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PubMed2003

Pathophysiology and pharmacological treatment of pulmonary hypertension in acute respiratory distress syndrome.

Pulmonary hypertension (PH) is a characteristic feature of the acute respiratory distress syndrome (ARDS). The magnitude of PH has been shown to correlate with the severity of lung injury in patients with ARDS independently of the severity of associated hypoxaemia and has an adverse prognostic significance. Early in the histopathological evolution of ARDS, pulmonary vasoconstriction, thromboembolism and interstitial oedema contribute to the development of PH, although pulmonary vascular remodelling probably occurs eventually. Intravenous vasodilator agents lead to an increase in intrapulmonary shunting and systemic hypotension, which can limit their therapeutic use, and have not been shown to improve survival. By contrast, rapidly metabolised vasodilators administered by inhalation induce selective pulmonary vasodilatation and decrease shunting, but again do not appear to confer a survival benefit. Research aimed at further understanding the mechanisms that underlie pulmonary hypertension, a characteristic feature of the acute respiratory distress syndrome, are expected to provide improvements in pharmacological interventions for the treatment of pulmonary hypertension in the acute respiratory distress syndrome.

Humans↗
PubMed1995

[Extracorporeal membrane oxygenation in adult respiratory distress syndrome. Experience in 2 patients].

We report two female patients with adult respiratory distress syndrome and severe respiratory failure in whom extracorporeal membrane oxygenation was used. Its indication was due to a bad response to conventional treatment with mechanical ventilation and high levels of positive end expiratory pressure. A 2.0 or 2.2 m2 membrane oxygenator in a veno-venous circuit with systemic anticoagulation was used, maintaining mechanical ventilation. In the first patient, the procedure was done early and was successful, increasing hemoglobin saturation from 39 to 87%. The patient was withdrawn from the procedure 48 hours later and died one week later due to a septic shock. The second patient was connected to the procedure after three weeks of respiratory distress syndrome and no increase in arterial oxygenation was achieved. The patient died due to an intracranial hemorrhage, probably hastened by systemic anticoagulation. The real benefits of extracorporeal membrane oxygenation are not defined yet.

Adult↗
PubMed1996

Severe pulmonary dysfunction following acute respiratory distress syndrome.

Recovery of lung function following the acute respiratory distress syndrome (ARDS) is thought to be related to the severity of the initial insult. We report a case demonstrating virtually complete functional recovery following severe ARDS. The significance of this and the need for comprehensive follow-up of such patients is discussed.

Accidental Falls↗
PubMedDate not supplied

[Long term of quality of life and mortality in acute respiratory distress syndrome (ARDS) patients].

INTRODUCTION: Although advanced technology and make many researches, the acute respiratory distress syndrome has been associated to high mortality. We prospectively evaluated the quality of life and mortality changes in patients with acute respiratory distress syndrome, was used quality of life indicators, as well as we determinated if positional strategie will be have an influence to falling-off in mortality. MATERIAL AND METHODS: We combined the Karnosfky scale, daily live activities index, and the perception of quality of life scale to assess previously quality of life before admission to the intensive care unit and 6 moths after realese for 59 patients with acute respiratory distress syndrome. Mortality was compared with age, stay, severity of disease, nine equivalent manpower score and quality of life indicators. We evaluated mortality according to position strategie supine-position or pron-position. RESULTS: Mortality was to the 57%. Three significant variables related with mortality were identified: age, nine equivalent manpower score and quality of life indicators. We didn't find any significant differentiate between positioning strategies. All of quality of life indicators were decrease six months after discharge to the intensive care unit. DISCUSSION: Mortality from patients acute respiratory distress syndrome is described between ratio for others authors, as well as it doesn't condittioned for positional estrategie used. The quality of life of survivors have deteriorated moderately, it was attributable to chronic disease.

Female↗
PubMed2002

Anti-interleukin-8 autoantibodies in patients at risk for acute respiratory distress syndrome.

