Adult respiratory distress syndrome.
Explore the source record for details and available documents.
Humans↗
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.
Incidence, clinical course, and outcome in 217 patients with acute respiratory distress syndrome.
OBJECTIVE: To assess prospectively acute respiratory distress syndrome incidence, etiologies, physiologic and clinical features, and mortality and its predictors in four intensive care units in Argentina. DESIGN: Prospective inception cohort. SETTING: Four general intensive care units in teaching hospitals. PATIENTS: All consecutive adult patients admitted between January 3, 1999, and January 6, 2000, that met the criteria of the American-European Consensus Conference for acute respiratory distress syndrome. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: A total of 235 patients developed acute respiratory distress syndrome, and 217 survived for >24 hrs; these were further analyzed. Main risk factors were: sepsis (44%, including 65 pneumonia cases), shock (15%), trauma (11%), gastric aspiration (10%), and other (34%). At admission, nonsurvivors had significantly higher Acute Physiology and Chronic Health Evaluation II, Sequential Organ Failure Assessment and McCabe scores, and lower oxygenation and pH. During the first week, Pao2/Fio2, Sequential Organ Failure Assessment, pH, base excess, and driving pressure consistently discriminated between survivors and nonsurvivors. Hospital mortality was 58%. One third of patients died early. Main causes of death were multiple organ dysfunction syndrome, sepsis, and septic shock; refractory hypoxemia was uncommon. Factors independently associated with mortality were organ dysfunctions on day 3, Pao2/Fio2 on day 3, and McCabe score. CONCLUSIONS: Acute respiratory distress syndrome was a frequent syndrome in this cohort. Sepsis was its leading cause, and pneumonia was the most common single diagnosis. Mortality was high but similar to most recent series that included serious comorbidities. Independent predictors of death 72 hrs after admission emphasize the importance of both extrapulmonary and pulmonary factors together with preexisting severe illnesses.
Adolescent↗
[Respiratory distress syndrome. Evidence based respiratory medicine: 2nd update workshop of the SPLF].
Explore the source record for details and available documents.
Humans↗
Pulmonary and extrapulmonary acute respiratory distress syndrome: are they different?
PURPOSE OF REVIEW: Acute respiratory distress syndrome has been considered a morphologic and functional expression of lung injury caused by a variety of insults. Two distinct forms of acute respiratory distress syndrome/acute lung injury are described, because there are differences between pulmonary acute respiratory distress syndrome (direct effects on lung cells) and extrapulmonary acute respiratory distress syndrome (reflecting lung involvement in a more distant systemic inflammatory response). This article will focus on the differences in lung histology and morphology, respiratory mechanics, and response to ventilatory strategies and pharmacologic therapies in pulmonary and extrapulmonary acute respiratory distress syndrome. RECENT FINDINGS: Many researchers recognize that experimental pulmonary and extrapulmonary acute respiratory distress syndrome are not identical. In addition, clinical studies have described the detection of differences radiographically, functionally, and by analysis of the responses to therapeutic interventions (ventilatory strategies, positive end-expiratory pressure, prone position, drugs). However, there are contradictions among the different studies addressing these issues, which could be attributed to the fact that the distinction between pulmonary and extrapulmonary acute respiratory distress syndrome is not always clear and simple. Furthermore, there may be frequent overlapping in pathogenetic mechanisms and morphologic alterations. SUMMARY: The understanding of acute respiratory distress syndrome needs to take into account its origin. If each pathogenetic mechanism were to be considered, clinical management would be more precise, and probably the outcome could include real amelioration.
Animals↗
Multiple organ system failure and infection in adult respiratory distress syndrome.
Patients with the adult respiratory distress syndrome and multiple organ system failure have a high mortality rate despite extensive supportive therapy. We evaluated the role of multiple organ system failure and infection in 37 consecutive survivors of the syndrome, and 47 consecutive nonsurvivors on whom autopsies were done. Failure of the central nervous, coagulation, endocrine, gastrointestinal, and renal systems was common in all patients but was more frequent in those who died. Major infections occurred in 46 nonsurvivors and 22 survivors. All patients with bacteremia who had a clinically identified site of infection survived, whereas all patients with bacteremia without a clinically identified site of infection died. Autopsy results of the latter group showed infections requiring surgical drainage for complete therapy. Patients clinically septic but without bacteremia and without a clear site of infection were shown at autopsy to have pneumonia. Multiple organ system failure was more common in infected (93%) than noninfected (47%) patients. Vigorous evaluation and treatment of infection in patients with the adult respiratory distress syndrome may improve survival.
