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PubMed1985

Reduction in intraventricular hemorrhage by elimination of fluctuating cerebral blood-flow velocity in preterm infants with respiratory distress syndrome.

In a previous study of preterm infants requiring mechanical ventilation for the respiratory distress syndrome, we demonstrated a striking association of fluctuating cerebral blood-flow velocity in the first day of life with the subsequent occurrence of intraventricular hemorrhage. Because this fluctuating pattern could be eliminated by muscle paralysis, we conducted a prospective study of preterm infants receiving mechanical ventilation for the respiratory distress syndrome in which we evaluated the effect of paralysis and this flow-velocity pattern on the incidence and severity of intraventricular hemorrhage. Twenty-four infants with the fluctuating pattern in the first hours of life were identified and randomly selected to serve as controls (10) or to be subjected to muscle paralysis (14). Intraventricular hemorrhage developed in all 10 control infants but in only 5 of the 14 infants subjected to muscle paralysis. Moreover, in 4 of the 5 paralyzed infants in whom hemorrhage developed, it did so after cessation of the paralysis. Seven of the 10 control infants had Grade III hemorrhage, the most severe variety of intraventricular hemorrhage, whereas none of the paralyzed infants had Grade III hemorrhage. We conclude that elimination of fluctuating cerebral blood-flow velocity in preterm infants with respiratory distress syndrome markedly reduces the incidence and severity of intraventricular hemorrhage.

Blood Flow Velocity↗
PubMed1979

Adult respiratory distress syndrome after venous air embolism.

Venous air embolism is not commonly believed to produce the adult respiratory distress syndrome. We present a nonsurgical case of venous air embolism followed by the development of this syndrome. Other causes of adult respiratory distress syndrome were excluded. Physicians should be alerted to its possible occurrence and the need for appropriate therapy.

Adult↗
PubMed1988

High postmortem levels of hypoxanthine in the vitreous humor of premature babies with respiratory distress syndrome.

To test whether or not premature babies at risk for retinopathy of prematurity have elevated hypoxanthine levels in the eye, the vitreous humor of 13 premature babies who died of severe respiratory distress syndrome and lung failure, was analyzed for hypoxanthine. Their hypoxanthine level was 459 +/- 171 mumol/L (mean +/- SD) compared with 54 +/- 71 mumol/L in seven newborn babies who died suddenly (P less than .001). In 53 adults who died suddenly, the hypoxanthine concentration was 136 +/- 119 mumol/L (P less than .001 when compared with babies with respiratory distress syndrome). Babies with respiratory distress syndrome underwent a significantly longer period with arterial PO2 levels less than 40 mm Hg (5.3 kPa) and they required supplementation with 100% oxygen significantly longer than control babies. The hypoxanthine concentration was correlated with the time during which the arterial PO2 was lower than 40 mm Hg (5.3 kPa) before death, and a significant positive correlation was found (R = .59, P less than .12). The study shows that high levels of hypoxanthine are found in vitreous humor of premature babies with respiratory distress syndrome. Because hypoxanthine is a potential oxygen radical generator and premature babies might have lower levels of antioxidants than full-term babies, it is suggested that the hypoxanthine accumulation in the eyes of premature babies with respiratory distress syndrome could play a pathogenetic role in the development of retinopathy of prematurity.

Aqueous Humor↗
PubMed2000

Surfactant phospholipids and surface activity among preterm infants with respiratory distress syndrome who develop bronchopulmonary dysplasia.

Our objective was to determine if preterm infants with respiratory distress syndrome who develop bronchopulmonary dysplasia have abnormalities in surfactant phospholipids and/or function. Tracheal aspirate samples obtained from preterm infants with respiratory distress syndrome on days 1, 3-5, 7-10, 14-17, 21-24 and 27-30 were analyzed for total phospholipids and phospholipids fractions by determination of total phospholipid phosphorus and thin layer chromatography, respectively. Surfactant properties were assessed with captive bubble surfactometer. Sixteen out of 56 (29%) infants died during the first 30 d of life. Infants who died were more immature, required more ventilatory support and had a surfactant with lower surface-tension-reducing properties than infants who survived (p < 0.05). Surviving infants were divided into group I (no bronchopulmonary dysplasia at 27-30 d, n = 25) and group II (with bronchopulmonary dysplasia at 27-30 d, n = 15). No significant differences in concentrations of surfactant phospholipids nor measurements of surface tension were noted among groups of infants. Surfactant therapy after birth was associated with a significant increase in concentrations of total phospholipids, lecithin, phosphatidylinositol and lower surface-tension measurements at 3-5 d of age among surviving infants (p < 0.01). Abnormalities in concentrations of surfactant phospholipids or surfactant function could not be demonstrated during the first month of life among preterm infants with respiratory distress syndrome who develop bronchopulmonary dysplasia.

