Inspiration-phased oxygen delivery.
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Biomedical subjects
Publications and source records attributed to R J Winter.
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10 patients (mean age 23.1, range 17.1-40.5 years), 8 with cystic fibrosis (CF), and 2 with advanced bronchiectasis without CF, were taught, while being treated in hospital for exacerbations of pseudomonas infection, how to continue to give themselves intravenous antibiotics at home. They were discharged after satisfactory antibiotic levels had been achieved, and 22 courses were given at home over a total of 116 patient-days. In 14 of these, the greater part of the course was given at home (mean duration 6.6, range 5-10 days); 2 of these were given without admission to hospital. In the 8 patients with two or more infective exacerbations within a 12-month period there was no difference between home and hospital treatments in clinical improvement or in relapse time, defined as the interval between completion of treatment and subsequent antibiotic therapy. Self-administration of antibiotics intravenously at home for selected adults with cystic fibrosis and severe bronchiectasis reduces hospital stay and does not seem to be associated with an increased rate of recurrent infection.
In many patients with chronic bronchitis and emphysema right and left ventricular ejection fractions (RVEF and LVEF) are reduced. A study was conducted using multiple gated equilibrium radionuclide ventriculography to compare the effects of oral salbutamol 4 mg and pirbuterol 15 mg on cardiac function in 12 patients with chronic bronchitis (forced expiratory volume in one second 0.86 (SEM 0.12) 1; arterial oxygen pressure 8.2 (SEM 0.5) kPa (61.7 (SEM 3.8) mm Hg)). Different doses of nebulised salbutamol (500 microgram and 5 mg) were also compared in nine of the patients. Both oral salbutamol and oral pirbuterol produced significant increases in RVEF and LVEF at 60 and 90 minutes after drug ingestion (p less than 0.01 in each case). There were no significant differences between salbutamol and pirbuterol in their effects on RVEF and LVEF. Inhaled salbutamol at doses commonly prescribed had no significant effect on RVEF and LVEF after 20 and 60 minutes. Salbutamol and pirbuterol given by mouth have similar actions on RVEF and LVEF. Further studies are necessary to assess the effects of long term B2 agonists in this group of patients.
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To study the selective effect of thyroid hormone and growth hormone, alone and in combination on plasma cholesterol, 12 children were monitored monthly during three 4-month treatment periods. Plasma cholesterol was unaltered by growth hormone therapy alone (mean +/- SD, basal cholesterol level: 202 +/- 26 mg/dL; cholesterol level after growth hormone 200 +/- 24 mg/dL). With thyroxine (T4) replacement alone, or combined with growth hormone, a significant (P less than 0.01) decrement in plasma cholesterol occurred. (Thyroxine alone: 172 +/- 11 mg/dL; thyroxine and growth hormone: 172 +/- 10 mg/dL). Basal thyroid function tests, including TRH stimulation, were normal. Serum thyroxine levels decreased and serum triiodothyronine (T3) levels increased in response to growth hormone therapy. Linear growth increased significantly in response to growth hormone alone and both therapies combined. Serum values of T4 and T3 were significantly (P less than 0.001) correlated with basal cholesterol, r = 0.84 and r = 0.83, respectively. Our experience with euthyroid growth hormone deficiency confirms that modest hypercholesterolemia is characteristic of that disorder, and that growth hormone therapy has no statistically significant effect on plasma cholesterol. The modest hypercholesterolemia that does respond to thyroid replacement is further evidence of a subtle abnormality of thyroid function in such individuals. The mechanism whereby thyroid hormone has its cholesterol lowering effect in these apparently euthyroid subjects is unclear.
In a combined mail and medical record survey of 121 non-diabetic and 90 diabetic girls greater than or equal to 9 years of age, the mean age of menarche in the control non-diabetic population was 13.0 +/- 1.2 years and 13.4 +/- 1.2 years in the diabetics. The diabetic group was divided into those whose onset was before or after age 11 years (DM less than 11, DM greater than or equal to 11). The DM greater than or equal to 11 group had a mean menarchal age of 14.0 +/- 1.2 years and the DM less than 11 group, 13.1 +/- 1.2 (p less than 0.005). The DM greater than or equal to 11 group also differed significantly from the control group. The difference between the two groups suggests that the onset of diabetes near the onset of puberty may have a more disruptive effect on hypothalamic-pituitary-gonadal axis maturation that does the prepubertal onset of diabetes.
