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PubMed1995

The modern version of adult respiratory distress syndrome.

Adult respiratory distress syndrome (ARDS) remains a highly lethal complication of autodestructive inflammation. This syndrome originally referred to a single organ failure but is now considered a component, usually the first, of the multisystem organ failure syndrome (MOFS). Cytokines, neutrophils, and endothelial adherence molecules initiate the disease process, with cell injury caused by oxidants and proteases released from inflammatory cells. ARDS, if progressive, will result in pulmonary fibrosis. Improved ventilatory support techniques have not been shown to decrease mortality. Pharmacologic manipulation of the inflammatory response is a more promising method of controlling the disease process.

Adult↗
PubMed1989

Proton nuclear magnetic resonance studies of plasma to determine metabolic status of patients with adult respiratory distress syndrome.

Adult respiratory distress syndrome (ARDS) is a non-cardiogenic pulmonary edema of various etiologies. Here we report the first application of proton nuclear magnetic resonance (NMR) for the detection of abnormal metabolites in plasma from patients with ARDS. By comparing plasma obtained from the systemic artery with that obtained from the pulmonary artery, we could study the metabolic status of the lung in patients with ARDS. Although their concentrations may vary, the peaks for acetate, acetoacetate, beta-hydroxybutyrate, phenylalanine, and other unidentified compounds in water-suppressed NMR of these patients' plasma were higher than in the normal controls. The proton NMR resonance at a chemical shift of about 7.4 ppm (relative to sodium tetradeutero-3-trimethyl-silylpropionate), presumably caused by phenylalanine and its related metabolites produced by a disordered amino acid metabolism, is detected in greater than 65% of the samples from ARDS patients. We discuss the detection of abnormal metabolites in terms of possible deranged metabolism of carbohydrates, lipids, or amino acids in this syndrome.

3-Hydroxybutyric Acid↗
PubMedDate not supplied

Defining adult respiratory distress syndrome.

Adult respiratory distress syndrome is a continuum of severe, evolving, diffuse lung injury, often complicated by multiorgan failure. Its pathophysiology is unclear and its treatment is empirical. It is diagnosed clinically using criteria that have no consensus and do not address underlying mechanisms.

Clinical Protocols↗
PubMed1997

Mechanical ventilation and adjuncts in acute respiratory distress syndrome.

Acute respiratory distress syndrome is a response of the lung to both direct and indirect insults. Although much knowledge has been gained in understanding the pathophysiology of the syndrome, overall mortality in the past 25 years remains unchanged. Application of scientific knowledge to present-day technology has yielded advances in ventilator and pharmacological support for the patient with ARDS. Emphasis is now made on the prevention of iatrogenic lung injury with the use of pressure-limited mechanical ventilation, permissive hypercapnia, and artificial means of gas exchange (discussed in the chapter by Dr Furukawa). The role of INO and surfactant, as well as antimediator therapy, in the armamentarium against ARDS appears promising but awaits definitive clinical trials. Only with progress and newer therapies will we be able to improve the outlook for patients and families in the future.

Administration, Inhalation↗
PubMed2004

Inflammation and the acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) is a clinical syndrome of non-cardiogenic pulmonary oedema associated with bilateral pulmonary infiltrates, stiff lungs and refractory hypoxaemia. ARDS is characterized by an explosive acute inflammatory response in the lung parenchyma, leading to alveolar oedema, decreased lung compliance and, ultimately, hypoxaemia. Although our understanding of the causes and pathophysiology of ARDS has increased, the mortality rate remains in the range of 30-50%. No major advances in pharmacological therapy have been achieved. Mechanical ventilation is the main therapeutic intervention in the management of ARDS. The only approach that has been shown to reduce the inflammatory response and mortality is the use of lung-protective ventilatory strategy with a low tidal volume and high positive-end expiratory pressure. This chapter will review the current state of the literature on the pathogenesis of ARDS and ventilatory and pharmacotherapy approaches to its management.

Acute Disease↗
PubMedDate not supplied

A surgeon's view of adult respiratory distress syndrome.

