Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “RESPIRATORY DISTRESS SYNDROME”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources
PubMed2000

Outcomes and cost-effectiveness of ventilator support and aggressive care for patients with acute respiratory failure due to pneumonia or acute respiratory distress syndrome.

PURPOSE: Many patients with acute respiratory failure die despite prolonged and costly treatment. Our objective was to estimate the cost-effectiveness of providing rather than withholding mechanical ventilation and intensive care for patients with acute respiratory failure due to pneumonia or acute respiratory distress syndrome. SUBJECTS AND METHODS: We studied 1,005 patients enrolled in a five-center study of seriously ill patients (the Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments [SUPPORT]) with acute respiratory failure (pneumonia or acute respiratory distress syndrome and an Acute Physiology Score > or =10) who required ventilator support. We estimated life expectancy based on long-term follow-up of SUPPORT patients. Utilities were estimated using time-tradeoff questions. Costs (in 1998 dollars) were based on hospital fiscal data and Medicare data. RESULTS: Of the 963 patients who received ventilator support, 48% survived for at least 6 months. At 6 months, survivors reported a median of 1 dependence in activities of daily living, and 72% rated their quality of life as good, very good, or excellent. Among the 42 patients in whom ventilator support was withheld, the median survival was 3 days. Among patients whose estimated probability of surviving at least 2 months from the time of ventilator support ("prognostic estimate") was 70% or more, the incremental cost per quality-adjusted life-year (QALY) saved by providing rather than withholding ventilator support and aggressive care was $29,000. For medium-risk patients (prognostic estimate 51% to 70%), the incremental cost-effectiveness was $44,000 per QALY, and for high-risk patients (prognostic estimate < or =50%), it was $110,000 per QALY. When assumptions were varied from 50% to 200% of baseline estimates, the results ranged from $19,000 to $48,000 for low-risk patients, from $29,000 to $76, 000 for medium-risk patients, and from $67,000 to $200,000 for high-risk patients. CONCLUSIONS: Ventilator support and intensive care for acute respiratory failure due to pneumonia or acute respiratory distress syndrome are relatively cost-effective for patients with >50% probability of surviving 2 months. However, for patients with an expected 2-month survival < or =50%, the cost per QALY is more than threefold greater at >$100,000.

APACHE↗
PubMed2003

What has been learnt from P/V curves in patients with acute lung injury/acute respiratory distress syndrome.

Mechanical impairment of the respiratory system was recognised soon after the description of acute respiratory distress syndrome. The analysis of the pressure/volume (P/V) curve of the respiratory system contributed a lot to the understanding of the pathophysiology of acute lung injury and formed the basis for lung protection. The lower and upper inflection points were regarded as points of interest to avoid cyclic derecruitment and overdistension and to optimise ventilatory settings. However, because of the heterogeneity of lung injury, reducing the mechanical properties of the whole respiratory system to a single curve is a schematic approach, which makes interpretation difficult. New data suggest that alveolar re-inflation occurs along the whole P/V curve that can, therefore, be considered as a recruitment curve. The lower inflection point has no relationship with alveolar opening and closure and does not indicate the positive end-expiratory pressure needed to prevent alveolar collapse. The shape of the P/V curve gives information about the extension and the homogeneity of lung injury, indicating the possibility of lung recruitment. The upper inflection point, classically seen as the beginning of overdistension, may also indicate the end of recruitment. The pressure/volume curve offers the unique opportunity of evaluating alveolar recruitment/derecruitment at the bedside that can be helpful for the identification of optimal ventilatory settings and makes the curve a valuable tool for the ventilatory management of acute lung injury.

Acute Disease↗
PubMed1985

Sleep apnoea profile in preterm infants recovering from respiratory distress syndrome.

