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PubMed1995

[Pathophysiology and Diagnosis of the acute respiratory distress syndrome].

We studied methods for diagnosing the acute respiratory distress syndrome (ARDS) based on its characteristic abnormalities. A gamma-ray external counting method with Tc-99m human serum albumin revealed that pulmonary microvascular permeability was abnormally high in patients with ARDS. With this method, ARDS could be distinguished from cardiogenic pulmonary edema. Levels of interleukin-8 in bronchoalveolar fluid from patients with septic ARDS, reexpansion pulmonary edema, and inhalation burn injury were abnormally high. In 21 patients with acute lung injury, 15 of whom had ARDS, plasma concentrations of three inflammatory markers were measured: thiobarbituric acid reactive material which reflects cell membrane lipid peroxidation; 7S collagen, a component of basement membrane; and the soluble form of P-selectin, an adhesion molecule. Levels of all three were abnormally high in patients with ARDS, and correlated with the degree of lung injury and with the outcome in these patients. We conclude that these measurements in plasma or bronchoalveolar lavage fluid may enable us to assess the severity of ARDS.

Biomarkers↗
PubMed1986

Maternal smoking and infant respiratory distress syndrome.

The relationship between maternal smoking and infant respiratory distress syndrome (RDS) was investigated among 550 premature (36 weeks or less) births delivered at the University of Washington Hospital from 1977 to 1980. Forty-five percent of the mothers were smokers. To avoid bias due to the reduced birth weight of infants of smokers, infants of smokers and nonsmokers were compared within small gestational age categories (two-week intervals) and not by birth weight categories. Infants of mothers who smoked had a reduced incidence of RDS for their gestation compared with infants of nonsmokers. The probability of RDS (adjusted for gestational age and method of delivery) was 25% for the infants of smokers versus 38% for the infants of nonsmokers (odds ratio = 0.55, P = .005), equivalent to approximately a 1.5-week acceleration in lung maturity for infants of smokers. The smoking effect was not explained by demographic differences between smokers and nonsmokers, nor by differences in the incidence of pregnancy complications between the two groups. This study adds support to the theory that adverse pregnancy conditions may lead to an acceleration in pulmonary maturity to allow earlier extrauterine adaptation.

Female↗
PubMed1988

Normal lung growth following antenatal dexamethasone treatment for respiratory distress syndrome.

Antenatal steroid therapy reduces the incidence of respiratory distress syndrome (RDS) in premature infants. However, animal studies showed a decrease in lung cell number and lower lung weights in fetal rabbits exposed to hydrocortisone. This prompted us to measure flows and lung volumes (by spirometry and helium-dilution method) in children greater than 6 years who were part of a study by the Collaborative Group on Antenatal Steroid Therapy. The effect of antenatal steroids on subsequent pulmonary function had not previously been studied. Of the 158 children originally enrolled before birth, a total of 8 dexamethasone (DEX)- and 11 placebo-treated children were still local residents and fulfilled the criteria of the study (gestational age, 28-34 weeks; DEX/placebo treatment 1-7 days before delivery). Mean heights and weights were normal with no significant differences between the groups. Pulmonary function tests showed no differences in lung volumes or expiratory flows between the children whose mothers had received antenatal DEX and those who had received placebo. These results indicate no adverse effect of antenatal DEX on subsequent lung volumes and expiratory flows in childhood.

Child↗
PubMed1993

Surfactant and adult respiratory distress syndrome.

