Infections and the inflammatory response in acute respiratory distress syndrome

Research output: Contribution to journalArticle

183 Citations (Scopus)

Abstract

Study objective: Systemic inflammatory response syndrome (SIRS) and infections are frequently associated with the development and progression of acute respiratory distress syndrome (ARDS) and multiple organ dysfunction syndrome (MODS). We investigated, at onset and during the progression of ARDS, the relationships among (1) clinical variables and biological markers of SIRS, (2) infections defined by strict criteria, and (3) patient outcome. Biological markers of SIRS included serial measurements of inflammatory cytokines (IC)-tumor necrosis factor-α (TNF-α) and interleukins (IL) 1β, 2, 4, 6, and 8 - in plasma and BAL fluid. Methods: We prospectively studied two groups of ARDS patients: 34 patients treated conventionally (group 1) and nine patients who received glucocorticoid rescue treatment for unresolving ARDS (group 2). Individual SIRS criteria and SIRS composite score were recorded daily for all patients. Plasma IC levels were measured by enzyme- linked immunosorbent assay on days 1, 2, 3, 5, 7, 10, and 12 of ARDS and every third day thereafter while patients received mechanical ventilation. Unless contraindicated, bilateral BAL was performed on day 1, weekly, and when ventilator-associated pneumonia was suspected. Patients were closely monitored for the development of nosocomial infections (NIs). Results: ICU mortality was similar among patients with and without sepsis on admission (54% vs 40%; p<0.45). Among patients with sepsis-induced ARDS, mortality was higher in those who subsequently developed NIs (71% vs 18%; p<0.05). At the onset of ARDS, plasma TNF-α, IL-1β, IL-6, and IL-8 levels were significantly higher (p<0.0001) in nonsurvivors (NS) and in those with sepsis (p<0.0001). The NS group, contrary to survivors (S), had persistently elevated plasma IC levels over time. In 17 patients, 36 definitive NIs (17 in group 1 and 19 in group 2) were diagnosed by strict criteria. No definitive or presumed NIs caused an increase in plasma IC levels above patients' preinfection baseline. Daily SIRS components and SIRS composite scores were similar among S and NS and among patients with and without sepsis-induced ARDS, were unaffected by the development of NI, and did not correlate with plasma IC levels. Conclusions: Sepsis as a precipitating cause of ARDS was associated with higher plasma IC levels. However, NIs were not associated with an increase in SIRS composite scores, individual SIRS criteria, or plasma IC levels above patients' preinfection baseline. SIRS composite scores over time were similar in S and NS. SIRS criteria, including fever, were found to be nonspecific for NI. Irrespective of etiology of ARDS, plasma IC levels, but not clinical criteria, correlated with patient outcome. These findings suggest that final outcome in patients with ARDS is related to the magnitude and duration of the host inflammatory response and is independent of the precipitating cause of ARDS or the development of intercurrent NIs.

Original languageEnglish (US)
Pages (from-to)1306-1321
Number of pages16
JournalChest
Volume111
Issue number5
StatePublished - Jan 1 1997

Fingerprint

Adult Respiratory Distress Syndrome
Systemic Inflammatory Response Syndrome
Cross Infection
Infection
Cytokines
Sepsis
Dimercaprol
Biomarkers
Interleukin-1
Tumor Necrosis Factor-alpha
Ventilator-Associated Pneumonia
Multiple Organ Failure
Mortality
Interleukin-8
Artificial Respiration
Glucocorticoids
Interleukin-2
Survivors
Interleukin-6

All Science Journal Classification (ASJC) codes

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine
  • Cardiology and Cardiovascular Medicine

Cite this

Infections and the inflammatory response in acute respiratory distress syndrome. / Headly, A. Stacey; Tolley, Elizabeth; Meduri, Gianfranco.

In: Chest, Vol. 111, No. 5, 01.01.1997, p. 1306-1321.

