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PubMed1993

In vitro effects of pentoxifylline on smooth muscle cell migration and blood monocyte production of chemotactic activity for smooth muscle cells: potential therapeutic benefit in the adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) is a severe lung condition characterized by an acute lung injury leading to a massive intra-alveolar fibrosis with rapid lung failure. ARDS intra-alveolar fibrosis results from the migration of mesenchymal cells (mainly smooth muscle cells [SMC]) into the alveoli through alveolar epithelial basement membrane gaps resulting from the injury. SMC migration is followed by their replication and production of extracellular matrix, which leads to fibrosis. Thus, any pharmacologic agent able to prevent SMC migration should prevent, at least in part, intra-alveolar fibrosis. SMC migration is thought to be due to the presence, in the alveolar spaces, of chemotactic factors for mesenchymal cells, such as fibronectin and platelet-derived growth factor (PDGF). The local presence of these chemotactic factors can be due to plasmatic leakage, platelet degranulation, and mononuclear phagocyte activation. Pentoxifylline is a methylxanthine interacting with the biology of several types of cells, including red blood cells, neutrophils, blood monocytes, and endothelial cells. Pentoxifylline prescription has been suggested in ARDS with respect to its activity on neutrophils, its inhibition of tumor necrosis factor-alpha (TNF) release by mononuclear phagocytes, and its prevention of TNF-induced lung injury. Since pentoxifylline can modulate the migration of several cell types, we hypothesized that it could interfere with mesenchymal cell migration. SMC migratory response was measured in vitro with modified Boyden chemotactic chambers in the presence of PDGF, fibronectin, "platelet extract," and activated blood monocyte supernatants. Pentoxifylline, at therapeutic levels, significantly reduced SMC migration in response to the presence of these chemotactic activities.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Platelets↗
PubMed1999

Damage to surfactant-specific protein in acute respiratory distress syndrome.

BACKGROUND: Acute respiratory distress syndrome (ARDS) develops in association with many serious medical disorders. Mortality is at least 40%, and there is no specific therapy. A massive influx of activated neutrophils, which damage pulmonary vascular endothelium and alveolar epithelium, leads to alveolar oedema and pulmonary surfactant dysfunction. In-vitro studies show that neutrophil elastase can cleave surfactant-specific proteins and impair surfactant function. If this happens in vivo in ARDS, the response to surfactant therapy will be limited. METHODS: Samples of pulmonary surfactant were obtained from the lungs of 18 patients with ARDS and six healthy controls by bronchoalveolar lavage. We separated proteins in these samples according to molecular weight by sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE). We then used western blotting with monoclonal antibody E8 to detect the major surfactant-specific protein A (SP-A). FINDINGS: By contrast with controls, 14 of 18 patients had evidence of in-vivo damage to SP-A that resembled damage caused to SP-A when it is cleaved by neutrophil elastase. Controls showed a single band of normal dimers at 66 kDa, whereas 14 of 18 patients showed multiple bands at 66 kDa, 55 kDA, and 30-36 kDa, and six showed additional bands at 36-40 kDa. INTERPRETATION: Direct damage to surfactant-specific proteins occurs in lungs of patients with ARDS, probably by proteolysis. Trials of protein-containing therapeutic surfactant are in progress in ARDS, and our results indicate that the frequent failure to maintain response may result from continuing damage to surfactant by products of activated neutrophils. A combination of surfactant and antiprotease therapy may improve therapeutic prospects.

Adolescent↗
PubMed2006

Open lung biopsy in early-stage acute respiratory distress syndrome.

