PROCALCITONIN KINETICS MAY INDICATE PRESENCE OF SECONDARY BACTERIAL INFECTIONS IN COVID-19 ARDS

PCT rise was observed in 35 (53.8%) of patients, CRP rise in 42 (67.4%) and WCC rise in 52 (80%) of the patients. VAP was the most common ICU-acquired infection, occurring in 28/65 (43.1%) patients, of whom 8/65 (12.3%) suffered both VAP and BSI during their ICU stay. B Introduction: b Secondary bacterial infection in Covid-19 is associated with increased mortality and disproportionately affects critically ill patients. [Extracted from the article] Copyright of Critical Care Medicine is the property of Lippincott Williams & Wilkins and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)

Procalcitonin Increase Is Associated with the Development of Critical Care-Acquired Infections in COVID-19 ARDS.

Secondary bacterial infection in COVID-19 patients is associated with increased mortality and disproportionately affects critically ill patients. This single-centre retrospective observational study investigates the comparative efficacy of change in procalcitonin (PCT) and other commonly available biomarkers in revealing or predicting microbiologically proven secondary infection in critical COVID-19 patients. Adult patients admitted to an intensive care unit (ICU) with confirmed SARS-CoV-2 infection between 9 March 2020 and 5 June 2020 were recruited to the study. For daily biomarker and secondary infection, laboratory-confirmed bloodstream infection (LCBI) and ventilator-associated pneumonia/tracheobronchitis (VAP/VAT) data were collected. We observed a PCT rise in 53 (81.5%) of the patients, a C-reactive protein (CRP) rise in 55 (84.6%) and a white blood cell count (WBC) rise in 61 (93.8%). Secondary infection was confirmed in 33 (50.8%) of the patients. A PCT rise was present in 97.0% of patients with at least one confirmed VAP/VAT and/or LCBI event. CRP and WBC rises occurred in 93.9% and 97.0% of patients with confirmed VAP/VAT and/or LCBI, respectively. Logistic regression analysis found that, when including all biomarkers in the same model, there was a significant association between PCT rise and the occurrence of LCBI and/or VAP/VAT (OR = 14.86 95%CI: 2.20, 342.53; p = 0.021). Conversely, no statistically significant relationship was found between either a CRP rise (p = 0.167) or a WBC rise (p = 0.855) and the occurrence of VAP/VAT and/or LCBI. These findings provide a promising insight into the usefulness of PCT measurement in predicting the emergence of secondary bacterial infection in ICU.

A cluster of children with facial nerve palsy in a high prevalence area for COVID-19.

BACKGROUND: COVID-19 is a disease of varying presentation and neurological sequelae of the disease are being studied. Following a cluster of paediatric facial nerve palsy (FNP) cases in an area of South Wales with a high prevalence of COVID-19, we conducted an opportunistic study to determine whether there has been an increase of incidence of FNP and if there is an association between the FNP and COVID-19 in children. METHODS: We performed a retrospective review of the incidence of FNP between 2015 and 2020 across two hospitals within the health board. The incidence was compared with that in 2020 including a cluster of six children in 14 weeks, presenting to Royal Glamorgan Hospital between June and October. RESULTS: There were 48 cases of children with FNP across both hospital within the study years. Seven (7) cases in 2020. The incidence was not statistically different in comparison to other years. Five out of six of these children in 2020 had antibody testing for COVID-19. All serology testing (100%) returned negative for SARS-CoV- 2 antibodies. CONCLUSIONS: In high prevalence area for COVID-19, cases of children with FNP have not shown a commensurate increase. we have found no causal link between COVID-19 and FNP in children. While this is a small study, larger cohort studies are needed to support this finding. As new strains of COVID-19 are being reported in UK, South Africa and Brazil, physicians need to continue to be vigilant for consistent pattern of signs and symptoms, especially in children.

A Cluster of Children with Facial Nerve Palsy in High Prevalence Area for COVID-19.

OBJECTIVES: COVID-19 is a disease of varying presentation and neurological sequelae of the disease are being studied. Following a cluster of paediatric facial nerve palsy (FNP) cases in an area of South Wales with a high prevalence of COVID-19, we conducted an opportunistic study to determine whether there has been an increase in incidence of FNP and if there is an association between the FNP and COVID-19 in children. STUDY DESIGN: A retrospective cohort study. Using the case series from 2020 and comparing it with previous years. METHODS: We reviewed the incidence of FNP between 2015-2020 across two hospitals within the health board. The incidence was compared with that in 2020 including a cluster of six children in 14 weeks, presenting to the Royal Glamorgan Hospital between June and October. RESULTS: There were 48 cases of children with FNP across both hospital within the study years. Seven (7) cases in 2020. The incidence was not statistically different in comparison to other years.Five out of six of these children in 2020 had antibody testing for COVID-19. All serology testing (100%) returned negative for SARS-CoV- 2 antibodies.In high prevalence area for COVID-19, cases of children with FNP have not shown a commensurate increase. we have found no causal link between COVID-19 and FNP in children. While this is a small study, larger cohort studies are needed to support this finding. CONCLUSION: As new strains of COVID-19 are being reported in UK, South Africa and Brazil, physicians need to continue to be vigilant for consistent pattern of signs and symptoms, especially in children.

