Background COVID‐19‐associated pulmonary aspergillosis (CAPA) has been widely reported but homogenous large cohort studies are needed to gain real‐world insights about the disease. Methods We collected clinical and laboratory data of 1161 patients hospitalised at our Institute from March 2020 to August 2021, defined their CAPA pathology, and analysed the data of CAPA/non‐CAPA and deceased/survived CAPA patients using univariable and multivariable models. Results The overall prevalence and mortality of CAPA in our homogenous cohort of 1161 patients were 6.4% and 47.3%, respectively. The mortality of CAPA was higher than that of non‐CAPA patients (hazard ratio: 1.8 [95% confidence interval: 1.1–2.8]). Diabetes (odds ratio [OR] 1.92 [1.15–3.21]); persistent fever (2.54 [1.17–5.53]); hemoptysis (7.91 [4.45–14.06]); and lung lesions of cavitation (8.78 [2.27–34.03]), consolidation (9.06 [2.03–40.39]), and nodules (8.26 [2.39–28.58]) were associated with development of CAPA by multivariable analysis. Acute respiratory distress syndrome (ARDS) (2.68 [1.09–6.55]), a high computed tomography score index (OR 1.18 [1.08–1.29]; p < .001), and pulse glucocorticoid treatment (HR 4.0 [1.3–9.2]) were associated with mortality of the disease. Whereas neutrophilic leukocytosis (development: 1.09 [1.03–1.15] and mortality: 1.17 [1.08–1.28]) and lymphopenia (development: 0.68 [0.51–0.91] and mortality: 0.40 [0.20–0.83]) were associated with the development as well as mortality of CAPA. Conclusion We observed a low but likely underestimated prevalence of CAPA in our study. CAPA is a disease with high mortality and diabetes is a significant factor for its development while ARDS and pulse glucocorticoid treatment are significant factors for its mortality. Cellular immune dysregulation may have a central role in CAPA from its development to mortality.

Background:Direct layngoscopy and endotracheal intubation is a noxious stimuli and induces sympathomimetic responses. Although well tolerated in healthy subjects, it may impose life threatening arrhythmias, left ventricular failure or rupture of cerebral aneurysm in susceptible patients. Esmolol, Labetalol and Lignocaine attenuate these responses but are associated with side effects of bradycardia, hypotension etc. In lower doses, chances of these side effects are comparatively low. So we designed this prospective clinical trial to assess the efficacy of intravenous esmolol, labetalol and lignocaine in low doses for attenuation of sympathomimetic responses to endotracheal intubation.Materials and Methods:Seventy-five consenting patients of ASA physical status I or II of age range 20 to 60 years, scheduled for different general surgical procedures were randomly assigned to one of the three groups; group ES, group LB and group LG. Participants of group ES, group LB and group LG was given esmolol HCL 0.5 mg/Kg, labetalol HCL 0.25 mg/kg and lignocaine HCL 1 mg/Kg body weight respectively. Outcome variables were HR, SBP, DBP, MAP and RPP. These variables were recorded just after intubation and thereafter at 1,3,5, 7 and 10 minutes of intubation.Results:There was no statistically significant difference regarding the demographic characteristics of the groups. Heart rate and systolic blood pressure was lower throughout the study period in labetalol group. But the values of study parameters were always higher than the baseline in esmolol and lignocaine group. Values of mean arterial pressure was slightly higher in labetalol group but it was much higher in two other groups throughout the study period. Diastolic blood pressure was higher in all the groups. Values of rate pressure product was higher during intubation and at 1minute after intubation in labetalol group but thereafter it was always lower than baseline values.Conclusion:Labetalol 0.25 mg Kg-1 is an effective and safe drug to be used for attenuation of sympathomimetic responses to endotracheal intubation. Esmolol 0.5 mg Kg-1 and lignocaine 1 mg Kg-1 are also effective to some extent and are safe.

Intravenous dexmedetomidine in combination with 25 mL of bupivacaine (0.5%) accelerated the onset of sensory and motor block and prolonged the duration of sensory and motor block when used for brachial plexus block, without resulting in any adverse events.