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PubMed2001

Current concepts in adult respiratory distress syndrome in children.

Acute respiratory distress syndrome (ARDS) is an acute form of severe alveolar-capillary injury that evolves after a direct or indirect lung insult. It begins as noncardiogenic pulmonary edema and develops into a neutrophilic alveolitis, and, later, pulmonary fibrosis. Mortality remains high among children with ARDS, particularly when serious underlying conditions co-exist, sepsis occurs, and when there is multi-organ failure. Lung function improves with time among survivors, but pulmonary fibrosis may persist. Advances in the care of children with ARDS include the use of lung-protective ventilator strategies, permissive hypercapnia, inhaled nitric oxide, high-frequency ventilation, and extra-corporeal life support. These approaches reduce ventilator-associated lung injury and may improve survival when used in combination with one another. Interventions that reduce alveolar inflammation, enhance alveolar fluid removal, and reduce pulmonary fibrosis will further improve survival and recovery from ARDS in the future.

Bronchodilator Agents↗
PubMed1976

Interruption of patent ductus arteriosus in premature infants with respiratory distress syndrome.

In infants with respiratory distress syndrome (RDS) hypoxemia inhibits closure of the patent ductus arteriosus (PDA), resulting in increased pulmonary blood flow with subsequent increased hypoxemia. In an attempt to interrupt this cycle 42 consecutive premature infants with RDS and PDA, weighing between 550 and 2,000 gm (average, 1,383 gm) and with an average gestational age of 31 weeks, were arbitrarily treated either medically (13 patients) or by interruption of the PDA (20 patients). Eleven patients who were initially treated medically could not be weaned from the respirator and later underwent operation. There were no operative or anesthetic deaths; late survival was 65% (20 patients). The last 31 patients were randomly divided into operative and nonoperative groups. Preliminary results revealed no significant differences in late survival between the two groups. Since the operative risk is minimal, further investigative efforts are indicated to settle this issue.

Digoxin↗
PubMed2001

The characteristics of bronchoalveolar lavage from a patient with antiphospholipid syndrome who developed acute respiratory distress syndrome.

The purpose of this study was to investigate the biochemical characteristics as well as the occurrence and specificity of antiphospholipid antibodies in the bronchoalveolar lavage (BAL) fluid from a patient with both antiphospholipid antibodies syndrome (APS) and acute respiratory distress syndrome (ARDS). Proteins, lipids, cells and autoantibodies were determined. Immunoglobulins were purified with affinity chromatography. Autoantibody identification was assessed with enzyme-linked immunosorbent assay (ELISA) and with electrophoresis, followed by immunoblotting and revelation with antihuman IgG-peroxidase conjugate. Antiphospholipid antibodies were found to be present in the BAL fluid as well as in the serum from a patient with APS. Specifically, antiphosphatidylserine and antiphosphatidic acid IgG antibodies in the BAL fluid and antiphosphatidylcholine and anticardiolipin IgG antibodies in the serum were detected at high levels. BAL fluid protein and the percentage of neutrophils were found to be increased. A quantitative as well as qualitative deficiency of surfactant phospholipids was also observed. Antibodies directed against surfactant phospholipids could cause surfactant abnormalities and an inflammatory reaction. These disorders may be one of the causes of the ARDS or a factor in the perpetuation of the inflammation.

Adult↗
PubMed1977

Maternal intravenous ethanol in the prevention of respiratory distress syndrome.

The occurrence of respiratory distress syndrome (RDS) was studied in 68 premature neonates whose mothers were treated with at least one six-hour course of intravenous ethyl alcohol within 48 hours before delivery. At the gestational interval of 28 to 32 weeks, significant differences were observed in the incidence of RDS (p = less than 0.05), in severe RDS (p = less than 0.005), and in the mortality rate from RDS ( = less than 0.05), when compared to premature neonates not treated with alcohol and delivered during the same time interval. Several high-risk factors were found unevenly distributed between treated and control groups of patients, and their relevance to RDS was discussed. Premature rupture of membranes of more than 24 hours did not protect infants from RDS in the patients studied. Explanations for possible mechanisms of action are discussed.