OBJECTIVE: To test the hypothesis that elevated concentrations of interleukin-8 associated with anti-interleukin-8 autoantibodies (anti-interleukin-8:interleukin-8 complexes) are found in patients at risk for acute respiratory distress syndrome who developed the disease. DESIGN: Measurement of anti-interleukin-8:interleukin-8 complex concentrations in previously collected bronchoalveolar lavage fluids. These fluids were obtained from patients at risk for acute respiratory distress syndrome who subsequently either recovered or developed acute respiratory distress syndrome. PATIENTS: A unique population of patients at risk for acute respiratory distress syndrome was studied. There were 26 patients at risk for acute respiratory distress syndrome who were divided into three groups. Group I patients had high interleukin-8 concentrations and developed acute respiratory distress syndrome, group II had high interleukin-8 concentrations and did not develop acute respiratory distress syndrome, and group III had low interleukin-8 concentrations and did not develop acute respiratory distress syndrome. These patients were selected to test the hypothesis that presence of elevated concentrations of anti-interleukin-8:interleukin-8 complexes differentiates patients at risk for acute respiratory distress syndrome who developed acute respiratory distress syndrome from patients who did not. MEASUREMENTS AND MAIN RESULTS: Bronchoalveolar lavage fluid concentrations of interleukin-8 associated with the anti-interleukin-8 autoantibodies were significantly different between groups (p <.03). The amount of interleukin-8 bound to the anti-interleukin-8 autoantibody was higher in group I than in group II and group III. CONCLUSIONS: Bronchoalveolar lavage fluid concentration of anti-interleukin-8:interleukin-8 complexes may serve as a marker of disease progression in patients at risk for acute respiratory distress syndrome.

Antigen-Antibody Complex↗
PubMed2001

Leukotoxin-diol: a putative toxic mediator involved in acute respiratory distress syndrome.

Leukotoxin is clinically associated with acute respiratory distress syndrome (ARDS). Recently, we found that leukotoxin-diol, the hydrated product of leukotoxin, is more toxic than the parent leukotoxin in vitro (Moghaddam and colleagues, Nature Med. 1997;3:562-566). To test if this difference in the toxicity of leukotoxin and leukotoxin-diol exists in vivo, Swiss Webster mice were administered leukotoxin or leukotoxin-diol. All mice treated with leukotoxin-diol died of ARDS-like respiratory distress, whereas the animals exposed to leukotoxin at the same dose survived. Histopathologic evaluation of the lungs revealed massive alveolar edema and hemorrhage with interstitial edema around blood vessels in the lungs of mice treated with leukotoxin-diol, whereas the lungs of mice treated with identical doses of leukotoxin had perivascular edema only and little change in alveolar spaces. Immunohistochemistry showed that the soluble epoxide hydrolase responsible for the hydrolysis of leukotoxin to its diol is concentrated in the vascular smooth muscle of small and medium-sized pulmonary vessels. In addition, 4-phenylchalcone oxide, an inhibitor of soluble epoxide hydrolase, was found to decrease the mortality induced by leukotoxin but had no effect on mortality induced by leukotoxin-diol. These studies provide strong in vivo evidence that leukotoxin may act as a protoxicant and that the corresponding diol is a putative toxic mediator involved in the development of ARDS.

Animals↗
PubMed2002

Adjunctive corticosteroids therapy in acute respiratory distress syndrome owing to disseminated coccidioidomycosis.

Coccidioides immitis causes a benign upper respiratory tract infection in endemic areas. Acute respiratory distress syndrome is a rare complication that is associated with high mortality. Corticosteroids have been avoided as adjunctive therapy to antifungals in the treatment of acute respiratory distress syndrome secondary to coccidioidomycosis because of the fear of enhancing fungal virulence, but they have been proven safe and effective in other infectious entities. We are presenting a case of severe acute respiratory distress syndrome owing to a fulminant coccidioidomycosis infection that responded to a short course of systemic corticosteroids in addition to the standard antifungal treatment.

Acute Disease↗
PubMed1979

How to manage adult respiratory distress syndrome.

The key clinical features of adult respiratory distress syndrome are increasing dyspnea, tachypnea, and work of breathing; diffuse pulmonary infiltrations on chest radiographs; severe hypoxemia; and absence of a classic diagnosis. Adequate tissue oxygenation is the cornerstone of therapy. Therapeutic modalities include mechanical ventilation, fluid restriction, diuretics, and cardiotonic and vasopressor agents.

Adult↗
PubMed1981

[Amniotic fluid testing - importance to prophylaxis against idiopathic respiratory distress syndrome (author's transl)].

For glucocorticoid prophylaxis against idiopathic respiratory distress syndrome, the authors feel that a decisive role is played by the waiting period following administration, depending on the results of amniotic fluid testing. They decided to wait 48 hours in cases of immature lung and 24 hours in cases of mature lung, both holding patterns under the protection of antibiotics. The incidence of idiopathic respiratory distress syndrome among their premature births over two years as well as mortality due to that cause were found to be lower than those in a control group. Antibiotic-protected holding before delivery did not aggravate the curves of maternal nor foetal infections.

