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PubMed1991

Adult respiratory distress syndrome.

The adult respiratory distress syndrome carries a mortality rate of 60-65% which has remained unchanged since its description more than 20 years ago. As our knowledge of the pathophysiology of ARDS improves, so does our ability to better define this disease entity. This is important since our therapy has been supportive with no change in outcome. The recent thinking is that ARDS is part of a multi-system disease process where there is activation of a total body inflammatory response. Identifying these inflammatory mediators and their role in the pathogenesis of ARDS may allow specific drugs to inhibit or modulate their release and action and hopefully alter the course of the disease. New therapeutic options, like exogenous surfactant, are emerging and undergoing clinical trails. Till a cure for ARDS is proven effective, prevention and support are our only current therapeutic options in battling ARDS.

Humans↗

PubMedDate not supplied

Plasma thrombomodulin levels in early respiratory distress syndrome.

Infants with respiratory distress syndrome (RDS) undergo hemodynamic alterations in both the pulmonary and systemic vascular beds that predispose these infants to microvascular damage. In addition, disseminated intravascular coagulation (DIC) is frequently encountered in preterm infants with advanced RDS. In preterm infants with RDS, the plasma status is not known. Therefore, we studied plasma thrombomodulin levels in 25 preterm infants who did or did not develop RDS within the first few hours of life. The mean plasma thrombomodulin levels were found to be similar in the two groups (8.12 +/- 10.20 ng/ml vs. 18.30 +/- 22.77 ng/ml, respectively, p > 0.05 by Mann-Whitney U Test). It seems that plasma thrombomodulin levels are normal in the earlier stages of RDS before the occurrence of severe vascular damage and DIC due to hypoxemia.

Birth Weight↗

PubMed2002

Role of the neutrophil in septic shock and the adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) is a serious complication of many medical and surgical conditions, most of which do not involve direct pulmonary injury. In surgical practice, septic shock has long been recognised as an important cause of ARDS and it presents many management challenges. Endotoxin released from dead and dying Gram-negative bacteria induces a generalised inflammatory response that results in multiple organ dysfunction, the lung being just one target of this injurious process. In recent years, with the discovery of several key inflammatory mediators, many aspects of this complex condition have been elucidated. The neutrophil has emerged as the central effector cell and possesses a formidable armamentarium of cytokines, enzymes, and oxygen radicals that are capable of inflicting damage to cells. In this review I examine the mechanisms underlying the recruitment and activation of neutrophils in ARDS.

Adult↗

PubMed1989

Roles of the neutrophil and other mediators in adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) and transfusion-related acute lung injury (TRALI) are characterized by diffuse, acute lung injury. Most likely, TRALI is a type of ARDS although it is associated with a much lower morbidity and mortality than found with classic ARDS. For years, the pathogenesis of ARDS has been explained by the complement hypothesis in which pulmonary neutrophilic sequestration and degranulation follow complement-mediated neutrophil chemotaxis. A definitive role for the neutrophil in diffuse, acute lung injury, however, has not been established. Although numerous chemoattractants for neutrophils are generated in the lungs and, through degranulation and formation of toxic oxygen free radicals, the neutrophil is fully capable of causing tissue injury, substantial evidence refutes the requirement for neutrophils in diffuse, acute lung injury. Other potential factors in the pathogenesis of ARDS include primary endothelial cell injury, alveolar macrophage activity, and hemostatic disorders.

Chemotaxis, Leukocyte↗

PubMed2003

Bench-to-bedside review: beta2-Agonists and the acute respiratory distress syndrome.

The acute respiratory distress syndrome (ARDS) is a devastating constellation of clinical, radiological and pathological signs characterized by failure of gas exchange and refractory hypoxia. Despite nearly 30 years of research, no specific pharmacological therapy has yet proven to be efficacious in manipulating the pathophysiological processes that underlie this condition. Several in vitro and in vivo animal or human studies suggest a potential role for beta2-agonists in the treatment of ARDS. These agents have been shown to reduce pulmonary neutrophil sequestration and activation, accelerate alveolar fluid clearance, enhance surfactant secretion, and modulate the inflammatory and coagulation cascades. They are also used widely in clinical practice and are well tolerated in critically ill patients. The present review examines the evidence supporting a role for beta2-agonists as a specific pharmacological intervention in patients with ARDS.

