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PubMed1993

Expression of tumor necrosis factor-alpha gene in alveolar macrophages from patients with the adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) is a complex syndrome in which pathogenesis is multifactorial. TNF-alpha, known to be pivotal in tissue damage, has been shown to have high levels in blood and alveolar fluid in ARDS. The identification of the cells responsible for this production in the alveolar milieu has not yet been reported. In order to evaluate the TNF-alpha gene expression in ARDS we have analyzed by in situ hybridization, using RNA probes, alveolar macrophages (AM) obtained by BAL from seven patients with ARDS, eight patients with miscellaneous respiratory diseases, and three control patients. In freshly collected AM from patients with ARDS, 66 +/- 14.5% cells expressed the TNF-alpha gene without in vitro stimulation. This TNF-alpha expression does not result from the BAL procedure itself since only a few unstimulated control AM contained TNF-alpha mRNA transcripts. TNF-alpha expression in AM is not restricted to patients with ARDS since it has also been observed in miscellaneous respiratory diseases; however, this expression is a constant feature in ARDS. These results demonstrated the major role of AM in the intra-alveolar production of TNF-alpha, and they point out the necessity in ARDS for a specific intra-alveolar therapy.

Adult↗

PubMed1980

Adult respiratory distress syndrome in children.

Respiratory distress syndrome is the clinical manifestation of injury to the terminal alveolar-capillary unit, and may result from a variety of nonpulmonary insults including shock, sepsis, and trauma. The clinical characteristics, pathophysiology, and treatment of respiratory distress syndrome in children are reviewed.

Biological Transport↗

PubMed2002

Comparative randomized study: administration of natural and synthetic surfactant to premature newborns with respiratory distress syndrome.

BACKGROUND: The respiratory distress syndrome (RDS) in premature newborns has been etiologically correlated to immature lungs and specifically with surfactant deficiency. Exogenous administration of surfactant is nowadays considered to be the treatment of choice. In this paper we attempt a comparison of clinical results from the administration of natural Alveofact and synthetic Exosurf surfactants in premature newborns with respiratory distress syndrome. METHODS: The study subjects were 92 premature newborns who had been hospitalized in the Department of Neonatology, of the University of Crete. A total of 42 subjects received synthetic surfactant and 50 subjects received natural surfactant. The surfactant was administered in one to three doses, depending on respiratory support requirements. RESULTS: The time of administration was a little longer for the natural surfactant group. The duration of mechanical ventilatory support, requiring oxygen, the duration of hospitalization and the percentage of increase of arterial alveolar partial pressure oxygen ratio (a/APO2) were slightly higher for the synthetic surfactant group. The mortality rate during the neonatal period (28th day) was higher for the synthetic surfactant group than for the natural surfactant group (38.1 vs 24%). A similar tendency was noticed also as regards to complications, e.g. pneumothorax (11.2 vs 5.2%; relative risk (RR) 0.27) intraventricular hemorrhage (34.6 vs 21.1%; RR 0.61), septicemia (11.5 vs 5.2%; RR 0.46) and bronchopulmonary dysplasia (12.5 vs 2.8%; RR 0.22). CONCLUSION: The use of natural surfactant seems to offer more advantages in comparison with its synthetic counterpart.

Drug Combinations↗

PubMed1997

Acute respiratory distress syndrome in pregnancy.

Acute respiratory distress syndrome is a serious sequelae of many serious illnesses during pregnancy. An understanding of acute respiratory distress syndrome is central to the proper care of a patient with the disorder. Acute respiratory distress syndrome results in diminished pulmonary compliance and respiratory shunt mediated hypoxemia. Furthermore, the initial pulmonary injury in acute respiratory distress syndrome may be further worsened by therapeutic hyperoxia and barotrauma. Limitation of peak-plateau airway pressure to less than 35 to 40 cm H2O may reduce barotrauma. Inflammatory mediator therapy may hold future promise in attenuation of lung injury induced by acute respiratory distress syndrome. Aggressive care may help those pregnant patients afflicted with acute respiratory distress syndrome.