Bronchopulmonary Dysplasia↗
PubMed1997

[Natural surfactant in routine treatment of neonatal respiratory distress syndrome. Experiences from two central hospitals].

Regular use of surfactant in the treatment of respiratory distress syndrome started in Norwegian neonatal intensive care units in 1992. The authors present the results for the first 70 babies with respiratory distress syndrome who were treated with natural surfactant from 1991 to 1994 at two level II hospitals. Median time of administration dropped from eight hours after birth in 1991 to three hours in 1994. Treatment soon after birth leads to a greater reduction in oxygen requirement. 12 children died, all of them very immature after complicated pregnancies. The total mortality in babies with a birth weight of less than 1,500 grams was 7%. The incidence of severe bronchopulmonary dysplasia was markedly reduced and the total number of days on a ventilator was reduced by 50%. Use of surfactant was not associated with more complications. Severe respiratory distress syndrome should be prevented with antenatal steroids, and treated early postnatally with natural surfactant.

Biological Products↗
PubMed1995

Short note: the potential of umbilical cord blood to increase tissue oxygenation in adult respiratory distress syndrome.

Umbilical blood, consisting mainly of fetal haemoglobin, has an increased oxygen affinity. Adult respiratory distress syndrome may be caused by any acute, diffuse, infiltrative lung lesion of diverse aetiologies and is characterized by severe arterial hypoxia. Mechanical ventilation with high FIO2 and elevated pressures is used to improve tissue oxygenation in these patients. Nevertheless, adult respiratory distress syndrome may be fatal. Our hypothesis suggests that transfusion of umbilical cord blood to adult respiratory distress syndrome patients may facilitate oxygen transport by increasing oxygen binding in the erythrocytes passing through the damaged lungs. The local hypoxia and the accompanied acidosis in the periphery may accelerate the oxygen unload to the tissues, thus augmenting overall oxygen delivery. Studies with animals and humans show that left-shifted oxyhaemoglobin dissociated curve confers a degree of adaptation to low-oxygen tension ambient. Umbilical cord blood is available in every hospital, and there are no contraindications to its use.

Adult↗
PubMed2004

Carboxyhemoglobin formation as an unexpected side effect of inhaled nitric oxide therapy in severe acute respiratory distress syndrome.

OBJECTIVE: To report an unexpected cause of carboxyhemoglobinemia associated with inhaled nitric oxide therapy in severe acute respiratory distress syndrome. DESIGN: Case report. SETTING: Medical critical care unit at Lausanne University Hospital. PATIENT: One female patient with acute respiratory distress syndrome treated with inhaled nitric oxide, who developed a simultaneous increase in blood methemoglobin and carboxyhemoglobin. CONCLUSIONS: Potential pathophysiologic mechanisms linking acute respiratory distress syndrome, inhaled nitric oxide, methemoglobin, and carboxyhemoglobin are discussed. Since carboxyhemoglobin has a negative influence on oxygen-carrying capacity, this effect may potentially offset the beneficial influence (if any) of inhaled nitric oxide on arterial PO2. This observation does not support the use of inhaled nitric oxide in the treatment of acute respiratory distress syndrome.

Administration, Inhalation↗
PubMed1989

[Respiratory distress syndrome in adults].

The pathogenesis of the adult respiratory distress syndrome is described discussing the present state of knowledge on this problem. The diagnostic problems and the modern therapeutic possibilities are mentioned.

Adult↗
PubMed1989

Hepatic dysfunction in the adult respiratory distress syndrome.

Multiple organ system failure is a major cause of mortality in the adult respiratory distress syndrome (ARDS). We serially evaluated parameters of multiple organ function in 24 patients during the first week after the diagnosis of ARDS and related them to outcome. The adult respiratory distress syndrome was associated with sepsis (n = 16), postoperation (n = 7), and trauma (n = 1). Fourteen of the 24 patients (58 percent) died. Although there were no significant differences in the indices of pulmonary or renal dysfunction between survivors and nonsurvivors, evidence of hepatic dysfunction was different in the two groups. On the day we identified ARDS, serum bilirubin was 1.2 mg/dl +/- 0.9 mg/dl in patients who survived, and was 2.3 mg/dl +/- 2.8 mg/dl (chi +/- SD) in those who died. Initial serum glutamic oxalacetic transaminase (SGOT) and alkaline phosphatase levels were lower in survivors than in those who died (71 +/- 44 IU/L vs 399 +/- 807 IU/L, and 121 +/- 53 IU/L vs 269 +/- 243 IU/L, respectively). These abnormalities persisted during the first week of respiratory failure, with significant differences in serum bilirubin and alkaline phosphatase between survivors and nonsurvivors (p less than 0.01). The degree of pulmonary and renal dysfunction was similar in both groups. These data suggest that liver function may be a major determinant of survival in patients with the adult respiratory distress syndrome.