Research output: Contribution to journalArticle

@article{7f4953bfba184d37a21c6ef580e6b2d8,
title = "Infections and the inflammatory response in acute respiratory distress syndrome",
abstract = "Study objective: Systemic inflammatory response syndrome (SIRS) and infections are frequently associated with the development and progression of acute respiratory distress syndrome (ARDS) and multiple organ dysfunction syndrome (MODS). We investigated, at onset and during the progression of ARDS, the relationships among (1) clinical variables and biological markers of SIRS, (2) infections defined by strict criteria, and (3) patient outcome. Biological markers of SIRS included serial measurements of inflammatory cytokines (IC)-tumor necrosis factor-α (TNF-α) and interleukins (IL) 1β, 2, 4, 6, and 8 - in plasma and BAL fluid. Methods: We prospectively studied two groups of ARDS patients: 34 patients treated conventionally (group 1) and nine patients who received glucocorticoid rescue treatment for unresolving ARDS (group 2). Individual SIRS criteria and SIRS composite score were recorded daily for all patients. Plasma IC levels were measured by enzyme- linked immunosorbent assay on days 1, 2, 3, 5, 7, 10, and 12 of ARDS and every third day thereafter while patients received mechanical ventilation. Unless contraindicated, bilateral BAL was performed on day 1, weekly, and when ventilator-associated pneumonia was suspected. Patients were closely monitored for the development of nosocomial infections (NIs). Results: ICU mortality was similar among patients with and without sepsis on admission (54{\%} vs 40{\%}; p<0.45). Among patients with sepsis-induced ARDS, mortality was higher in those who subsequently developed NIs (71{\%} vs 18{\%}; p<0.05). At the onset of ARDS, plasma TNF-α, IL-1β, IL-6, and IL-8 levels were significantly higher (p<0.0001) in nonsurvivors (NS) and in those with sepsis (p<0.0001). The NS group, contrary to survivors (S), had persistently elevated plasma IC levels over time. In 17 patients, 36 definitive NIs (17 in group 1 and 19 in group 2) were diagnosed by strict criteria. No definitive or presumed NIs caused an increase in plasma IC levels above patients' preinfection baseline. Daily SIRS components and SIRS composite scores were similar among S and NS and among patients with and without sepsis-induced ARDS, were unaffected by the development of NI, and did not correlate with plasma IC levels. Conclusions: Sepsis as a precipitating cause of ARDS was associated with higher plasma IC levels. However, NIs were not associated with an increase in SIRS composite scores, individual SIRS criteria, or plasma IC levels above patients' preinfection baseline. SIRS composite scores over time were similar in S and NS. SIRS criteria, including fever, were found to be nonspecific for NI. Irrespective of etiology of ARDS, plasma IC levels, but not clinical criteria, correlated with patient outcome. These findings suggest that final outcome in patients with ARDS is related to the magnitude and duration of the host inflammatory response and is independent of the precipitating cause of ARDS or the development of intercurrent NIs.",
author = "Headly, {A. Stacey} and Elizabeth Tolley and Gianfranco Meduri",
year = "1997",
month = "1",
day = "1",
language = "English (US)",
volume = "111",
pages = "1306--1321",
journal = "Chest",
issn = "0012-3692",
publisher = "American College of Chest Physicians",
number = "5",

}

TY - JOUR

T1 - Infections and the inflammatory response in acute respiratory distress syndrome