Apgar Score↗
PubMed2005

Low-dose steroid therapy at an early phase of postoperative acute respiratory distress syndrome.

BACKGROUND: The acute respiratory distress syndrome (ARDS) that develops after thoracic surgery is usually lethal. The use of corticosteroids to treat ARDS has been the subject of great controversy. METHODS: Therefore we compared conventional therapy with early low-dose steroid therapy in the treatment of postoperative ARDS. Methylprednisolone was given daily as an intravenous push every 6 hours and was changed to a single oral dose or discontinued, with a loading dose of 2 mg/kg followed by 2 mg/kg per day. RESULTS: Over 2.5 years, 523 major thoracic operations were performed with postoperative ARDS developing in 20 patients (3.8%), of which 8 were treated with conventional therapy and 12 with early low-dose steroid therapy. Early low-dose steroid therapy significantly reduced postoperative mortality, with 7 patients (58.3%) recovering without mechanical ventilation. CONCLUSIONS: We believe this is the first clinical study of low-dose methylprednisolone at an early phase of postoperative ARDS. The beneficial effects of the use of early low-dose steroids in ARDS are consistent with the hypothesis that fibroproliferation is an early response to lung injury, which is inhibited by early low-dose steroid therapy without disturbing operative wound healing.

Administration, Oral↗
PubMed2001

Enhanced systolic function of the right ventricle during respiratory distress syndrome in newborn lambs.

Respiratory distress syndrome (RDS) causes pulmonary hypertension. It is often suggested that this increased afterload for the right ventricle (RV) might lead to cardiac dysfunction. To examine this, we studied biventricular function in an experimental model. RDS was induced by lung lavages in seven newborn lambs. Five additional lambs served as controls. Cardiac function was quantified by indexes derived from end-systolic pressure-volume relations obtained by pressure-conductance catheters. After lung lavages, a twofold increase of mean pulmonary arterial pressure (from 15 to 34 mmHg) was obtained and lasted for the full 4-h study period. Stroke volume was maintained (5.2 +/- 0.6 ml at baseline and 6.1 +/- 1.4 ml at 4 h of RDS), while RV end-diastolic volume showed only a slight increase (from 6.5 +/- 2.3 ml at baseline to 7.7 +/- 1.3 ml at 4 h RDS). RV systolic function improved significantly, as indicated by a leftward shift and increased slope of the end-systolic pressure-volume relation. Left ventricular systolic function showed no changes. In control animals, pulmonary arterial pressure did not increase and right and left ventricular systolic function remained unaffected. In the face of increased RV afterload, the newborn heart is able to maintain cardiac output, primarily by improving systolic RV function through homeometric autoregulation.

Algorithms↗
PubMed1993

Four markers of collagen metabolism as possible indicators of disease in the adult respiratory distress syndrome.

During the adult respiratory distress syndrome (ARDS), an irreversible fibrotic process can occur extremely rapidly. To establish indices of ARDS in pneumonia as well as the severity of the lung fibrosis, we have undertaken for the first time a study of four markers of collagen metabolism obtained from both bronchoalveolar lavage fluid (BALF) and serum: Type I (CI), Type III (CIII), N-terminal peptide of Type III procollagen (PIIINP), and galactosylhydroxylysylglucosyltransferase activity (GGT). We studied 61 patients (13 coma controls, 29 with pneumonia, and 19 with ARDS). In BALF, the average values of CI, CIII, PIIINP, and GGT were significantly higher in ARDS than in the control patients. The values for patients with pneumonia, although increased, were significantly lower than those in ARDS for CI, CIII, and PIIINP. In serum, the mean CI and PIIINP were significantly increased in pneumonia and ARDS, but the mean CIII was significantly increased only in ARDS compared with the control group. Significant positive linear correlations were observed for ARDS between CI and CIII or PIIINP and CIII in BALF and serum. Such correlations were observed for pneumonia only in serum. Molecular mass determinations demonstrated that CI- and CIII-related antigens in BALF were essentially intact triple helices of collagens or procollagens. Among patients with histologically defined interstitial fibrosis, the level of PIIINP in BALF was significantly higher for those with an additional intraalveolar fibrosis. In conclusion, measurements of these collagen markers may be useful for assessing disease activity and reflecting the flux of collagen molecules in the lung.