INTRODUCTION: Acute respiratory distress syndrome (ARDS) has heterogeneous etiologies, rapid progressive change and a high mortality rate. To improve the outcome of ARDS, accurate diagnosis is essential to the application of effective early treatment. The present study investigated the clinical effects and safety of open lung biopsy (OLB) in patients with early-stage ARDS of suspected non-infectious origin. METHODS: We undertook a retrospective study of 41 patients with early-stage ARDS (defined as one week or less after intubation) who underwent OLB in two medical intensive care units of a tertiary care hospital from 1999 to 2005. Data analyzed included baseline characteristics, complication rate, pathological diagnoses, treatment alterations, and hospital survival. RESULTS: The age of patients was 55 +/- 17 years (mean +/- SD). The average ratio of arterial partial pressure of oxygen (PaO2) to fraction of inspired oxygen (FiO2) was 116 +/- 43 mmHg (mean +/- SD) at biopsy. Seventeen patients (41%) were immunocompromised. Postoperative complications occurred in 20% of patients (8/41). All biopsies provided a pathological diagnosis with a diagnostic yield of 100%. Specific pathological diagnoses were made for 44% of patients (18/41). Biopsy findings led to an alteration of treatment modality in 73% of patients (30/41). The treatment alteration rate was higher in patients with nonspecific diagnoses than in patients with specific diagnoses (p = 0.0024). Overall mortality was 50% (21/41) and was not influenced by age, gender, pre-OLB oxygenation, complication rate, pathological results, and alteration of treatment. There was no surgery-related mortality. The survival rate for immunocompromised patients was better than that for immunocompetent patients (71% versus 33%; p = 0.0187) in this study. CONCLUSION: Our retrospective study suggests that OLB was a useful and acceptably safe diagnostic procedure in some selected patients with early-stage ARDS.

Adult↗
PubMed1998

Elevated transforming growth factor-alpha levels in bronchoalveolar lavage fluid of patients with acute respiratory distress syndrome.

The acute respiratory distress syndrome (ARDS) frequently results in a fibroproliferative response that precludes effective alveolar repair. Transforming growth factor-alpha (TGF-alpha), a potent epithelial and mesenchymal cell mitogen, may modulate the response to lung injury. In this study, we determined whether bronchoalveolar lavage fluid (BALF) concentrations of TGF-alpha are increased during the first 2 wk after the onset of ARDS and, if so, whether increased TGF-alpha levels in lavage fluid are associated with increased levels of procollagen peptide III (PCP III), a biological marker of fibroproliferation, and with increased fatality rates. We enrolled 74 consecutive patients with ARDS prospectively identified on admission to the intensive care unit of a tertiary care hospital, and 11 patients with chronic interstitial lung disease. Thirteen healthy volunteers served as control subjects. TGF-alpha concentrations were measured in BALF recovered on Days 3, 7, and 14 after the onset of ARDS (total of 130 lavage samples). TGF-alpha was detected in the lavage fluid of 90% of patients with ARDS (67 of 74), and in 100% of patients with idiopathic pulmonary fibrosis (IPF) (10 of 10), but in none of 13 normal volunteers. At each day tested, the median lavage TGF-alpha level of patients with ARDS was significantly higher than that of normals. The overall fatality rate was 45% (33 of 74 patients). In a univariate analysis, the median TGF-alpha levels in nonsurvivors were 1.5-fold higher at Day 7 (p = 0.06) and 1.8-fold higher at Day 14 (p = 0.048). The fatality rate was 4 times higher (CI 1.6, 17.5) for patients with both increased lavage TGF-alpha and PCP III concentrations at Day 7 than for patients with low TGF-alpha and PCP III values, indicating a synergistic relationship between TGF-alpha and PCP III. We conclude that increased levels of TGF-alpha in BALF are common in patients with ARDS and that lavage TGF-alpha is associated with a marker of the fibroproliferative response in sustained ARDS.

Adolescent↗
PubMed2026

Rare genetic variant risks in patients with sepsis-associated acute respiratory distress syndrome.

BACKGROUND: Acute respiratory distress syndrome (ARDS) is a complex, heterogeneous, and deadly condition often resulting from pulmonary lesions due to sepsis, among other causes. There is a lack of targeted therapies to specifically treat the patients. Common genetic factors in the population (frequency&#x2009;>&#x2009;1%) have been associated with ARDS susceptibility, but systematic genetic screens of the role of rare genetic variants are lacking. We used the network of known molecular interactions to identify ARDS risks from clusters of biologically related genes containing qualifying variants (QVs) with frequency&#x2009;<&#x2009;1% likely affecting function. METHODS: We conducted whole-exome sequencing in sepsis patients from the GEN-SEP cohort (n&#x2009;=&#x2009;822, of which 272 developed ARDS). A network-based heterogeneity clustering algorithm was used to discover significant gene clusters (p&#x2009;<&#x2009;1&#x2009;&#xd7;&#x2009;10&#x2013;5). Gene-set enrichment analysis and logistic regression models aggregating QVs were used for cross-verification to confirm consistency and deepen understanding of the effect sizes of gene clusters. RESULTS: We identified 19 significant clusters (plowest&#x2009;=&#x2009;3.29&#x2009;&#xd7;&#x2009;10&#x2013;10), each containing an average of 102 genes (11.6% mean similarity). QVs in nine gene clusters were associated with sepsis-associated ARDS (plowest&#x2009;=&#x2009;1&#x2009;&#xd7;&#x2009;10&#x2013;5) but were not associated with 28-day survival. Clusters were enriched in several biological pathways, notably the Toll-like receptor cascades. CONCLUSIONS: These results support a marked genetic heterogeneity underlying ARDS susceptibility and the presence of rare risk variants involving multiple biological processes that are associated with sepsis outcomes. Particularly, they underscore the importance of rare variants in genes of the Toll-like receptor cascades in the risk for sepsis-associated ARDS.

