Biomedical subjects
Publications and source records attributed to I Gur.
Two historical cohorts (1993-1994 and 2001) of preterm infants ventilated for respiratory distress syndrome were compared. Dexamethasone administration fell from 22% to 6%. Chronic lung disease in survivors rose slightly from 13% to 17%, and mortality fell from 21% to 15% (other causes). The effect of restriction of dexamethasone use on chronic lung disease and mortality remains to be seen.
OBJECTIVE: To study the long term neurodevelopmental outcome of children who participated in a randomised, double blind, placebo controlled study of early postnatal dexamethasone treatment for prevention of chronic lung disease. METHODS: The original study compared a three day course of dexamethasone (n = 132) with a saline placebo (n = 116) administered from before 12 hours of age in preterm infants, who were ventilated for respiratory distress syndrome and had received surfactant treatment. Dexamethasone treatment was associated with an increased incidence of hypertension, hyperglycaemia, and gastrointestinal haemorrhage and no reduction in either the incidence or severity of chronic lung disease or mortality. A total of 195 infants survived to discharge and five died later. Follow up data were obtained on 159 of 190 survivors at a mean (SD) age of 53 (18) months. RESULTS: No differences were found between the groups in terms of perinatal or neonatal course, antenatal steroid administration, severity of initial disease, or major neonatal morbidity. Dexamethasone treated children had a significantly higher incidence of cerebral palsy than those receiving placebo (39/80 (49%) v. 12/79 (15%) respectively; odds ratio (OR) 4.62, 95% confidence interval (95% CI) 2.38 to 8.98). The most common form of cerebral palsy was spastic diplegia (incidence 22/80 (28%) v. 5/79 (6%) in dexamethasone and placebo treated infants respectively; OR 4.45, 95% CI 1.95 to 10.15). Developmental delay was significantly more common in the dexamethasone treated group (44/80 (55%)) than in the placebo treated group (23/79 (29%); OR 2. 87, 95% CI 1.53 to 5.38). Dexamethasone treated infants had more periventricular leucomalacia and less intraventricular haemorrhage in the neonatal period than those in the placebo group, although these differences were not statistically significant. Eleven children with cerebral palsy had normal ultrasound scans in the neonatal period; all 11 had received dexamethasone. Logistic regression analysis showed both periventricular leucomalacia and drug assignment to dexamethasone to be highly significant predictors of abnormal neurological outcome. CONCLUSIONS: A three day course of dexamethasone administered shortly after birth in preterm infants with respiratory distress syndrome is associated with a significantly increased incidence of cerebral palsy and developmental delay.
It has been suggested that the high rates of prematurity, low birth weight, perinatal morbidity and mortality in in-vitro fertilization (IVF) infants are due to the increased frequency of multiple gestations in this population. The aim of our study was to test this hypothesis by comparing the outcome of IVF twins with that of twins born after spontaneously conceived pregnancies. The perinatal outcome of 40 IVF twins was compared with that of 80 control twins, matched for maternal age, parity and ethnic origin. IVF twins had a higher rate of prematurity (P = 0.03), their mean birth weight was significantly lower (P < 0.01) and the frequency of very low birth weight infants was much higher (P < 0.003). There was no neonatal mortality in the control group, whereas four IVF twins died (P < 0.01). Neonatal morbidity was significantly greater in IVF twins (P < 0.05). Oxygen therapy and mechanical ventilation were administered more frequently to IVF twins (P < 0.007 and P < 0.05). We conclude that twins conceived by IVF are at a significantly higher risk for prematurity and associated neonatal morbidity and mortality than spontaneously conceived twins.
The present study describes the use of simple video games for a 5-week regimen of respiratory muscle training in 15 patients with Duchenne muscular dystrophy (DMD) at various stages of the disease. The games were re-arranged to be operated and driven by the respiratory efforts of the patient and to incorporate accurate ventilation and time measurements. Improvement in respiratory performance was determined by maximum voluntary ventilation (MVV), maximal achieved ventilation (VEmax) during a progressive isocapnic hyperventilation manoeuvre (PIHV) and the PIHV duration. The actual training period was 23 +/- 4 days (mean +/- S.D.) at ventilatory effort of 46 +/- 6% MVV, for 10 +/- 3 min day-1. Patients with moderate impairment of lung function tests (LFT) showed an improvement in MVV, VEmax, and duration of PIHV of 12 +/- 7% (p < 0.02), 53 +/- 25% (p < 0.001) 57 +/- 21% (p < 0.01), respectively. Improvements correlated with actual training time and ventilation level, %MVV, but negatively correlated with years of immobilization and with the initial MVV. We conclude that computerized respiratory games may be applied for breathing exercises and may improve respiratory performance in recently immobilized children with DMD who have moderate impairment of LFT.
