleated cells with 94% lymphocytes. Cultures and cytology were unrevealing. Given the profound lymphocytic component, a COVID-19 nasal swab was obtained and resulted positive. Prior to contracting COVID-19, the patient's weekly INR levels were consistently at goal. DISCUSSION: The global pandemic of the COVID-19 continues to identify extrapulmonary manifestations of the disease. A rising number of publications have implicated COVID-19 with causing myocarditis, pericardial effusions, and hemorrhagic cardiac tamponade(1). Hemorrhagic cardiac effusions are typically seen with malignancy, tuberculosis, trauma, recent cardiac procedures, post-myocardial infarction, and are also seen in Coxsackie viral infections. Multiple studies implicate COVID-19 interactions with oral-vitamin K antagonists as the cause of unpredictable INR's which can lead to spontaneous bleeding2. There are fewer than 10 reported instances of hemorrhagic pericardial effusions with tamponade physiology in COVID-19 patients;however, none of the other cases presented with a super-therapeutic INR. We are also the first to demonstrate a primary lymphocytic component of the pericardial fluid suggesting viral etiology. Profound coagulopathies in COVID-19 result in an increased mortality(3). CONCLUSIONS: We propose that based on the increase in publications of case-reports describing COVID-19 viral infections and hemorrhagic pericardial effusions, that SARS-CoV-2 should be added to the list of known viral etiologies. Further, COVID-19 patients who are systemic anticoagulation with vitamin K antagonists should be monitored closely for abrupt changes in their INR. Reference #1: 1. Gupta A, Madhavan MV, Sehgal K, et al. Extrapulmonary manifestations of COVID-19. Nature Medicine. 2020;26(7):1017-1032. Reference #2: 2. Camilleri E, Van Rein N, Van Der Meer FJM, Nierman MC, Lijfering WM, Cannegieter SC. Stability of vitamin K antagonist anticoagulation after COVID-19 diagnosis. Research and Practice in Thrombosis and Haemostasis. 2021;5(7) Reference #3: 3. Tang N, Li D, Wang X, Sun Z. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia. Journal of Thrombosis and Haemostasis. 2020;18(4):844-847. DISCLOSURES: No relevant relationships by Gregory Hicks No relevant relationships by Daniel Kissau No relevant relationships by Andrew Labelle No relevant relationships by Scott Mayer No relevant relationships by Dmitriy Scherbak

