From ventilator-induced lung injury to multiple organ dysfunction?

1998 ◽  
Vol 24 (2) ◽  
pp. 102-104 ◽  
Author(s):  
D. Dreyfuss ◽  
G. Saumon
Keyword(s):  
Lung Injury ◽  
Organ Dysfunction ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction ◽  
Ventilator Induced Lung Injury

scholarly journals NOX2 protects against progressive lung injury and multiple organ dysfunction syndrome

2014 ◽  
Vol 307 (1) ◽  
pp. L71-L82 ◽  
Author(s):  
Laura C. Whitmore ◽  
Kelli L. Goss ◽  
Elizabeth A. Newell ◽  
Brieanna M. Hilkin ◽  
Jessica S. Hook ◽  
...  
Keyword(s):  
Lung Injury ◽  
Organ Dysfunction ◽  
Systemic Inflammation ◽  
Multiple Organ Dysfunction Syndrome ◽  
Murine Model ◽  
Oxidant Stress ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction ◽  
Cellular Analysis ◽  
Deficient Mice

Systemic inflammatory response syndrome (SIRS) is a common clinical condition in patients in intensive care units that can lead to complications, including multiple organ dysfunction syndrome (MODS). MODS carries a high mortality rate, and it is unclear why some patients resolve SIRS, whereas others develop MODS. Although oxidant stress has been implicated in the development of MODS, several recent studies have demonstrated a requirement for NADPH oxidase 2 (NOX2)-derived oxidants in limiting inflammation. We recently demonstrated that NOX2 protects against lung injury and mortality in a murine model of SIRS. In the present study, we investigated the role of NOX2-derived oxidants in the progression from SIRS to MODS. Using a murine model of sterile systemic inflammation, we observed significantly greater illness and subacute mortality in gp91phox−/y(NOX2-deficient) mice compared with wild-type mice. Cellular analysis revealed continued neutrophil recruitment to the peritoneum and lungs of the NOX2-deficient mice and altered activation states of both neutrophils and macrophages. Histological examination showed multiple organ pathology indicative of MODS in the NOX2-deficient mice, and several inflammatory cytokines were elevated in lungs of the NOX2-deficient mice. Overall, these data suggest that NOX2 function protects against the development of MODS and is required for normal resolution of systemic inflammation.

TNF but not IL-1 in dogs causes lethal lung injury and multiple organ dysfunction similar to human sepsis

1991 ◽  
Vol 71 (5) ◽  
pp. 1979-1989 ◽  
Author(s):  
P. Q. Eichacker ◽  
W. D. Hoffman ◽  
A. Farese ◽  
S. M. Banks ◽  
G. C. Kuo ◽  
...  
Keyword(s):  
Septic Shock ◽  
Lung Injury ◽  
Organ Dysfunction ◽  
Time Course ◽  
Interleukin 1 ◽  
Multiple Organ ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Multiple Organ Dysfunction ◽  
Arterial Po2

We compared the early and late pulmonary effects of human recombinant tumor necrosis factor (TNF) and interleukin 1 (IL-1) challenges in awake dogs with chronic tracheostomies. Serial blood gas analysis, bronchoalveolar lavage (BAL) with cell and protein analysis, intravascular catheter hemodynamics, and radionuclide left ventricular ejection fractions (LVEF) were determined before and after infusion of TNF (60 micrograms/kg body wt, n = 8), IL-1 (1,000 micrograms/kg body wt, n = 6), or heat-inactivated IL-1 (n = 6, controls). Controls given heat-inactivated IL-1 had no changes (P = NS) in any pulmonary parameter throughout the study. Animals given IL-1 had a transient increase (P less than 0.05) in BAL neutrophil concentration 1 day after infusion but no other changes (P = NS) in pulmonary function throughout the study. Animals given TNF had early (0–4 h) decreases (P less than 0.05) in arterial PO2, increases (P less than 0.05) in physiological shunt fraction and alveolar-to-arterial PO2 gradient, and a high mortality rate (50%). In TNF animals, volume challenges at 4 h were associated (P less than 0.05) with death and noncardiogenic pulmonary edema. In TNF survivors, hypoxemia persisted for 2–3 days and was associated with increases (P less than 0.05) in alveolar protein and neutrophil concentration on days 1 and 3, respectively, which in survivors returned to near normal over 6–21 days. Animals challenged with TNF and not IL-1 had reversible depression of LVEF similar in time course to abnormalities in arterial PO2. In this study, TNF (but not IL-1) challenges were lethal and produced acute pulmonary dysfunction sustained over days (reversible in survivors) that was similar to that seen in human septic shock. The ability of TNF to induce pulmonary injury similar to bacterial shock suggests that TNF is a key mediator of sepsis-induced lung injury. Furthermore, because TNF challenge induced both sustained pulmonary and cardiac injury, TNF may be a common pathway for the multiple organ dysfunction that occurs during septic shock.