In order to determine if the Adult Respiratory Distress Syndrome (ARDS) is associated with a shortage of pulmonary surfactant, we have examined a series of 155 undiluted tracheal aspirates obtained from 23 patients with ARDS and from 30 patients without ARDS, all 53 needing ventilatory support. The unfixed and unstained specimens were examined by polarized light microscopy for the presence of pulmonary surfactant. Free surfactant particles were present in the aspirates of 50 patients (95%). Within minutes of obtaining the specimen, in addition to showing surfactant, the examination of these undiluted, unfixed tracheal aspirates by light microscopy showed the presence of bacterial and fungal infection. As fibrinogen/fibrin inactivates surfactant, the undiluted aspirates of 21 patients with ARDS and of 30 patients without ARDS were stained for the presence of these proteins by a new slide method using 0.01 ml of tracheal aspirate. Fibrinogen/fibrin was found in the aspirates from 20 of 21 patients with ARDS and in only five of 30 patients without ARDS; these five had bronchopneumonia. The method has a sensitivity of 0.95 and a specificity of 0.83. The role of plasma proteins and of neutrophil leucocytes in causing ARDS is discussed.

Adolescent↗
PubMed2000

Chorioamnionitis decreased incidence of respiratory distress syndrome by elevating fetal interleukin-6 serum concentration.

Respiratory distress syndrome (RDS) of newborns is one of the most important factors determining neonatal morbidity and mortality. The interleukin-6 (IL-6) titre in cord sera of RDS-free neonates born to mothers with histological chorioamnionitis was significantly higher than that in RDS-complicated neonates without chorioamnionitis. Maternal administration of glucocorticoid suppressed the IL-6 concentrations in the cord sera of fetuses with chorioamnionitis. The fetuses without chorioamnionitis who suffered from RDS even after maternal glucocorticoid administration showed a similar IL-6 titre to that of RDS-affected neonates without chorioamnionitis. Examination of the mechanism by which IL-6 decreased the incidence of fetal RDS revealed that H441-4, a human pulmonary adenocarcinoma cell line, stimulated with recombinant (r)-IL-6 started the synthesis of mRNA and protein of pulmonary surfactant protein (SP)-A. The present study shows that IL-6 elevation in fetuses with chorioamnionitis promotes fetal lung maturation by inducing SP-A synthesis, thereby decreasing the incidence of RDS in the preterm neonates.

Cell Line↗
PubMed2001

Best compliance during a decremental, but not incremental, positive end-expiratory pressure trial is related to open-lung positive end-expiratory pressure: a mathematical model of acute respiratory distress syndrome lungs.

A mathematical model of the acute respiratory distress syndrome (ARDS) lung, incorporating simulated gravitational superimposed pressure and alveolar opening and closing pressures, was used to study the mean tidal pressure-volume (PV) slope ("effective compliance") during incremental and decremental positive end-expiratory pressure (PEEP) trials with constant tidal volume (VT) "ventilation." During incremental PEEP, the PEEP giving maximum mean tidal PV slope did not coincide with "open lung PEEP" (minimum PEEP preventing end expiratory collapse of 97.5% of alveoli inflated at end-inspiration), and it varied greatly with varying VT and "lung mechanics." Incremental PEEP with a low VT tests recruitment by the peak pressure, not prevention of collapse by PEEP. During decremental PEEP with a low VT, maximum mean tidal PV slope occurred with PEEP 2-3.5 cm H2O below open-lung PEEP, unless closing pressure was high. High VT, high "specific compliance," and high opening pressures caused slightly greater underestimation of open-lung PEEP. Maximum mean tidal PV slope was always higher (e.g., 93.7 versus 16.69 ml/cm H2O), and the variation in PV slope with PEEP was greater, during decremental PEEP. The maximum PV slope during a decremental PEEP trial with a low VT may be a useful method to determine open-lung PEEP in ARDS, and should be studied clinically.

Lung Compliance↗
PubMed2006

Acute respiratory distress syndrome associated with rabies: a case report.

