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Systemic Steroids for evolving severe CLD Pharmacologic doses of steroids have been shown to effect acute improvements in respiratory status in babies with severe inflammatory chronic lung changes. Acutely steroids improve pulmonary mechanics and gas exchange often leading to a reduction in requirements for assisted ventilation. (Halliday and Ehrenkrantz. Cochrane Database of Systematic Reviews. 2000) Long-term decreases in mortality or BPD have not been substantiated. However, accumulating evidence suggests that pharmacologic doses of steroids given to premature infants may have significant long-term adverse effects on neurodevelopment. Particularly, the incidence of cerebral palsy is increased in former preterm infants who received postnatal steroids. A recent systematic review suggests that 1 in 7 to 11 infants treated with postnatal steroids will suffer a subsequent neurodevelopmental disability (Barrington. Pediatrics 2001;107:1425-6.) Hydrocortisone has similar short-term adverse effects as seen with dexamethasone. However, studies have not observed neurodevelopmental delay and cerebral palsy in children exposed to hydrocortisone early in life but this needs to be further evaluated. Click to review the Pediatrics journal article "Hydrocortisone Treatment in Extremely Low Birth Weight Infants: Growth and Neurodevelomental Outcomes After Early Low-Dose" This effect may be due to hydrocortisone having less glucocorticoid potency than dexamethasone. Hydrocortisone has both glucocorticoid and mineralocorticoid activity. Glucocorticoid potency may result in apoptosis and neuronal death perhaps leading to the poor neurological outcomes seen with dexamethasone. Therefore, postnatal steroid use should be limited to only the most severely ill infants who are most likely to benefit from their use. Only the lowest doses possible and shortest courses should be employed. Vanderbilt’s systemic steroid protocol is designed to target only those infants with evolving severe CLD who have a 80% risk of mortality from CLD without the use of postnatal steroids. Given the current controversy surrounding systemic steroid usage, parents should be informed of the risks and benefits of and indications for postnatal steroid usage before dexamethasone is prescribed. Patient criteria
Exclusion criteria
Steroid course:
See order set in Wiz Order for Dexamethasone. Each daily dose of dexamethasone should be administered in two divided doses at 12 hour intervals by bolus intravenous infusion. HCT should be administered in three divided doses at 8 hour intervals. Other interventions during postnatal steroid therapy Supplemental vitamin A- Supplemental vitamin A should be held during the 8 days of systemic steriod treatment and for 1 week following the dexamethasone or hydrocortisone course. This precautionary withholding of supplemental vitamin A is based on the observation that postnatal dexamethasone treatment is associated with an increase in plasma vitamin A concentrations in VLBW neonates (Shenai. Pediatrics 2000;106:547) and may therefore predispose these infants to the potential risk of vitamin A toxicity. Protein intake- Protein intake should be increased to 4 g/kg/d during the 8 days of systemic steroid treatment. This measure is intended to counteract the catabolic effect of dexamethasone treatment on protein metabolism (Brownlee, et al. Arch Dis Child 1992;67:1). BUN should be monitored closely during this time. Famotidine (Pepcid) treatment- Famotidine should be administered at a dose of 1 mg/kg/dose q 12 hours by IV or OG administration. Alternatively, famotidine may be added to the TPN solution to provide a dose of 2 mg/kg/day. This measure is intended to prevent gastrointestinal complications resulting from systemic steroid treatment. (Kelly et al. Arch Dis Child 1993;69:37). Unless contraindicated based on clinical findings, continuation or initiation of low-volume OG feeds may be desirable during dexamethasone treatment. Triglycerides- Postnatal steroid administration has been associated with hypertriglyceridemia. Serum triglyceride levels should therefore be monitored during systemic steroid treatment and Intralipid administration decreased accordingly, if