Adult↗
PubMedDate not supplied

Acute effects of upright position on gas exchange in patients with acute respiratory distress syndrome.

Patients with acute respiratory distress syndrome (ARDS) have dorsal atelectasis of the lungs. This is probably caused by several mechanisms: compression on dependent lung zones, purulent secretions in alveoli, and upward shift of the diaphragm. An upright position (UP) of the patient (the whole body in a straight line at 40 to 45 degrees) can theoretically ameliorate these mechanisms. The objective was to evaluate whether there was an improvement of gas exchange during UP of ARDS patients and to evaluate the hemodynamic effects. A prospective interventional study was performed in the surgical and medical ICUs and the burn unit of the Ghent University Hospital, a tertiary care center. Included were ARDS patients with onset of ARDS within 48 hours before start of the study. Patients were excluded when there was hemodynamic instability or when the PaO2/FiO2 ratio deteriorated during the 2 hours preceding UP. After a 2-hour observation period in a semirecumbent position, patients were put in UP for 12 hours. Respiration and hemodynamic data were recorded at the start and end of the 2-hour observation period, and after 1, 4, and 12 hours in UP. Eighteen patients were included in the study. There was a significant increase of the PaO2/FiO2 ratio during UP (P < .001). Except for the need for volume resuscitation in 5 patients (27.8%), there was no significant change in the hemodynamic profile of the patients. Upright positioning of patients with ARDS, a relatively simple maneuver, resulted in an improvement of gas exchange and was tolerated hemodynamically relatively well during a 12-hour observation period.

Adolescent↗
PubMed1998

Inflammatory mediators in bronchoalveolar lavage fluid and plasma in leukocytopenic patients with septic shock-induced acute respiratory distress syndrome.

OBJECTIVES: The acute respiratory distress syndrome (ARDS) is a frequent complication of severe sepsis and a major cause of death in patients with hematologic malignancy during chemotherapy-induced leukocytopenia. Inflammatory mediators are important modulators of host response to injury and have been found to be increased in the bronchoalveolar lavage (BAL) fluid of nonleukocytopenic patients with ARDS. Since inflammatory cytokines in plasma of nonleukocytopenic patients seem to be efficient predictors of the course of ARDS, we examined this hypothesis in leukocytopenic patients with septic shock-induced ARDS. DESIGN: Prospective, observational study. SETTING: Intensive care unit (ICU) of a university hospital. PATIENTS: Nineteen patients with leukocytopenia (white blood cell count of <1/nL) following cytoreductive chemotherapy for malignant disorders and severe sepsis with shock-induced ARDS (Murray score of >2.5). INTERVENTIONS: BAL and plasma sampling and ICU management. MEASUREMENTS AND MAIN RESULTS: The proinflammatory cytokines tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-8 were measured in the BAL aspirates and in plasma samples, both obtained within 18 hrs after onset of ARDS. Hemodynamic and oxygen metabolism data were measured immediately before plasma samples were taken and BAL was performed. Of the 19 patients studied, nine patients responded to ICU treatment (e.g., mechanical ventilation as indicated by PaO2/FIO2, FIO2, shunt volume, and course of pulmonary infiltrates), whereas ten patients did not respond. BAL cytokine concentrations were significantly increased in nonresponders in comparison with responding patients (TNF-alpha, p = .021; IL-6, p = .008; IL-8, p = .019). In contrast, we did not observe any differences between the groups in terms of plasma cytokine concentrations. CONCLUSION: Determination of cytokine concentrations in BAL samples may be useful for evaluation of severity and course of ARDS in leukocytopenic patients, whereas measurement of plasma cytokines is not helpful.