Acute respiratory distress syndrome (ARDS) is the first potentially lethal complication in rabies virus infection, although its occurrence is rare. We report on a fatal case of rabies virus infection in a 45-year-old woman from Hu-Nan Province, China. The neurologic signs of limb numbness and water phobia occurred from 61 days after the dog bite; the clinical course was progressive, with the most severe clinical manifestations being fever, encephalitis, and ARDS. The woman expired 12 days after admission to the hospital. An autopsy proved rabies encephalitis, mainly involving the medulla oblongata, the thalamus, part of the pons, the cerebellum, and the hippocampus. The lung pathologic examination revealed the organizing phase of ARDS with diffuse alveolar damage, hyaline membrane formation, type II alveolar cell hyperplasia accompanied by proliferation of fibroblasts and infiltration of mononuclear cells into the interstitial space. Immunohistochemistry stain and reverse transcription-polymerase chain reaction for rabies virus failed to demonstrate the organism in the lung tissue. Strong expression of inducible nitric oxide synthase (iNOS) was detected in the alveolar macrophages. An immunologic mechanism with iNOS expression in the absence of direct invasion of the organism may participate in the pathogenesis of ARDS associated with rabies.

Female↗
PubMed2004

Pilot study of the effects of ONO-5046 in patients with acute respiratory distress syndrome.

Evidence has linked neutrophil elastase to acute respiratory distress syndrome (ARDS), suggesting that inhibiting the activity of this enzyme could prevent the development and progression of ARDS. However, few clinical trials have examined this notion. We therefore examined the effects of ONO-5046 (sivelestat, a specific inhibitor of neutrophil elastase; sodium N-[2-[4-(2,2-dimethylpropionyloxy) phenylsulfonylaminobenzoyl]amino-acetate tetrahydrate]) in a randomized, double-blinded trial in patients with ARDS. We randomly assigned 24 patients with ARDS to groups that received conventional therapy without or with sivelestat (0.2 mg. kg(-1). h(-1)) for 14 days. The variables of interest associated with clinical outcome were the duration of mechanical ventilation; changes in oxygenation from baseline; changes in cytokine levels from baseline; number of patients alive at 30 days who did not need mechanical ventilation; and mortality rate. The length of intensive care unit stay, number of ventilation days, and mortality rates did not statistically differ between groups. ARDS was more persistent in the control than in the sivelestat group (control, 19.5 +/- 7.4 days; sivelestat, 13.5 +/- 5.9 days; P = 0.039). Neutrophil elastase activity significantly differed between groups at 72 h after treatment. Levels of interleukin-6 were lower in the sivelestat group than in the controls at 24, 48, and 72 h after treatment. ONO-5046 apparently did not affect survival or the duration of mechanical ventilation.

Adult↗
PubMed1996

Mucosal tumor necrosis factor-alpha production and extensive disruption of sulfated glycosaminoglycans begin within hours of birth in neonatal respiratory distress syndrome.

Many of the clinicopathologic features of neonatal respiratory distress syndrome (RDS) may be related to the inflammatory response mounted by the affected infant, although little is known about the interstitial component of this response. We have thus studied the local inflammatory response in this condition by immunohistochemical analysis of whole lung lobes, obtained at postmortem from 40 infants who died from acute RDS in the first week of life. All had demonstrated classical clinical history and histologic features. An archival subgroup from the early 1970s had never received ventilatory support. Immunohistochemical analysis demonstrated rapid temporal increase from birth in the mucosal density of CD68+ macrophages, MAC-387+ monocytes/macrophages, polymorphonuclear neutrophils, and tumor necrosis factor-alpha-immunoreactive cells, maximal in those dying at or after 72 h. Using a cationic probe specific for sulfated glycosaminoglycans (GAGs), the inflammatory infiltration was seen to be associated with striking loss of endothelial, basement membrane, and interstitial GAGs, which was almost complete by 48-72 h. GAG degradation products were found within hyaline membranes in all infants dying after 48 h. This study confirms that neonatal RDS is characterized by intense interstitial inflammation, significantly underestimated on routine staining. This begins within hours of birth and is maximal by 72 h of age. Breakdown of sulfated GAGs within the extracellular matrix follows the same time course and may explain much of the physiologic derangement characteristic of this condition.