Amniotic Fluid↗
PubMed1994

Adult respiratory distress syndrome: outcome in a community hospital.

BACKGROUND: Published reports indicate that survival rates of patients with adult respiratory distress syndrome have not improved dramatically since the first report of the condition in 1967. However, changes in ventilator strategies and improved critical care management may result in better survival rates in patients with well-defined, severe adult respiratory distress syndrome. OBJECTIVES: To report the outcomes of patients with adult respiratory distress syndrome treated in a community hospital and compare these findings with those in previously published reports. METHODS: A retrospective study design was used. All patients diagnosed with adult respiratory distress syndrome (N = 47) over a 2-year period were studied. RESULTS: For the study patients, the survival rate was 64%; 29% died from respiratory failure alone. Analysis demonstrated that advanced age was not associated with mortality. Pressure-control ventilation was used for 31 patients and there was no significant difference in the presence of barotrauma in the pressure-control mode vs volume ventilation. CONCLUSION: This survival rate exceeds most recently reported rates and thus supports the idea that improvement in treatment of adult respiratory distress syndrome is occurring.

Adult↗
PubMed2004

Acute respiratory distress syndrome in children with severe motor and intellectual disabilities.

We report 13 severely disabled children with acute respiratory distress syndrome, who were treated at the Department of Pediatrics, Niigata City General Hospital between 1995 and 2002. The children ranged in age from 1 year to 16 years. All were non-ambulant. Chronic aspiration and gastro-esophageal reflux were recognized in 12 patients. Patients had the rapid onset of dyspnea refractory to oxygen therapy. Diffuse bilateral lung infiltrates were present on chest X-ray. Predisposing events included sepsis (3 patients), pneumomia (7 patients), pancreatitis (1 patient) and two children with other infections. All required mechanical ventilation for periods of 3-26 days and received oxygen for 5-64 days. Steroid therapy and surfactant therapy were given to eight and three patients, respectively. Only one patient developed an air leak complication. Despite intensive care, three children died, one underwent tracheostomy and nine recovered completely. Acute respiratory distress syndrome is a commonly recognized cause of acute respiratory failure following a variety of insults. It is characterized by the acute onset of dyspnea refractory to oxygen therapy, and diffuse lung infiltrates. Children with severe motor and intellectual disabilities had various complications. In this study, chronic aspiration and gastro-esophageal reflux are considered to be one of predisposing factors triggering acute respiratory distress syndrome in children with severe motor and intellectual disabilities. Although acute respiratory distress syndrome was considered to be a not infrequent occurrence, its mortality rate might be low despite the severity of the disease in children with severe motor and intellectual disabilities. Acute respiratory distress syndrome can be a complication seen in severely disabled children.

Adolescent↗
PubMed2000

Treatment with exogenous surfactant stimulates endogenous surfactant synthesis in premature infants with respiratory distress syndrome.

OBJECTIVE: Treatment of preterm infants with respiratory distress syndrome (RDS) with exogenous surfactant has greatly improved clinical outcome. Some infants require multiple doses, and it has not been studied whether these large amounts of exogenous surfactant disturb endogenous surfactant metabolism in humans. We studied endogenous surfactant metabolism in relation to different amounts of exogenous surfactant, administered as rescue therapy for RDS. DESIGN: Prospective clinical study. SETTING: Neonatal intensive care unit in a university hospital. PATIENTS: A total of 27 preterm infants intubated and mechanically ventilated for respiratory insufficiency. INTERVENTIONS: Infants received a 24-hr infusion with the stable isotope [U-13C]glucose starting 5.3 +/- 0.5 hrs after birth. The 13C-incorporation into palmitic acid in surfactant phosphatidylcholine (PC) isolated from serial tracheal aspirates was measured. Infants received either zero (n = 5), one (n = 4), two (n = 15), or three (n = 3) doses of Survanta (100 mg/kg) when clinically indicated. MEASUREMENTS AND MAIN RESULTS: Using multiple regression analysis, the absolute synthesis rate (ASR) of surfactant PC from plasma glucose increased with 1.3 +/- 0.4 mg/kg/day per dose of Survanta (p = .007) (mean +/- SEM). The ASR of surfactant PC from glucose was increased by prenatal corticosteroid treatment with 1.3 +/- 0.4 mg/kg/day per dose corticosteroid (p = .004), and by the presence of a patent ductus arteriosus with 2.1 +/- 0.7 mg/ kg/day (p = .01). CONCLUSION: These data are reassuring and show for the first time in preterm infants that multiple doses of exogenous surfactant for RDS are tolerated well by the developing lung and stimulate endogenous surfactant synthesis.