AU - Headly, A. Stacey

AU - Tolley, Elizabeth

AU - Meduri, Gianfranco

PY - 1997/1/1

Y1 - 1997/1/1

N2 - Study objective: Systemic inflammatory response syndrome (SIRS) and infections are frequently associated with the development and progression of acute respiratory distress syndrome (ARDS) and multiple organ dysfunction syndrome (MODS). We investigated, at onset and during the progression of ARDS, the relationships among (1) clinical variables and biological markers of SIRS, (2) infections defined by strict criteria, and (3) patient outcome. Biological markers of SIRS included serial measurements of inflammatory cytokines (IC)-tumor necrosis factor-α (TNF-α) and interleukins (IL) 1β, 2, 4, 6, and 8 - in plasma and BAL fluid. Methods: We prospectively studied two groups of ARDS patients: 34 patients treated conventionally (group 1) and nine patients who received glucocorticoid rescue treatment for unresolving ARDS (group 2). Individual SIRS criteria and SIRS composite score were recorded daily for all patients. Plasma IC levels were measured by enzyme- linked immunosorbent assay on days 1, 2, 3, 5, 7, 10, and 12 of ARDS and every third day thereafter while patients received mechanical ventilation. Unless contraindicated, bilateral BAL was performed on day 1, weekly, and when ventilator-associated pneumonia was suspected. Patients were closely monitored for the development of nosocomial infections (NIs). Results: ICU mortality was similar among patients with and without sepsis on admission (54% vs 40%; p<0.45). Among patients with sepsis-induced ARDS, mortality was higher in those who subsequently developed NIs (71% vs 18%; p<0.05). At the onset of ARDS, plasma TNF-α, IL-1β, IL-6, and IL-8 levels were significantly higher (p<0.0001) in nonsurvivors (NS) and in those with sepsis (p<0.0001). The NS group, contrary to survivors (S), had persistently elevated plasma IC levels over time. In 17 patients, 36 definitive NIs (17 in group 1 and 19 in group 2) were diagnosed by strict criteria. No definitive or presumed NIs caused an increase in plasma IC levels above patients' preinfection baseline. Daily SIRS components and SIRS composite scores were similar among S and NS and among patients with and without sepsis-induced ARDS, were unaffected by the development of NI, and did not correlate with plasma IC levels. Conclusions: Sepsis as a precipitating cause of ARDS was associated with higher plasma IC levels. However, NIs were not associated with an increase in SIRS composite scores, individual SIRS criteria, or plasma IC levels above patients' preinfection baseline. SIRS composite scores over time were similar in S and NS. SIRS criteria, including fever, were found to be nonspecific for NI. Irrespective of etiology of ARDS, plasma IC levels, but not clinical criteria, correlated with patient outcome. These findings suggest that final outcome in patients with ARDS is related to the magnitude and duration of the host inflammatory response and is independent of the precipitating cause of ARDS or the development of intercurrent NIs.

AB - Study objective: Systemic inflammatory response syndrome (SIRS) and infections are frequently associated with the development and progression of acute respiratory distress syndrome (ARDS) and multiple organ dysfunction syndrome (MODS). We investigated, at onset and during the progression of ARDS, the relationships among (1) clinical variables and biological markers of SIRS, (2) infections defined by strict criteria, and (3) patient outcome. Biological markers of SIRS included serial measurements of inflammatory cytokines (IC)-tumor necrosis factor-α (TNF-α) and interleukins (IL) 1β, 2, 4, 6, and 8 - in plasma and BAL fluid. Methods: We prospectively studied two groups of ARDS patients: 34 patients treated conventionally (group 1) and nine patients who received glucocorticoid rescue treatment for unresolving ARDS (group 2). Individual SIRS criteria and SIRS composite score were recorded daily for all patients. Plasma IC levels were measured by enzyme- linked immunosorbent assay on days 1, 2, 3, 5, 7, 10, and 12 of ARDS and every third day thereafter while patients received mechanical ventilation. Unless contraindicated, bilateral BAL was performed on day 1, weekly, and when ventilator-associated pneumonia was suspected. Patients were closely monitored for the development of nosocomial infections (NIs). Results: ICU mortality was similar among patients with and without sepsis on admission (54% vs 40%; p<0.45). Among patients with sepsis-induced ARDS, mortality was higher in those who subsequently developed NIs (71% vs 18%; p<0.05). At the onset of ARDS, plasma TNF-α, IL-1β, IL-6, and IL-8 levels were significantly higher (p<0.0001) in nonsurvivors (NS) and in those with sepsis (p<0.0001). The NS group, contrary to survivors (S), had persistently elevated plasma IC levels over time. In 17 patients, 36 definitive NIs (17 in group 1 and 19 in group 2) were diagnosed by strict criteria. No definitive or presumed NIs caused an increase in plasma IC levels above patients' preinfection baseline. Daily SIRS components and SIRS composite scores were similar among S and NS and among patients with and without sepsis-induced ARDS, were unaffected by the development of NI, and did not correlate with plasma IC levels. Conclusions: Sepsis as a precipitating cause of ARDS was associated with higher plasma IC levels. However, NIs were not associated with an increase in SIRS composite scores, individual SIRS criteria, or plasma IC levels above patients' preinfection baseline. SIRS composite scores over time were similar in S and NS. SIRS criteria, including fever, were found to be nonspecific for NI. Irrespective of etiology of ARDS, plasma IC levels, but not clinical criteria, correlated with patient outcome. These findings suggest that final outcome in patients with ARDS is related to the magnitude and duration of the host inflammatory response and is independent of the precipitating cause of ARDS or the development of intercurrent NIs.

UR - http://www.scopus.com/inward/record.url?scp=0030905548&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030905548&partnerID=8YFLogxK

M3 - Article

VL - 111

SP - 1306

EP - 1321

JO - Chest

JF - Chest

SN - 0012-3692

IS - 5

ER -