TUBERCULOUS TAMPONADE WITH A TWIST: A CASE OF TB AND COVID-19

SESSION TITLE: Critical Care Presentations of TB SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: We present a case of tuberculous pericarditis and cardiac tamponade due to suspected sequela of SARS-Coronavirus 19 (COVID-19) infection. It is important for clinicians to include tuberculosis (TB) in the differential diagnoses for patients presenting with presumptive viral pericarditis and tamponade. CASE PRESENTATION: A 52-year-old Hispanic man with chronic kidney disease not on hemodialysis was admitted with shortness of breath, fluid overload, hypoxemia and concern for uremic pericarditis. The patient tested positive for COVID-19 to which the symptoms were initially attributed, and he was treated with steroids, remdesevir, tocilizumab and hemodialysis. The patient incidentally had a positive QuantiFERON gold test obtained before initiating hemodialysis. On day 60 of hospitalization, the clinical exam abruptly deteriorated with stuporous mentation, hypotension, and cool skin. Bedside point of care echocardiography revealed a new large circumferential pericardial effusion with right ventricular diastolic collapse and increased respiratory variation in peak E-wave mitral inflow velocity consistent with tamponade physiology. Emergent pericardiocentesis was performed, and hemodynamic instability resolved immediately after aspiration of 750 milliliters of frank pus. Empiric antibiotics were initially given for pyogenic pericarditis. When the pericardial fluid later tested positive for acid-fast bacilli and adenosine deaminase, anti-TB therapy was started. The hospitalization was further complicated by septic shock and cardiac arrest. Though found to have a re-accumulated pericardial effusion on bedside ultrasound peri-arrest, there was no tamponade physiology (suggestive of at least a partial response to the TB treatment in the setting of overall poor underlying reserve). DISCUSSION: The coexistence of COVID-19 and tuberculous pericarditis with tamponade has been reported to date in one other case to our knowledge. COVID-19 with massive pericardial tamponade is rare and a careful diagnostic approach involving multi-modality imaging with bedside echocardiogram is invaluable in the evaluation and treatment of obstructive shock. In this case, we hypothesize that the COVID-19 infection may have led to re-activation of latent TB despite treatment of COVID-19 with corticosteroids (which are an adjunct tuberculostatic treatment in patients with tuberculous pericarditis). Tuberculous pericarditis with tamponade is a relatively uncommon manifestation of extrapulmonary TB and is a major cause of cardiovascular death and morbidity. Even with aggressive antituberculosis therapy, 30-60% of patients may need surgical pericardiectomy for constrictive pericarditis. CONCLUSIONS: This case highlights the need to consider possibility of concomitant viral and TB pericarditis in the diagnostic differential for tamponade. More histopathologic or post-mortem examinations of COVID-19 pericarditis cases are needed. Reference #1: Asif T, Kassab K, Iskander F, Alyousef T. Acute pericarditis and cardiac tamponade in a patient with COVID19: a therapeutic challenge. Eur J Case Rep Intern Med. 2020 May 6;7(6):001701. Reference #2: Barrett et al. Increase in disseminated TB during the COVID19 pandemic. Int J Tuberc Lung Dis. 2021 Feb 1;25(2):160-166. Reference #3: Wong SW, Ng J. K.X., Chia YW. Tuberculous pericarditis with tamponade diagnosed concomittantly with COVID19: a case report. Eur Heart J Case Rep. 2020 Dec 28;5(1):ytaa491. eCollection 2021 Jan. DISCLOSURES: No relevant relationships by Jaskiran Khosa No relevant relationships by Walter Klein No relevant relationships by Amy Tran No relevant relationships by Michael Ulrich