Female↗

PubMed1996

Pathogenesis and treatment of the adult respiratory distress syndrome.

The adult respiratory distress syndrome is an acute clinical illness characterized by noncardiogenic pulmonary edema and refractory hypoxemia. Injury to the alveolar-capillary barrier and lung inflammation lead to intrapulmonary shunting of blood, surfactant depletion, and pulmonary vascular obstruction. Numerous mediators contribute to the pathologic response. Conventional therapy includes treating underlying causes and positive pressure mechanical ventilation. Concern about pressure-induced lung injury had led to new strategies to accomplish adequate gas exchange. Novel therapeutic interventions have included extracorporeal support techniques, use of compounds designed to neutralize proinflammatory cytokines, and administration of surfactants, but these efforts have not definitely affected mortality in randomized trials. Potent antioxidant agents have shown promise in animal models of acute lung injury, but human studies are lacking. Inhaled nitric oxide appears to have temporary effects on pulmonary artery pressure and on ventilation or perfusion relationships, but longer-term efficacy and safety in patients suffering from adult respiratory distress syndrome is unknown and awaits results of ongoing clinical trials.

Adult↗

PubMed1995

Role of surfactant in the pathophysiology of the acute respiratory distress syndrome (ARDS).

Acute respiratory distress syndrome (ARDS) has become a well-recognized condition that can result from a number of different causes that lead to injury of the alveolar-capillary membrane. This results in high-permeability pulmonary oedema that disturbs the pulmonary surfactant system. In ARDS, the treatments available are still inadequate and morbidity, mortality, and costs remain unacceptably high. In the last 15 yrs, the morbidity and mortality rates of premature infants suffering from the respiratory distress syndrome (RDS) due to surfactant deficiency, have been reduced by exogenous surfactant therapy, and this treatment is now routinely used in most neonatal intensive care units. At this moment, only a few case reports and results of limited clinical pilot studies are available, in which patients with ARDS are treated with exogenous surfactant. Although the results from these studies are not consistent, the best results have been seen in patients treated with high concentrations or multiple doses of surfactant. It has been suggested that the increased permeability changes, along with the inflammatory response, lead to accumulation of plasma components in the alveolar space, causing inhibition of the instilled surfactant in a dose-dependent way. Thus, for treatment of ARDS, a high concentration of surfactant is required to overcome the inhibitory effect of plasma components. However, a few questions remain unanswered, including: When should surfactant treatment start? Which dosage? Of which type of surfactant? Which method of administration should be used, in combination with which type of ventilatory support, etc.?

Humans↗

PubMed2004

KL-6 levels are elevated in plasma from patients with acute respiratory distress syndrome.

The acute respiratory distress syndrome (ARDS) is an extreme form of lung injury characterised by disruption to the alveolar epithelium. KL-6 is a mucin-like glycoprotein expressed on type II pneumocytes. Circulating levels of KL-6 have diagnostic and prognostic significance in a number of interstitial lung diseases, and when elevated are thought to indicate disruption of the alveolar epithelial lining. In this study, the authors sought to determine whether plasma KL-6 levels were elevated in patients with ARDS and whether these were associated with aetiology, disease severity, outcome or ventilatory strategy. Plasma samples were collected from 28 patients with ARDS, nine ventilated controls of matched illness severity and 10 healthy individuals. KL-6 concentrations were measured by enzyme-linked immunosorbent assay. Patients with ARDS had higher plasma levels of KL-6 (median 537 U x mL(-1), interquartile range (IQR) 383-1,119), as compared to ventilated controls (median 255 U x mL(-1), IQR 83-338) and normal individuals (median 215 U x mL(-1), IQR 149-307). In patients with ARDS, plasma KL-6 levels were higher in nonsurvivors than survivors, and correlated positively with oxygenation index and negatively with arterial oxygen tension:inspiratory oxygen fraction ratio. There were also significant positive correlations with mean and peak airway pressures. Elevated levels of plasma KL-6 may provide a useful marker for acute respiratory distress syndrome in ventilated patients and have possible prognostic significance. Alveolar epithelial cell damage may be influenced by the nature of mechanical ventilatory support.