Anti-Inflammatory Agents↗
PubMed1992

Release of eicosanoids and endothelin in an experimental model of adult respiratory distress syndrome.

In an experimental model of adult respiratory distress syndrome (ARDS) we have investigated the release of several vasoactive mediators since the rapid and severe increase in pulmonary arterial pressure is known to be a key feature in this condition. Intravenous injection of oleic acid (OA) into rats resulted in the development of a syndrome similar to ARDS characterized by severe hypoxia. As early as 15 min after OA injection elevated levels of 11-deoxy-15-keto-13,14-dihydro-11,16-cyclo-prostaglandin (PG) E2 (DKH2-cyclo-PGE2) as an indicator of endogenous PGE2 formation could be observed. Similarly, elevated levels of cysteinyl-leukotrienes (LT), determined as immunoreactive (ir) LTE4, and ir-endothelin (ET) could be detected. These mediators were found to be elevated in plasma samples for at least 3 h. In addition, rather large amounts of ir-ET could be detected in bronchoalveolar lavage (BAL) fluid samples between 1 h and 3 h. Thus, it seems possible that cysteinyl-LT and peptides of the ET family, both known for their vasoactivity, might be involved in the pathophysiological process of ARDS.

Animals↗
PubMed2004

Protective ventilation of patients with acute respiratory distress syndrome.

The majority of patients with acute respiratory distress syndrome (ARDS) require mechanical ventilation. This support provides time for the lungs to heal, but the adverse effects of mechanical ventilation significantly influence patient outcome. Traditionally, these were ascribed to mechanical effects, such as haemodynamic compromise from decreased venous return or gross air leaks induced by large transpulmonary pressures. More recently, however, the ARDS Network study has established the clinical importance of lowering the tidal volume to limit overdistension of the lung when ventilating patients with ARDS. This study suggests that ventilator-associated lung injury (VALI) caused by overdistension of the lung contributes to the mortality of patients with ARDS. Moreover, the results from clinical and basic research have revealed more subtle types of VALI, including upregulation of the inflammatory response in the injured and overdistended lung. This not only damages the lung, but the overflow of inflammatory mediators into the systemic circulation may explain why most patients who die with ARDS succumb to multi-organ failure rather than respiratory failure. The results of these studies, the present understanding of the pathophysiology of VALI, and protective ventilatory strategies are reviewed.

Barotrauma↗
PubMed2004

Bile acid pneumonia: a "new" form of neonatal respiratory distress syndrome?

We describe 3 cases of neonatal respiratory distress syndrome (RDS) in near-term infants, born from mothers with severe intrahepatic cholestasis of pregnancy. Common pictures of the cases were: good indices of lung maturity in the amniotic fluid; severe RDS requiring mechanical ventilation; high serum bile acid (BA) levels in the early days of life; no meconium aspiration; negative cultures; and absence of indirect laboratory signs of infection. After the first case, we hypothesized that abnormally high BA levels could have reversed the action of phospholipase A2 in the lungs, causing a degradation of phosphatidylcholines to lysophosphatidylcholines and the consequent lack of surfactant activity, leading to the severe respiratory distress. Consequently, in cases 2 and 3, we gave intratracheal surfactant to the infants, which, although administered around the first 24 hours of life, showed to be helpful. Our experience suggests that a high level of attention in the management of newborn infants (even near-term infants) born from women with intrahepatic cholestasis of pregnancy is necessary to detect as soon as possible signs and symptoms of this "unexpected" RDS, which can assume a very severe clinical picture. In such instances, we recommend that the diagnosis of BA pneumonia be kept in mind and that exogenous surfactant be given as soon as possible, even in the presence of indices of normal lung maturity in the amniotic fluid. Finding high levels of BA and lysophosphatidylcholines in the bronchoalveolar lavage of affected infants would aid in support of the diagnosis.

Bile Acids and Salts↗
PubMed2003

[Acute respiratory distress syndrome].

Current literature on acute respiratory distress-syndrome (ARDS) is reviewed with characteristics of the terms "acute pulmonary lesion" and "ARDS". Clinical and x-ray classifications of ARDS are presented. Etiology and pathogenesis, epidemiology, clinical manifestations and principles of current treatment are discussed. Use of mechanical ventilation of the lungs in ARDS patients is physiologically validated. Much attention is payed to application of natural and artificial surfactants.

Humans↗