PERICARDITIS EVOLVING INTO CARDIAC TAMPONADE IN A 76-YEAR-OLD PATIENT WITH COVID-19

SESSION TITLE: Cardiovascular Complications in Patients with COVID-19 SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Cardiac tamponade is a medical emergency that requires rapid diagnosis and intervention to prevent hemodynamic collapse. Although COVID-19 typically manifests with pulmonary symptoms, cardiac involvement is becoming better studied through increasingly frequently reported cases [1]. We present a case of COVID-19 cardiac involvement presenting as a rapidly progressive pericardial effusion turning into tamponade. This highlights the importance of a high index of suspicion for patients who develop sudden and atypical respiratory compromise with hypotension in the setting of COVID-19 infection. CASE PRESENTATION: A 76-year-old male with a history of ESRD presented with fatigue after missing hemodialysis. Laboratory investigations revealed a mild troponin elevation and positive SARS-CoV-2 PCR. Initial TTE demonstrated an EF of 60-65% with a small pericardial effusion and thickened calcified pericardium. After a few days, the patient was noted to be encephalopathic and hypotensive. Labs revealed leukocytosis, lactic acidosis as well as an elevated troponin and D-dimer. Chest CTA was significant for a large pericardial effusion with reduced size of the right ventricle, concerning for cardiac tamponade. Repeat TTE had a moderate pericardial effusion and right atrial collapse, consistent with tamponade. Given significantly elevated INR in the setting of anticoagulation, pericardiocentesis was deferred while the patient was transfused FFP. The patient subsequently suffered PEA arrest and expired despite attempted hemodynamic stabilization. DISCUSSION: Cardiac tamponade is a result of accumulating pericardial fluid culminating in decreased cardiac output and shock. Clinicians should be prompted by characteristic findings, including Beck’s triad (JVD, hypotension, and muffled heart sounds) and Kussmaul’s sign of paradoxically elevated JVP with inspiration [2]. However, the diagnosis of tamponade based solely on clinical finding is difficult and may lead to unnecessary intervention [3]. Ultimately, a diagnosis of tamponade requires both hemodynamic instability and pericardial effusion. Echocardiography, including TTE and POCUS, plays a central role in the identification of cardiac tamponade. While it is essential to note the presence of a pericardial effusion, it is important to be familiar with core echocardiographic signs of tamponade: systolic RA collapse (earliest sign), diastolic RV collapse, IVC with minimal respiratory variation, and exaggerated respiratory cycle changes in MV and TV in-flow velocities (a surrogate for pulsus paradoxus) [3]. CONCLUSIONS: Despite the classic association between COVID-19 and pulmonary manifestation, pericardial involvement has been noted in 20% of COVID-19 patients. It is therefore imperative to maintain a high index of suspicion and familiarity of characteristic echocardiogram findings of tamponade to prompt intervention and curtail cardiac hemodynamic collapse. Reference #1: Lala A, Johnson KW, Januzzi JL, et al. Prevalence and Impact of Myocardial Injury in Patients Hospitalized With COVID-19 Infection. J Am Coll Cardiol. 2020;76(5):533-546. doi:10.1016/j.jacc.2020.06.007 Reference #2: Stashko E, Meer JM. Cardiac Tamponade. [Updated 2021 Dec 21]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing;2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK431090/ Reference #3: Alerhand S, Carter JM. What echocardiographic findings suggest a pericardial effusion is causing tamponade?. Am J Emerg Med. 2019;37(2):321-326. doi:10.1016/j.ajem.2018.11.004 DISCLOSURES: No relevant relationships by Christopher Allahverdian No relevant relationships by John Javien No relevant relationships by Vishal Patel No relevant relationships by Sarah Youkhana

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

To drain, or not to drain: Diagnostic and therapeutic challenges associated with cardiac tamponade in Right heart sided heart failure and pulmonary hypertension

Background: In clinical practice, cardiac tamponade is not an all-or-none phenomenon, but rather a continuum of hemodynamic impairment. Diagnosis depends on an overall assessment of clinical and echocardiographic findings, hemodynamic measurements, and other corresponding patient-level variables must be considered to make a diagnosis to initiate timely intervention.1 The identification of cardiac tamponade in the presence of severe pulmonary hypertension and right ventricular failure can be even more challenging, because the classic findings are often not observed. Our patient clearly had hemodynamic compromise (orthostatic collapses and then persistent hypotension from a large pericardial effusion but did not exhibit the common features of tamponade on ECHO. This can be explained by the preexisting, markedly elevated right-sided pressures, which prevented typical findings of pulsus paradoxus, right atrial and ventricular diastolic collapse, and equalization of diastolic pressures.1 Case presentation: 44 Years old lady background of Interstitial lung disease, pulmonary artery hypertension, Right heart failure and anti-synthetase syndrome. Recently required Intensive care admission for COVID pneumonitis and was discharged on home oxygen. Now admitted to hospital after she boarded the flight without oxygen and became unwell. She was treated on lines of exacerbation of interstitial lung disease, Right heart failure and moderate pericardial effusion without signs of tamponade in ECHO and was given adequate diuresis and responded very well to it. Her oxygen requirement came down and she clinically improved. Few days after, she developed diarrhea and prerenal Acute kidney injury while in ward and became borderline hypotensive which improved after her diuretic doses were reduced and then held. She then after few days started to develop orthostatic collapses with hypotension and then became persistently hypotensive. Her CT Pulmonary angiogram showed unchanged moderate circumferential pericardial effusion, and no Pulmonary embolism. She was reviewed by Critical care outreach team and an urgent bedside Echocardiogram was performed to rule out features of tamponade which showed moderate pericardial effusion, severely dilated Right heart with massive Right ventricular pressures compressing her Left ventricle. She was urgently reviewed by cardiology and was taken to Intensive care unit for invasive hemodynamic monitoring, where she was given inotropes and inhaled pulmonary artery vasodilators. The decision was taken to cautiously diurese and not to drain the pericardial effusion due to risk of developing further instability by increasing right ventricular expansion causing further collapse and pressure on Left ventricle. Discussion and conclusion: Our case stresses on the importance of Bedside Echocardiogram in timely identifying the atypical features of cardiac tamponade and to understand the different hemodynamics and mechanism of obstructive shock in patients with pre-existing right sided heart failure. After the establishing that patient was in obstructive cardiogenic shock with atypical findings of tamponade, the next most important step was to decide whether to drain the pericardial effusion or not. In our literature search, we found that the drainage of a large pericardial effusion in patients with pulmonary hypertension has been accompanied by catastrophic, sudden hemodynamic collapse and it has been postulated that the presence of pericardial fluid limits right ventricular distension in response to pressure and volume overload. When the pericardial fluid is removed, rapid enlargement of the right ventricle causes: (1) reduced right ventricular systolic function due to muscle fiber distension;and (2) compression of the left ventricle, which leads to impaired diastolic filling and left ventricular outflow track obstruction.1.

