Chest
Clinical Investigations in Critical CareInfections and the Inflammatory Response in Acute Respiratory Distress Syndrome
Section snippets
Patients
The study was conducted between January 1992 and May 1993 at the Medical ICU of the Regional Medical Center and the University of Tennessee Medical Center, Memphis. The protocol was approved by the University of Tennessee institutional review board, and informed consent was obtained before entrance into the study. We prospectively studied 43 consecutive patients who developed medical ARDS. Thirty-eight patients were admitted to the ICU directly from the emergency department, and five patients
Clinical Variables at the Onset of ARDS for Groups 1 and 2
Demographics and clinical variables at the onset of ARDS for groups 1 and 2 are shown in Table 1. No significant difference was found between the two groups except for sex, LIS, cardiovascular dysfunction, and the presence of shock. Causes of direct lung injury for group 1 included 17 pneumonia (7 with bacteremia), two chemical aspiration, and one bleomycin-oxygen toxic reaction. Causes of direct lung injury for group 2 included two pneumonia and three chemical aspiration. Causes of indirect
DISCUSSION
The host defense response to an insult is similar, regardless of the tissue involved, and consists of an interactive network of simultaneously activated pathways that act in synergy to increase the chance of survival. The host defense is essentially a protective response of tissues and serves to destroy, dilute, or wall off injurious agents21 and to repair any tissue damage. This repair consists of replacing injured tissue by regenerating parenchymal cells and filling defects with fibroblastic
CONCLUSIONS
Survival 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 NI. We have found no evidence of amplification of the host inflammatory response, as measured by clinical SIRS score or biological plasma IC levels, in the presence of documented or suspected NI. Downregulation in the presence of NI most likely represents cytoprotection from overwhelming cytokinemia and
ACKNOWLEDGMENTS
We wish to thank Drs. John P. Griffin and David Armbruster for editorial assistance; Reba Umberger, RN, and Stephanie Carson, RN, for assistance with data collection; Vicky Franke for secretarial support; and the UT Division of Pulmonary and Critical Care Medicine for assistance with patient recruitment.
REFERENCES (42)
- et al.
Inflammatory cytokines in the BAL of patients with ARDS: persistent elevation over time predicts poor outcome
Chest
(1995) - et al.
Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis
Chest
(1992) - et al.
Diagnosis of nosocomial bacterial pneumonia in acute, diffuse lung injury
Chest
(1981) - et al.
The adult respiratory distress syndrome: a report of survival and modifying factors
Chest
(1992) - et al.
The standardization of bronchoscopic techniques for ventilator-associated pneumonia
Chest
(1992) - et al.
Causes of fever and pulmonary densities in patients with clinical manifestations of ventilator-associated pneumonia
Chest
(1994) - et al.
Persistent elevation of inflammatory cytokines predicts a poor outcome in ARDS: plasma IL-1β and IL-6 are consistent and efficient predictors of outcome over time
Chest
(1995) - et al.
Plasma and BAL cytokine response to corticosteroid rescue treatment in late ARDS
Chest
(1995) Inflammatory cytokines
Clin Immunol Immunopathol
(1992)- et al.
The acute phase response
Immunol Today
(1994)
Does drainage of intra-abdominal pus reverse multiple organ failure?
Am J Surg
Downregulation of proinflammatory cytokine release in whole blood from septic patients
Blood
Risk with predispositions
Ann Intern Med
Indications of risk, course, and prognosis in adult respiratory distress syndrome [editorial]
Am Rev Respir Dis
Extracorporeal support for respiratory insufficiency: collaborative study
Causes of mortality in patients with the adult respiratory distress syndrome
Am Rev Respir Dis
Incidence, site, and outcome of infections in patients with the adult respiratory distress syndrome
Am Rev Respir Dis
Multiple organ system failure and infection in adult respiratory distress syndrome
Ann Intern Med
New Horizons
Toward a theory regarding the pathogenesis of the systemic inflammatory response syndrome: what we do and do not know about cytokine regulation
Crit Care Med
APACHE II: a severity of disease classification system
Crit Care Med
Cited by (215)
Prolonged glucocorticoid treatment in ARDS: Pathobiological rationale and pharmacological principles
2023, Stress: Immunology and Inflammation: Handbook of Stress Series Volume 5General adaptation in critical illness 1: The glucocorticoid signaling system as master rheostat of homeostatic corrections in concerted action with nuclear factor-κB
2023, Stress: Immunology and Inflammation: Handbook of Stress Series Volume 5Innate Immunity and Pulmonary Inflammation: A Balance Between Protection and Disease
2018, Translational Inflammation
This study was supported by Clinical Research Center grant 5M01RR00211 and Baptist Health Care Foundation grant 9506. This study won a 1994 DuPont Pharmaceuticals American College of Chest Physicians Young Investigator Award (Dr. Headley).