Autopsy↗
Mechanical ventilation in the management of acute respiratory distress syndrome.
The occurrence of acute respiratory distress syndrome (ARDS), is now common in intensive care units throughout the world. The diagnosis of ARDS is based on a definition that includes bilateral pulmonary infiltrates on chest radiographs, impaired oxygenation, and the absence of clinical evidence of elevated left atrial pressure. ARDS is the clinical result of a group of diverse processes, which range from physical or chemical injury, to extensive activation of innate inflammatory response. All these processes damage the integrity of the alveolar-capillary barrier causing increased alveolar-capillary permeability and an influx of protein-rich fluid into the alveolar space. This alveolar flooding results in hypoxemia, inactivated surfactant, intrapulmonary shunt, and impaired alveolar ventilation. The treatment of acute respiratory distress syndrome is largely supportive in nature, keeping patients alive while allowing their lungs to heal, and minimizing further pulmonary insult. In 1994 the National Heart, Lung, and Blood Institute (NHLBI) established the ARDS Network for the conduct of clinical trials. This is a network, supported by the National Institutes of Health, that provided the infrastructure for well-designed, multicenter, randomized trials of therapies for ARDS. The first study from this group in 2001 produced landmark data demonstrating mortality improvements in ARDS with particular mechanical ventilation strategies. Specifically, low tidal volume mechanical ventilation was demonstrated to reduce mortality by 22%. Other strategies such as high positive end expiratory pressure and prone positioning have not been shown to reduce mortality. Clinicians who are involved in the care of patients with ARDS should have a basic understanding of mechanical ventilation and the evidence guiding the mechanical ventilation strategies of these patients. Until further evidence is published, providers should adopt the use of a volume and pressure limited approach to mechanical ventilation.
High-Frequency Ventilation↗
The validity and reliability of the functional impairment checklist (FIC) in the evaluation of functional consequences of severe acute respiratory distress syndrome (SARS).
Severe acute respiratory distress syndrome (SARS) contributed to significant mortality and morbidity worldwide. We aimed to establish the validity, reliability and responsiveness of the functional impairment checklist (FIC) as a measurement tool for physical dysfunction in SARS survivors. One hundred and sixteeen (65 females and 51 males, mean age 45.6) patients who joined the SARS rehabilitation programme were analysed. The factor analysis yielded two latent factors. The mean FIC-symptom and FIC-disability score were 24.12 (SD +/- 20.2) and 26.11 (SD +/- 27.32), respectively. Based on the item-scale correlation coefficients, the Cronbach's alpha coefficients reflecting the internal consistency reliability of scale score were 0.75 for FIC-symptom and 0.86 for FIC-disability. Test-retest reliability in 23 patients showed no statistical significant difference in the FIC scores between tests with intraclass correlation coefficient (ICC) 0.49-0.57. The FIC scales correlated both with 6 munute walking test (6MWT) distance (-0.26 and -0.38) and handgrip strength (HGS) (-0.20 and -0.27). Moreover, the FIC scales correlated with St. George's respiratory questionnaire (SGRQ) (0.19 to 0.52) and short form 36 Hong Kong (SF-36) domains (-0.19 to -0.59). Both FIC scales correlated stronger with physical component summary (PCS) (-0.41 and -0.55) than with mental component summary (MCS) (-0.30 and -0.23). FIC reduced significantly at 6 months while the SF-36 PCS and MCS did not show any change. In conclusion, the study results indicate the FIC is reliable, valid and responsive to change in symptom and disability as a consequence of SARS, suggesting it may provide a means of assessing health related quality of life (HRQOL) outcomes in a longitudinal follow up.
Adult↗
[Comparison of high-frequency jet ventilation and conventional ventilation in the adult respiratory distress syndrome].