Humans↗
PubMed2000

Inhibition of p38 mitogen activate kinase attenuates the severity of pancreatitis-induced adult respiratory distress syndrome.

OBJECTIVE: Adult respiratory distress syndrome (ARDS) is responsible for a significant portion of the morbidity and mortality during severe acute pancreatitis. Because inflammatory mediators such as tumor necrosis factor (TNF)-alpha and nitric oxide (NO) produced within the lungs have been implicated in sepsis-induced ARDS, we aimed to determine the role of these mediators in pancreatitis-induced ARDS using a model whereby ascites from animals with pancreatitis is transferred to otherwise healthy animals resulting in pulmonary injury. DESIGN: Prospective, randomized, controlled trial. SETTING: Research laboratory at a university medical school. SUBJECTS: Pathogen-free Sprague-Dawley rats weighing 225-250 g. INTERVENTIONS: Sterile, endotoxin- and cytokine-free pancreatic ascites tested for interleukin (IL)-1beta , TNF-alpha, interferon-gamma, and IL-6 was obtained from rats 18 hrs after the induction of severe, acute pancreatitis. Ascites was subsequently administered intravenously (20 mL/kg) to healthy rats. Sham animals were administered intravenous saline. Healthy animals administered intravenous ascites were randomized to receive a single intraperitoneal injection of the p38 mitogen activated kinase inhibitor CNI-1493 (1 mg/kg) or vehicle. MEASUREMENTS: Pulmonary injury was assessed at 24 hrs by histology and leukocyte and protein concentrations via bronchoalveolar lavage. Pulmonary TNF-alpha protein was detected by immunohistochemistry. Serum nitrite, as a measure of NO production, was measured utilizing the Griess reaction. MAIN RESULTS: After the intravenous administration of pancreatic ascites, the number of leukocytes and the protein concentration within the bronchoalveolar fluid were increased and pulmonary histology was worsened consistent with acute lung injury (all p < .001 vs. sham). Each of these variables of pulmonary injury was lessened in animals receiving CNI-1493 and intravenous ascites (p < .05 vs. vehicle). Pulmonary TNF-alpha protein and serum nitrites were decreased with the administration of CNI-1493 (p < .005 vs. vehicle). CONCLUSIONS: A component of pancreatic ascites other than endotoxin, bacteria, or cytokines (IL-1beta, TNF, interferon-gamma, or IL-6) is capable of inducing ARDS in healthy animals. Inhibition of p38 mitogen activated kinase decreases the pulmonary injury through attenuated production of TNF-alpha and NO suggesting a primary role for these mediators in pancreatitis-induced ARDS.

Analysis of Variance↗
PubMed2004

Partial liquid ventilation for the prevention of mortality and morbidity in paediatric acute lung injury and acute respiratory distress syndrome.