Aged↗
PubMed2004

Oxidative and inflammatory parameters in respiratory distress syndrome of preterm newborns: beneficial effects of melatonin.

Reactive oxygen species play an important role in the pathogenesis of respiratory distress syndrome and its complications. This study was conducted to determine if treatment with the antioxidant melatonin would influence interleukin-6, interleukin-8, tumor necrosis factor alpha, and nitrite/nitrate levels in newborns with grade III or IV respiratory distress syndrome (radiographically confirmed) diagnosed within the first 6 hours of life. Prior to treatment, a blood sample was collected from the umbilical cord or a peripheral vein of each newborn. Second, third, and fourth blood samples were collected at 24 hours, 72 hours, and 7 days, respectively, after beginning treatment with melatonin or placebo. Compared with the melatonin-treated respiratory distress syndrome newborns, in the untreated infants the concentrations of interleukin-6, interleukin-8, and tumor necrosis factor alpha were significantly higher at 24 hours, 72 hours, and at 7 days after onset of the study. in addition, nitrite/nitrate levels at all time points were higher in the untreated respiratory distress syndrome newborns than in the melatonin-treated babies. Following melatonin administration, nitrite/nitrate levels decreased significantly, whereas they remained high and increased further in the respiratory distress syndrome infants not given melatonin.

Antioxidants↗
PubMed1976

[Morphological investigation of the neonatal lung with respiratory distress syndrome which was maximally distended with Somentor 33 and formalin (author's transl)].

The importance of morphological immaturity of the lung in the development of the respiratory distress syndrome was investigated. Atelectatic lungs of newborns were maximally expanded with a mineral oil of low kinematic viscosity (Somentor 33) or 10% Formalin. With this method, surface active forces of peripheral air spaces should not impede expansion of the lungs. 27 lungs of neonates who died of respiratory distress syndrome and 10 lungs of neonates without primary respiratory problems were examined. Following maximal expansion of the lungs with the respiratory distress syndrome show a hypercellular densely cellular tissue of the pulmonary segments, much like glanduloid hyperplasia with small peripheral air spaces and long distances for diffusion of the respiratory gases. The lungs of newborns without respiratory distress syndromes are well alveolar following expansion and show an optimal morphology for gas diffusion. A lack of a surfactant should have significant consequences in small air spaces.

Formaldehyde↗
PubMed1994

Respiratory distress syndrome in New Zealand: evidence from the OSIRIS trial of exogenous surfactant (Exosurf).

AIMS: To assess the impact, mortality, morbidity and economic costs, of respiratory distress syndrome severe enough to warrant ventilation in one year in New Zealand. METHODS: Review of data from all five New Zealand regional neonatal intensive care units' participation in the international OSIRIS trial of exogenous surfactant (Exosurf) treatment for respiratory distress syndrome (involving 6700 infants in 21 countries), and extrapolation of these data to a full year. RESULTS: There were 265 New Zealand infants entered in the OSIRIS trial; the mean birthweight was 1335 g and mean gestation 29 weeks; 61% of infants were less than 30 weeks gestation. Forty-seven infants (17.7%) died prior to discharge from hospital, 40 deaths being attributed to prematurity or respiratory distress syndrome. One hundred and two infants (38.5% of the cohort; 45% of surviving infants) were oxygen dependent and 36 infants (13.6%) were dead at 28 days of age. Thirty-four infants (12.8% of the cohort; 15% of surviving infants) were oxygen dependent and 40 infants (15%) were dead at the expected date of delivery. Infants were intubated for a mean 12.5 days, with surviving infants of less than 27 weeks gestation intubated for a disproportionately long period of time. Seventy-two infants (29% of the 246 infants examined) had an abnormality detected by cranial ultrasound scan at 1 or 6 weeks of age and in 23 (9%) this was a major abnormality. Of surviving infants 16 (7.5% of 213 examined) had a major abnormality on cranial ultrasound scan. Amongst infants at high risk for respiratory distress syndrome (gestation less than 30 weeks) 53% received antenatal steroids, compared with 22% in the OSIRIS trial overall. In a full year the cost of caring for infants with respiratory distress syndrome sufficiently severe enough to warrant ventilation is estimated to be NZ$12.5 million. The average cost of caring for a surviving infant was roughly NZ$52,500 and a nonsurviving infant was NZ$24,500. CONCLUSIONS: In a full year (total births 60,000) approximately 350 New Zealand infants may require ventilation for respiratory distress syndrome. Increasing the percentage of infants who receive antenatal steroids is likely to be extremely cost effective. In the era of antenatal steroids and exogenous surfactant, 85% of infants with respiratory distress syndrome requiring ventilation survive to discharge home and over 90% of survivors are likely to be healthy normal adults.