Adult↗
PubMed1997

Relative production of tumour necrosis factor alpha and interleukin 10 in adult respiratory distress syndrome.

BACKGROUND: The adult respiratory distress syndrome (ARDS) may be regarded as an example of an uncontrolled or excessive inflammatory response in which tumour necrosis factor alpha (TNF-alpha) has been proposed to play a central role. Interleukin 10 (IL-10) has been identified as an important regulator of this response. The potential role for IL-10 in this context was investigated by measuring the relative production of IL-10 and TNF-alpha protein in the plasma, bronchoalveolar lavage (BAL) fluid, and alveolar macrophage culture supernatants of patients with, or at risk of developing, ARDS. METHODS: Twenty six patients were studied from three groups at risk of or with ARDS: sepsis (n = 12), multiple trauma (n = 8), and perforated bowel (n = 6). Ten patients had ARDS. Bronchoalveolar lavage and venepuncture were performed within 24 hours of arrival on the intensive therapy unit or of diagnosis of ARDS. IL-10 and TNF-alpha protein were detected in the plasma, BAL fluid, and alveolar macrophage supernatants by sandwich enzyme linked immunoabsorbent assays. RESULTS: The median IL-10 concentrations in the plasma and BAL fluid of patients with ARDS were significantly lower than the concentrations detectable in the plasma (median difference-17.5, 95% CI -52.4 to 1.31, p < 0.05) and BAL fluid of at risk patients (median difference -32.1, 95% CI -47.5 to 2.3, p < 0.05). There was a tendency towards enhanced concentrations of TNF-alpha detectable in the alveolar macrophage supernatants and the BAL fluid of patients with ARDS compared with at risk patients, although this did not reach statistical significance. No difference was observed in the plasma concentrations of TNF-alpha between the two groups. The ratios of TNF-alpha to IL-10 protein in the BAL fluid of patients with ARDS and at risk patients were 3.52 and 0.85, respectively (median difference 1.44, 95% CI 0.07 to 5.01, p < 0.01). There was no difference in alveolar macrophage production of IL-10 between the two groups. CONCLUSIONS: This study highlights the potential importance of the pro-inflammatory versus the anti-inflammatory imbalance in ARDS which may be reflected by the ratio of IL-10 and TNF-alpha in the lung.

Bronchoalveolar Lavage Fluid↗
PubMed2001

Metalloproteinase inhibition prevents acute respiratory distress syndrome.

BACKGROUND: The acute respiratory distress syndrome (ARDS) occurs in patients with clearly identifiable risk factors, and its treatment remains merely supportive. We postulated that patients at risk for ARDS can be protected against lung injury by a prophylactic treatment strategy that targets neutrophil-derived proteases. We hypothesized that a chemically modified tetracycline 3 (COL-3), a potent inhibitor of neutrophil matrix metalloproteinases (MMPs) and neutrophil elastase (NE) with minimal toxicity, would prevent ARDS in our porcine endotoxin-induced ARDS model. METHODS: Yorkshire pigs were anesthetized, intubated, surgically instrumented for hemodynamic monitoring, and randomized into three groups: (1) control (n = 4), surgical instrumentation only; (2) lipopolysaccharide (LPS) (n = 4), infusion of Escherichia coli lipopolysaccharide at 100 microg/kg; and (3) COL-3 + LPS (n = 5), ingestion of COL-3 (100 mg/kg) 12 h before LPS infusion. All animals were monitored for 6 h following LPS or sham LPS infusion. Serial bronchoalveolar lavage (BAL) samples were analyzed for MMP concentration by gelatin zymography. Lung tissue was fixed for morphometric assessment at necropsy. RESULTS: LPS infusion was marked by significant (P < 0.05) physiological deterioration as compared with the control group, including increased plateau airway pressure (P(plat)) (control = 15.7 +/- 0.4 mm Hg, LPS = 23.0 +/- 1.5 mm Hg) and a decrement in arterial oxygen partial pressure (P(a)O(2)) (LPS = 66 +/- 15 mm Hg, Control = 263 +/- 25 mm Hg) 6 h following LPS or sham LPS infusion, respectively. Pretreatment with COL-3 reduced the above pathophysiological changes 6 h following LPS infusion (P(plat) = 18.5 +/- 1.7 mm Hg, P(a)O(2) = 199 +/- 35 mm Hg; P = NS vs control). MMP-9 and MMP-2 concentration in BAL fluid was significantly increased between 2 and 4 h post-LPS infusion; COL-3 reduced the increase in MMP-9 and MMP-2 concentration at all time periods. Morphometrically LPS caused a significant sequestration of neutrophils and monocytes into pulmonary tissue. Pretreatment with COL-3 ameliorated this response. The wet/dry lung weight ratio was significantly greater (P < 0.05) in the LPS group (10.1 +/- 1.0 ratio) than in either the control (6.4 +/- 0.5 ratio) or LPS+COL-3 (7.4 +/- 0.6 ratio) group. CONCLUSIONS: A single prophylactic treatment with COL-3 prevented lung injury in our model of endotoxin-induced ARDS. The proposed mechanism of COL-3 is a synergistic inhibition of the terminal neutrophil effectors MMPs and NE. Similar to the universal practice of prophylaxis against gastric stress ulceration and deep venous thromboses in trauma patients, chemically modified tetracyclines may likewise be administered to prevent acute lung injury in critically injured patients at risk of developing ARDS.