Adult↗

PubMed1999

Surfactant replacement therapy in RSV-induced acute respiratory distress syndrome (ARDS).

Acute respiratory distress syndrome (ARDS) associated with severe respiratory syncytial virus infection is rare. We report a 5-month-old Indian girl who was admitted to our intensive care ward with severe respiratory failure who fulfilled the criteria for ARDS using both Murray's Lung Injury Score of > 2.5 and the American-European Consensus Conference definition for ARDS. She developed diffuse bilateral alveolar infiltrates, severe hypoxaemia (PaO2/FiO2 < 100) and required high PEEP (> 15 cm H2O) 24 hours after admission. RSV was isolated from her nasopharyngeal secretion. She also had clinical features suggestive of a primary immunodeficiency and had laboratory evidence of combined T and B cell defect. There was unsustained clinical improvement with a dose of surfactant administered at 36 hours of PICU stay, and she continued to deteriorate and succumbed after 19 days in the PICU.

Fatal Outcome↗

PubMed2003

[Death risk factors of severe acute respiratory syndrome with acute respiratory distress syndrome].

OBJECTIVE: To discuss the possible death risk factors of severe acute respiratory syndrome (SARS) with acute respiratory distress syndrome (ARDS). METHODS: Twenty-five patients suffered from SARS with ARDS in the intensive care unit were retrospectively analyzed from December 2002 to April 2003. Statistical analysis was made using SPSS 10.0 and forward stepwise (wald) logistic regression analysis were used to determine the interrelationships between multiple variables and death. P<0.05 was considered statistically significant. RESULTS: The following factors were associated with a significantly higher mortality rate in the SARS with ARDS patients, including age increase (OR=1.203, CI=1.036 to 1.396, P=0.016), long-time hypoxia(OR=1.067, CI=1.014 to 1.122, P=0.013), thrombocytopenia(OR=111.932, CI=6.096 to 2 055.252, P=0.001), hypernatremia (OR=26.667, CI=2.242 to 317.147, P=0.009), and elevation of serum creatinine levels (OR=111.932, CI=6.096 to 2 055.252, P=0.001). CONCLUSION: More attention should be paid to deal with these risk factors and to prevent the development of serious complications associated with SARS.

Adult↗

PubMed1993

Late adult respiratory distress syndrome.

Late adult respiratory distress syndrome (ARDS) refers to the clinical stage of ARDS when the lung attempts to repair the initial or persistent injury to the endothelial and epithelial lining of the respiratory units. Histologically, it is characterized by the replacement of damaged epithelial cells and the striking accumulation of mesenchymal cells (fibroproliferative phase) and their connective tissue products in the air spaces and walls of the intra-acinar microvessels. Unfortunately, this reparative process is frequently ineffective, leading directly or indirectly to the patient's death. Its evolution appears to be determined by the extent of initial insult to the lung and by the presence of a protracted inflammatory response. Continuous injury may result from persistent release of inflammatory cytokines in the lung. In late ARDS, injury to the endothelial surface appears to be the pathogenic mechanism behind persistent bronchoalveolar lavage neutrophilia and diffuse pulmonary uptake of gallium. Ineffective repair is characterized by progressive proliferation of myofibroblast and deposition of collagen in the alveoli, thereby producing worsening gas exchange and lung mechanics. Prolonged mechanical ventilation predisposes the patient to the development of pulmonary and extrapulmonary infections. Moreover, release of inflammatory cytokines from the lung with fibroproliferation causes fever and leukocytosis, making clinical distinction from pulmonary or extrapulmonary infections difficult, if not impossible. Anecdotal reports suggest that corticosteroid treatment may accelerate recovery in late ARDS.