Age of Onset↗
PubMed2000

Pilot study of nebulized surfactant therapy for neonatal respiratory distress syndrome.

Thirty-four spontaneously breathing newborns with respiratory distress syndrome (RDS) requiring nasal continuous positive airway pressure (CPAP) and an arterial-to-alveolar oxygen tension ratio (a/A PO2) of 0.15-0.22 were randomized to treatment with nebulized surfactant (Curosurf) or to serve as controls. All children were first supported by nasal CPAP according to normal clinical routines. Surfactant was administered using a modified Aiolos nebulizer, and a total of 480 mg was aerosolized in each case. The control group received no nebulized material, but had the same CPAP support. Acid-base status and a/A PO2 were determined at regular intervals before, during and after surfactant administration. Both groups included in the study were similar with regard to gestational age, birthweight, steroids given before birth, sex and Apgar scores as well as a/A PO2 when entering the study. There were no significant differences between the groups in a/A PO2 1-12 h after randomization, number of infants needing mechanical ventilation, time on ventilator or CPAP. Two children in the treated group developed bronchopulmonary dysplasia. No side effects of the surfactant therapy were noted. No beneficial effects of aerosolized surfactant were demonstrated in our trial, contrary to data from animal experiments. This finding probably reflects differences in administration techniques. Our findings do not justify large clinical trials with the same protocol. Further work is needed to optimize delivery of aerosolized surfactant to the neonatal lung in clinical practice.

Aerosols↗
PubMed1987

Growth and development of infants surviving respiratory distress syndrome: a 2-year follow-up.

In a regional birth cohort of 5,356 live-born infants, during 12 consecutive months, 46 (0.9%) infants suffered from respiratory distress syndrome. Ten of them died before the age of 2 years. The cause of death was respiratory distress syndrome in two cases, intracerebral hemorrhage in four cases, asphyxia in one case, and congenital erythropoietic anemia in one case. Of the 36 survivors, 34 could be traced for the follow-up. Growth and development of the survivors with respiratory distress syndrome were compared with that of 3,375 term infants in the birth cohort with birth weights at the tenth percentile or above with no risk factors recognized during pregnancy, labor, delivery, or the neonatal period. Normal development was found in 85% of the survivors with respiratory distress syndrome and 99% of the control infants at the age of 2 years. Intracerebral hemorrhage and low one- and five-minute Apgar scores were associated with unfavorable outcome at 2 years in the survivors with respiratory distress syndrome. The developmental scores were significantly poorer than those of the controls at 2 years for gross motor, audiovisual, and psychosocial categories, whereas for fine motor development, the difference disappeared by the 2 years of age. The growth of the survivors with respiratory distress syndrome was satisfactory even if their heights remained below that of their control peers.

Anthropometry↗
PubMed1993

Immunogold localization of SP-A in lungs of infants dying from respiratory distress syndrome.

Prematurely born infants can develop the neonatal respiratory distress syndrome (RDS) because of a deficiency of pulmonary surfactant. This lipoprotein complex synthesized by type II pneumocytes has different ultrastructural forms--intra- and extracellular lamellar bodies, which within the alveoli are transformed into tubular myelin, and this in turn gives rise to the surface monolayer, the functionally active form of surfactant. We have previously shown that at autopsy RDS lungs lack tubular myelin and have decreased immunoreactivity for antisera to surfactant protein A (SP-A), an important component of tubular myelin. Therefore, we proposed a role for SP-A in the conversion of lamellar bodies to tubular myelin and in the pathogenesis of RDS. To explore this possibility further, we compared in 14 RDS and 14 control lungs the distribution of SP-A in ultrathin sections, using affinity-purified rabbit anti-human-SP-A IgG and goat anti-rabbit IgG-conjugated with 10 nm colloidal gold particles. In controls, gold label was present in lamellar bodies, endoplasmic reticulum, on the cytoplasmic membrane of type II cells, and on lamellar bodies and tubular myelin either within alveoli or macrophages. In RDS lungs, reduced label was present in the same intracellular compartments and organelles, except in tubular myelin, which is absent. It is postulated that if SP-A is indeed necessary for the conversion of lamellar bodies to tubular myelin, in RDS either there is a deficiency of adequate amounts of functional SP-A or some other important component of surfactant is missing.