Dilated cardiomyopathy with intraventricular thrombosis is a rare disease, most frequently encountered in adults. It rarely occurs in infants. We report here the case of a 2-year-old boy with intraventricular thrombosis due to dilated cardiomyopathy and emphasize the importance of prophylactic anticoagulant therapy in this case.
Neonatal hyponatremia can be caused by increased sodium losses, inadequate sodium intake, increased maternal or neonatal water load or by water retention secondary to excess of ADH release. Cocaine use by pregnant women has not as yet been reported to correlate with hyponatremia in the newborn infant. We present a case of an infant whose mother used cocaine regularly during the last stages of pregnancy and who developed hyponatremia in the first week of life. A mechanism is proposed and discussed.
Respiratory heat loss (RHL) or water loss (RWL) have been proposed as possible triggering factors in exercise and hyperventilation-induced asthma (EIA and HIA). It has recently been demonstrated that exercise intensity and climatic factors are both important in determining the severity of EIA. Eight young asthmatics performed both exercise and isocapnic hyperventilation (IHV) manoeuvres under identical climatic conditions, as part of our investigation of these interactive factors which determine the severity of the asthmatic response. It was found that, when challenged at low ventilatory levels, exercise produced a significantly attenuated asthmatic response compared to IHV. The fall in forced expired volume in 1 sec (delta FEV1) following exercise was 15 +/- 4% as compared with 27 +/- 3% after IHV (p less than 0.002). It is concluded that while the hypernoea in exercise may serve as a trigger, exercise per se introduces an additional factor which serves to limit the full response seen with IHV. This attenuated response is revealed at low ventilatory levels but is masked at high levels.
Recent studies have shown some evidence that exercise-induced asthma (EIA) may not be entirely explained by respiratory heat loss (RHL). We investigated the interrelationship between heat exchange, exercise intensity and EIA. In order to differentiate between the effects of RHL and exercise intensity, we arranged for tests to be performed with the same RHL, but with different intensities of exercise and inspired air conditions. Each of 8 asthmatic children exercised twice in random order for 6 min on a cycle ergometer. One test consisted of exercise performed at a greater level of effort while breathing room air, mean (+/- SE) air conditions being 25.0 +/- 0.4 degrees C and 15.7 +/- 0.2 mg H2O/L. The other test was performed at a lesser level of effort while breathing cold (0.0 +/- 0.5 degrees C) and dry air (O mg H2O/L). The mean ratio of minute ventilations in the 2 exercise tests was 1.78 +/- 0.03, but the RHL was similar in both tests. The EIA after the exercise at the greater level was more severe than after the lesser level, the percent fall in FEV2 from baseline being 36 +/- 7% and 21 +/- 5%, respectively (p less than 0.025). We conclude that the exercise level has a major role in determining the severity of EIA and that climatic conditions act as modifying factors.
Obstructive jaundice due to inspissated bile is usually a self-limited disease caused by hemolytic disease of the newborn. We present a case where disseminated intravascular coagulation caused an obstruction of the biliary tree, requiring surgical intervention for reestablishment of bile flow.
To evaluate the effect of positive ionisation of inspired air on bronchial reactivity, 12 asthmatic children were twice challenged by exercise in random order. During one test positively ionised air (5-10 X 10(5) ions/cm) was breathed. All challenges were matched in terms of basal lung function and exercise tests were matched in terms of ventilation and respiratory heat loss. Exercise induced asthma was significantly aggravated by exposure to positively ionised air, the postexercise fall in FEV1 (delta FEV1) being 24.7% (SEM and 5.3%) and 35.3% (5%) after the control and ionised air tests respectively (p less than 0.04). It is concluded that positive ionisation aggravates the bronchial response to exercise.
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Two children with the unusual condition known as Apert's syndrome are presented. Both have the typical manifestations of the syndrome: craniosynostosis, exorbitism, hypertelorism, maxillary hypoplasia, dental malocclusion, cleft palate, compound syndactyly of the hands and simple syndactyly of the feet. A review of the latest surgical procedures for correction of these defects is presented and the importance of early physical and social rehabilitation is stressed.
