Posterior Mediastinal Mass: Unraveling a Non-Traumatic Herniation of the Caudate Lobe of the Liver

Introduction: Posterior mediastinal mass is most likely due to neurogenic tumor, meningocele or thoracic spine lesions. Caudate lobe of the liver herniation presenting as posterior mediastinal mass is a rare occurrence. Diaphragmatic herniation (DH) of the caudate lobe presents in various way including dyspnea, dyspepsia or incidental finding on imaging. We present a case of diaphragmatic hernia of the caudate lobe of the liver presenting as a posterior mediastinal mass found during evaluation of dyspnea. Case Description/Methods: A 75-year-old female presented to her physician with worsening shortness of breath from her baseline of 3 days duration. She had a history of sarcoidosis, COVID pneumonia over 1 year ago, COPD, diastolic heart failure, and hypertension. She was initially evaluated for COVID re-infection, which was negative and a CT of the chest with contrast to check for sarcoidosis flare revealed posterior mediastinal mass measuring 4.5 x 6.5 x 6.4 cm. Further work up with CT chest and abdomen with contrast revealed that the posterior mediastinal mass had similar attenuation as the liver and appears continuous with the caudate lobe of the liver. This was confirmed by NM scan of liver. Review of her records from an outside organization revealed similar finding on imaging a few years ago. Patient denied any history of trauma and laboratory work up revealed normal liver functions. After pulmonologist evaluation she was started on 2 L home oxygen following six-minute walk test, and also CPAP following a positive sleep study. Pulmonary function tests were performed and inhalers were continued. Given the chronicity of her symptoms and co-morbidities with stable caudate lobe herniation, conservative management was advised with surgery warranted if symptoms persist despite treatment (Figure 1). Discussion(s): DH is typically found on the left side with stomach or intestine while the right side is usually guarded by the liver. Isolated herniation of part of the liver into the thoracic cavity is rarely reported and is mostly acute from traumatic or spontaneous rupture requiring immediate repair. Our patient was initially evaluated for the posterior mediastinal mass for concerns of tumor, followed by the finding of what was thought to be acute herniation of the caudate lobe of liver into the thoracic cavity. Review of records showed this to be a stable lesion, we suspect that the patient had congenital diaphragmatic defect. Chronic and stable liver herniation into thoracic cavity can be managed conservatively if uncomplicated.

Effusive Constrictive Pericarditis, a Heart Failure Mimicker

Background Effusive constrictive pericarditis can initially mimic heart failure and ultimately result in cardiogenic shock. Case Patient is a 57-year-old female with history of recent massive pulmonary embolism status post systemic alteplase, chronic diastolic heart failure, and history of COVID-19 infection presenting with increasing dyspnea on exertion and weakness despite compliance to outpatient diuretics. Patient was noted to be hypotensive, and fluid overloaded on exam. Decision-making Due to concern for constriction right heart catheterization (RHC) was completed and showed cardiac index of 1.1 with elevated filling pressures, discordant variation of right ventricle (RV) and left ventricle (LV) pressure tracings, diastolic equalization of pressure, and dip and plateau pattern of RV and LV diastolic tracing suggestive of constrictive physiology. Transesophageal echocardiogram showed no pericardial effusion with increased echo-density of the pericardium. Cardiac MRI showed mild diffuse thickening and subtle enhancement of the pericardium with septal bounce and no significant pericardial effusion consistent with constrictive pericarditis. Due to persistent hypotension requiring milrinone infusion, the patient underwent pericardiectomy with improvement of hemodynamics and symptoms. Conclusion Effusive constrictive pericarditis can mimic heart failure and should be ruled out in those with evidence of low cardiac output to avoid cardiovascular morbidity and mortality. [Formula presented]Copyright © 2023 American College of Cardiology Foundation

COVID-19: A CONFOUNDING MIMICKER OF HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS

SESSION TITLE: Challenging Cases of Hemophagocytic Lymphohistiocytosis SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Hemophagocytic lymphohistiocytosis (HLH) is a rare syndrome involving pathologic immune activation that is often fatal. The link between the cytokine storm related to COVID-19 and development of HLH has been reported since the onset of the pandemic, but little is known about clinical manifestations of HLH, thereby delaying treatment. CASE PRESENTATION: A 50 year-old male presented with a several day history of progressive weakness in the setting of missed dialysis session. Medical history was significant for ESRD on dialysis and diastolic heart failure (EF 35%). Initial vitals were unremarkable. Physical exam was notable for peripheral edema bilaterally. Laboratory studies were consistent with hyperkalemia, elevated ferritin (28,383) and elevated liver function tests. COVID-19 PCR was positive upon admission. Chest x-ray, CTA chest and a right upper quadrant ultrasound were unremarkable. He was admitted to the medical ICU for emergent dialysis. Soon after arrival to the ICU, he became lethargic and confused with increasing oxygen requirements and a subsequent a code blue was called. Cardiopulmonary resuscitation was immediately initiated, with a first rhythm consistent with ventricular fibrillation. He was shocked and placed on an amiodarone infusion with return of spontaneous circulation. TTE revealed a severely reduced EF <10%. Despite initiation of advanced COVID-19 therapies with Solu-Medrol and tocilizumab he remained ventilator dependent. Due to hemodynamic instability and persistent metabolic acidosis, he was transitioned to continuous renal replacement. Further blood work showed worsening inflammatory markers (ferritin 33,500, LDH 6981). Because of the significantly elevated ferritin, there were concerns for possible HLH. Triglycerides and IL-2 receptor were 395 mg/dL and 9300 pg/mL respectively. Total NK cells were decreased to 1.2%. He remained persistently unstable despite aggressive measures. He suffered a second cardiopulmonary arrest, which was unable to achieve return of spontaneous circulation and he ultimately passed away. DISCUSSION: HLH is characterized by uncontrolled activation and proliferation of benign macrophages in reticuloendothelial organs. This results in histiocytic hemophagocytosis, worsening peripheral blood cytopenia(s), cytokine storm, and cytokine mediated biochemical alteration ultimately culminating in multiorgan dysfunction and disseminated intravascular coagulation. Although a distinctive constellation of features has been described for HLH, diagnosis remains challenging as patients have diverse presentations associated with a variety of triggers. CONCLUSIONS: As HLH is a medical emergency with poor prognosis, prompt recognition and early treatment is crucial for improving clinical outcomes. We hope this case will create increased awareness and timely diagnosis of cytokine storm syndromes in patients with severe COVID-19 infection. Reference #1: Meazza Prina M, Martini F, Bracchi F, Di Mauro D, Fargnoli A, Motta M, Giussani C, Gobbin G, Taverna M, D'Alessio A. Hemophagocytic syndrome secondary to SARS-Cov-2 infection: a case report. BMC Infect Dis. 2021 Aug 13;21(1):811. doi: 10.1186/s12879-021-06532-7. PMID: 34388982;PMCID: PMC8361241. Reference #2: Schnaubelt, Sebastian MDa,*;Tihanyi, Daniel MDb;Strassl, Robert MDc;Schmidt, Ralf MDc;Anders, Sonja MDb;Laggner, Anton N. MDa;Agis, Hermine MDd;Domanovits, Hans MDa Hemophagocytic lymphohistiocytosis in COVID-19, Medicine: March 26, 2021 - Volume 100 - Issue 12 - p e25170 doi: 10.1097/MD.0000000000025170 DISCLOSURES: No relevant relationships by Garrett Fiscus No relevant relationships by Niala Moallem No relevant relationships by Resham Pawar

Respiratory symptoms of the 2019 novel coronavirus when the source of the symptoms is intra-cardiac thrombus not the pneumonia

Case Report The 2019 Novel Coronavirus (COVID-19) is currently causing a global pandemic. Common symptoms are fever, cough, myalgia, fatigue, headache, dyspnea, sore throat, vomiting, and diarrhea. Patients may present with end-organ failure, ARDS, shock, acute kidney injury, or even death. We present a case of COVID-19 with shortness of breath caused by an intra-cardiac thrombus. Case presentation An 84-year-old woman with COPD and diastolic heart failure presented with shortness of breath. She had hypoxemia on room air upon presentation. Lungs were clear on physical examination. COVID-19 PCR was positive. Her chest radiograph demonstrated no pulmonary infiltrates. Transthoracic echocardiography (TTE) demonstrated a large, irregularly shaped echogenic mass in both the right atrium and right ventricle consistent with a large thrombus. The mass in the right atrium was 3.9∗3.6 cm;the portion in the ventricle was 3.2∗2.2 cm. A previous TTE study in this patient did not reveal an intra-cardiac thrombus. No deep venous thrombosis was found. She was begun on anticoagulation and refused catheter-directed therapy. She improved and was discharged to her home. Discussion Thromboembolic complications of COVID-19 have been described in the literature. The most common are deep venous thrombosis and pulmonary embolism in critically ill patients despite the use of prophylactic anticoagulation. Several studies have reported post-mortem biopsies with widespread microthrombi. Arterial thrombosis with stroke and limb ischemia has also been described. Our case had an unusual presentation since the cause of her shortness of breath was the intra-cardiac thrombus. The pathogenesis beyond the hypercoagulability in COVID is not well understood. Some studies propose direct endothelial injury by the COVID-19 virus, causing microvascular inflammation, endothelial exocytosis, and endothelitis. Some experts propose a hypercoagulable state in COVID-19 patients based on elevated factor VIII, elevated fibrinogen, circulating prothrombotic microparticles, and neutrophil extracellular traps (NETs). Yet, no definitive mechanism has been identified. (Figure Presented).