Adrenergic beta-2 Receptor Agonists↗

PubMed1993

Oxidized glutathione is increased in the alveolar fluid of patients with the adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) is a devastating clinical illness characterized by refractory hypoxemia and high-permeability pulmonary edema. Reactive oxygen species may play a key role in the pathogenesis of the acute lung injury. Glutathione is a tripeptide that is able to react with and effectively neutralize oxidants, such as hydrogen peroxide. The present study found that the alveolar epithelial lining fluid of patients with ARDS was deficient in total glutathione compared with that of normal subjects (31.5 +/- 8.4 versus 651.0 +/- 103.1 microM, p = 0.0001) and patients with cardiogenic pulmonary edema (31.5 +/- 8.4 versus 154.1 +/- 52.4 microM, p = 0.001). In addition, a greater percentage of total glutathione was in the oxidized form in patients with ARDS compared with normal subjects (30.6 +/- 6.1 versus 6.4 +/- 2.9%, p = 0.03). This deficiency of reduced glutathione in the alveolar fluid may predispose these patients to enhanced lung cell injury.

Adult↗

PubMed1999

Corticosteroid rescue in late paediatric acute respiratory distress syndrome.

Late acute respiratory distress syndrome (ARDS) is associated with a mortality of more than 80%. Recent reports in adults have shown improved survival in late ARDS treated with prolonged course of steroids, however little data are available in children concerning its safety and efficacy. We report the successful treatment of a child dying from refractory late ARDS using a prolonged course of high-dose methylprednisolone instituted after 12 days of advanced mechanical ventilation. Progressive improvement was seen from days 3, 7, 10 and 14 after treatment with improvement in PaO2/fraction of inspired oxygen (FiO2) ratios, lung injury score and chest radiographical score. Treatment was complicated by a fungal urinary tract infection that was easily controlled. There were no major metabolic side effects. Steroid therapy can be considered in the treatment of children with refractory late ARDS but larger prospective studies are needed to define indications, timing, dosing and safety of this mode of treatment in children.

Glucocorticoids↗

PubMed1998

The American-European Consensus Conference on ARDS, part 2: Ventilatory, pharmacologic, supportive therapy, study design strategies, and issues related to recovery and remodeling. Acute respiratory distress syndrome.

The acute respiratory distress syndrome (ARDS) continues as a contributor to the morbidity and mortality of patients in intensive care units throughout the world, imparting tremendous human and financial costs. During the last 10 years there has been a decline in ARDS mortality without a clear explanation. The American-European Consensus Committee on ARDS was formed to re-evaluate the standards for the ICU care of patients with acute lung injury (ALI), with regard to ventilatory strategies, the more promising pharmacologic agents, and the definition and quantification of pathologic features of ALI that require resolution. It was felt that the definition of strategies for the clinical design and coordination of studies between centers and continents was becoming increasingly important to facilitate the study of various new therapies for ARDS.

Europe↗

PubMedDate not supplied

[Effects on the pulmonary function after single dose of exogenous pulmonary surfactant in children with acute respiratory distress syndrome].

The Acute Respiratory Distress Syndrome (ARDS) is a pulmonary lesion of multifactorial cause in which the surfactant system is altered owing to inactivation and impairment of composition and metabolism. The use of exogenous pulmonary surfactant is a therapeutic option with the objective to maintain alveolar stability thus improving the pulmonary compliance (increasing the residual functional capacity), oxygenation and ventilatory mechanics. A study carried out on two pediatric patients with ARDS submitted to mechanic pulmonary ventilation, applying a single dose of exogenous pulmonary surfactant is described. The patients were evaluated using arterial and venous gasometry before and after the use of surfactant, observing increment in oxygenation, reduction of shunt fraction, improvement in ventilation immediately after exogenous pulmonary surfactant instillation and return to the previous situation after 240 minutes in case 1 and 120 minutes in case 2. More prospective clinical and randomized studies are needed to effectively evaluate this therapeutic modality.