Extracellular Space↗
PubMed1996

Plasminogen activator activity in preterm infants with respiratory distress syndrome: relationship to the development of bronchopulmonary dysplasia.

Respiratory distress syndrome (RDS) is characterized by the presence of fibrin-rich exudates in the alveoli. Fibrin and its degradation products may play an important role in the pathogenesis of bronchopulmonary dysplasia (BPD). The purpose of this study was to test the hypothesis that preterm neonates with RDS have depressed alveolar fibrinolytic activity and that those with RDS progressing to BPD have an even greater impairment in alveolar fibrinolysis. Serial tracheal aspirate (TA) samples from intubated neonates--9 control and 46 with RDS--were analyzed for fibrinolytic activity. In neonates with RDS, 26 resolved, 18 progressed to BPD, and 2 died before 28 d. Plasminogen activator (PA) and its inhibitor (PAI) were identified in TA by reverse fibrin autography and immunoblotting. Net PA/plasmin activity in TA was significantly depressed on d 1 of life in patients with self-resolved RDS (median = 20.85 ng/mL, p < 0.05) and RDS progressing to BPD (median = 4.97 ng/mL, p < 0.001) compared with control patients (median = 87.1 ng/mL). In addition, neonates progressing to BPD had significantly lower PA/plasmin activity on day one of life compared with neonates with self-resolved RDS (p < 0.001). ELISA for specific PA and PAI were not significantly different. We speculate that depressed fibrinolytic activity may place preterm neonates at risk for RDS and that the degree of this depression may predict the progression to BPD. In infants < or = 30 wk of gestation at birth with RDS, a PA/plasmin activity < or = 10.0 ng/mL on the 1st d of life had a positive predictive value of 80% (12/15) and a negative predictive value of 82% (9/11) for the progression to BPD.

Amino Acid Sequence↗
PubMed2006

The impact of endotracheal suctioning on gas exchange and hemodynamics during lung-protective ventilation in acute respiratory distress syndrome.

OBJECTIVE: To evaluate the respiratory and hemodynamic effects of open suctioning (OS) versus closed suctioning (CS) during pressure-control (PC) and volume-control (VC) ventilation, using a lung-protective ventilation strategy in an animal model of acute respiratory distress syndrome (ARDS). SETTING: Animal laboratory in a university hospital. DESIGN: Randomized cross-over evaluation. ANIMALS: Eight female Dorset sheep. INTERVENTIONS: Lung lavage was used to simulate ARDS. We applied VC and PC mechanical ventilation with a tidal volume of 6 mL/kg and positive end-expiratory pressure (PEEP), adjusted based on a table of PEEP versus fraction of inspired oxygen (FIO2). Suctioning was performed for 10 s with a suction pressure of -100 mm Hg, during both OS and CS. OS and CS were randomly performed with each animal. Hemodynamics and arterial blood gases were recorded before, during, and after endotracheal suctioning. RESULTS: The PaO2/FIO2 ratios before suctioning were similar in all groups, as were the PEEP and FIO2. PaO2/FIO2 was lower after OS than after CS/VC or CS/PC. There was no post-suctioning difference in oxygenation between CS/VC and CS/PC. PaCO2 recorded 10 min after suctioning was greater than the presuctioning value, in all groups. Intrapulmonary shunt fraction increased between baseline and 10 min post-suctioning with OS and CS/VC, but did not significantly increase with CS/PC. There were no significant changes in hemodynamics pre-suctioning versus post-suctioning with OS, CS/VC, or CS/PC. CONCLUSION: PaO2/FIO2) was better maintained during CS with both VC and PC modes during lung-protective ventilation for ARDS, as compared with OS, and shunt fraction post-suctioning changed least with PC.