Focused Ultrasound in Critical Care Outreach for acutely ill and deteriorating patients on the wards

Introduction: Focused Ultrasound in Intensive Care (FUSIC) refers to the use of ultrasound by a trained bedside clinician to guide patient management in real-time. Ultrasound is widely applied in practice and there is growing consensus that it is an essential tool for managing acutely ill patients in the intensive care unit (ICU). The Critical Care Outreach Team uses FUSIC as an additional assessment tool to guide management and decision-making plan for deteriorating patients on the wards. Objectives: To investigate whether how often information gained fromFUSICimaging had an impact on patient care and management decisions in a critical care outreach setting. Methods: A single-centre observational study at an academic tertiary referral institution. We included all patients reviewed by critical care outreach who were assessed by ultrasound during a 12-month period. Routine procedures for teaching purposes were not included. Results: Forty-six patients were assessed and supported by a combined focused lung and heart ultrasound performed at the patient bedside on the wards. In 46 patients FUSIC was instrumental in the differential diagnostic workup and in guiding the clinical management. In 32 (70%) patients FUSIC aided fluid therapy or diuresis (in case of pulmonary oedema) and helped targeting fluid balance. In three patients though to have consolidation on chest x-ray we were able to identify significant pleural effusions without needing an additional CT scan. In four patients with hypotension, an additional CT-PA was warranted due to dilated right ventricle (RV) with abnormal septal motion and decreased left ventricle (LV) size ratio (i.e. sign of right heart strain) as highly suspicious of pulmonary embolus. In two young patients with Coronavirus disease 2019 (COVID-19), using FUSIC we identified severe LV dysfunction which was subsequentially diagnosed as myocarditis and Angiotensin-converting enzyme (ACE) inhibitors therapy was commenced within 24 hours. Further diagnosis included cardiac tamponade (n = 2) requiring pericardiocentesis and pneumothorax (n =1). In all cases, the use of ultrasound helped in promptly referring patients to the specialist team (i.e. respiratory or cardiology) and to the ICU consultant. Conclusions: In our critical care outreach practice, FUSIC is considered an indispensable tool for safe and accurate management of acutely ill and deteriorating patients on the wards.