Polygraphic recordings were made on 10 preterm infants recovering from respiratory distress syndrome and 12 healthy preterm control infants at 40, 52, and 64 weeks' conceptual age to study the influence of respiratory distress syndrome on the development of the sleep apnoea profile. Two significant differences were found: infants with respiratory distress syndrome not only had a lower incidence of non-obstructive apnoea and periodic breathing at 40 weeks but also a persistently higher incidence of obstructive and mixed apnoea at 52 and 64 weeks' conceptual age; the latter finding being related to non-rapid eye movement sleep only. While the lower incidence of both types of apnoea at 40 weeks suggests an advanced maturation of respiratory drive, the persistence of obstructive and mixed apnoea related to non-rapid eye movement sleep may reflect the impact of respiratory distress syndrome on airway structures.

Humans↗
PubMed2002

Respiratory distress syndrome: principles and current therapy.

Acute respiratory distress syndrome (ARDS) describes a clinicopathologic disease process that occurs in association with a variety of clinical situations. The severity and outcome of this syndrome varies. Prolonged hospital stay, significant early morbidity and mortality, and long-term pulmonary parenchymal changes that result in reduced, often debilitating, pulmonary functions, typify the outcome of severe form of ARDS. Treatment is supportive with ventilatory assistance and adjunctive use of supplemental oxygen and end expiratory airway pressure (PEEP). Oxygen therapy and PEEP, though dramatically improve lung mechanics and oxygenation, are not innocuous and may adversely affect cardiovascular function and even induce pulmonary parenchymal injury. Over the years a variety of "lung protective" treatment modalities have been introduced and proved as effective and safe in the treatment of this syndrome

Adult↗
PubMedDate not supplied

[Impairment of the fibrinolytic function of the lungs in the respiratory distress syndrome in patients with peritonitis].

Adult respiratory distress syndrome (ARDS) is accompanied by disseminated intravascular coagulation syndrome (DICS), its development causing progressing signs of the shock lung. The loss of the so far high pulmonary fibrinolytic activity promotes the onset of DICS in mixed venous and arterial blood. This metabolic pulmonary function is retained in patients with ARDS, stage I, is slightly damaged in patients with ARDS, stage II and is completely impaired in patients with ARDS, stages III and IV.

Disseminated Intravascular Coagulation↗
PubMedDate not supplied

Adult respiratory distress syndrome associated with adult epiglottitis.

Adult respiratory distress syndrome (ARDS) is an increased permeability pulmonary edema syndrome known to be associated with a variety of direct and indirect pulmonary insults. ARDS occurred in a 37-year-old woman during an episode of epiglottitis. The patient was treated with endotracheal intubation and mechanical ventilation and recovered, to be discharged from the hospital 1 week after presentation. There are only two cases of ARDS reported in this setting, and in each case, pulmonary edema followed cardiac arrest and the patients had a fatal outcome.

Adult↗
PubMed2006

Clinical epidemiology of acute lung injury and acute respiratory distress syndrome: incidence, diagnosis, and outcomes.

Acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) are clinical syndromes characterized by the sudden onset of severe hypoxemia and diffuse bilateral pulmonary infiltrates in the absence of left atrial hypertension. Although advances have been made in the understanding of the etiology, pathophysiology, and epidemiology of both entities, many questions remain regarding their incidence, diagnosis, and outcomes. This article reviews the currently used definition of ARDS and ALI, different studies that have advanced the understanding of the epidemiology and outcomes of these entities, and several diagnostic issues that are important for both clinicians and researchers.

Biopsy↗
PubMed1991

Evaluation of two endotracheal suction regimes in babies ventilated for respiratory distress syndrome.

All low birthweight babies ventilated for the respiratory distress syndrome during a period of fourteen months were randomised to receive endotracheal suction 12-hourly or 6-hourly. There were no significant differences in respiratory outcome between the groups. These observations suggest that it is safe to aspirate endotracheal tubes infrequently during the first few days in uncomplicated respiratory distress syndrome.

Humans↗
PubMed1995

Cardiorespiratory effects of positive end-expiratory pressure during progressive tidal volume reduction (permissive hypercapnia) in patients with acute respiratory distress syndrome.