Sixteen adult patients with respiratory distress syndrome requiring mechanical respiratory assistance entered this study, the purpose of which was to obtain the same blood gas values under high frequency jet ventilation as under conventional ventilation. When high frequency jet ventilation without spontaneous breathing was compared to continuous positive pressure ventilation, peak airway pressure was the same, but mean airway pressure, positive end-expiratory pressure and pleural pressure were higher and cardiac index lower. When high frequency jet ventilation with spontaneous breathing was compared to intermittent mandatory ventilation, peak airway pressure was lower, mean airway pressure and positive end-expiratory pressure were higher, and pleural pressure and cardiac index were not different.
Adult↗
Adult respiratory distress syndrome in pediatric patients. II. Management.
Adult respiratory distress syndrome, a clinical syndrome of respiratory failure that follows many kinds of insults, often in patients with no previous pulmonary disease, occurs in pediatric patients. This group of disorders has a typical clinical, pathologic, and pathophysiologic course, the hallmark of which is injury to the alveolar-capillary membrane with increased permeability of the pulmonary vasculature and pulmonary edema. Resolution may occur at any stage, but most patients die and many develop chronic lung disease requiring respiratory support for weeks or months. Multiple organ system failure, secondary infection, and irreversible respiratory dysfunction are responsible for the poor outcome. The underlying mechanisms that relate injury to the development of pulmonary disease are unclear. In some cases there may be direct injury to the lung, but in others, such as septic shock, there are mediators that link the initial insult to the subsequent lung injury. The leukocyte may have a central role in this process, although this is uncertain. Therapeutic measures needed to support the patient, especially increased inspired oxygen, are additional factors in the progression of lung disease. Current therapy, as summarized in Table II, is primarily supportive. Efforts to treat ARDS after it is clinically apparent have been disappointing. The pathogenic mechanisms that lead to ARDS are probably well advanced by the time the syndrome is diagnosed on the basis of the usual clinical signs. Therefore an emphasis on understanding the mechanisms of lung injury so that specific markers can be used to predict which patients will develop ARDS, allowing intervention in the early stages of the process, may prove rewarding.
Cardiac Output↗
Pathophysiology of shock and adult respiratory distress syndrome.
The respiratory failure that develops in surgical patients is usually caused by a surgical problem--shock, trauma, sepsis, pulmonary contusion, aspiration, pulmonary emboli or pain, with its attendant ventilatory compromise. Although the underlying pathophysiology for the respiratory failure in these conditions is not precisely known, the means for prevention are well known. Patients subjected to trauma should be aggressively resuscitated from shock. They should have the chance of being cared for in a facility where an operation can be performed promptly. The respiratory failure of sepsis is best treated by seeking out foci of pus or devitalized tissue and surgically ablating these foci when found. Adherence to these basic surgical principles--aggressive resuscitation of patients in shock and prompt attention to their surgical problems--will alleviate much of the respiratory distress of surgical patients, no matter what the pathophysiology or etiology may be.
Animals↗
[Adult respiratory distress syndrome--etiology and pathogenesis].
Adult respiratory distress syndrome (ARDS) is not a specific lung disease. It represents an acute respiratory insufficiency syndrome in patients with non-injured lung as a result of severe multiple lung lesions of different etiology and pathogenesis. ARDS is provoked by a great number of etiologic factors of two main groups: 1) etiologic factors directly injuring the alveolo-capillary wall and 2) etiologic factors indirectly injuring the alveolo-capillary wall. ARDS develops in three phases: phase of exudation, phase of injury of the alveolocapillary wall and phase of proliferation (chronic phase).
Adult↗
Pharmacotherapy of acute lung injury and the acute respiratory distress syndrome.
Acute lung injury and the acute respiratory distress syndrome are common syndromes with a high mortality rate that affect both medical and surgical patients. Better understanding of the pathophysiology of acute lung injury and the acute respiratory distress syndrome and advances in supportive care and mechanical ventilation have led to improved clinical outcomes since the syndrome was first described in 1967. Although several promising pharmacological therapies, including surfactant, nitric oxide, glucocorticoids and lysofylline, have been studied in patients with acute lung injury and the acute respiratory distress syndrome, none of these pharmacological treatments reduced mortality. This article provides an overview of pharmacological therapies of acute lung injury and the acute respiratory distress syndrome tested in clinical trials and current recommendations for their use as well as a discussion of potential future pharmacological therapies including beta(2)-adrenergic agonist therapy, keratinocyte growth factor, and activated protein C.