Adult respiratory distress syndrome (ARDS) is of interest to the cardiac surgeon because cardiopulmonary bypass has been considered to be both a cause and a treatment of ARDS. One simple resolution of this paradox is that neither belief can be supported on the available evidence. However, the position is not clear-cut.

Cardiopulmonary Bypass↗
PubMed2006

G protein-coupled receptor for asthma susceptibility associates with respiratory distress syndrome.

BACKGROUND: Respiratory distress syndrome (RDS) and bronchopulmonary dysplasia (BPD) have some common features with asthma. AIM: To study whether G protein-coupled receptor for asthma susceptibility (GPRA) contributes to RDS or BPD. METHODS: A haplotype association study was performed in a case-control setting of 521 Finnish infants (including 176 preterm neonates with RDS and 37 with BPD). Immunoreactivity of GPRA isoforms A and B was determined in pulmonary samples of fetuses, term infants and preterm infants with RDS or BPD. GPRA mRNA expression was determined by quantitative real-time polymerase chain reaction (PCR) in samples from nasal respiratory epithelium of adults, term infants and preterm infants. RESULTS: In infants with RDS born at 32-35 weeks of gestation, GPRA haplotype H1 was significantly underrepresented in RDS, whereas haplotype H4/H5 was associated with an increased risk. As in asthma, GPRA B isoform was induced in bronchial smooth muscle cells in RDS and BPD. In nasal respiratory epithelium, relative GPRA mRNA expression was strong in adults, weak in preterm and slightly higher in term samples. CONCLUSIONS: The results suggest that near-term RDS and asthma share the same susceptibility and protective GPRA haplotypes. Altered GPRA expression may play a role in the pathogenesis of RDS and BPD in preterm infants.

Adult↗
PubMed1997

Acute respiratory distress syndrome.

Acute Respiratory Distress Syndrome (ARDS) occurs in a wide range of adult and pediatric critical care settings. This article provides an overview of ARDS including the controversies in definition, a summary of pathophysiology, diagnosis, clinical presentation, and management options. The article also attempts to emphasize new management options in the management of ARDS, and highlights differences between adults and children.

Adrenal Cortex Hormones↗
PubMed2003

[Acute respiratory distress syndrome].

Acute respiratory distress syndrome (ARDS) - is a life-threatening acute clinical syndrome of pulmonary insufficiency with high mortality. The causes of the syndrome are of every description - from crustacean poisoning to cardiopulmonary bypass. The rate of ARDS is not clear, because of diagnostical variety of ARDS and acute pulmonary dysfunction. The discussion on ARDS diagnostical criteria lasted for many years. The clinical criteria depend on how the essence of the disease is understood, on the size of lung infiltration, lung compliance and failure as well as degree of hypoxemia. The risk of ARDS increases with the increase of number of predisposing factors. The investigation data depend mainly on used datum-point for diagnostics of ARDS. It is obvious that non-cardiogenic light pulmonary edema is found very often, and serious lung lesions are rare enough. The aim of nowadays treatment is to cure the disease that causes the syndrome and to sustain vital functions. The early diagnostics of ARDS predisposing factors and minimization of their influence, the prevention, early diagnostics and timely treatment of complications are essential. In many cases ARDS caused by collateral factors is the constituent of multiple organ dysfunction syndrome. Anyway the ARDS predisposed by direct factors is often complicated by other organ (cardiovascular, renal, hepatic, hematogenous, central nervous system, gastrointestinal tract, etc.) dysfunction. In this case the treatment becomes more difficult and includes therapy correcting the function of other systems. In spite of intensive treatment, mortality of this syndrome still remains 50-90% according to the literature data. Though some authors state that recently the ARDS mortality decreased, but most of the authors did not notice any improvement during the last 20 years. The prognosis is determinated not only by pulmonary insufficiency itself (the cause of death in 5% of patients), but by the ARDS predisposing factor (the worst is sepsis and septic shock), multiple organ dysfunction syndrome, difficult physical state of the patient, sepsis as a cause or as a complication of ARDS, nosocomial pneumonia, progressive fibroproliferation in the lung. Considering the actuality of ARDS, the diagnostical criteria of ARDS, pathogenesis, clinical course and new treatment methods are reviewed in the publication.