necessary. Monitoring- Sequential monitoring of blood gases is indicated to allow for maximal and rapid weaning from mechanical ventilation and supplemental oxygen during systemic steroid treatment. This should prevent barotrauma with sudden improvements in compliance and lung function. Sequential monitoring of blood pressure and blood glucose concentration is also indicated during dexamethasone treatment to detect acute side-effects of systemic hypertension and hyperglycemia. The anti-inflammatory actions of dexamethasone and hydrocortisone result in immunosuppression, and therefore close surveillance for symptoms of sepsis is warranted. Steroid rebound- As the systemic effects of steroids wear off, the patient often experiences a deterioration in respiratory function. This set-back should be anticipated 3-4 days after the last dose of dexamethasone. However, infection must still be considered in the differential diagnosis at this time. Indomethacin- an alarmingly frequent incidence of spontaneous GI perforation (11-13%) has been reported in <1000g infants receiving simultaneous postnatal dexamethasone or hydrocortisone and indomethacin. (Stark et al. Pediatrics 1999;104:739A.) This combination of medications should be avoided in this population. Protocol revisited and re-approved at Clinical Division Meeting 12/17/01. References American Academy of Pediatrics. Postnatal corticosteroids to treat or prevent chronic lung disease in preterm infants. Pediatrics 2002; 109: 330-338 Halliday HL, Ehrenkranz RA. Moderately early (7–14 days) postnatal corticosteroids for preventing chronic lung disease in preterm infants. Cochrane Systematic Reviews. http://www.nichd.nih.gov/cochrane/Hallida2/Halliday.htm Soll RF, et al. Early postnatal dexamethasone for the prevention of chronic lung disease. Pediatr Res 1999;45:226A. Stark AR, et al. Adverse effects of early dexamethasone treatment in extremely-low-birth-weight infants. N Engl J Med 2001; 344:95-101. Shinwell ES, et al. Early Dexamethasone Therapy is Associated with Increased Incidence of Cerebral Palsy. Hot Topics in Neonatology, Washington DC, 1999. Barrington KJ. The adverse neuro-developmental effects of postnatal steroids in the preterm infant: a systematic review of RCTs. BioMed Central Pediatr 2001;1:1. http://www.biomedcentral.com/1471-2431/1/1 Thebaud B, et al. Postnatal glucocorticoids in very preterm infants: "the good, the bad, and the ugly"? Pediatrics. 2001:107:413-15. Barrington KJ. Postnatal steroids and Neurodevelopmental Outcomes: A Problem in the Making. Pediatrics 2001; 107:1425-6. Stark AR, Carlo W, Bauer C, et al. Complications of early steroid therapy in a randomized controlled trial [abstract]. Pediatrics. 1999;104:739A Soll RF; Vermont Oxford Network Steroid Study Group. Early postnatal dexamethasone therapy for the prevention of chronic lung disease [abstract]. Pediatr Res. 1999;42:123A Papile LA, Tyson JE, Stoll BJ, et al. A multicenter trial of two dexamethasone regimens in ventilator-dependent premature infants. N Engl J Med. 1998;338:1112–1118 Stoll BJ, Temprosa M, Tyson JE, et al. Dexamethasone therapy increases infection in very low birth weight infants. Pediatrics. 1999;104(5). Available at: www.pediatrics.org/cgi/content/full/104/5/e63 Amin SB, Sinkin RA, McDermott MP, et al. Lipid intolerance in neonates receiving dexamethasone for bronchopulmonary dysplasia. Arch Pediatr Adolesc Med. 1999;153:795–800 Van Goudoever JB, Wattimena JD, Carnielli VP, Sulkers EJ, Degenhart HJ, Sauer PJ. Effect of dexamethasone on protein metabolism in infants with bronchopulmonary dysplasia. J Pediatr. 1994;124:112–118. Leitch CA, Ahlrichs J, Karn C, Denne SC. Energy expenditure and energy intake during dexamethasone therapy for chronic lung disease. Pediatr Res. 1999;46:109–113 Berry MA, Abrahamowicz M, Usher RH. Factors associated with growth of extremely premature infants during initial hospitalization. Pediatrics. 1997;100:640–646 Kari MA, Heinonen K, Ikonen RS, Koivisto M, Raivio KO. Dexamethasone treatment in preterm infants at risk for bronchopulmonary dysplasia. Arch Dis Child. 1993;68:566–569 Hallman M, Peltoniemi O, Saarela T. Early Neonatal Hydrocortisone: Study Rather Than Treat. Pediatrics. 2006;118:2540-2542 |
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