BACKGROUND: In patients with acute respiratory distress syndrome (ARDS), the ventilatory approach is based on tidal volume (VT) of 10-15 ml/kg and positive end-expiratory pressure (PEEP). To avoid further pulmonary injury, decreasing VT and allowing PaCO2 to increase (permissive hypercapnia) has been suggested. Effects of 10 cmH2O of PEEP on respiratory mechanics, hemodynamics, and gas exchange were compared during mechanical ventilation with conventional (10-15 ml/kg) and low (5-8 ml/kg) VT. METHODS: Nine sedated and paralyzed patients were studied. VT was decreased gradually (50 ml every 20-30 min). Static volume-pressure (V-P) curves, hemodynamics, and gas exchange were measured. RESULTS: During mechanical ventilation with conventional VT, V-P curves on PEEP 0 (ZEEP) exhibited an upward convexity in six patients reflecting a progressive reduction in compliance with inflating volume, whereas PEEP resulted in a volume displacement along the flat part of this curve. After VT reduction, V-P curves in the same patients showed an upward concavity, reflecting progressive alveolar recruitment with inflating volume, and application of PEEP resulted in alveolar recruitment. The other three patients showed a V-P curve with an upward concavity; VT reduction increased this concavity, and application of PEEP induced greater alveolar recruitment than during conventional VT. With PEEP, cardiac index decreased by, respectively, 31% during conventional VT and 11% during low VT (P < 0.01); PaO2 increased by 32% and 71% (P < 0.01), respectively, whereas right-to-left venous admixture (Qs/Qt) decreased by 11% and 40%, respectively (P < 0.01). The greatest values of PaO2, static compliance, and oxygen delivery and the lowest values of Qs/Qt (best PEEP) were obtained during application of PEEP with low VT (P < 0.01). CONCLUSIONS: Although PEEP induced alveolar hyperinflation in most patients during mechanical ventilation with conventional VT, at low VT, there appeared to be a significant alveolar collapse, and PEEP was able to expand these units, improving gas exchange and hemodynamics.

Female↗
PubMed2000

Treatment of acute (Adult) respiratory distress syndrome. The holy grail of surfactant therapy.

The treatment of neonatal respiratory distress syndrome with surfactant represents a successful culmination of decades of basic and clinical research. In many babies, respiratory distress syndrome is a relatively pure expression of surfactant deficiency. Acute respiratory distress syndrome (ARDS) is a more common disease that is most frequently seen in adults, but the processes are common to lung injuries in newborns and children as well. While some impairment of production and secretion of surfactant constituents may be present in ARDS, surfactant inactivation is probably a more important factor in this disease. Until recently, surfactants available for human use have been easily susceptible to inactivation and this may explain why they have been less successful for treatment of ARDS than for neonatal respiratory distress syndrome. This review outlines recent information on surfactant inactivation and describes initiatives that may result in 'inactivation-proof' surfactants that may be of increased benefit in ARDS.

Acute Disease↗
PubMed1995

Prevention and therapy of the adult respiratory distress syndrome.

The complex pathophysiology of adult respiratory distress syndrome (ARDS) makes preventive and therapeutic concepts difficult. Ample experimental evidence indicates that ARDS can be prevented by blocking systemic inflammatory agents. Clinically, only heparin, for inhibition of coagulation phenomena, is presently used among this array of approaches. Corticosteroids have not proven to be beneficial in ARDS. Alternative antiinflammatory agents are being proposed and are under current clinical investigation (e.g. indomethacin, acetylcysteine, alpha 1-proteinase inhibitor, antitumor necrosis factor, interleukin 1 receptor antagonist, platelet-activating factor antagonists). Symptomatic therapeutic strategies in early ARDS include selective pulmonary vasodilation (preferably by inhaled vasorelaxant agents) and optimal fluid balance. Transbronchial surfactant application, presently tested in pilot studies, may be available for ARDS patients in the near future and may have acute beneficial effects on gas exchange, pulmonary mechanics, and lung hemodynamics; its impact on survival cannot be predicted at the present time. Strong efforts should be taken to reduce secondary nosocomial pneumonia in ARDS patients and thus avoid the vicious circle of pneumonia, sepsis from lung infection, and perpetuation of multiple organ dysfunction syndrome. Optimal respirator therapy should be directed to ameliorate gas-exchange conditions acutely but at the same time should aim at minimizing potentially aggravating side effects of artificial ventilation (barotrauma, O2 toxicity). Several new techniques of mechanical ventilation and the concept of permissive hypercapnia address these aspects. Approaches with extracorporeal CO2 removal and oxygenation are being used in specialized centers.