Animals↗
PubMed1965

THE CURRENT STATUS OF THE RESPIRATORY DISTRESS SYNDROME OF THE NEWLY BORN.

The respiratory distress syndrome (RDS) occurs in 14% of premature infants and is twice as common and twice as lethal in males as in females. Recent work suggests that, during the intrauterine period a disturbance in nutrition of the lung resulting from fetal pulmonary vascular constriction results in alveolar-cell damage and a decrease in pulmonary surface activity with resultant atelectasis. Data on respiratory work levels, oxygen consumption and arterial oxygen tension suggest that there is an oxygen debt in the acute stage of the disease. Such data have further clarified the pathogenesis of the metabolic and respiratory components of the acidosis and the secondary effects thereof. In prevention, prophylaxis of prematurity is of major importance. A program of treatment designed to combat the various aspects of the pathophysiological disturbances is described in the form of a case profile. Modern methods of observation, biochemical control and treatment, as well as the necessity for critical evaluation, suggest that infants with RDS are best cared for in special centres.

Acidosis↗
PubMed1983

Surfactant function in respiratory distress syndrome.

Airway samples from infants with respiratory distress syndrome were recovered by suction immediately after tracheal intubation for respiratory failure. The minimum surface tension of these airway samples was 27.3 +/- 3.0 dynes/cm. Surfactant with low surface tension (1.4 +/- 1.0 dynes/cm) was recovered from these samples by centrifugation; the supernatant fractions from the samples had high minimum surface tensions. The supernatant fractions contained soluble proteins that inhibited the surface tension-lowering properties of natural sheep surfactant. Similar supernatant fractions collected from infants intubated for reasons other than respiratory distress syndrome were much less inhibitory to sheep surfactant. The minimum surface tension of sequential daily airway samples from infants with respiratory distress syndrome fell progressively to 5.7 +/- 2.4 dynes/cm on the day of extubation. These results document the presence of proteins in the airways of infants with respiratory distress syndrome that inhibit the surface tension-lowering properties of surfactant.

Animals↗
PubMed1992

[Pneumoperitoneum in a premature, non-ventilated neonate with respiratory distress syndrome leading to respiratory failure. What is the etiology?].

The authors describe the finding of extensive tensive pneumoperitoneum which developed during distension therapy (CNP) in an immature neonate. The absence of another extraalveolar cumulation of air made the authors use PO2 analysis in the peritoneal air by means of a transcutaneous electrode. Because the PO2 rose after connection of the electrode to the catheter draining the abdominal cavity, the authors assumed a respiratory aetiology of the pneumoperitoneum and did not consider laparatomy. They assume that the above test may be valuable in the differential diagnosis between respiratory and gastrointestinal pneumoperitoneum in those instances where it is not possible to assess the aetiology of pneumoperitoneum unequivocally.

