Pub Date : 2020-04-22DOI: 10.1201/9780429154805-29
Keith Hopcroft, V. Forte
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, fl uid 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 in fl ow 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 fl uid 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).
{"title":"Chest","authors":"Keith Hopcroft, V. Forte","doi":"10.1201/9780429154805-29","DOIUrl":"https://doi.org/10.1201/9780429154805-29","url":null,"abstract":"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, fl uid 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 in fl ow 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 fl uid 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).","PeriodicalId":331681,"journal":{"name":"Symptom Sorter","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133683616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-04-22DOI: 10.1201/9780429154805-106
Keith Hopcroft, V. Forte
which enabled the differentiation and relative quantification of proteins between samples, including their phosphorylation levels. Results: The TMT system detected 2675 proteins and 778 phos-phorylated peptides. Compared with the uninfected placenta, in the infected placentae, several essential pathways, including the innate and acquired immune systems, were upregulated. The phosphorylation levels of these pathways were also activated. The complement cascade, VEGF signaling, and RHO GTPase signaling were also changed. In patients with IUFD, SARS-CoV-2 infection-related pathways were still enriched in the placentae, while the effects of postmortem tissue degradation could not be ruled out. Conclusion: SARS-CoV-2 infection during pregnancy affects placental protein expression and phosphorylation. SARS-CoV-2 infection must cause both histopathological and functional changes in the placenta in addition to direct cytotoxicity. Analysis of the local immune responses and mechanisms of the placental barrier enables the rescue of placental dysfunction in infected mothers and subsequent fetal well-being.
{"title":"Oral","authors":"Keith Hopcroft, V. Forte","doi":"10.1201/9780429154805-106","DOIUrl":"https://doi.org/10.1201/9780429154805-106","url":null,"abstract":"which enabled the differentiation and relative quantification of proteins between samples, including their phosphorylation levels. Results: The TMT system detected 2675 proteins and 778 phos-phorylated peptides. Compared with the uninfected placenta, in the infected placentae, several essential pathways, including the innate and acquired immune systems, were upregulated. The phosphorylation levels of these pathways were also activated. The complement cascade, VEGF signaling, and RHO GTPase signaling were also changed. In patients with IUFD, SARS-CoV-2 infection-related pathways were still enriched in the placentae, while the effects of postmortem tissue degradation could not be ruled out. Conclusion: SARS-CoV-2 infection during pregnancy affects placental protein expression and phosphorylation. SARS-CoV-2 infection must cause both histopathological and functional changes in the placenta in addition to direct cytotoxicity. Analysis of the local immune responses and mechanisms of the placental barrier enables the rescue of placental dysfunction in infected mothers and subsequent fetal well-being.","PeriodicalId":331681,"journal":{"name":"Symptom Sorter","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127522341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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