Humans↗
PubMedDate not supplied

Fibrinolytic agents: a new approach to the treatment of adult respiratory distress syndrome.

Nineteen patients suffering from adult respiratory distress syndrome (ARDS) secondary to trauma or sepsis, or both, failed to respond to treatment with mechanical ventilation with oxygen and positive end-expiratory pressure. On the premise that ARDS may be caused by the microclots of disseminated intravascular coagulation obstructing the pulmonary microcirculation, the patients were treated with either streptokinase or urokinase. Eighteen patients responded with significant improvement in PaO 2 value. No bleeding occurred and clotting parameters remained normal.

Adolescent↗
PubMed1990

[Development of acute interstitial pulmonary edema in the respiratory distress syndrome].

Acute interstitial pulmonary edema in Respiratory distress syndrome with serious functional insufficiency is frequently accidental, and presents a process which develops rapidly in the alveolar-capillary structure, especially within the surfactant system. Its biogenic anti-atelectatic activity is initially diminished, and becomes excluded in the end. Mechanical ventilation with positive end-expiratory pressure is the logical way of treatment, based on the pathophysiological principle. Our clinical experience is accordant regarding the good effects of mechanical ventilation with positive end-expiratory pressure (PEEP).

Acute Disease↗
PubMed1994

Plasma concentration of elastase-alpha 1-proteinase inhibitor complex in surfactant-treated preterm neonates with respiratory distress syndrome.

Although exogenous surfactant replacement improves respiratory distress syndrome (RDS) of immature neonates, it may not prevent subsequent lung damage and development of bronchopulmonary dysplasia associated with polymorphonuclear neutrophil (PMN)-activation. We therefore wanted to assess whether surfactant administration would be associated with activation of circulating PMNs. Since elastase-alpha 1-proteinase inhibitor (E-alpha 1-PI) has proved to be a sensitive indicator of intravascular PMN activation, we studied E-alpha 1-PI plasma concentration in preterm neonates during the treatment of RDS with a bovine surfactant preparation (group I: n = 23). Results were compared with those from a retrospective control group treated by ventilation alone (group II: n = 13), and with a reference group of 92 newborns (group III). Following surfactant administration, median E-alpha 1-PI concentration increased significantly (day 1 80.5 vs Day 2,234 micrograms.l-1), and exceeded the upper limit of the reference range of 274 micrograms.l-1 in seven patients, with a maximal value of 1,881 micrograms.l-1 after multiple surfactant administrations. In contrast, 12 infants from Group II showed no increase in median E-alpha 1-PI levels (Day 1,107 vs Day 2,107 micrograms.l-1), and remained within the reference range (Day 1,125 micrograms.l-1; Day 2,107 micrograms.l-1) of the 92 newborns without respiratory impairment, infection, birth-trauma or asphyxia. From these results, it is concluded that surfactant may trigger a transient, mainly local, inflammatory response, reflected by increased levels of E-alpha 1-PI, and may exert a dose-related pathogenic influence on the course and prognosis of RDS.(ABSTRACT TRUNCATED AT 250 WORDS)

Bronchopulmonary Dysplasia↗
PubMed2000

High serum cardiac troponin T concentrations in preterm infants with respiratory distress syndrome.