Humans↗
PubMed1996

[Value of surfactant in the treatment of acute respiratory distress syndrome in a child].

BACKGROUND: Adult respiratory distress syndrome has a high mortality rate, despite treatment including mechanical ventilation with positive end-expiratory pressure, increase of the inspiratory time and high inspiratory oxygen concentration. Exogenous surfactant, a well established treatment in premature newborns with neonatal respiratory distress syndrome has only been occasionally evaluated in adult respiratory distress syndrome. CASE REPORT: A 3 year-old child suffered from adult respiratory distress secondary to respiratory syncytial virus infection. Both mechanical ventilation and inhaled nitric oxide failed to improve the respiratory distress. Two doses of intratracheal surfactant application immediately improved pulmonary functions, transiently after the first instillation on day 13 and definitely after the second one, on day 16. CONCLUSION: Exogenous surfactant appeared to be useful for the survival of our patient but prospective evaluation of this treatment in adult respiratory distress syndrome is needed.

Acute Disease↗
PubMed2002

Acute respiratory distress syndrome epidemiology and pathophysiology.

Acute respiratory distress syndrome is a devastating syndrome of lung injury following known risk factors, with a persistently high mortality. A consensus conference definition of ARDS has been adopted by clinical researchers, but potential problems remain. ARDS may represent more than one entity, and radiographic and mechanical differences between pulmonary versus extrapulmonary initiated ARDS have been described. There is increasing recognition of inflammatory mediators in the pathophysiology of acute lung injury. Surfactant abnormalities contribute to the associated lung dysfunction. A growing body of evidence supports the presence of VILI and a potential mechanism for developing MOSF, and has led to new management strategies. The importances of apoptosis to the repair process, and mechanisms that may lead to persistent fibrosis, such as the activation of the coagulant pathway with fibrin deposition, are increasingly recognized.

Animals↗
PubMed1982

Ischemic necrosis of both lower extremities as a result of the microembolism syndrome complicating the adult respiratory distress syndrome caused by Escherichia coli pneumonia and septicemia.

Extensive gangrene of both lower extremities necessitating bilateral above-the-knee amputations complicated the adult respiratory distress syndrome (ARDS) caused by Escherichia coli pneumonia and septicemia in a 52-yr-old man. Concurrent with the evolution of tissue necrosis, peripheral blood leukocyte and platelet counts fell, and pulmonary vascular resistance increased. Adequacy of the cardiac output was confirmed by repeated thermodilution cardiac output measurements, and major vascular occlusion was excluded surgically. Fibrin degradation products and thrombocytopenia were present, but the other usual criteria for disseminated intravascular coagulation were absent. Small vessel thrombosis by fibrin and leukocytes was observed histologically in the amputated extremities. These findings suggest that gangrene was due to the "microembolism syndrome"--diffuse small vessel occlusion by fibrin thrombi complicating ARDS. This unusual complication of ARDS may occur without abnormalities suggestive of diffuse intravascular coagulation in routine laboratory tests of blood coagulation. It should be suspected and treated promptly to avoid severe disability in survivors.

Escherichia coli Infections↗
PubMed1999

The first case of H5N1 avian influenza infection in a human with complications of adult respiratory distress syndrome and Reye's syndrome.

Avian influenza virus was not known to cause systemic infection in humans before. We report a 3-year-old boy with good past health who developed pneumonia caused by H5N1 avian influenza A virus (A/Hong Kong/156/97). The virus was isolated from a tracheal aspirate. There were complications of Reye's syndrome, adult respiratory distress syndrome, and multiple organ system failure. He had a history of receiving aspirin. His adult respiratory distress syndrome did not respond to endotracheal surfactant replacement therapy. He died 6 days after admission. Clinicians should be alert to the importance of a new human influenza strain.

Child, Preschool↗