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To investigate the physical and psychological factors associated with labile diabetic control, 30 children and adolescents with recurrent diabetic ketoacidosis were included in a retrospective longitudinal review covering an 8-year period. The details of the ketoacidosis episodes and the psychosocial characteristics of the patient and his family were summarized from the medical record. Only a minority of the ketoacidosis episodes were overtly and solely related to intercurrent illness or poor compliance. A majority of the subjects studied lived in families with substantial psychosocial dysfunction, including chronic unresolved interpersonal conflict, inadequate parenting, father not in home, financial stress, and lack of family involvement with the diabetes. Many of the children displayed behavioral and personality problems. In most of these 30 cases, there was evidence that these dysfunctions existed prior to the onset of diabetes. These psychosocial problems were not immediately apparent in many instances, thus requiring more comprehensive psychosocial assessment and involvement by a social worker and/or a psychologist. Ongoing emotional support and counseling were instrumental in reversing the pattern of recurrent ketoacidosis, in coordination with care by all members of the diabetes team. The findings from this experience suggest that recurrent ketoacidosis warrants prompt evaluation from a psychosocial as well as a physical perspective.
We have compared the effects of oral theophylline and salbutamol on right and left ventricular function in twelve patients with chronic bronchitis and emphysema. Right and left ventricular ejection fraction (RVEF and LVEF) were measured using multiple gated radionuclide ventriculography. Theophylline 600 mg and salbutamol 4 mg both produced increases in RVEF and LVEF. There were no significant changes in blood gases after either drug. The clinical significance of the effects of oral bronchodilators on cardiac function in patients with chronic bronchitis and emphysema has yet to be determined.
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Twenty-four hr glucose and hormonal monitoring was conducted in 34 randomly selected children with insulin dependent diabetes. Asymptomatic nocturnal hypoglycemia was present in 18% (6/34). The nocturnal plasma glucose decline of 20-25 mg/dl/hr reached a mean nadir of 50 mg/dl. The mean rebound hyperglycemia of 300 mg/dl over the subsequent 6.4 hrs. was significantly greater than any glucose excursion in diabetic children with daytime, symptomatic hypoglycemia (n = 5) or in those with non-hypoglycemic profiles (n = 23). Coincident with the nocturnal decline, but preceding the glucose nadir, was a marked release of growth hormone which was significantly greater (p less than .05) than that observed in the other diabetic groups. This release of growth hormone, and the nocturnal hypoglycemia, were reflected in the ratio of awake/sleep mean concentrations of glucose and growth hormone. These data support the speculation that growth hormone release contribute to the hyperglycemic rebound observed. Mean 24 hr growth hormone concentrations varied considerably from patient to patient such that a generalization for growth hormone concentrations in insulin dependent diabetes cannot be made. Asymptomatic nocturnal hypoglycemia is a frequent complication of the therapy of insulin dependent diabetes. Subsequent hyperglycemic rebound (the "Somogyi Effect") is associated with exuberant counterregulatory release of growth hormone. The precise pathophysiological role of this growth hormone release is unclear.
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To test the hypothesis that hyperlipidemia is characteristic of growth hormone deficiency in childhood, we have measured serum cholesterol and triglyceride concentrations in 24 euthyroid children with growth hormone deficiency. Although modest elevations of cholesterol and/or triglyceride above the 95th percentile for age, race, and sex were present in 46% of the children studied, the mean (+/- 1 SD) cholesterol of 173 +/- 36 mg/dl and the mean triglyceride of 80 +/- 42 mg/dl were not significantly different from published normal mean values. Administration of human growth hormone for 4 mo to 15 of these subjects did not alter these mean cholesterol and triglyceride values, but did result in a marked improvement in the growth rate. Some individuals (n = 6) with a subnormal growth response to therapy and/or a low serum thyroxine and high serum cholesterol were treated for an additional 4 mo with growth hormone and thyroid hormone together. There was a statistically significant decrement in serum cholesterol in this group. We conclude that modest hyperlipidemia does exist in some children with growth hormone deficiency. Subclinical hypothyroidism may play a role in the hypercholesterolemia of some children, as may growth hormone deficiency itself. Any association of growth hormone and lipid metabolism remains to be clarified.
To test the hypothesis that somatomedin activity is influenced by diabetes and its metabolic regulation, the relationship between somatomedin activity and diabetic control as assessed by hemoglobin A1C was investigated in 40 children with insulin-dependent diabetes. An inverse correlation between hemoglobin A1C and serum somatomedin activity was statistically significant. The data suggest that abnormalities of linear growth, which can occur in children with poorly controlled diabetes, may involve abnormalities in net somatomedin activity.