Background: Coronavirus disease 2019 (COVID-19) has rapidly become a global pandemic. Because the severity of the disease is highly variable, predictive models to stratify patients according to their mortality risk are needed. Objective: Our aim was to develop a model able to predict the risk of fatal outcome in patients with COVID-19 that could be used easily at the time of patients' arrival at the hospital. Methods: We constructed a prospective cohort with 611 adult patients in whom COVID-19 was diagnosed between March 10 and April 12, 2020, in a tertiary hospital in Madrid, Spain. The analysis included 501 patients who had been discharged or had died by April 20, 2020. The capacity of several biomarkers, measured at the beginning of hospitalization, to predict mortality was assessed individually. Those biomarkers that independently contributed to improve mortality prediction were included in a multivariable risk model. Results: High IL-6 level, C-reactive protein level, lactate dehydrogenase (LDH) level, ferritin level, D-dimer level, neutrophil count, and neutrophil-to-lymphocyte ratio were all predictive of mortality (area under the curve >0.70), as were low albumin level, lymphocyte count, monocyte count, and ratio of peripheral blood oxygen saturation to fraction of inspired oxygen (SpO 2 /FiO 2). A multivariable mortality risk model including the SpO 2 /FiO 2 ratio, neutrophil-to-lymphocyte ratio, LDH level, IL-6 level, and age was developed and showed high accuracy for the prediction of fatal outcome (area under the curve 0.94). The optimal cutoff reliably classified patients (including patients with no initial respiratory distress) as survivors and nonsurvivors with 0.88 sensitivity and 0.89 specificity. Conclusion: This mortality risk model allows early risk stratification of hospitalized patients with COVID-19 before the appearance of obvious signs of clinical deterioration, and it can be used as a tool to guide clinical decision making. (J Allergy Clin Immunol 2020;146:799-807.)
Diagnosis of fungal pneumonia (FP) in critically ill patients is challenging. Circulating biomarkers for the diagnosis of FP have limitations and the combination of different assays in serum samples and directly from the target organ may further improve the diagnosis of FP. We prospectively assessed the diagnostic utility of paired galactomannan (GM) in bronchoalveolar lavage fluid (BAL) and serum GM and (1→3)-β-D-glucan (BG) assays in critically ill patients at risk of FP. Patients with FP were classified according to European Organisation for Research and Treatment of Cancer-Mycoses Study Group criteria, with modifications. Out of 847 admissions, 51 patients were eligible. There were nine invasive aspergillosis (IA) cases (four proven, five probable), three proven Pneumocysitis jirovecii pneumonia (PJP) cases and one mixed FP case (probable IA and proven PJP). The diagnostic accuracy as given by the area under the receiver operating characteristic curve in IA cases (proven and probable) for GM in BAL was 0.98 (95% CI, 0.94-1.00), whilst for GM and BG in serum it was 0.85 (95% CI, 0.74-0.96) and 0.815 (95% CI, 0.66-0.96), respectively. For IA cases (proven and probable) AUC for GM in BAL was significantly higher than GM and BG in serum (p 0.025 and p 0.032, respectively). In one of four proven and one of six probable IA cases, GM in serum remained negative, whereas GM in BAL was positive. In patients with IA, GM (90%) and BG (80%) appeared a mean of 4.3 days (range, 1-10 days) before Aspergillus was cultured. GM detection in BAL appears to improve the diagnosis of IA in critical patients.
PCT has a high negative predictive value (94%) and lower PCT levels seems to be a good tool for excluding coinfection, particularly for patients without shock.
Our findings suggest that early oseltamivir administration was associated with favourable outcomes among critically ill ventilated patients with 2009 H1N1 virus infection.
Antimicrobial stewardship programmes promote excellence in the use of antimicrobials by selecting the appropriate antimicrobial agent and the correct dose, route of administration and duration of treatment. However, there is limited experience with such programmes targeting antifungal treatments. We present the results of a non-compulsory programme for the control of antifungals. For 12 months, prescriptions of oral voriconazole or intravenous voriconazole, caspofungin and liposomal amphotericin B were reviewed, and non-compulsory recommendations were made. The incidence and outcome of fungal infections were examined. The results for the dispensed defined daily doses (DDDs) and expenditure on antifungals were compared with those for the previous 12 months. The number of antifungal treatments reviewed was 662. A recommendation to change treatment was made in 29% of the cases, including a change from intravenous to oral treatment (15%), cessation of antifungal treatment (8%), and a change to fluconazole (6%). The DDDs of intravenous voriconazole and caspofungin were reduced by 31.4% and 20.2%, respectively. The DDDs of oral voriconazole and dispensed vials of liposomal amphotericin B were increased by 8.2% and 13.9%, respectively. Expenditure on antifungals was reduced by US$370681.78 (11.8% reduction). The programme was not related to significant increases in the incidence of candidaemia, percentage of persistent/relapsing candidaemia cases, percentage of fluconazole-resistant Candida species, incidence of infections by filamentous fungi, or 12-month mortality in patients with filamentous fungal infections. In conclusion, a stewardship programme targeting antifungals achieved a reduction in antifungal expenditure without reducing the quality of care provided.
Clinicians select the empirical antibiotic regimen after classifying patients according to likely pathogens and prognosis. The inclusion of a macrolide as part of the initial therapeutic regimen for SCAP appears to be as safe and effective as alternative options. Addition of a macrolide agent to a betalactam/betalactamase inhibitor or using a macrolide alone was a marker for less severe disease.
Coronavirus disease 2019 (COVID‐19) can lead to a massive cytokine release. The use of the anti‐interleukin‐6 receptor monoclonal antibody tocilizumab (TCZ) has been proposed in this hyperinflammatory phase, although supporting evidence is limited. We retrospectively analyzed 88 consecutive patients with COVID‐19 pneumonia that received at least one dose of intravenous TCZ in our institution between 16 and 27 March 2020. Clinical status from day 0 (first TCZ dose) through day 14 was assessed by a 6‐point ordinal scale. The primary outcome was clinical improvement (hospital discharge and/or a decrease of ≥2 points on the 6‐point scale) by day 7. Secondary outcomes included clinical improvement by day 14 and dynamics of vital signs and laboratory values. Rates of clinical improvement by days 7 and 14 were 44.3% (39/88) and 73.9% (65/88). Previous or concomitant receipt of subcutaneous interferon‐β (adjusted odds ratio [aOR]: 0.23; 95% confidence interval [CI]: 0.06‐0.94;
P
= .041) and serum lactate dehydrogenase more than 450 U/L at day 0 (aOR: 0.25; 95% CI: 0.06‐0.99;
P
= .048) were negatively associated with clinical improvement by day 7. All‐cause mortality was 6.8% (6/88). Body temperature and respiratory and cardiac rates significantly decreased by day 1 compared to day 0. Lymphocyte count and pulse oximetry oxygen saturation/FiO
2
ratio increased by days 3 and 5, whereas C‐reactive protein levels dropped by day 2. There were no TCZ‐attributable adverse events. In this observational single‐center study, TCZ appeared to be useful and safe as immunomodulatory therapy for severe COVID‐19 pneumonia.
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