Sickle cell intrahepatic cholestasis (SCIC) is a rare but potentially fatal complication of sickle cell disease (SCD), with high mortality, observed mainly in patients with homozygous sickle cell anemia. Herein, we have reported a case of severe SCIC with a poor outcome despite aggressive measures including exchange transfusion and use of vasopressors.The patient was admitted with generalized weakness, confusion, rigors, chills, and signs of hepatic failure, such as hyperbilirubinemia, hypoalbuminemia, and coagulopathy. There was no evidence of viral hepatitis or biliary obstruction. The patient received two exchange transfusions, but he continued to deteriorate clinically despite exchange transfusion and developed hemorrhagic shock and multiorgan failure. The patient was made comfort care as per family wishes. This case emphasizes the importance of early diagnosis of sickle cell intrahepatic cholestasis and poor prognosis despite aggressive measures.

Graves' disease accounts for one of the most common causes of thyrotoxicosis. Most patients with Graves' disease present with classic signs and symptoms of hyperthyroidism. Psychosis and mood symptoms secondary to hyperthyroidism are rare. Here we report the case of a 37-year-old male with a history of Graves' disease with poor medication adherence who presented to the emergency department with psychotic features and hyperexcitability. He had excessive agitation, paranoia, and hyperactivity requiring restraints. He also endorsed insomnia and weight loss. He was admitted to the inpatient unit, and laboratory investigations were significant for a low thyroid-stimulating hormone, and elevated T3, T4, thyroidstimulating antibodies, and thyroid peroxidase antibodies. The initial assessment was a primary psychiatric illness. The patient never had a personal or family history of psychiatric illness. Psychiatry and endocrinology were consulted for further recommendations. The patient was started on methimazole 30 mg, propranolol 100 mg, and hydrocortisone 100 mg, which resolved his symptoms.

Tricuspid valve endocarditis with recurrent septic pulmonary emboli is an indication for surgery. In this report, we present a case of right-sided infective endocarditis (RSIE) in a female patient with a history of intravenous drug use (IVDU). The patient was admitted with multiple chief complaints of fatigue, chills, fever, cough, chest pain, and shortness of breath. She was found to have a large 1.8 cm (W) x 2.4 cm (L) mobile tricuspid valve vegetation on transthoracic echocardiogram (TTE). Despite being on appropriate antibiotics, the patient failed to improve clinically. Cardiothoracic surgery (CTS) evaluated the patient for surgical management of infective endocarditis (IE) given the size of vegetation, persistent bacteremia, and clinical deterioration. However, the risk/benefit ratio for open-heart surgery was high, given the history of active IVDU and hemodynamic instability. The patient underwent percutaneous extraction of the vegetation using suction filtration and veno-venous bypass and her condition significantly improved clinically afterward. We discuss the importance of suction filtration and veno-venous bypass in managing tricuspid valve endocarditis as an alternative in patients who are not ideal candidates for surgery and the need for more evidence regarding its effectiveness compared to surgery.

Introduction: SARS-Cov-2 virus has been shown to inflict damage on native cardiac valvular tissue. We present the index case of prosthetic mitral valve (MV) dehiscence secondary to SARS-Cov-2 virus as evidenced by histopathologic analysis of peri-valvular annular tissue . Case: 63-year-old male with history of MV replacement 2 years ago presented with complaint of dyspnea for 2 weeks. He was asymptomatic on a cardiology appointment a month ago and had an unremarkable transthoracic echocardiography (TTE) at that time. On arrival, he was hypoxic to 80% on room air and chest exam revealed bibasilar crackles. Complete blood count and electrolytes were within normal ranges. He tested positive for SARS-Cov-2 virus RNA and had a recent family history of COVID-19. Chest X-ray revealed bilateral pulmonary vascular congestion. He was given supplemental oxygen through nasal cannula with improvement in pulse oximetry. Repeat TTE revealed mitral paravalvular leak with suspicion for prosthetic dehiscence. Transesophageal echocardiogram showed multiple jets of severe paravalvular regurgitation and disruption of the MV apparatus. No vegetations were detected on echocardiography. He underwent a pre-operative right heart catheterization which confirmed severe MV regurgitation with pulmonary artery (PA) capillary wedge pressure of 45mmHg (Normal: <12) and a PA pressure of 40mmHg (Normal:<20). Intra-operatively, we found near-complete dehiscence of prosthetic MV with surrounding annular calcifications. Our patient underwent surgical MV replacement with a biosynthetic valve. Histopathologic analysis of the annular tissue revealed myxomatous degeneration and an inflammatory infiltrate of CD4 T helper cells consistent with subacute to chronic inflammation. Of note, neutrophils were not detected which usually signify acute bacterial endocarditis. Tissue and blood cultures remained sterile. Our patient improved hemodynamically after MV replacement and was discharged home in stable condition. Conclusion: We propose that SARS-Cov-2 virus may cause prosthetic MV dehiscence through CD4 T cell-mediated damage to annular tissue. Such cases would require surgical valve replacement to manage the resulting hemodynamic compromise.

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