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Biomedical subjects

J W Kendig

Publications and source records attributed to J W Kendig.

28 records · Page 2Linked to original sources
PubMed1989

Surfactant replacement therapy: impact on hospital charges for premature infants with respiratory distress syndrome.

Surfactant replacement therapy for neonatal respiratory distress syndrome has the potential to reduce morbidity and mortality of very premature infants. To investigate whether surfactant replacement therapy will also reduce hospital charges for these infants, we compared the hospital charges incurred by a group of patients treated with surfactant with charges of control patients. Mortality in the surfactant-treated group (8%) was significantly decreased compared with the control patients (29%). Average daily hospital charges in the surfactant-treated patients were 25% less than for the control patients. Most of the savings in daily hospital charges were due to a 52% reduction in daily charges for laboratory, x-ray, respiratory therapy, and other ancillary services. Similarly, ancillary charges for the first full week of hospitalization were significantly reduced by $1,883 for patients who received surfactant therapy. Analysis of the charges for the entire hospitalization revealed that surfactant-treated patients had a significantly smaller proportion of their charges that resulted from ancillary services and an increased proportion due to room charges. The average total hospital charges for the two groups were similar, but the total hospital charges to produce a surviving infant were $18,500 less in the surfactant-treated group than the charges to produce a survivor from the control group. It is likely that, in addition to a reduction in neonatal mortality and morbidity from respiratory distress syndrome, surfactant replacement therapy may also significantly reduce charges for ancillary services for these patients. In this way, surfactant therapy may be cost-effective by improving survival without increasing overall hospital costs.

Economics, Hospital↗
PubMed1988

Changes in pulmonary mechanics after the administration of surfactant to infants with respiratory distress syndrome.

We assessed pulmonary mechanics in 35 premature infants with respiratory distress syndrome just before and one hour after the administration of 90 mg of surfactant to each infant. Transpulmonary pressure was measured between the airway opening and an esophageal balloon with use of a differential transducer, and flow rates were measured by a pneumotachometer. Values for pulmonary mechanics were then calculated by microcomputer processing. The administration of surfactant produced a large decrease (56 percent) in the mean (+/- SEM) ratio of alveolar to arterial oxygen, from 7.1 +/- 0.5 to 3.1 +/- 0.2 (P less than 0.0001)--a change that indicates improvement in gas exchange. Associated changes in pulmonary mechanics were not demonstrable when 10 of the infants were studied during continuous mechanical ventilation. However, in the 25 infants examined during spontaneous breathing with continuous positive airway pressures (identical airway pressures before and after treatment), large and consistent improvements in pulmonary mechanics were found after the administration of surfactant. Tidal volume increased by 32 percent (P less than 0.03), minute ventilation by 38 percent (P less than 0.02), dynamic compliance by 29 percent (P less than 0.004), and inspiratory flow rates by 54 percent (P less than 0.01). We conclude that significant improvement in pulmonary mechanics results from surfactant-replacement therapy for respiratory distress syndrome, but that these mechanical changes are apparent only during spontaneous respiration and can be masked if measurements are made during mechanical ventilation.

Humans↗
PubMed1988

The effect of surfactant replacement therapy on conditions associated with respiratory distress syndrome: patent ductus arteriosus, intraventricular hemorrhage, and bronchopulmonary dysplasia.

In assessing the current experience with SRT, both considering its effects on respiratory function and on associated problems, there are strong suggestions that this therapy has the potential to have a major impact on the morbidity and mortality of premature infants. The studies to date have not disclosed any serious adverse reactions, and there are strong trends toward improvements in short-term respiratory function and in long-term outcomes. In particular, SRT does not seem to adversely effect cardiopulmonary circulatory status and worsen the effects of the patent ductus arteriosus. There are no adverse effects on intraventricular hemorrhage and some possibility that it may lead to a reduction in hemorrhages. The use of SRT will likely have its biggest effect on reducing the incidence and severity of bronchopulmonary dysplasia.

Bronchopulmonary Dysplasia↗
PubMed1988

Surfactant replacement therapy at birth: final analysis of a clinical trial and comparisons with similar trials.

A randomized trial of surfactant replacement therapy at birth was conducted at the University of Rochester between June 1983 and November 1985. Thirty-four premature infants, 25 to 29 weeks' gestational age, received a preventilatory dose of a calf lung surfactant extract in saline prepared at the University of Rochester. A control group of 31 infants received a preventilatory dose of saline alone. The major finding of this trial is that a single preventilatory dose of calf lung surfactant extract reduces the severity of the respiratory distress syndrome during the first 24 hours of life. The beneficial effects, however, are not sustained in many infants and diminish after 24 hours of life. The survival rate was 71% in both the control and surfactant-treated groups. There was a lower incidence of pneumothorax in the surfactant-treated group. There were no differences in the incidence of bronchopulmonary dysplasia, patent ductus arteriosus, and intraventricular hemorrhage. No adverse effects of surfactant replacement therapy were identified. Results of this study suggest that multiple postventilatory doses of surfactant will be required for optimal therapy.

Clinical Trials as Topic↗
PubMed1987

Exogenous lung surfactant: effect on radiographic appearance in premature infants.

