Incidence and risk factors for secondary pulmonary infections in patients hospitalized with coronavirus disease 2019 pneumonia.
COVID-19
Coronavirus disease 2019
SARS-CoV-2
Secondary bacterial infections
Secondary pulmonary infections
Severe acute respiratory syndrome coronavirus 2
Journal
The American journal of the medical sciences
ISSN: 1538-2990
Titre abrégé: Am J Med Sci
Pays: United States
ID NLM: 0370506
Informations de publication
Date de publication:
06 2022
06 2022
Historique:
received:
02
08
2020
revised:
04
01
2021
accepted:
15
04
2021
pubmed:
25
4
2021
medline:
18
5
2022
entrez:
24
4
2021
Statut:
ppublish
Résumé
Secondary pulmonary infections (SPI) have not been well described in COVID-19 patients. Our study aims to examine the incidence and risk factors of SPI in hospitalized COVID-19 patients with pneumonia. This was a retrospective, single-center study of adult COVID-19 patients with radiographic evidence of pneumonia admitted to a regional tertiary care hospital. SPI was defined as microorganisms identified on the respiratory tract with or without concurrent positive blood culture results for the same microorganism obtained at least 48 h after admission. Thirteen out of 244 (5%) had developed SPI during hospitalization. The median of the nadir lymphocyte count during hospitalization was significantly lower in patients with SPI as compared to those without SPI [0.4 K/uL (IQR 0.3-0.5) versus 0.6 K/uL (IQR 0.3-0.9)]. Patients with lower nadir lymphocyte had an increased risk of developing SPI with odds ratio (OR) of 1.21 (95% CI: 1.00 to 1.47, p = 0.04) per 0.1 K/uL decrement in nadir lymphocyte. The baseline median inflammatory markers of CRP [166.4 mg/L vs. 100.0 mg/L, p = 0.01] and d-dimer (18.5 mg/L vs. 1.4 mg/L, p<0.01), and peak procalcitonin (1.4 ng/mL vs. 0.3 ng/mL, p<0.01) and CRP (273.5 mg/L vs. 153.7 mg/L, p<0.01) during hospitalization were significantly higher in SPI group. The incidence of SPI in hospitalized COVID-19 patients was 5%. Lower nadir median lymphocyte count during hospitalization was associated with an increased OR of developing SPI. The CRP and d-dimer levels on admission, and peak procalcitonin and CRP levels during hospitalization were higher in patients with SPI.
Sections du résumé
BACKGROUND
Secondary pulmonary infections (SPI) have not been well described in COVID-19 patients. Our study aims to examine the incidence and risk factors of SPI in hospitalized COVID-19 patients with pneumonia.
METHODS
This was a retrospective, single-center study of adult COVID-19 patients with radiographic evidence of pneumonia admitted to a regional tertiary care hospital. SPI was defined as microorganisms identified on the respiratory tract with or without concurrent positive blood culture results for the same microorganism obtained at least 48 h after admission.
RESULTS
Thirteen out of 244 (5%) had developed SPI during hospitalization. The median of the nadir lymphocyte count during hospitalization was significantly lower in patients with SPI as compared to those without SPI [0.4 K/uL (IQR 0.3-0.5) versus 0.6 K/uL (IQR 0.3-0.9)]. Patients with lower nadir lymphocyte had an increased risk of developing SPI with odds ratio (OR) of 1.21 (95% CI: 1.00 to 1.47, p = 0.04) per 0.1 K/uL decrement in nadir lymphocyte. The baseline median inflammatory markers of CRP [166.4 mg/L vs. 100.0 mg/L, p = 0.01] and d-dimer (18.5 mg/L vs. 1.4 mg/L, p<0.01), and peak procalcitonin (1.4 ng/mL vs. 0.3 ng/mL, p<0.01) and CRP (273.5 mg/L vs. 153.7 mg/L, p<0.01) during hospitalization were significantly higher in SPI group.
CONCLUSIONS
The incidence of SPI in hospitalized COVID-19 patients was 5%. Lower nadir median lymphocyte count during hospitalization was associated with an increased OR of developing SPI. The CRP and d-dimer levels on admission, and peak procalcitonin and CRP levels during hospitalization were higher in patients with SPI.
Identifiants
pubmed: 33894182
pii: S0002-9629(21)00137-3
doi: 10.1016/j.amjms.2021.04.007
pmc: PMC8058139
pii:
doi:
Substances chimiques
Procalcitonin
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
476-483Informations de copyright
Copyright © 2021. Published by Elsevier Inc.
Déclaration de conflit d'intérêts
Conflicts of Interest Dr. Feustel received funding as a statistical consultant for Transonic Systems and is a scientific advisor with shares in Penrose TherapeuTx, LLC. The remaining authors have disclosed that they do not have any potential conflicts of interest.
Références
Lancet Microbe. 2020 May;1(1):e11
pubmed: 32835323
JAMA. 2020 Mar 17;323(11):1061-1069
pubmed: 32031570
N Engl J Med. 2020 Apr 30;382(18):1708-1720
pubmed: 32109013
Am J Respir Crit Care Med. 2020 Jul 15;202(2):284-287
pubmed: 32412787
Eur Radiol. 2020 Aug;30(8):4381-4389
pubmed: 32193638
Lancet. 2020 Feb 15;395(10223):497-506
pubmed: 31986264
Clin Infect Dis. 2020 Dec 3;71(9):2459-2468
pubmed: 32358954
Open Forum Infect Dis. 2016 Aug 10;3(3):ofw171
pubmed: 27704024
EBioMedicine. 2020 May;55:102763
pubmed: 32361250
Lancet. 2020 Feb 15;395(10223):507-513
pubmed: 32007143
Lancet Respir Med. 2020 May;8(5):475-481
pubmed: 32105632
Crit Care Explor. 2020 Jun 15;2(6):e0143
pubmed: 32696006
Lancet. 2020 May 9;395(10235):1517-1520
pubmed: 32311318
Emerg Microbes Infect. 2020 Dec;9(1):727-732
pubmed: 32196410
Lancet. 2020 Mar 28;395(10229):1054-1062
pubmed: 32171076
Am J Respir Crit Care Med. 2020 Jul 1;202(1):132-135
pubmed: 32396381
Lancet Infect Dis. 2016 Jul;16(7):819-827
pubmed: 26947523
Infect Control Hosp Epidemiol. 2020 Sep;41(9):1124-1125
pubmed: 32317036
Front Microbiol. 2017 Jun 23;8:1041
pubmed: 28690590
Am J Emerg Med. 2013 Jan;31(1):137-44
pubmed: 22944552
JAMA. 2020 May 26;323(20):2085-2086
pubmed: 32293646
Eur Respir J. 2020 May 7;55(5):
pubmed: 32269088
Influenza Other Respir Viruses. 2016 Sep;10(5):394-403
pubmed: 27232677