Administration, Inhalation↗
Iron and iron-related proteins in the lower respiratory tract of patients with acute respiratory distress syndrome.
OBJECTIVE: An increased oxidative stress in the lower respiratory tract of individuals with acute respiratory distress syndrome is considered to be one mechanism of lung injury in these patients. Cell and tissue damage resulting from an oxidative stress can ultimately be the consequence of a disruption of normal iron metabolism and an increased availability of catalytically active metal. Using bronchoalveolar lavage fluid, we quantified concentrations of iron and iron-related proteins in the lower respiratory tract in patients with acute respiratory distress syndrome and healthy volunteers. DESIGN: A clinical study to quantify iron and iron-related proteins in the lower respiratory tract in patients with acute respiratory distress syndrome and healthy volunteers. PATIENTS: We studied 14 patients with acute respiratory distress syndrome and 28 healthy volunteers. MAIN RESULTS: Comparable to previous investigation, protein, albumin, and cytokine concentrations in the bronchoalveolar lavage fluid were significantly increased in acute respiratory distress syndrome patients. The concentrations of total and nonheme iron were also increased in the lavage fluid of patients. Concentrations of hemoglobin, haptoglobin, transferrin, transferrin receptor, lactoferrin, and ferritin in the bronchoalveolar lavage fluid were all significantly increased in acute respiratory distress syndrome patients. CONCLUSIONS: We conclude that bronchoalveolar lavage fluid indices reflect a disruption of normal iron metabolism in the lungs of acute respiratory distress syndrome patients. Increased concentrations of available iron in acute respiratory distress syndrome may participate in catalyzing oxidant generation destructive to the tissues of the lower respiratory tract. However, increased metal availability is also likely to elicit an increased expression of transferrin receptor, lactoferrin, and ferritin in the lower respiratory tract which will function to diminish this oxidative stress.
Adult↗
Pulmonary function and health-related quality of life in survivors of acute respiratory distress syndrome.
Although survival rates for acute respiratory distress syndrome have increased, there is only limited information regarding the quality of life and the relationship between quality of life and pulmonary function after survival. We prospectively measured pulmonary function, emotional function, and health-related quality of life in a cohort of acute respiratory distress syndrome survivors recruited from patients who were enrolled in a randomized clinical trial of high versus low tidal volume mechanical ventilation at 1 year after their recovery. No significant differences were found between the patients treated with high and low tidal volumes on any pulmonary function measure. Approximately 80% of the patients in both groups demonstrated reduced diffusing capacity; 20% had airflow obstruction, and 20% had chest restriction. Scores on measures of depression and anxiety were within the normal ranges, suggesting that they did not have significant affective symptoms. However, both groups reported decreased health-related quality of life in physical functioning, physical ability to maintain their roles (role-physical), bodily pain, general health, and vitality (energy) on the Medical Outcome Study Short Form Health Survey with similar physical limitations reported on the Sickness Impact Profile questionnaire. The pulmonary function abnormalities correlated with decreased health-related quality of life for domains reflecting physical function. Acute respiratory distress syndrome survivors treated with high and low tidal volumes have abnormal pulmonary function that was related to decreased health-related quality of life 1 year after hospital discharge.
APACHE↗
Sepsis syndrome, the adult respiratory distress syndrome, and nosocomial pneumonia. A common clinical sequence.
