ABSTRACT
Covid-19 (SARS-CoV-2) is a new coronavirus. Since the declaration of a global pandemic, a lot has been learnt about its spread, disease pattern, diagnosis and management. The lungs remain the prime organs to incur serious insult and when lung complications embark, significant morbidity and mortality is observed. Predominantly, patchy and peripheral lung distribution in the Covid-19 pneumonia has been described in the radiology experience and literature. There are a range of imaging modes useable in diagnosis, prognosis, monitoring, and therapy of Covid-19. However, when it comes to the appropriateness and the potential benefits of imaging, resource utilization and infectious risk must be considered. The use of ultrasound during this pandemic has provided us with an alternate imaging modality that is easily performed at the bedside, with real time images available to the clinician. This case highlights the role played by the thoracic ultrasound in the diagnosis and progression of Covid-19 pneumonia.
ABSTRACT
BACKGROUND: Eosinopenia is considered a surrogate of inflammation in several disease settings. Following ST-segment elevation myocardial infarction, eosinopenia is presumed to be a marker of infarct severity. We sought to study the relationship between eosinopenia and infarct severity and how this relationship determined the long-term outcomes following ST-segment elevation myocardial infarction. METHODS: Six hundred and six consecutive patients undergoing primary percutaneous coronary interventions from a large volume single center were enrolled. Low eosinophil count was defined as < 40 cells/mL from samples within 2 hours after reperfusion. Primary endpoint was defined as composite of death, myocardial infarction, stroke, unplanned revascularization, and readmission for heart failure over 3.5 years' follow-up. RESULTS: Sixty-five percent of the patients had eosinopenia. Patients in the low eosinophil group had larger infarct size as measured by troponin value (2934 vs 1177 ng/L, P < .001) and left ventricle systolic function on echocardiography (48% vs 50%, P = 0.029). There was a weak correlation between eosinophil count and both troponin (r = -0.25, P < 0.001) and ejection fraction (r = 0.10, P = .017). The primary endpoint was higher in eosinopenic patients (28.8% vs. 20.4%; hazard ratio [HR] 1.49, 95% confidence interval [CI] 1.05 to 2.13, P = .023). A discordance between eosinopenia and severe left ventricle systolic dysfunction was observed in 55.6% of cases. Compared with normal count, eosinopenia was associated with worse clinical outcomes in patients with non-severe left ventricle dysfunction (24.1% vs 16.2%; HR 1.58, 95% CI 1.01 to 2.45, P = .044) but not in those with severe left ventricle dysfunction (42.3% vs. 38.9%; HR 1.10, 95% CI 0.59 to 2.03, P = .77) (P < .01 for interaction). CONCLUSIONS: Eosinopenia is an easily determined marker that reflects worse clinical outcomes over long-term follow-up.