BACKGROUND: Acute lung injury, and acute respiratory distress syndrome, are syndromes of severe respiratory failure. Children with acute lung injury or acute respiratory syndrome have high mortality and significant morbidity. Partial liquid ventilation is proposed as a less injurious form of respiratory support for these children. Uncontrolled studies in adults have shown improvement in gas exchange and lung compliance with partial liquid ventilation A single uncontrolled study in six children with acute respiratory syndrome showed some improvement in gas exchange during three hours of partial liquid ventilation. OBJECTIVES: To assess whether partial liquid ventilation reduces either mortality or morbidity, or both, in children with acute lung injury or acute respiratory syndrome. SEARCH STRATEGY: We searched The Cochrane Central Register of Controlled Trials (CENTRAL), The Cochrane Library issue 2, 2003; MEDLINE (1966 to April 2003); and CINAHL (1982 to April 2003); intensive care journals and conference proceedings; reference lists and 'grey literature'. SELECTION CRITERIA: Randomized controlled trials which compared partial liquid ventilation with other forms of ventilation, in children (28 days - 18 years) with acute lung injury or acute respiratory syndrome, reporting one or more of the following: mortality; duration of mechanical ventilation, respiratory support, oxygen therapy, stay in the intensive care unit, or stay in hospital; infection; or long term cognitive impairment or neurodevelopmental progress or other long term morbidities. DATA COLLECTION AND ANALYSIS: Two reviewers independently evaluated the quality of the relevant studies and extracted the data from the included studies. MAIN RESULTS: Only one study enrolling 182 patients (only reported as an abstract in conference proceedings) was identified and found eligible for inclusion: the authors report only limited results. The trial was stopped prematurely and therefore under-powered to detect any significant differences. The only outcome of clinical significance available was 28 day mortality: there was no statistically significant difference between groups with a relative risk for 28 day mortality in the partial liquid ventilation group of 1.54 (95% confidence intervals of 0.82 to 2.9). REVIEWERS' CONCLUSIONS: There is no evidence from randomized controlled trials to support or refute the use of partial liquid ventilation in children with acute lung injury or acute respiratory syndrome: adequately powered, high quality randomized controlled trials are still needed to assess its efficacy. Clinically relevant outcome measures should be assessed (mortality at discharge and later, duration of respiratory support and hospital stay, and long-term neurodevelopmental outcomes) and the studies should be published in full.

Adolescent↗
PubMed1996

Acute respiratory distress syndrome (ARDS) in neonates and children.

ARDS remains a syndrome which despite all efforts poses problems in exact definition (cause, course and severity). Most of the existing information comes from clinical observations and uncontrolled studies and is therefore of limited value. Despite the advent of new treatment modalities mortality from ARDS has remained high and is influenced or caused by several factors like underlying disease, previous health status, presence of MOSF, complications of therapy or ultimate failure of gas exchange. Therapy is directed at elimination of the cause of ARDS if possible, but then mainly supportive, considering all organs and systems. With the introduction of gentler respiratory support techniques (small tidal volumes and pressure limitation, permissive hypercapnia and HFO) and appropriate measures to reduce oxygen toxicity (titration of PEEP, possibly NO), iatrogenic lung injury, indistinguishable from ARDS, can be reduced, and this might improve survival rates. For the future, modulation of the host's inflammatory response may hold great promises for prevention and treatment of ARDS, but such strategies need to be explored with well controlled clinical trials, respecting the complexity of the issue.

Child↗
PubMedDate not supplied

Acute respiratory distress syndrome update.

Respiratory failure and eventual ventilator dependence are hallmarks of the acute respiratory distress syndrome (ARDS). ARDS carries a significant mortality in all patient populations and the treatment strategies are largely supportive in nature. Despite years of clinical experience, ARDS continues to pose a substantial threat and no definitive therapy has yet to be described. We will present an overview of management options.

Adult↗
PubMed1975

Iatrogenic respiratory distress syndrome. An analysis of obstetric events preceding delivery of infants who develop respiratory distress syndrome.

The obstetric events leading to the birth of infants who developed respiratory distress syndrome (RDS) were evaluated. In a retrospective study of 100 consecutive cases it was determined that untimely or unwarranted physician intervention in the pregnancy was responsible for 15 per cent of cases and possibly responsible for another 18 per cent. Recommendations for prevention of "iatrogenic" RDS are made.

Cesarean Section↗
PubMed2006

Relationship between pressure-volume curve and markers for collagen turn-over in early acute respiratory distress syndrome.

OBJECTIVE: In acute respiratory distress syndrome, the relationships between changes in the elastic behavior of the respiratory system and biological markers of extra-cellular matrix or surfactant turn-over could give some insights into its pathophysiological determinants. DESIGN AND MEASUREMENTS: In 17 patients with acute respiratory distress syndrome, we assessed the relationship between chord compliance measured on pressure-volume curves obtained at two levels of positive end-expiratory pressure (0 and 10[Symbol: see text]cm[Symbol: see text]H(2)O) and biological markers of collagen turn-over or surfactant degradation in bronchoalveolar lavage fluid obtained simultaneously in the early phase of the disease (first 4 days). MAIN RESULTS: The compliance of the respiratory system obtained from the pressure-volume curves was significantly correlated with markers for collagen turn-over (type III procollagen peptide and matrix metalloproteinase 2) and with markers of surfactant degradation (type-IIA secretory phospholipase A2). The correlations were stronger when the curve was traced from positive end-expiratory pressure, suggesting that this condition may improve the assessment of tissue mechanics. A logarithmic relationship best described the correlation between compliance and type III procollagen peptide, in agreement with a collagen-dependent model of maximal distension. The marker for surfactant degradation was associated with ongoing alveolar inflammation (cellularity of bronchoalveolar lavage fluid and tumor necrosis factor-alpha concentration). Interleukin-10, an anti-inflammatory mediator, showed no correlation with compliance. CONCLUSION: These preliminary data suggest that a severe reduction in compliance in the early phase of acute respiratory distress syndrome is associated with both collagen deposition and surfactant degradation.