APACHE↗
PubMed2002

Angiotensin converting enzyme insertion/deletion polymorphism is associated with susceptibility and outcome in acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) is an often fatal condition for which a genetic predisposition is postulated, although no specific genes have been identified to date. Angiotensin converting enzyme (ACE) has a potential role in the pathogenesis of ARDS via effects on pulmonary vascular tone/permeability, epithelial cell survival, and fibroblast activation. Forty-seven percent of the variance in plasma ACE activity is accounted for by the ACE insertion/deletion (I/D) polymorphism, the D allele being associated with higher activity. We therefore hypothesized that the presence of the D allele would be associated with the development of ARDS. Ninety-six white patients fulfilling American/European Consensus Committee criteria for ARDS were genotyped for the ACE polymorphism together with individuals from three comparison groups: 88 white patients with non-ARDS respiratory failure ventilated in the intensive care unit (ICU), 174 ICU patients undergoing coronary artery bypass grafting, and 1,906 individuals from a general population group. DD genotype frequency was increased in the patients with ARDS compared with the ICU (p = 0.00008), coronary artery bypass grafting (p = 0.0009), and general population group (p = 0.00004) control groups and was significantly associated with mortality in the ARDS group (p < 0.02). These data suggest a potential role for renin-angiotensin systems in the pathogenesis of ARDS and for the first time implicate genetic factors in the development and progression of this syndrome.

Acute Disease↗
PubMed1993

Postinjury multiple organ failure: role of extrathoracic injury and sepsis in adult respiratory distress syndrome.

Adult respiratory distress syndrome (ARDS) and multiple organ failure (MOF) occur as a result of an unbridled systemic inflammatory response (i.e., severe systemic inflammatory response syndrome [SIRS]). Early epidemiologic studies concluded that infection with systemic sepsis was the common pathway for the development of ARDS and eventual MOF. As a consequence, research investigation from 1977 to 1987 focused on later clinical events (e.g., immunosuppression, persistent hypercatabolism, and bacterial translocation). Now, it is believed that an initial massive traumatic insult can create severe SIRS independent of infection (one-hit model). Alternatively, a less severe traumatic insult can create an inflammatory environment (i.e., primes the host) such that a later, otherwise innocuous, secondary inflammatory insult precipitates severe SIRS (two-hit model). As a result of these newer inflammatory models, research interest over the last 5 yrs has shifted to investigating earlier clinical events (e.g., unrecognized flow-dependent oxygen consumption, ischemia/reperfusion, and priming/activation of the inflammatory response). The traditional infection models of ARDS and MOF are applicable to current research and patient care efforts. However, the inflammatory models emphasize the pivotal role of the initial traumatic insult. Moreover, while ARDS occurs earlier than other types of overt organ failure, it is now believed that simultaneous organ injury is occurring, presumably via similar inflammatory mechanisms.

Adult↗
PubMed2003

The pathophysiology of acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) is a heterogeneous process that results in diffuse alveolar damage. It is associated with a variety of causative factors that can be grouped into two general categories, those associated with direct lung injury through the airways and those associated with indirect lung injury through the blood stream. Regardless of whether injury originates within or outside the lung, a systematic inflammatory response is triggered. This article reviews some of the physiologic alterations associated with ARDS before focusing on the derangement in the cellular environment.

Humans↗
PubMed1987

Trauma and pulmonary insufficiency: mediators and modulators of adult respiratory distress syndrome.

Adult respiratory distress syndrome is a complex disease resulting in lung dysfunction secondary to a primary nonpulmonary catastrophic event. Many mediators are involved in the destructive chain of events occurring at the cellular level. Investigation of ARDS continues, with efforts directed toward blocking those mediators and thereby alleviating the lung damage and hypoxia once this cascade has been initiated. Even with these advances, however, current optimal therapy is directed toward reversing the primary inciting event and providing the supportive care required to survive the acute episode.