Acute Disease↗

PubMed2001

Surfactant alteration and replacement in acute respiratory distress syndrome.

The acute respiratory distress syndrome (ARDS) is a frequent, life-threatening disease in which a marked increase in alveolar surface tension has been repeatedly observed. It is caused by factors including a lack of surface-active compounds, changes in the phospholipid, fatty acid, neutral lipid, and surfactant apoprotein composition, imbalance of the extracellular surfactant subtype distribution, inhibition of surfactant function by plasma protein leakage, incorporation of surfactant phospholipids and apoproteins into polymerizing fibrin, and damage/inhibition of surfactant compounds by inflammatory mediators. There is now good evidence that these surfactant abnormalities promote alveolar instability and collapse and, consequently, loss of compliance and the profound gas exchange abnormalities seen in ARDS. An acute improvement of gas exchange properties together with a far-reaching restoration of surfactant properties was encountered in recently performed pilot studies. Here we summarize what is known about the kind and severity of surfactant changes occurring in ARDS, the contribution of these changes to lung failure, and the role of surfactant administration for therapy of ARDS.

Animals↗

PubMed1990

Right ventricular performance in adult respiratory distress syndrome.

In adult respiratory distress syndrome (ARDS), the pulmonary artery hypertension is followed by increases in right ventricular diastolic and systolic volumes and a decreased ejection fraction. The stroke volume is preserved by the Frank-Starling mechanism as preload increases, even in the presence of severe pulmonary artery hypertension. In contrast, if there coexists a depression of the right ventricle contractility, as during right ventricular contusion, septic shock or a viral myocarditis, the compensatory Frank-Starling mechanism, that maintains right ventricular pump function, seems limited. Thus, it appears that the contractile state of the right ventricle can influence the clinical course of ARDS. In addition, patients with ARDS require mechanical ventilation with positive end-expiratory pressure (PEEP), which has a detrimental effect on right ventricular loading conditions. Most investigators agree that the most important effect is a decreased right ventricular preload, secondary to the increased pleural pressure due to PEEP. However, in patients with severe pulmonary artery hypertension, the PEEP-induced increase in right ventricular afterload may become more preponderant, and inotropic support to maintain right ventricular stroke volume may be necessary.

Humans↗

PubMed1990

Potential of N-acetylcysteine as treatment for the adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS), often referred to as non-cardiac pulmonary oedema, is now regarded as a very complicated inflammatory process with oedema being only one facet. In recognition of this, pharmacologic therapy with anti-inflammatory corticosteroids was used widely until the completion of randomized clinical trials. Unfortunately, corticosteroids have not been proved to be useful in preventing ARDS in septic patients nor in patients with established ARDS and this has led to investigations with pharmacologic agents which are safer and more specifically targeted to certain parts of the inflammatory process. We have examined the role of the glutathione anti-oxidant system in the sheep model of ARDS as well as in patients with established ARDS through use of intravenous N-acetylcysteine (NAC). We have found that the response to endotoxin is markedly blunted in sheep treated with NAC. In our controlled clinical trials with NAC we found that patients with ARDS have depressed plasma and red cell glutathione concentrations, that these levels are substantially increased by therapy with intravenous NAC and there are measurable clinical responses to treatment with regard to increased oxygen delivery, improved lung compliance and resolution of pulmonary oedema.

Acetylcysteine↗

PubMed1991

Deficiency of alveolar fluid glutathione in patients with sepsis and the adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) is a devastating clinical illness characterized by refractory hypoxemia and high-permeability pulmonary edema. Reactive oxygen species such as hydrogen peroxide and hypochlorous acid may play a key role in the pathogenesis of the acute lung injury. Glutathione (GSH) is a tripeptide that is able to react with and effectively neutralize oxidants such as hydrogen peroxide and hypochlorous acid. The present study found that the alveolar epithelial lining fluid of patients with ARDS was deficient in total GSH compared to normal subjects (21.7 mumols +/- 7.8 mumols vs 91.8 mumols +/- 14.5 mumols; p = 0.002). In addition, if GSH was measured in unconcentrated bronchoalveolar lavage (BAL) fluid and indexed to total BAL protein, there was also a deficiency in patients with ARDS compared to normal subjects (0.004 +/- 0.003 nmol of GSH per microgram of total protein vs 0.026 +/- 0.005 nmol of GSH per microgram of total protein; p = 0.002). Since patients with ARDS are subjected to an increased burden of oxidants in the alveolar fluid, principally released by recruited neutrophils, this deficiency of GSH may predispose these patients to enhanced lung cell injury.

