Rare case of infective aortitis with aortic rupture and cardiac tamponade in a young child.

Aortitis and aortic dissection are very rare in children. The clinical presentation of aortitis varies across a spectrum, ranging from incidental findings to fatal aortic dissection and rupture. A high index of suspicion is needed to establish an accurate and timely diagnosis. Here, we present an unfortunate case of fatal infective aortitis with aortic rupture and cardiac tamponade in a healthy toddler. Postmortem report implicated Kingella kingae as the causative organism of aortic pseudoaneurysm and rupture, leading to the instantaneous death of the child.

A rare complication of pericardiocentesis: Pneumopericardium.

Pneumopericardium is the presence of air in the pericardial sac. Pneumopericardium after pericardiocentesis has been rarely reported in the literature. In the present case, we report a patient who presented with tamponade physiology during COVID-19 and developed pneumopericardium after emergency pericardiocentesis. Immediate recognition and treatment are crucial and chest x-ray, thorax computerized tomography, and transthoracic echocardiography (TTE) are used for diagnosis.

Cardiac tamponade and massive pleural effusion in a young COVID-19-positive adult.

COVID-19 has a broad spectrum of cardiac manifestations, and cardiac tamponade leading to cardiogenic shock is a rare presentation. A 30-year-old man with a history of COVID-19-positive, reverse transcription polymerase chain reaction (RT-PCR) done 1 week ago and who was home-quarantined, came to the emergency department with palpitations, breathlessness and orthopnoea. His ECG showed sinus tachycardia with low-voltage complexes, chest X-ray showed cardiomegaly and left pleural effusion and two-dimensional echocardiography showed large pericardial effusion with features suggestive of cardiac tamponade. He was taken up for emergency pericardiocentesis which showed haemorrhagic pericardial fluid. Intercostal drainage insertion was done for left-sided large pleural effusion. After ruling out all the other causes for haemorrhagic pericardial effusion, the patient was started on colchicine, steroids, ibuprofen and antibiotics to which he responded. Both pericardial and pleural effusions resolved completely on follow-up.

Pericardial Diseases in COVID19: a Contemporary Review.

PURPOSE OF REVIEW: Coronavirus disease 2019 (COVID19) involves the heart, including pericardium. This article reviews the possible pathophysiological mechanisms in pericardial involvement in COVID19 and pericardial manifestations of COVID19. It also summarizes the patients with pericarditis secondary to COVID19 and outlines the contemporary treatment strategies in this patient population. RECENT FINDINGS: A high degree of suspicion is required to identify the pericardial involvement in COVID19 patients. It is proposed that an underlying hyperinflammatory reaction in COVID19 leads to pericardial inflammation. Acute pericarditis with or without myocardial involvement is diagnosed on clinical presentation, serum inflammatory markers, electrocardiogram, and echocardiogram. Multimodality imaging may also have an additional diagnostic value. Patients are usually managed medically, but some patients develop a life-threatening pericardial tamponade necessitating pericardial drainage. Pericardial involvement is an important clinical manifestation of COVID19 requiring a proper workup. Timely diagnosis and a specific management plan based on the presentation and concomitant organ involvement usually lead to a complete recovery.

Coronavirus disease 2019 (COVID-19)-associated constrictive pericarditis.

This report documents a rare case of COVID-19-associated constrictive pericarditis (CP) in the setting of a recent COVID-19 infection. A 55-year-old man with a history of hypertension and gout presented with acute hypoxic respiratory failure and was diagnosed with COVID-19 pneumonia with progression to acute respiratory distress syndrome. His hospital course was complicated by a large pericardial effusion; an emergent bedside transthoracic echocardiography was concerning for cardiac tamponade, so pericardiocentesis was performed. A workup with cardiac magnetic resonance imaging showed changes consistent with a diagnosis of CP. Viral and idiopathic aetiologies are the most common cause of CP in the developed world, with COVID-19 now a proposed predisposing viral illness. The virus induces systemic inflammation and pericardial changes that can lead to CP physiology. Imaging modalities including echocardiogram and cardiac magnetic resonance play an integral role in confirming the diagnosis.

Concomitant new diagnosis of systemic lupus erythematosus and COVID-19 with possible antiphospholipid syndrome. Just a coincidence? A case report and review of intertwining pathophysiology.

In the midst of the COVID-19 pandemic, further understanding of its complications points towards dysregulated immune response as a major component. Systemic lupus erythematosus (SLE) is also a disease of immune dysregulation leading to multisystem compromise. We present a case of new-onset SLE concomitantly with COVID-19 and development of antiphospholipid antibodies. An 18-year-old female that presented with hemodynamic collapse and respiratory failure, progressed to cardiac arrest, and had a pericardial tamponade drained. She then progressed to severe acute respiratory distress syndrome, severe ventricular dysfunction, and worsening renal function with proteinuria and hematuria. Further studies showed bilateral pleural effusions, positive antinuclear and antidouble-stranded DNA antibodies, lupus anticoagulant, and anticardiolipin B. C3 and C4 levels were low. SARS-Cov-2 PCR was positive after 2 negative tests. She also developed multiple deep venous thrombosis, in the setting of positive antiphospholipid antibodies and lupus anticoagulant. In terms of pathophysiology, COVID-19 is believed to cause a dysregulated cytokine response which could potentially be exacerbated by the shift in Th1 to Th2 response seen in SLE. Also, it is well documented that viral infections are an environmental factor that contributes to the development of autoimmunity; however, COVID-19 is a new entity, and it is not known if it could trigger autoimmune conditions. Additionally, it is possible that SARS-CoV-2, as it happens with other viruses, might lead to the formation of antiphospholipid antibodies, potentially contributing to the increased rates of thrombosis seen in COVID-19.