Animals↗
PubMed2003

Differential role for T cells in the development of fibrotic lesions associated with reovirus 1/L-induced bronchiolitis obliterans organizing pneumonia versus Acute Respiratory Distress Syndrome.

Bronchiolitis obliterans organizing pneumonia (BOOP) and Acute Respiratory Distress Syndrome (ARDS) are two pulmonary diseases with fibrotic components. BOOP is characterized by perivascular/peribronchiolar leukocyte infiltration leading to the development of intra-alveolar fibrosis. ARDS is a biphasic disease that includes an acute phase, consisting of severe leukocyte infiltration, edema, hemorrhage, and the formation of hyaline membranes, and a chronic phase, which is characterized by persistent intra-alveolar and interstitial fibrosis. CBA/J mice infected with 1 x 10(6) plaque-forming units (pfu) reovirus 1/L develop follicular bronchiolitis and intra-alveolar fibrosis similar to BOOP. In contrast, CBA/J mice infected with 1 x 10(7) pfu reovirus 1/L develop histologic characteristics of ARDS including diffuse alveolar damage, hyaline membranes, and intra-alveolar fibrosis. In this report, we demonstrate a differential role for T lymphocytes in the development of fibrosis associated with BOOP versus ARDS. Neonatally thymectomized CBA/J mice infected with 1 x 10(7) pfu (ARDS) reovirus 1/L still develop the hallmark characteristics of ARDS, including a severe viral pneumonia with cellular infiltrates comprised mainly of macrophages and neutrophils, hyaline membrane formation, and hemorrhage during the acute phase of the disease and persistent intra-alveolar fibrosis during the chronic phase of the disease. In contrast, neonatally thymectomized CBA/J mice infected with 1 x 10(6) pfu (BOOP) reovirus 1/L do not develop intra-alveolar fibrosis associated with BOOP. Therefore, while T cells are necessary for the development of intraluminal fibrosis associated with BOOP, they are not necessary for the development of intraluminal fibrosis associated with ARDS. Furthermore, we suggest that interferon-gamma plays a key role in the fibrotic process and that elevated levels of interferon-gamma are associated with a continuum from least to more severe fibrosis.

Animals↗
PubMed1985

Complement activation and clearance in acute illness and injury: evidence for C5a as a cell-directed mediator of the adult respiratory distress syndrome in man.

The appearance of the adult respiratory distress syndrome (ARDS) during the course of acute illness is believed to result, in part, from intrapulmonary neutrophil sequestration and degranulation induced by circulating inflammatory mediators. To evaluate the role of complement-neutrophil interactions in the pathogenesis of ARDS in man, 34 patients suffering from intra-abdominal sepsis (seven), multisystem trauma (15), or acute pancreatitis (12) were serially studied with regard to neutrophil migratory responses to C5a and F-Met-Leu-Phe, lysosomal content of beta-glucuronidase and lysozyme, and simultaneously obtained plasma levels of immunoreactive C3adesArg and C5adesArg. Nineteen patients developed ARDS. In these patients, plasma C3adesArg levels obtained within 72 hours of admission to the hospital were elevated to 305 +/- 35 ng/ml compared with 145 +/- 16 ng/ml for patients who did not develop ARDS (p less than 0.0005). C5adesArg levels were not elevated in either group. In vitro studies showed that neutrophils from normal persons were able to clear all of the C5a/C5adesArg generated in up to 5% zymosan-activated serum, while no clearance of C3adesArg was identified. Patient migratory responses could be divided into three groups based on their initial (less than 72 hour) samples: (1) hyperresponsive to both N = formyl-methionyl-leucyl-phenylalanine (FMLP) and C5a, (2) specifically deactivated to C5a, and (3) deactivated to both C5a and FMLP. Patients in the latter two groups developed ARDS. Enzyme content of neutrophils from patients who developed ARDS showed a substantial fall in beta-glucuronidase and lysozyme levels. The finding of elevated plasma C3a levels and deactivation of migratory response to C5a support the contention that complement activation had occurred in these patients and that their neutrophils had been exposed to C5a/C5adesArg in vivo. The finding of nonspecific migratory dysfunction associated with lysozymal enzyme loss, a circumstance not reproducible in vitro by C5a exposure, suggests that other stimuli produced degranulation of neutrophils made hyperresponsive by prior exposure to C5a.