Adult↗

PubMed1990

Functional loss of chemotactic factor inactivator in the adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) is often characterized by a neutrophilic alveolitis, which may be mediated in part by the neutrophil chemoattractant, C5a. Chemotactic factor inactivator (CFI) can decrease C5a-directed neutrophil chemotaxis. Thus, a loss of CFI activity in the ARDS lung could lead to an increased ability of C5a to attract neutrophils. Lung CFI levels were measured antigenically and functionally in bronchoalveolar lavage (BAL) fluid obtained from 29 patients with ARDS and in 14 normal control subjects. Antigenic levels of CFI were found to be markedly elevated in ARDS BAL fluid (1,855 +/- 437 ng/ml) compared with that in normal BAL (29 +/- 10 ng/ml, p less than 0.005), but, in contrast, CFI functional activity was markedly decreased in ARDS BAL fluid compared with that in normal BAL fluid (31 +/- 7% inhibition versus 76 +/- 5% inhibition, p less than 0.01). Furthermore, although purified CFI readily inhibited the ability of C5a to attract neutrophils (92% inhibition), this activity was decreased when BAL fluid from patients with ARDS was incubated with CFI (47 +/- 10%, p less than 0.01). These findings suggest that patients with ARDS are functionally deficient in CFI, leading to an increased ability of C5a to attract neutrophils.

Aminopeptidases↗

PubMedDate not supplied

Videodensitometry and chest radiography in the evaluation of pulmonary blood flow and pulmonary oedema in a porcine model of early adult respiratory distress syndrome.

The adult respiratory distress syndrome was induced in pigs (n = 11) by a continuous infusion of E. coli endotoxin in order to evaluate the use of radiographic videodensitometry and chest radiography for assessment of pulmonary circulation and pulmonary oedema. A further aim was to determine the effect of an ionic contrast medium, Urografin 60%, on extravascular lung water (EVLW). The infusion resulted in a decline in arterial oxygen tension. Mean pulmonary arterial pressure increased, and cardiac output decreased, resulting in a marked rise in pulmonary vascular resistance. EVLW increased moderately. The corresponding variables in control animals (saline infusion; n = 5) changed very little. Good correlations were found (r = 0.87-1.0) between absolute flows as measured by the thermodilution technique and relative flows as determined by videodensitometry in animals with pulmonary damage. In the endotoxin group there was a significant correlation (r = 0.75) between the change in EVLW from baseline to the final measurement (at 6 hours) and the corresponding change in radiographic density. Radiographic signs of pulmonary damage were sparse. Only 3 of 11 animals displayed increased radiographic density of the lung parenchyma indicative of pulmonary oedema. Pleural effusion developed in 4 animals. Injection of Urografin 60%, 1 ml X kg-1, caused a slight but significant decrease in EVLW. We propose that at this concentration and dosage the contrast medium acts mainly as an osmotic diuretic.

Absorptiometry, Photon↗

PubMed1980

Role of complement activation in a model of adult respiratory distress syndrome.