Mysterious cause of hypotension in MIS-C

Case Report Multisystem inflammatory syndrome (MIS-C) involves severe multi-organ inflammatory injury 2-6 weeks after COVID-19 infection. Seventy to 85% of patients have cardiovascular involvement, including diminished left ventricular ejection fraction (EF), coronary aneurysm, arrhythmias, valvular dysfunction, and pericardial effusion. Here we present a patient who arrived to the pediatric emergency department (ED) with MIS-C and suspected cardiogenic shock, though without the echocardiogram abnormalities commonly associated with MIS-C. A 7 year old African American male presented for a third time to our ED over the course of 4 days of febrile illness and was found to have MIS-C. During this time, he had no chest pain, palpitations, shortness of breath, or abnormal cardiopulmonary exam. At the first 2 ED visits, he was generally well appearing and after treating fever, had vital signs normal for his age. At his third visit, his vital signs were notable for borderline hypotension 86/48 (threshold 83/39 for his height of 1.25 meters). Troponins, chest X-ray, and EKG were normal. Bedside ultrasound was normal, with EF 55-60% so the hypotension was presumed to be secondary to hypovolemia and sepsis. However, despite 40 mL/kg of fluid boluses and maintenance fluid x1.5, his blood pressure continued to downtrend to a nadir of 79/39. He soon developed an S3 gallop and facial edema indicating fluid overload. His proBNP 4986 pg/mL also resulted at this time, suggesting cardiac injury was present. A formal cardiology echocardiogram confirmed the bedside ultrasound findings, noting normal ventricular size and motion, trivial pericardial effusion, and normal coronary artery size. However, it also detected diastolic dysfunction evident in mildly elevated E/e' of 10.86 of lateral mitral annulus, and 12.7 at medial mitral annulus. Three hours after starting solumedrol for treatment of MIS-C, his blood pressure improved to 110/52. The patient had no further episodes of hypotension, though it is unclear if steroids had resolved this by alleviating the underlying inflammation or as a secondary effect. We present a case of MIS-C that led to diastolic heart failure detected by mild hypotension, elevated proBNP, and subtle findings on formal echocardiogram. Although less common than systolic dysfunction in MIS-C, early recognition of diastolic heart failure is important for effective fluid management and initiation of vasoactive agents in criticallly 'ill patients. Diastolic heart failure with preserved systolic function has been seen on echo of MIS-C patients, and is hypothesized to be the subacute period after recovery of systolic function. However, we did not find clinical symptoms of systolic heart failure prior to the patient's development of diastolic heart failure. It is therefore essential to recognize that a patient with MIS-C may present with diastolic heart failure without preceding symptoms or echo findings of other cardiac anomalies.

Heart failure with preserved ejection fraction in coronavirus disease 2019 patients: the promising role of diuretic therapy in critically ill patients.

The impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on diastolic function is less known. We describe a 46-year-old man with a history of mild hypertension who presented to the emergency department with fever, cough, and myalgia for 2 days. The patient was tested positive for SARS-CoV-2. He was admitted and started on a combination of antiviral and antimicrobial therapy. He developed respiratory distress 2 days later, and O2 saturation declined. Blood tests showed an increased N-terminal pro-B type natriuretic peptide (NT-proBNP) level, and echocardiography showed normal left ventricular ejection fraction and E/e' ratio of 16. Computed tomography scan showed interstitial pulmonary oedema and prominent peripheral pulmonary vascular markings. Given these findings, heart failure with preserved ejection fraction (HFpEF) was considered. Low-dose diuretic was started, and fluid administration was restricted, resulting in a decrease in NT-proBNP level, clinical and haemodynamic stabilization, and improved oxygenation. This case highlights the occurrence of HFpEF in coronavirus disease 2019.