Adrenal Cortex Hormones↗

PubMed2002

Adenoviral transfer of HSP-70 into pulmonary epithelium ameliorates experimental acute respiratory distress syndrome.

The acute respiratory distress syndrome (ARDS) provokes three pathologic processes: unchecked inflammation, interstitial/alveolar protein accumulation, and destruction of pulmonary epithelial cells. The highly conserved heat shock protein HSP-70 can limit all three responses but is not appropriately expressed in the lungs after cecal ligation and double puncture (2CLP), a clinically relevant model of ARDS. We hypothesize that restoring expression of HSP-70 using adenovirus-mediated gene therapy will limit pulmonary pathology following 2CLP. We administered a vector containing the porcine HSP-70 cDNA driven by a CMV promoter (AdHSP) into the lungs of rats subjected to 2CLP or sham operation. Administration of AdHSP after either sham operation or 2CLP increased HSP-70 protein expression in lung tissue, as determined by immunohistochemistry and Western blot hybridization. Administration of AdHSP significantly attenuated interstitial and alveolar edema and protein exudation and dramatically decreased neutrophil accumulation, relative to a control adenovirus. CLP-associated mortality at 48 hours was reduced by half. Modulation of HSP-70 production reduces pathologic changes and may improve outcome in experimental ARDS.

Adenoviridae↗

PubMed2003

Update on pediatric acute respiratory distress syndrome.

Pediatric acute respiratory distress syndrome (ARDS) remains an important challenge for the intensive care clinician. ARDS, which can result from either direct lung injury or from a "downstream" inflammatory process, is manifested by profound hypoxemia and respiratory failure. The care of pediatric ARDS is based on a meticulous, multidisciplinary, intensive care team approach. This review discusses the changing definition of ARDS and available intensive care treatment modalities, including newer lung-protective mechanical ventilation strategies and adjunct therapies. The prognosis of children suffering pediatric ARDS is examined with a look toward areas of potential future intervention in this often deadly disease.

Acute Disease↗

PubMed2004

The epidemiology of posttraumatic adult respiratory distress syndrome.

BACKGROUND: Although adult respiratory distress syndrome is an important early complication of blunt trauma, the epidemiology and risk factors for its development remain poorly defined. The aims of this study were to determine the prevalence and demographics of this complication in a prospective cohort series of patients admitted to the hospital following injury. We also assessed the contribution of the severity and pattern of the injury to the risk of this complication developing. By identifying factors associated with the highest risk of the development of adult respiratory distress syndrome, we aimed to produce guidelines to facilitate earlier detection. METHODS: We prospectively studied 7192 patients admitted to a single university hospital, over an eight-year period, for treatment of a traumatic injury. With the exception of patients who had sustained a hip fracture or who had been discharged within seventy-two hours after admission, all patients who required hospital admission following trauma, were older than thirteen years of age, and were a resident within the catchment area were included in the analysis. The prevalence and demographics of posttraumatic adult respiratory distress syndrome were identified for patients who had sustained musculoskeletal, thoracic, abdominal, and head injuries, either in isolation or in combination. The relative risks of this condition developing were calculated according to the injury pattern. Multiple logistic regression analysis was performed to identify the most highly significant predictors of the development of adult respiratory distress syndrome. RESULTS: Adult respiratory distress syndrome developed in thirty-six (0.5%) of the patients. The prevalence was significantly higher among younger patients (p = 0.002), and 83% of the cases followed high-energy trauma. The prevalence of adult respiratory distress syndrome after isolated thoracic, head, abdominal, or extremity injury was <1%. Patients with injuries to two anatomical regions had a higher prevalence (up to 2.9%), and those with injuries to three anatomical regions had an even higher prevalence (up to 10.2%). Multiple logistic regression analysis showed the Injury Severity Score, the presence of a femoral fracture, the combination of abdominal and extremity injuries, and observations of compromised physiological function on admission each to be an independent predictor of the later development of adult respiratory distress syndrome. CONCLUSIONS: The prevalence of adult respiratory distress syndrome increases with injury severity and combinations of injuries to more than one anatomical region. We have been able to quantify the importance and relative risks associated with these injuries. The implications of our findings with regard to facilitating early detection of this complication are discussed.