Adult↗
PubMed2000

[Incidence of respiratory distress syndrome in premature twins].

Respiratory distress syndrome (RDS) is a syndrome of respiratory malfunction occurring in pre-term newborns. Twin pregnancy is a risk factor for the occurrence of RDS. The objective of our study is to analyse RDS incidence in pre-term twins and to determine the mortality in this group of newborns compared to single pregnancy pre-term babies. The study is based on the data collected in Clinic for Gynaecology and Obstetrics, Neonatology Department in the year 1999. RDS was diagnosed on the basis of clinical status and radiology findings. In the course of the test period, 544 pre-terms were born, 91 (16.7%) of them being from twin pregnancies. RDS developed in 132 newborns from single pregnancies (29.1%), in 28 newborns from twin pregnancies with RDS developed in both twins (30.7%) and in 19 babies whose twin siblings did not have RDS. If we consider gestation age, RDS developed in 28.6% twins born between 32nd and 36th gestation week and in 20.45% single newborns of the same age. The results were similar in younger gestation age. Mortality rate in the tested group was 17.8% and 9% in the control group. These results lead us to the conclusion that pre-term newborns from twin pregnancies tend to develop RDS, a more difficult clinical status, have more complications and higher mortality rate than the newborns from single pregnancies.

Diseases in Twins↗
PubMed1976

Managing respiratory distress syndrome in adults.

Respiratory distress syndrome in adults may be produced by any of a number of causes resulting in similar pathophysiologic changes and having identical therapeutic implications. The most important factors in treatment are early recognition and early institution of therapy.

Adrenal Cortex Hormones↗
PubMed2001

Mechanical ventilation in acute respiratory distress syndrome.

The acute respiratory distress syndrome occurs commonly in critical care. There is an increasing volume of clinical and experimental evidence that poor ventilatory technique that is injurious to the lungs can propagate the systemic inflammatory response and adversely affect mortality. Many ventilatory techniques have been hypothesized to 'protect' the lungs during mechanical ventilation, including tidal volume limitation, high positive end-expiratory pressure, pressure-controlled inverse ratio ventilation, and prone positioning. Experimental techniques include liquid ventilation, surfactant administration and extracorporeal gas exchange. Despite excellent rationale for their use, few techniques, apart from tidal volume limitation, have been shown to improve survival in randomized controlled trials.

Journal Article↗
PubMed1991

Lung surfactant in respiratory distress syndrome.

Severe respiratory failure is always associated with a defect in the surfactant system. Surfactant substitution in newborn infants with respiratory distress syndrome (RDS) has gained worldwide acceptance. In the present study, we have evaluated whether surfactant diagnostics are of use in choosing recipients of exogenous surfactant. In addition, we studied whether factors apparently unrelated to surfactant influence the degree of respiratory failure and surfactant responsiveness. In small preterm infants, the surfactant indices in amniotic fluid (L/S ratio and phosphatidylglycerol), within 3 days of birth, predicted the risk of RDS with a sensitivity of 90-100%, and a specificity of 50-85%. The surfactant indices, measured in BAL, predicted the risk of ARDS (which became evident 1 to 7 days later) with a sensitivity of 50-60% and a specificity of 59-65%. In small preterm infants with RDS, the amount of fluids given during the first day correlated positively with the degree of respiratory failure and negatively with the degree of surfactant responsiveness. According to an experimental study, in hydrostatic lung edema, exogenous surfactant is diluted by edema fluid and becomes sensitive to inhibitors of surfactant function. Beside dosage, quality, and time of administration, the management of patients largely dictates the responsiveness to exogenous surfactant.

Humans↗