The adult respiratory distress syndrome is characterized by arterial hypoxemia as a result of increased alveolar capillary permeability to serum proteins in the setting of normal capillary hydrostatic pressures. Because bacterial sepsis is prominent among the various diverse conditions associated with altered alveolar capillary permeability, we studied the effect of bacteremia with attendant complement activation on the sequestration of microorganisms and the leakage of albumin in the lungs of guinea pigs. Pneumococci were injected intravenously into guinea pigs and their localization was studied. Unlike normal guinea pigs, complement-depleted guinea pigs did not localize injected bacteria to the lungs. Preopsonization of organisms did not correct this defect in pulmonary localization of bacteria in complement-depleted animals, suggesting that a fluid-phase component of complement activation was required. Genetically C5-deficient mice showed no pulmonary localization of bacteria. C5-sufficient mice demonstrated the usual pulmonary localization, thus further suggesting that the activation of C5 might be important in this localization. The infusion of activated C5 increased alveolar capillary permeability to serum proteins as assayed by the amount of radioactive albumin sequestered in the lung. Neutropenic animals did not develop altered capillary permeability after challenge with activated C5. Thus, complement activation through C5, in the presence of neutrophils, induces alterations in pulmonary alveolar capillary permeability and causes localization of bacteria to the pulmonary parenchyma. Complement activation in other disease states could potentially result in similar clinical manifestations.

Capillary Permeability↗

PubMed1998

Interleukin 10 inhibits alveolar macrophage production of inflammatory mediators involved in adult respiratory distress syndrome.

BACKGROUND: Adult respiratory distress syndrome (ARDS) causes severe morbidity and mortality in trauma patients. One potential method to attenuate the lung injury is to inhibit alveolar macrophage production of proinflammatory mediators. The purpose of this study was to investigate the cellular mechanism of interleukin 10 (IL-10) inhibition on LPS-stimulated macrophage (Mphi). We hypothesized that IL-10 inhibited phospholipase C signal pathways in Mphi. IL-10 inhibition would be restored by calcium ionophores and protein kinase C (PKC) activation. METHODS: Rabbit alveolar Mphi were obtained by bronchoalveolar lavage. Mphi were treated with Escherichia coli LPS (10 ng/ml) in the presence of various concentrations of human IL-10. Cell lysates and supernatant were analyzed for proagulants (PCA) and tumor necrosis factor (TNF), respectively. TNF mRNA expression of alveolar Mphi was also measured by Northern Blot assay. Macrophage PGE2 production was measured by ELISA. RESULTS: IL-10 inhibited the production of both TNF and PCA by LPS-stimulated Mphi. In addition, IL-10 also reduced TNF mRNA expression. Similarly, PGE2 production by LPS-stimulated Mphi was also attenuated by IL-10. An increase in the intracellular [Ca2+] induced by A23187 failed to reverse this IL-10-mediated inhibition. In comparison, phorbol myristate acetate, a protein kinase C (PKC) activator, restored TNF and PCA production despite the presence of IL-10. CONCLUSIONS: IL-10 inhibits Mphi production of inflammatory mediators. This inhibition is, at least in part, mediated by modulating the PKC activity.

Animals↗

PubMed1989

The incidence of the adult respiratory distress syndrome.

Although adult respiratory distress syndrome (ARDS) has been a recognized entity for over 20 years, estimates of its incidence have been very controversial. The most quoted figure is from a 1972 National Heart and Lung Institute Task Force, which estimated 150,000 cases/year in the United States, an incidence of about 75 cases/100,000 population. No experimental study, however, has adequately addressed this issue. We were in a unique position to answer this controversy because the hospital of one of the investigators is located on an island (Las Palmas, Canary Islands, population 700,000). All patients who required mechanical ventilation (other than during anesthesia and immediate postoperative care) were admitted to the same adult intensive care unit. A prospective study to determine the incidence of ARDS was carried out over a 3-yr period. Inclusion criteria were: (1) a known predisposing illness for ARDS; (2) PaO2 less than or equal to 55 mm Hg with FIO2 greater than 0.5 with 5 cm H2O PEEP, without improvement in 24 h; (3) bilateral pulmonary infiltrates; (4) no evidence of left ventricular failure. An average of ten patients per year, representing an incidence of 1.5 cases/100,000 population, were diagnosed as having ARDS and the mortality rate was 70%. Using a more liberal clinical criterion of PaO2 less than or equal to 75 mm Hg with FIO2 greater than or equal to 0.5, 44 more patients with ARDS, representing a total incidence of 3.5 cases/100,000 population, were identified. In conclusion, the overall incidence of ARDS was 1.5 to 3.5 cases/100,000 population, an incidence that is much lower than most previously published estimates.

Adult↗