ACUTE PERICARDITIS in TIMES of COVID

Background: The most common etiology of acute pericarditis is usually infectious, especially viral. When its cause is infammatory (up to 7% of cases), it can be presented as an isolated process or be a clinical manifestation in the context of multiple systemic autoimmune diseases (SAD), therefore it is necessary to make a broad differential diagnosis. Nowadays, an increased incidence has been described in relation to SARS-CoV-2 infection, and especially in global vaccination against this one. This represents a clinical challenge when we have to identify the cause of this pathology with a not insignifcant comorbidity. Objectives: To describe the characteristics of a series of patients with acute pericarditis and its association with SAD. Methods: Retrospective and descriptive observational study. Digitalised records of patients with acute pericarditis evaluated in the Rheumatology unit of a tertiary hospital in Seville during 2021 were reviewed. Demographic, epidemiological, clinical and therapeutic variables were analysed. Results: Eight cases of acute pericarditis were detected. The average age of the patients was 51.50 ± 18.601 years. 62.5% were women. 50% had previous rheumatological pathology: two rheumatoid arthritis (RA), one systemic lupus erythematosus (SLE) and one limited systemic sclerosis (LSS);with an average disease duration of 8.63 ± 2.387 months. Of these, 3 were on treatment with steroids and DMARDs (lefunomide or hydroxychloroquine) and 1 had previously received rituximab. Pericardial effusion was moderate in 50% of cases, severe in 33.3% and mild in 16.7%. One patient had cardiac tamponade. Five patients had pleural effusion, which was moderate in 80%, and in one case associated with pneumonia. As complications, one patient developed heart failure and the patient with ESL was diagnosed with pulmonary arterial hypertension. Two patients had previous COVID19 and 7 were vaccinated against Sars-CoV2. Treatment was colchicine in 57.15% of cases, steroids in 85.7%, DMARDsc in 85.8% (3 hydroxychloroquine and 3 azathioprine) and DMARDsb in 42.9% (1 anakinra, 1 tocilizumab and 1 rituximab). Pericarditis resolved in all patients. Table 1. Conclusion: In the previous year, an increase in consultations from other departments for acute pericarditis with suspected infammatory origin was observed. The possibility of a correlation with COVID19 or vaccination against COVID was initially considered, but it could not be demonstrated, since vaccination was later in vaccinated patients, and in those who had been infected, the time interval until the development of pericarditis was too long for it in order to be attributed to COVID19. Finally, in 5 of the 8 patients, pericarditis was related to SAD, in particular with the rheumatic pathologies most associated with this clinical manifestation (RA and SLE). Therefore, in the middle of the COVID pandemic, in addition to considering COVID19 or its vaccine in the differential diagnosis of acute pericarditis, we must not forget to include SAD in this diagnosis.

ACUTE MYOPERICARDITIS COMPLICATED WITH CARDIAC TAMPONADE IN COVID-19

CASE: 68yo Caucasian female with no significant cardiac history presented with worsening dyspnea and fatigue started around 7 days ago. She denied having any travel or known history of tuberculosis or any other autoimmune conditions. COVID RT-PCR test was positive on the day soon after admission. Initial vitals include SpO2 of 96% on 2L, BP 118/72 mmHg and HR in 110s/min Sinus. EKG revealed sinus tachycardia with non-specific ST-T changes. Labs showed c-reactive protein 2.0 mg/dl, ferritin 1061 ng/ml, LDH 300 EnzU/L;cardiac markers-troponin 212-261 ng/L and proBNP of 11,497 pg/mL. ECHO showed EF of 30-45% with global hypokinesis, and circumferential pericardial effusion with fibrinous strands. Within 48 hours, the patient sustained cardiac arrest with recurrent hemodynamically unstable tachyarrhythmia requiring multiple cardioversions. Repeat Bedside ECHO revealed larger effusion compared to prior, worrisome for cardiac tamponade. Emergent pericardiocentesis yielded 200ml of serous fluid improving the hemodynamics in form of improved SBP to 140mmHg from 70mmHg. Although this improvement appeared promising, it was only transient with rapid decline. Her ferritin levels went up 10-fold correlating with the worsening status. Her pressor requirement gradually worsened to the point of requiring IMPELLA, intercepting the initiation of RRT for acute renal failure. Unfortunately, with higher risk of poor outcome, the family opted to respect the patient's wishes and further care was withdrawn. IMPACT/DISCUSSION: As of January 2022, there have been close to 300 million confirmed COVID-19 cases all over the world. This ongoing pandemic disease, although primarily occur as respiratory illness, the florid symptoms with increasing mortality are due to its systemic inflammatory response causing multiorgan failure. Hence the symptoms can be anywhere from mild febrile illness to sudden death. As such, Cardiac involvement in form of Myo-pericarditis is less recognized in such scenario and often underestimated. The onset can vary as the primary presenting symptom to late presentation following respiratory course. While the association of pericarditis with COVID has been documented, the global presentation as Myo-pericarditis is still less known. Our case depicts one such occurrence where cardiac presentation is the key finding having led to poor prognosis more than the lung damage. The management is still the same using NSAIDs / Colchicine like any other type of pericarditis. If there were signs of cardiac tamponade, pericardiocentesis is warranted. In some cases, especially in the setting of recurrent effusions, pericardial window will be useful. CONCLUSION: Myo-pericarditis in COVID-19 can predispose to life threatening arrhythmias which would increase mortality. With the cytokine storm and inflammatory response associated with COVID being the primary offender, it can be challenging to treat them as any other type as the treatment should also focus on removal of inciting factors simultaneously.