Chemotaxis, Leukocyte↗
PubMed1998

Additive effect of nitric oxide inhalation on the oxygenation benefit of the prone position in the adult respiratory distress syndrome.

BACKGROUND: The response to inhaled nitric oxide and prone positioning was investigated in 47 patients with adult respiratory distress syndrome to test the hypothesis that inhalation of nitric oxide when in the prone position would result in additive improvement in oxygenation. METHODS: The authors prospectively studied patients of both genders who were 15 to 75 yr old and had adult respiratory distress syndrome confirmed by computed tomography (lung injury score, 3.1+/-1). RESULTS: Compared with baseline values in the supine position (T1), inhalation of 10 ppm nitric oxide for 1 h (T2) decreased the mean pulmonary artery pressure from 33+/-9 mmHg to 28+/-6 mmHg (P < 0.05; T2 vs. T1) and increased the ratio of the partial pressure of oxygen in arterial blood (PaO2) to inspired oxygen concentration (FiO2) from 115 (median first quartile [Q1] 97, median third quartile [Q3] 137) to 148 (Q1 132, Q3 196) (P < 0.05; T2 vs. T1). Cessation of nitric oxide brought the values back to baseline (T3). Two hours of prone positioning (T4) significantly increased the PaO2:FiO2 ratio (T4 vs. T3). However, after an additional hour of nitric oxide inhalation in the prone position (T5), a significant decrease of the venous admixture (from 33+/-6% to 25+/-6%; P < 0.05) and an increase of the PaO2:FiO2 ratio (from 165 [Q1 129, Q3 216] to 199 [Q1 178, Q3 316] [P < 0.05; T5 vs. T4]) were observed. CONCLUSIONS: In patients with isolated severe adult respiratory distress syndrome, inhalation of nitric oxide in the prone position significantly improved oxygenation compared with nitric oxide inhalation in the supine position or in the prone position without nitric oxide. The combination of the prone position with nitric oxide inhalation in the treatment of severe adult respiratory distress syndrome should be considered.

Adolescent↗
PubMed1979

Saturated phosphatidylcholine in amniotic fluid and prediction of the respiratory-distress syndrome.

The lecithin/sphingomyelin (L/S) ratio in amniotic fluid is widely used to predict the risk of respiratory-distress syndrome. However, the results are unreliable if the specimen is contaminated or obtained during a complicated pregnancy. We therefore compared the predictive value of the L/S ratio with that of the concentration of saturated phosphatidylcholine (SPC) in 322 amniotic-fluid samples, 75 per cent of which were contaminated or obtained during complicated pregnancies or both. A positive result is one that predicted the development of respiratory-distress syndrome, taken as an L/S ratio equal to or less than 2/1 or an SPC below 500 mug per deciliter. The respiratory-distress syndrome was correctly predicted in 25 of 45 cases (55.5 per cent) with L/S ratios equal to or less than 2/1, and in 35 of 42 cases (82 per cent) with SPC's less than 500 mug per deciliter. When L/S ratios were greater than 2/1, there were 13 of 277 (4.7 per cent) false negatives, and when SPC's were above 500 mug per deciliter, there were three of 280 (1.1 per cent) false negatives. We conclude that determination of SPC is both more specific and more sensitive as a predictor of the respiratory-distress syndrome than the techniques currently in use.

Acetone↗