Thirteen asthmatic children aged 9-14 years participated in a double blind randomised trial to compare the effectiveness and duration of action of 2 formulations of sodium cromoglycate; one a 20 mg capsule of powdered sodium cromoglycate delivered by turbo inhaler (spinhaler), and the other 1 mg of aerosolised sodium cromoglycate delivered by pressurised cannister inhaler (aerosol). The children performed exercise tests on each of 3 days in a 10 day period--15 minutes, 2 hours, and 6 hours after inhalation of powder, aerosol, or a placebo. Two patients were not protected from exercise induced asthma by either formulation of sodium cromoglycate. Among the remaining patients both formulations gave good protection from exercise induced asthma 15 minutes after inhalation, and the effect of both wore off steadily over the next 6 hours. The spinhaler gave appreciably better protection than the aerosol at 15 minutes after inhalation, and was the only formulation to provide good protection at 2 hours and 6 hours. The more limited effectiveness of the aerosol may be explained by the lower dose of sodium cromoglycate and the more complicated inhalation technique required.
To compare the refractory period that follows exercise and isocapnic hyperventilation, 10 asthmatic children performed two pairs of challenge tests in random order at least six hours apart. In pair A a hyperventilation challenge was followed by an exercise challenge and in pair B the order was reversed. Both pairs of tests were done while the children were breathing cold dry air. Tests were matched in terms of work load, ventilation, and end tidal carbon dioxide tension (PCO2). The mean percentage fall in FEV1 (delta FEV1) after the first challenge (hyperventilation) of pair A and the first challenge (exercise) of pair B were the same (30% (SEM 2%)) and 30% (4%) respectively). The mean delta FEV1 of the exercise test following hyperventilation in pair A and of hyperventilation following exercise in pair B was 22% (4%) and 18% (4%) respectively. Both these latter results were significantly lower than the respective delta FEV1 when the challenge was the first test of the pair. Although the mean refractoriness index (reduction in induced asthma in the second test of each pair compared with the first test) was greater when exercise was the first challenge, the difference was not significant.
Thirteen children each exercised for 6 min by running on a treadmill and by tethered swimming, breathing air at room temperature and either 8% or 99% relative humidity continuously. Ventilation, gas exchange and heart rate were closely matched in all four tests in each child, with a mean oxygen consumption of 32.3 +/- 1.7 ml x min-1 x kg-1. The post-exercise fall in FEV1 expressed as a percentage of the baseline FEV1 (delta FEV1) was significantly greater after running compared with swimming breathing either humid or dry air. The delta FEV1 was also related to respiratory heat loss (RHL) calculated from measurements of inspired and expired gas temperature and humidity. At a standardised RHL, the difference between running and swimming was highly significant [delta FEV1 (%) +/- SE = 39 +/- 5 and 28 +/- 4 respectively, p less than 0.01]. These experiments suggest that the type of exercise influences the severity of exercise-induced asthma even under conditions of the same metabolic stress and respiratory heat loss.
To study the pattern of lymphokines in bleomycin-induced lung injury, T cells were isolated from lung interstitial tissue (LIL), peribronchial lymphatic tissue (PBLT), and bronchoalveolar lavage (BAL) fluid of bleomycin-"sensitive" C57Bl/6 and bleomycin-"resistant" BALB/c mice at 3, 6, and 14 days following intratracheal instillation of bleomycin or saline. After 48 hours in culture, conditioned media were collected and assayed with specific enzyme-linked immunosorbent assay (ELISA) for interferon (IFN)-gamma, interleukin (IL)-2, IL-4 and IL-5. In bleomycin-treated C57B1/6 mice, IFN-gamma production was increased up to 20-fold at 3 and 6 days in LIL, and at 3 days in PBLT lymphocytes. IL-4 production was slightly decreased in LIL and PBLT lymphocytes at 14 days. IL-2 and IL-5 were not changed by bleomycin. In BALB/c mice, IFN-gamma production was increased 5-fold at 14 days, and IL-2 production at 6 days, in LIL but not PBLT. IL-4 and IL-5 were not significantly changed. The increase in IFN-gamma may play a role in the pathogenesis of bleomycin-induced lung injury. Differences in the cytokine pattern between the strains of mice may contribute to the variable strain susceptibility in bleomycin-induced lung injury.