Under Pressure: Spontaneous Pneumomediastinum with Resultant Cardiac Tamponade Influencing the Decision to Initiate Extra-Corporeal Membrane Oxygenation

IntroductionWe present a case of a rare but serious adverse consequence of Acute Respiratory Distress Syndrome (ARDS) secondary to COVID-19 infection: spontaneous pneumomediastinum and pneumopericardium resulting in cardiac tamponade. Case descriptionA 35 year old unvaccinated female with a history of degenerative disc disease, Sjogren's disease, and mild persistent asthma presented with COVID-19 pneumonia. On admission, she required near-maximum heated high flow oxygen, yet desaturated with minimal movement. Three days later, she noted sharp chest pain with worsening oxygenation. Chest radiograph revealed diffuse subcutaneous air with concern for bilateral pneumothoraces, and follow up CT revealed pneumomediastinum, pneumopericardium, and extensive subcutaneous emphysema. She was subsequently intubated. She ultimately developed signs of obstructive shock, and an emergent chest CT demonstrated tamponade physiology on the heart from the mediastinal air. Bedside echocardiogram was unable to be performed due to air surrounding the heart. At this time, her Murray score was 3.8, and discussions began regarding transfer to a referral center for Extracorporeal Membrane Oxygenation (ECMO). Given her tenuous hemodynamics and the prospect of transfer in a low-pressure aircraft, a mediastinotomy tube was placed with a large air leak, tidaling of the tube, and improvement in hemodynamics. On arrival at the ECMO center (Saint Joseph Hospital), her tamponade physiology had improved, but she was requiring progressively higher ventilator pressures due to her severe ARDS. Her extensive pneumomediastinum, pneumoperitoneum, and subcutaneous emphysema would likely only be worsened by higher positive end-expiratory pressures. Due to this complex physiology, she was deemed a VVECMO candidate and was cannulated the day after transfer. Following cannulation, her pneumomediastinum and pneumoperitoneum improved, and eventually her mediastinotomy tube no longer demonstrated an air leak or tidaling. As such, it was removed and her hemodynamics remained stable with no evidence of recurrent tamponade. DiscussionThis presented a unique case in which the choice for VVECMO was influenced not only by severity of ARDS, but also by the complicating factor of positive pressure ventilation causing worsening tamponade physiology due to spontaneous tension pneumomediastinum. Additionally, this case adds to the reports of spontaneous pneumomediastinum in COVID-19 infection, as our patient had no history of trauma or barotrauma before this occurred. On literature review, we have only found one other case report in which a tension pneumomediastinum in COVID-19 required bedside mediastinotomy. Physicians should be aware of this potentially fatal complication and expedite referral to an ECMO center.