Differences in Inflammatory Marker Kinetics between the First and Second Wave of COVID-19 Patients Admitted to the ICU: A Retrospective, Single-Center Study.

BACKGROUND: We sought to determine if there was a difference in the longitudinal inflammatory response measured by white blood cell count (WBC), C-reactive protein (CRP), procalcitonin (PCT), and ferritin levels between the first and the second COVID-19 wave of ICU patients. METHODS: In a single-center retrospective observational study, ICU patients were enrolled during the first and second waves of the COVID-19 pandemic. Data were collected on patient demographics, comorbidities, laboratory results, management strategies, and complications during the ICU stay. The inflammatory response was evaluated using WBC count, CRP, PCT, and Ferritin levels on the day of admission until Day 28, respectively. Organ dysfunction was measured by the SOFA score. RESULTS: 65 patients were admitted during the first and 113 patients during the second wave. WBC and ferritin levels were higher in the second wave. CRP and PCT showed markedly different longitudinal kinetics up until day 28 of ICU stay between the first and second wave, with significantly lower levels in the second wave. Steroid and immunomodulatory therapy use was significantly greater in the second wave. Mortality was similar in both waves. CONCLUSIONS: We found that there was a significantly reduced inflammatory response in the second wave, which is likely to be attributable to the more widespread use of immunomodulatory therapies.

Prevalence of phenotypes of acute respiratory distress syndrome in critically ill patients with COVID-19: a prospective observational study.

BACKGROUND: In acute respiratory distress syndrome (ARDS) unrelated to COVID-19, two phenotypes, based on the severity of systemic inflammation (hyperinflammatory and hypoinflammatory), have been described. The hyperinflammatory phenotype is known to be associated with increased multiorgan failure and mortality. In this study, we aimed to identify these phenotypes in COVID-19-related ARDS. METHODS: In this prospective observational study done at two UK intensive care units, we recruited patients with ARDS due to COVID-19. Demographic, clinical, and laboratory data were collected at baseline. Plasma samples were analysed for interleukin-6 (IL-6) and soluble tumour necrosis factor receptor superfamily member 1A (TNFR1) using a novel point-of-care assay. A parsimonious regression classifier model was used to calculate the probability for the hyperinflammatory phenotype in COVID-19 using IL-6, soluble TNFR1, and bicarbonate levels. Data from this cohort was compared with patients with ARDS due to causes other than COVID-19 recruited to a previous UK multicentre, randomised controlled trial of simvastatin (HARP-2). FINDINGS: Between March 17 and April 25, 2020, 39 patients were recruited to the study. Median ratio of partial pressure of arterial oxygen to fractional concentration of oxygen in inspired air (PaO2/FiO2) was 18 kpa (IQR 15-21) and acute physiology and chronic health evaluation II score was 12 (10-16). 17 (44%) of 39 patients had died by day 28 of the study. Compared with survivors, patients who died were older and had lower PaO2/FiO2. The median probability for the hyperinflammatory phenotype was 0·03 (IQR 0·01-0·2). Depending on the probability cutoff used to assign class, the prevalence of the hyperinflammatory phenotype was between four (10%) and eight (21%) of 39, which is lower than the proportion of patients with the hyperinflammatory phenotype in HARP-2 (186 [35%] of 539). Using the Youden index cutoff (0·274) to classify phenotype, five (63%) of eight patients with the hyperinflammatory phenotype and 12 (39%) of 31 with the hypoinflammatory phenotype died. Compared with matched patients recruited to HARP-2, levels of IL-6 were similar in our cohort, whereas soluble TNFR1 was significantly lower in patients with COVID-19-associated ARDS. INTERPRETATION: In this exploratory analysis of 39 patients, ARDS due to COVID-19 was not associated with higher systemic inflammation and was associated with a lower prevalence of the hyperinflammatory phenotype than that observed in historical ARDS data. This finding suggests that the excess mortality observed in COVID-19-related ARDS is unlikely to be due to the upregulation of inflammatory pathways described by the parsimonious model. FUNDING: US National Institutes of Health, Innovate UK, and Randox.