UNLABELLED: In preterm infants with respiratory distress syndrome (RDS), cardiac function is negatively influenced by the severity of the lung disease. On day 2 of life, cardiac troponin T (cTnT), biochemical marker of myocardial injury, was measured in 46 preterm infants (gestational age < or =32 wk), 26 with RDS and 20 without: median (range) 0.38 (0.02-1.57) microg/L vs 0.13 (0.02-0.85) microg/L, respectively. CONCLUSION: High cTnT concentrations in preterm infants with RDS suggest the presence of myocardial damage in this group of high-risk patients.

Female↗
PubMed2006

Vascular endothelial growth factor (VEGF) in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS): paradox or paradigm?

Acute respiratory distress syndrome (ARDS), the most severe form of acute lung injury (ALI), remains a devastating condition with a high mortality. It is characterised by alveolar injury and increased pulmonary vascular permeability. Vascular endothelial cell growth factor (VEGF) was identified by its properties to increase permeability and act as a cellular growth factor, hence its potential for a key role in the pathogenesis of ALI/ARDS. This review describes the basic biology of VEGF and its receptors as an essential prerequisite to discussing the available and sometimes paradoxical published data, before considering a paradigm for the role of VEGF in the human lung.

Humans↗
PubMed2000

Association between the surfactant protein A (SP-A) gene locus and respiratory-distress syndrome in the Finnish population.

Respiratory-distress syndrome (RDS) in the newborn is a major cause of neonatal mortality and morbidity. Although prematurity is the most-important risk factor for RDS, the syndrome does not develop in many premature infants. The main cause of RDS is a deficiency of pulmonary surfactant, which consists of phospholipids and specific proteins. The genes underlying susceptibility to RDS are insufficiently known. The candidate-gene approach was used to study the association between the surfactant protein A (SP-A) gene locus and RDS in the genetically homogeneous Finnish population. In the present study, 88 infants with RDS and 88 control infants that were matched for degree of prematurity, prenatal glucocorticoid therapy, and sex were analyzed for SP-A genotypes. We show that certain SP-A1 alleles (6A2 and 6A3) and an SP-A1/SP-A2 haplotype (6A2/1A0) were associated with RDS. The 6A2 allele was overrepresented and the 6A3 allele was underrepresented in infants with RDS. These associations were particularly strong among small premature infants born at gestational age <32 wk. In infants protected from RDS (those that had no RDS, despite extreme prematurity and lack of glucocorticoid therapy), compared with infants that had RDS develop despite having received glucocorticoid therapy, the frequencies of 6A2 (.22 vs.71), 6A3 (.72 vs.17), 6A2/1A0 (.17 vs.68), 6A3/1A1 (.39 vs.10), and 6A3/1A2 (.28 vs.06) in the two groups, respectively, were strikingly different. According to the results of conditional logistic-regression analysis, diseases associated with premature birth did not explain the association between the odds of a particular homozygous SP-A1 genotype (6A2/6A2 and 6A3/6A3) and RDS. In the population evaluated in the present study, SP-B intron 4 variant frequencies were low and had no detectable association with RDS. We conclude that the SP-A gene locus is an important determinant for predisposition to RDS in premature infants.

Alleles↗
PubMed2004

[Acute respiratory distress syndrome. Role of steroids].

The acute respiratory distress syndrome (ARDS) represents 7.7% of the intensive care population, and is associated with great morbidity and mortality (58%). Frequently, the mortality can be attributed to more than one cause. Refractory hypoxemia is uncommon (15%) and most of the patients also have multiple organic dysfunction, sepsis or septic shock. Although there are many publications concerning series of cases and clinical trials using steroids as a part of the treatment of ARDS, this issue remains controversial. In this article the role of steroids in the ARDS is evaluated by analysis of the available literature. We conclude that steroids are useful in a subgroup of patients with unresolving ARDS, after ruling out an active infection or after treatment with antibiotics.

Humans↗