Birth Weight↗
PubMed1993

Management of bronchopleural fistula in the adult respiratory distress syndrome.

Bronchopleural fistula occurring as a complication in patients with the adult respiratory distress syndrome typically appears after 1 to 2 wks of illness, and is associated with a poor prognosis. Whether the bronchopleural fistula per se worsens outcome is not known because of the lack of studies on its natural history. There are several potential adverse effects of bronchopleural fistula in adult respiratory distress syndrome (e.g., incomplete lung expansion, loss of effective tidal volume or positive end-expiratory pressure, inability to remove CO2, etc.), but the actual frequency of these problems among patients with this complication appears to be low, and their magnitude and clinical impact remain uncertain. Most of the literature consists of anecdotal reports of innovative measures for reducing the leak, such as manipulation of chest tube suction, high-frequency jet ventilation, independent lung ventilation, and various maneuvers using the fiberoptic bronchoscope. Controlled studies are lacking, however, and the application of sound, general management principles is of primary importance. The great majority of patients can be managed satisfactorily without resort to unfamiliar, labor-intensive, potentially hazardous measures.

Adult↗
PubMed2003

Acute respiratory distress syndrome in the septic surgical patient.

The acute respiratory distress syndrome (ARDS) is a process of acute inflammatory lung injury that affects a diverse array of surgical and medical patients. The syndrome is mediated by a complex and interacting system of chemical mediators produced by several types of pulmonary cells. Regardless of the predisposing causes, activation of the nuclear factor kappa B seems to be, at the molecular level, a signature event of ARDS, leading to the rapid activation of intracellular signaling pathways, which coordinate the induction of multiple genes encoding inflammatory mediators. There are at least two compelling reasons for promoting an understanding of these interactions and their molecular mediators and second messengers: new therapies intended to modulate these factors continue to be developed, and the levels of some of these molecules, most notably cytokines, may serve as early indicators of the onset of ARDS.

Cytokines↗
PubMed1976

Continuous positive airway pressure in the prophylaxis of the adult respiratory distress syndrome.

After an operation upon the abdomen, certain patients have a high risk of developing acute respiratory failure or the adult respiratory distress syndrome. These patients at high risk have been mechanically ventilated during the postoperative period in an attempt to prevent the onset of respiratory insufficiency. As a method of prophylaxis, continuous positive airway pressure has the advantages of increasing the functional residual capacity with minimal effects on the cardiac output, low potential for barotrauma and simplicity of equipment. Alternate patients at risk following an operation on the upper part of the abdomen were placed on 8 centimeters of water continuous positive airway pressure for the first 24 hours postoperatively. Fifty-six controls and 56 patients receiving continuous positive airway pressure were studied. In ten controls, adult respiratory distress syndrome developed, and three died in respiratory failure. Only one of the group receiving continuous positive airway pressure met standard criteria for the diagnosis of adult respiratory distress syndrome. In addition, in 25 patients serving as controls, respiratory complications other than adult respiratory distress syndrome developed compared with the development in only 11 receiving continuous positive airway pressure9

Abdomen↗
PubMed1981

Elastolytic activity in pulmonary lavage fluid from patients with adult respiratory-distress syndrome.

To test the hypothesis that adult respiratory-distress syndrome (ARDS) is related to increased activity of the proteolytic enzyme elastase released from neutrophils in the lung, we determined the differential white-cell count, the elastolytic activity, the source of elastase, and the concentration and activity of the endogenous protease inhibitor alpha-1-antiprotease (alpha-1-AP) in bronchoalveolar lavage fluid from 23 patients with ARDS and from 55 patients without this syndrome. Neutrophil predominance (> 80 per cent) was observed in 18 of 23 patients with ARDS. High elastolytic activity of neutrophil origin was found in 12 of 23 patients with ARDS (52 per cent), in none of 16 normal nonsmokers (P < 0.01), in two of 17 normal smokers, and in three of 22 patients with chronic obstructive pulmonary disease. Although there were no significant differences in alpha-1-AP concentrations, its activity was reduced in eight of nine patients with ARDS and high elastolytic activity. We conclude that in many patients with ARDS, high levels of neutrophil elastolytic activity in the lungs are associated with reduced alpha-1-AP function.

Aged↗