Systemic sepsis and pneumonia are common predisposing factors for ARDS, which can serve as the initial manifestation of the multisystem organ failure syndrome. Primary pneumonia that necessitates ICU admission leads to ARDS in approximately 10% of patients. Systemic infection can also lead to ARDS, but when bacteremia alone is present, the risk is low (probably less than 5%). If the septic syndrome with a hemodynamic and end-organ response develops, the ARDS may follow in as many as 40% of patients. When multiple risk factors for acute lung injury are present, the risk of developing ARDS rises dramatically. The septic syndrome, acute lung injury, and multiorgan failure are closely tied to one another because bacterial cell walls can activate inflammatory mediators, such as interleukin-1 and tumor necrosis factor, which can in turn lead to the septic syndrome and inflammatory injury to the lung. Clinical features, more than serum markers, have been the best predictors of whether lung injury will follow sepsis, indicating that the mere presence of mediators alone cannot cause ARDS and that there are individual susceptibility factors in the effects of these mediators. With the advent of monoclonal antibodies and new anti-inflammatory drugs, prevention of progression from sepsis to multiorgan failure may become possible. Pneumonia is the most common infection that complicates ARDS once it is established, and the mortality rate may approach 90%. The existence of acute lung injury, its predisposing conditions, coexisting illnesses, and the therapeutic interventions used for patients with lung injury all can interfere with lung host defenses and set the stage for bacterial infection of the already-injured lung. This infection appears to add to the propagation of the multiple system organ failure that has already begun. In the future, it may become possible to prevent this infection, which would be a welcome development, because currently, we are stymied in our efforts to diagnose and treat pneumonia in the setting of acute lung injury. Preventive efforts will follow from an understanding of the pathogenesis of pneumonia and in the future may include topical antibiotics, selective digestive decontamination, and prophylactic passive immunotherapy.
Acute Disease↗
Elective bone marrow transplantation in a child with X-linked hyper-IgM syndrome presenting with acute respiratory distress syndrome.
We describe a 10-month-old boy diagnosed with X-linked hyper-IgM syndrome (XHIM) after suffering from life-threatening acute respiratory distress syndrome (ARDS) caused by Pneumocystis carinii pneumonia (PCP), although his previous clinical history and first level laboratory tests investigating immunological function did not indicate immunodeficiency. When the patient's overall condition was good, elective bone marrow transplantation from an HLA-matched older brother was performed successfully. We describe how correct diagnosis and successful treatment were made possible thanks to the involvement of a network of specialists.
Bone Marrow Transplantation↗
Decreased angiotensin-converting enzyme in the adult respiratory distress syndrome.
Using hippuryl-L-histidyl-L-leucine as substrate, serum angiotensin-converting enzyme was measured in 13 patients who had adult respiratory distress syndrome, eight patients with respiratory failure without adult respiratory distress syndrome, and two groups of controls: 24 healthy blood donors and 24 hospitalized patients with a variety of conditions but without respiratory failure or adult respiratory distress syndrome. Serum angiotensin-converting enzyme expressed in units/ml was 14.60 +/- 5.60 for adult respiratory distress syndrome compared with 28.92 +/- 6.60 for the blood donors, 20.76 +/- 5.87 for the patients with respiratory failure without adult respiratory distress syndrome and 20.20 +/- 5.94 in the hospitalized patients without respiratory failure or adult respiratory distress syndrome. These differences were significant, P less than .001 when adult respiratory distress syndrome was tested against the blood donors and P less than .01 against the other two groups. The significance of these findings is not clear, but the possibility is raised that the decrease of angiotensin-converting enzyme in adult respiratory distress syndrome results from a loss of pulmonary endothelial cells, which are known both to produce angiotensin-converting enzyme and to be damaged in adult respiratory distress syndrome.
Adolescent↗
[Acute respiratory distress syndrome].
The pathophysiology of acute respiratory distress syndrome (ARDS) is characterized by pulmonary edema due to extravasation from capillary lesions in the endothelium. A clinical diagnosis is made when there is a predisposing cause (sepsis and pneumonia being the most common) that gives rise to acute respiratory insufficiency (PaO2/FiO2 ratio (3/4) 200 mmHg, bilateral infiltrates visible on a chest film and hemodynamic or other clinical signs of left cardiac insufficiency). Most patients require invasive support ventilation at a high FiO2 and positive end-expiratory pressure (PEEP). The only therapeutic approach available at this time associated with a highly significant decrease in mortality in patients with ARDS is ventilation at low flow volumes (6 ml/kg) and moderate levels of PEEP (approximately 10 cmH2O).
Arachidonic Acids↗