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Bronchopulmonary dysplasia

Autoimmune nephrotic syndromes Bronchopulmonary dysplasia Mineral dust pneumoconiosis... [Pg.200]

Daily energy requirements for children are approximately 150% of basal metabolic rate with additional calories to support activity and growth (Table 57-5). Requirements increase with fever, sepsis, major surgery, trauma, burns, long-term growth failure, and chronic conditions (e.g., bronchopulmonary dysplasia, congenital heart disease, and cystic fibrosis). [Pg.664]

Pearson, E., Bose, C., Snidow, T., Ransom, L., Young, T., Bose, G., and Stiles, A. (1992). Trial of vitamin A supplementation in very low birth weight infants at risk for bronchopulmonary dysplasia. /. Pediatr. 121, 420-427. [Pg.215]

Palivizumab is used to prevent serious lower respiratory tract infection due to RSV. It is used only in high-risk children who are younger than 24 months of age and have bronchopulmonary dysplasia or chronic lung disease that required treatment in the previous 6 months. It is also indicated for premature infants (less than 32 weeks gestation) until the age of 6 to 12 months. Palivizumab can reduce the incidence of RSV-related hospitalization by approximately half. The safety and efficacy of palivizumab in the treatment of RSV disease have not been established. [Pg.581]

B. Indications and use Synagis is indicated for the prevention of serious lower respiratory tract disease caused by RSV in infants and children with bronchopulmonary dysplasia (BPD) or a history of premature birth (< 35 weeks gestation) who are under 24 months of age at the time of first administration. [Pg.306]

Prevention of serious lower respiratory tract infection caused by respiratory syncytial virus in children less than 24 months of age with bronchopulmonary dysplasia or a history of prematurity (less than or equal to 35 weeks gestation)... [Pg.569]

On the other hand, there are many reports of hypertension (394), and electrocardiographic and other studies have often confirmed the presence of a disproportionately serious and bilateral hypertrophic obstructive cardiomyopathy, which unless it proves fatal is, in general, reversible once the glucocorticoids are withdrawn (SEDA-18, 386). Although the issue is confounded by the possibility that infants with bronchopulmonary dysplasia may be innately hypertensive, there seems no doubt as to the effect. [Pg.44]

The use of postnatal glucocorticoids in very premature infants is controversial although dexamethasone reduces bronchopulmonary dysplasia, it has been associated with severe adverse effects (407). In 220 infants with a birth-weight of 501-1000 g randomized to placebo or dexamethasone (0.15 mg/kg/day for 3 days and tapering over a period of 7 days) the relative risk of death or chronic lung disease... [Pg.45]

Amin SB, Sinkin RA, McDermott MP, Kendig JW. Lipid intolerance in neonates receiving dexamethasone for bronchopulmonary dysplasia. Arch Pediatr Adolesc Med 1999 153(8) 795-800. [Pg.58]

Palivizumab is a humanized monoclonal antibody directed against the F glycoprotein on the surface of RSV. It was recently approved for the prevention of RSV infection in high-risk infants and children such as premature infants and those with bronchopulmonary dysplasia. A placebo-controlled trial utilizing once-monthly intramuscular injections (15 mg/kg) for 5 months beginning at the start of the RSV season demonstrated a 55% reduction in the risk of hospitalization for RSV in treated patients. The major observed adverse effect has been elevation in serum aminotransferase levels. [Pg.1152]

Latini G, Avery GB. 1999. Materials degradation in endotracheal tubes a potential contributor to bronchopulmonary dysplasia. Acta Paediatr 88 1174-1175. [Pg.275]

Case 1. On July 13, 1995, a 7-month-old girl was brought to an emergency department because of respiratory arrest but could not be resuscitated. The cause of death was listed by MCMEO as bronchopulmonary dysplasia associated with environmental hyperthermia. She had been receiving home nursing care for congenital respiratory impairment. A window air conditioner was being installed at the time of her death. [Pg.344]

Strange RC, Cotton W, Fryer AA, Jones P, Bell J, Hume R. Lipid peroxidation and expression of copper-zinc and manganese superoxide dismutase in lungs of premature infants with hyaline membrane disease and bronchopulmonary dysplasia. J Lab Clin Med 116 (1990) 666-673. [Pg.249]

Wilson DC, McClure G, Halliday HL, Reid MM, Dodge JA. Nutrition and bronchopulmonary dysplasia. Arch Dis Child 1991 66(1 Spec No) 37-8. [Pg.2722]

Wagenaar GTM, ter Horst SAJ, van Gastelen MA, I. cijscr LM, Mauad T, van der Velden PA, de Heer E, Hiemstra PS, Poorthuis BJHM, Walther FJ. Gene expression profile and histopathology of experimental bronchopulmonary dysplasia induced by prolonged oxidative stress. Free Rad Biol Med 2004 36(6) 782-801. [Pg.136]

Shenai JP, Kennedy KA, Chytil F, Stahlman MT. Clinical trial of vitamin A supplementation in infants susceptible to bronchopulmonary dysplasia. J Pediatr 1987 111 269-77. [Pg.1160]

Dosimetry Drug dose and distribution/response to therapy 1 -5 pm Asthma, cystic fibrosis, COPD, bronchopulmonary dysplasia, respiratory syncytial virus, diabetes, adult respiratory distress syndrome... [Pg.191]

Fok TF, Monkman S, Dolovich M, Gray S, Coates G, Paes B, et al. Efficiency of aerosol medication delivery from a metered-dose inhaler versus jet nebulizer in infants with bronchopulmonary dysplasia. Pediatr Pulmonol 1996 21(5) 301 -309. [Pg.227]

Premature infants and children with chronic cholestasis may develop spontaneous vitamin E deficiency. In premature infants, the deficiency manifests itself as increased red cell fragility and mild hemolytic anemia. It has been claimed, but not established, that these infants respond to administration of vitamin E. The anemia is not prevented by vitamin E, and only small improvements in red cell indices follow vitamin E treatment. A role has been claimed for vitamin E in prophylaxis of retrolental fibroplasia and bronchopulmonary dysplasia, two types of oxygen-induced tissue injury that occur in premature infants treated aggressively with oxygen. [Pg.913]

The fully parameterized model elucidated thus far was subject to the backward elimination procedure to achieve parsimony. When a parameter was removed from the model, an objective function value increase of at least 7.88, corresponding to a nominal significance level of 0.005, was required for retention of the covariate relationship quantified by the parameter. Ultimately, the effect of RACE on Kant was removed, as was the effect of gestational age on PRE and The influence of bronchopulmonary dysplasia was also determined to be insignificant. Removal of these covariates resulted in the final PD model as follows ... [Pg.711]


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Bronchopulmonary

Dysplasia

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