At birth, premature infants of 25-29 weeks gestation, at high risk for development of neonatal respiratory distress syndrome (RDS), were given a single dose (90 mg) of calf lung surfactant extract (CLSE) by intratracheal instillation. The frequency and severity of RDS were assessed with use of a simple radiographic scoring system in which pulmonary parenchymal densities and the prominence of the air-bronchogram effect were used as indicators of widespread atelectasis. Radiographs were obtained in surfactant-treated and control infants within the first 90 minutes of life as part of an initial evaluation of their pulmonary status. Subsequent examinations were performed at less than 24 hours and less than 48 hours of age. Radiographic assessment of lung disease compared consistently with coordinated data on oxygen and mean airway pressure requirements of the infants. Both indicated a significantly decreased frequency and severity of RDS in the infants treated with surfactant. The results provide supporting evidence of the effectiveness of exogenous lung surfactant replacement in mitigating RDS in very premature infants.

Animals↗
PubMed1986

Differential sensitivity of neural cells to bilirubin toxicity.

Two established neural cell lines were used to examine the cytotoxicity of bilirubin in vitro. N2AB-1 is a subclone of Neuro 2a from the original C1300 mouse neuroblastoma and C6 glioma is a rat astrocytoma cell line. These cells were grown in monolayer cultures in medium with 10% fetal calf serum containing doses of 5 to 42 microM bilirubin. Morphologic and biochemical characteristics of cell viability were monitored for 72 h. Additional cultures of N2AB-1 were differentiated by treatment with prostaglandin E1/cyclic adenosine monophosphate before exposure to various bilirubin concentrations. The cells were examined every 24 h by phase contrast microscopy and protein synthesis was measured by incorporation of tritiated leucine for appropriate times. N2AB-1 cells were extremely sensitive to bilirubin within 24 h at doses greater than 11 microM. Cells showed swelling, vacuole formation, pigment accumulation, and lift off from the growing surface. Growth of N2AB-1 over 3 days was inhibited in a dose-dependent manner. Moreover, protein synthesis 6 h after bilirubin exposure and 24 h after bilirubin exposure was inhibited in the same dose dependency as cell growth. In contrast, N2AB-1 cells morphologically differentiated by drug treatment showed no effect of bilirubin exposure. Also, mitotically active rat glial cells were resistant to bilirubin toxicity under similar conditions. This study demonstrates that marked differences exist among neural cells in susceptibility in vitro to bilirubin toxicity and that mitotically active neuronal cells are more sensitive to bilirubin treatment than "mature" neurons.

Animals↗
PubMed1986

Oliguria and tolazoline pharmacokinetics in the newborn.

Tolazoline treatment of neonates has been reported since 1965. Dosages increased from pulse doses of 1 to 2 mg/kg to continuous infusions of 10 mg/kg X h before neonatal plasma tolazoline concentrations were measured. We developed a microassay for tolazoline and determined neonatal distribution volume, 1.61 +/- 0.21 L/kg, and disposition rate constant (beta), 0.0027 +/- 0.005 min-1 (mean +/- SEM). Half-life (gamma) ranged from 1.47 to 41.25 (median = 4.43) hours and correlated inversely with urine output (x); y (h) = -0.46 + 7.63/x (mL/kg X h), r = .61, P less than .05. The highest plasma tolazoline concentration in a neonate was 20.3 mg/L. Lethal tolazoline concentrations in lambs ranged from 21.8 to 56.8 mg/L. Initial tolazoline concentrations during infusions and after 1- to 2-mg/kg pulse doses ranged from 0.35 to 2.3 mg/L and PaO2 increased greater than or equal to 15 mm Hg in 64% of 14 treatments. The average neonatal pharmacokinetics predict that each 1 mg of tolazoline HCl per kilogram pulse dose will increase the plasma concentration of tolazoline base by 0.5 mg/L. The plasma concentration should remain constant with infusion dose increments of 0.16 mg of tolazoline HCl per kilogram per hour for every 1.0-mg/kg loading dose. Tolazoline dose requirements for specific patients will vary, especially with renal dysfunction. Reduced tolazoline doses were used to treat two patients, concentrations remained constant, and PaO2 was maintained. Tolazoline doses derived from neonatal kinetics are less than current infusion doses and may avoid high concentrations.

Animals↗
PubMed1985

Effect of bilirubin on brainstem auditory evoked potentials in the asphyxiated rat.

We measured brainstem auditory evoked responses (BAER) in four groups of paralyzed, ventilated, adult rats. Group A (n = 2) received intravenous albumin; group B (n = 5) received bilirubin in albumin; group C (n = 7) was asphyxiated and then received albumin; and group D (n = 19) was asphyxiated and received bilirubin in albumin. When compared with control values, no changes in BAER occurred in groups A or B and only slight changes were found in group C. In group D, seven rats died and seven suffered a marked secondary deterioration of the BAER following recovery, a phenomenon that did not occur in group C (p = 0.02). Bilirubin toxicity appears to be responsible for the changes in BAER but prior asphyxia was necessary for this effect to occur. Because the changes that occurred in group D involved all four major waves, it is not possible to separate out a toxic effect of bilirubin, localized to the auditory nerve and the auditory pathway, from a generalized systemic effect which could cause attenuation of the entire response. The BAER may be useful, however, as a noninvasive means of identifying bilirubin toxicity in the newborn.

Animals↗