Adolescent↗

PubMed1989

Adult respiratory distress syndrome.

The Adult Respiratory Distress Syndrome (ARDS) is a fulminant form of respiratory failure affecting many seriously ill patients. The early manifestations of ARDS are caused by increased permeability of the alveolo-capillary barrier leading to pulmonary edema, stiff lungs, and a large right-to-left intrapulmonary shunt. Polymorphonuclear leukocytes (PMNS) are involved in the pathogenesis of most ARDS, and multiple PMN mechanisms can effect pulmonary injury; interactions between PMN adherence, proteolytic enzyme release, and oxygen radical production are emphasized. ARDS therapy remains largely supportive and has had little impact on mortality. The complications of infection and multiorgan failure play important roles in determining ARDS outcome.

Adrenal Cortex Hormones↗

PubMed1986

Successful spontaneous vaginal delivery during mechanical ventilatory support for the adult respiratory distress syndrome.

The adult respiratory distress syndrome is a common cause of acute hypoxemic respiratory failure in the adult that is associated with a high mortality. There is a limited experience with managing this entity in the gravid patient. A case of successful management of mother and fetus through spontaneous delivery is presented, followed by a discussion of the principles of supportive therapy.

Adult↗

PubMed1984

The adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) is a common form of acute respiratory failure that has been increasingly reported as associated with a wide variety of medical conditions. Unlike other identifiable pathological events causing severe lung injury, it is now recognized that ARDS is not a single disease, but a complex interaction of pathophysiological events that result in diffuse injury to lung parenchyma. Only through a thorough understanding of ARDS pathophysiology, pathogenesis, and clinical course can medical intervention be instituted in a judicious and timely manner. This review article is intended to provide an overview of the suspected precipitating causes, discrete pathophysiologic changes, and monitorable clinical events associated with ARDS. With mortality from ARDS high, significant attention is being given to improving therapeutic intervention with such conventional measures as mechanical ventilation, positive end-expiratory pressure, and fluid management, along with corticosteroids and several new experimental pharmacologic approaches.

Adult↗

PubMed2000

[Pulmonary repair after adult respiratory distress syndrome].

The adult respiratory distress syndrome (ARDS) represents a particulary dangerous form of acute respiratory failure. The processes of reparation of the lungs start in the course of several hours following the acute pulmonary damage and ARDS. They imply: 1) lysis of intraalveolar fibrin, phagocytosis of the necrotic products and resorption of the edematous fluid from the alveolar lumen and the pulmonary interstitium. 2) reparation of the pneumocytes and the bronchiolar Clara cells. 3) reparation of the pulmonary interstitium (pulmonary fibrosis and sclerosis). These processes of reparation in the lung are modulated by cell adhesion molecules of the integrin group and a number of growth factors (PDGF, AMDGF, EGF, FGF, IGF-I). Apoptosis is the main factor that controls the correct outcome of the processes of pulmonary reparation.

Adult↗

PubMed1983

The adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) is an extreme form of noncardiogenic pulmonary edema associated with alveolar-capillary damage. Clinical features include acute respiratory distress, dyspnea and tachypnea, severe hypoxemia refractory to oxygen therapy, and diffuse bilateral pulmonary infiltrates. Any number of serious disorders can cause ARDS, but the processes leading to the alveolar permeability defect are not understood. Therefore, therapy remains nonspecific and supportive. Treatment includes positive end-expiratory pressure, careful fluid management, steroid therapy, and adequate nutrition. Unfortunately, even with the most sophisticated intensive care, the mortality of ARDS is still greater than 50%.

Adult↗