Humans↗
PubMed1994

Typhoid fever associated with adult respiratory distress syndrome.

Adult respiratory distress syndrome (ARDS) is rarely reported in association with typhoid fever despite the fact that sepsis is a common manifestation and endotoxemia has been described in this multisystem condition. We describe the course of a patient with ARDS and typhoid fever. With conventional treatment of the lung injury and with specific antimicrobial therapy, the patient survived. Recent consensus definitions of sepsis and ARDS simplified reporting of this case. Clinicians caring for individuals from or recent visitors to developing countries should be aware of the association of typhoid fever, sepsis, and ARDS.

Adult↗
PubMed1993

Blood transfusion related adult respiratory distress syndrome.

Adult respiratory distress syndrome (ARDS) is a rare but important complication of blood transfusion because it has a mortality rate of 50-60%. ARDS is characterised by noncardiogenic pulmonary oedema and is often associated with major trauma and/or sepsis. Clinical features include dyspnoea, tachypnoea, chills and extensive crepitations. The pathogenesis has not been elucidated completely and a number of hypotheses have been proposed. Factors which have been implicated include neutrophil sequestration and complement activation, macrophages, metabolites of the arachidonic acid cascade and cytokines, all of which contribute to the amplification of the inflammatory process. In particular, leucoagglutinins have been implicated with blood transfusions. Treatment is generally supportive as specific therapeutic strategies remain largely unproven.

Adult↗
PubMed1994

Peritoneal ventilation: an animal model of extrapulmonary ventilation in experimental adult respiratory distress syndrome.

Adult respiratory distress syndrome (ARDS) is a critical medical problem in which severe arterial hypoxemia is often poorly responsive to conventional modes of mechanical ventilation. We studied the efficiency of mechanical ventilation of the peritoneal cavity in rabbits with experimental ARDS caused by lung lavage. The study shows that peritoneal ventilation is significantly effective in oxygenation of hypoxemic animals with ARDS and is also effective for carbon dioxide elimination. Peritoneal ventilation may be considered as an investigational method for extrapulmonary oxygenation in severe intractable hypoxemia caused by ARDS.

Animals↗
PubMed2005

Constitutive activation of prosurvival signaling in alveolar mesenchymal cells isolated from patients with nonresolving acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) is a clinical syndrome characterized by stereotypic host inflammatory and repair cellular responses; however, mechanisms regulating the resolution of ARDS are poorly understood. Here, we report the isolation and characterization of a novel population of mesenchymal cells from the alveolar space of ARDS patients via fiber-optic bronchoscopy with bronchoalveolar lavage (BAL). BAL was performed on 17 patients during the course of ARDS. Immunofluorescence staining and multiparameter flow cytometric analysis defined a population of alveolar mesenchymal cells (AMCs) that are CD45-/prolyl-4-hydroxylase+/alpha-smooth muscle actin+/-. AMCs proliferated in ex vivo cell culture for multiple passages; early passage (3-5) cells were subsequently analyzed in 13 patients. AMCs isolated from patients with persistent or nonresolving ARDS (ARDS-NR, n = 4) demonstrate enhanced constitutive activation of prosurvival signaling pathways involving PKB/Akt, FKHR, and BCL-2 family proteins compared with AMCs from patients with resolving ARDS (ARDS-R, n = 9). Exogenous transforming growth factor-beta1 markedly induces PKB/Akt activation in AMCs from ARDS-R. ARDS-NR cells are more resistant to serum deprivation-induced apoptosis compared with ARDS-R. This study identifies a novel population of mesenchymal cells that can be isolated from the alveolar spaces of ARDS patients. AMCs in patients with ARDS-NR acquire an activational profile characterized by enhanced prosurvival signaling and an antiapoptotic phenotype. These findings support the concept that apoptosis of mesenchymal cells may be an essential component of normal repair and resolution of ARDS and suggest that dysregulation of this process may contribute to persistent ARDS.

Actins↗