VOLATILE ANESTHETIC MODULATION OF LUNG INJURY AND OUTCOME IN A MURINE MODEL OF MULTIPLE ORGAN DYSFUNCTION SYNDROME

Shock ◽  
1995 ◽  
Vol 4 (1) ◽  
pp. 61-67 ◽  
Author(s):  
Jay R. Shayevitz ◽  
Jorge L. Rodriguez ◽  
Lori Gilligan ◽  
Kent J. Johnson ◽  
Alan R. Tait
Keyword(s):  
Lung Injury ◽  
Organ Dysfunction ◽  
Multiple Organ Dysfunction Syndrome ◽  
Murine Model ◽  
Volatile Anesthetic ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction

scholarly journals Study of etiology and scoring system in acute lung injury and acute respiratory distress syndrome patients

2018 ◽  
Vol 5 (4) ◽  
pp. 854 ◽  
Author(s):  
Praveen Chabukswar ◽  
Jaya Baviskar
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Lung Injury ◽  
Organ Dysfunction ◽  
Distress Syndrome ◽  
Multiple Organ ◽  
Lung Injury Score ◽  
Tropical Diseases ◽  
Multiple Organ Dysfunction ◽  
Injury Score ◽  
Multiple Organ Dysfunction Score

Background: The acute respiratory distress syndrome (ARDS) is a clinical disorder characterized by injury to the alveolar epithelium and endothelial barriers of the lung, acute inflammation, and protein rich pulmonary edema leading to respiratory failure. Present study was carried out to investigate the mortality pattern of ALI/ARDS in the patients and to study the etiological factors leading to ALI/ARDS also to study the clinical pattern in patients with ALI/ARDS.Methods: All patients fulfilling the inclusion criteria as per the 1994 American European Consensus Conference on ARDS/ALI definition of ARDS/ALI were included in the study. On clinical examination the vital parameters were recorded. The respiratory system, abdominal, cardiovascular and central nervous systems were examined in detail. The severity of the illness was measured by the acute physiology and Chronic Health Evaluation (APACHE) Score, Multiple Organ Dysfunction score (MODS), lung injury score (LIS) and Sequential Organ Dysfunction Assessment (SOFA score). These scores were calculated on admission to our intensive care unit.Results: Out of the 65 patients 35 survived and 30 died. A multiple organ dysfunction Score of less than or equal to 4 was seen in 29 patients and more than 4 in 36 patient and a score of less than or equal to 4 was seen in 21 survivors and 8 dead patients, while a score of more than four was found in 14 patients who survived versus 22 patients who died. A lung injury score of less than or equal to 2 was seen in patients and more than 2 in 46 patients and a score of less than or equal to 2 was seen in 14 survivors and 5 non-survivors patients, while a score of more than 2 was found in 21 patients who survived versus 25 patients who died.Conclusions: The commonest etiological conditions leading to ALI/ARDS are pneumonia and tropical diseases including malaria, leptospirosis and dengue. The scoring systems, MODS, LIS and APACHE II are good indicators of the outcome of this condition. They are useful in tropical diseases as well.

Disseminated intravascular coagulation in meningococcal sepsis

2003 ◽  
Vol 23 (03) ◽  
pp. 125-130 ◽  
Author(s):  
S. Zeerleder ◽  
R. Zürcher Zenklusen ◽  
C. E. Hack ◽  
W. A. Wuillemin
Keyword(s):  
Organ Dysfunction ◽  
Disseminated Intravascular Coagulation ◽  
Skin Necrosis ◽  
Multiple Organ ◽  
Meningococcal Sepsis ◽  
Multiple Organ Dysfunction ◽  
Intravascular Coagulation ◽  
Therapeutic Concepts ◽  
New Therapeutic Concepts ◽  
Coagulation And Fibrinolysis

SummaryWe report on a man (age: 49 years), who died from severe meningococcal sepsis with disseminated intravascular coagulation (DIC), multiple organ dysfunction syndrome and extended skin necrosis. We discuss in detail the pathophysiology of the activation of coagulation and fibrinolysis during sepsis. The article discusses new therapeutic concepts in the treatment of disseminated intravascular coagulation in meningococcal sepsis, too.

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