Ronald I Clyman1, Andrea Wickremasinghe2, T Allen Merritt3, Tabitha Solomon3, Patrick McNamara4, Amish Jain4, Jaideep Singh5, Alison Chu5, Shahab Noori6, Krishnamurthy Sekar6, Pascal M Lavoie7, Joshua T Attridge8, Jonathan R Swanson8, Maria Gillam-Krakauer9, Jeff Reese9, Sara DeMauro10, Brenda Poindexter11, Sue Aucott12, Monique Satpute12, Erika Fernandez13, Richard J Auchus14. 1. Department of Pediatric, Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA. Electronic address: clymanr@peds.ucsf.edu. 2. Department of Pediatric, Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA. 3. Department of Pediatrics, Loma Linda University, Loma Linda, CA. 4. Department of Pediatrics, Hospital for Sick Children, Toronto, Canada. 5. Department of Pediatrics, University of Chicago, Chicago, IL. 6. Department of Pediatrics, University of Oklahoma, Oklahoma City, OK. 7. Department of Pediatrics, Children's & Women's Health Center of British Columbia, Vancouver, Canada. 8. Department of Pediatrics, University of Virginia, Charlottesville, VA. 9. Department of Pediatrics, Vanderbilt University, Nashville, TN. 10. Department of Pediatrics, Children's Hospital of Philadelphia and University of Pennsylvania Perelman School of Medicine, Philadelphia, PA. 11. Department of Pediatrics, Indiana University, Indianapolis, IN. 12. Department of Pediatrics, Johns Hopkins University, Baltimore, MD. 13. Department of Pediatrics, University of New Mexico, Albuquerque, NM. 14. Department of Medicine, University of Michigan, Ann Arbor, MI.
Abstract
OBJECTIVE: To test the hypothesis that an impaired adrenal response to stress might play a role in the hypotension that follows patent ductus arteriosus (PDA) ligation. STUDY DESIGN: We performed a multicenter study of infants born at <32 weeks' gestation who were about to undergo PDA ligation. Serum adrenal steroids were measured 3 times: before and after a cosyntropin (1.0 μg/kg) stimulation test (performed before the ligation), and at 10-12 hours after the ligation. A standardized approach for diagnosis and treatment of postoperative hypotension was followed at each site. A modified inotrope score (1 × dopamine [μg/kg/min] + 1 × dobutamine) was used to monitor the catecholamine support an infant received. Infants were considered to have catecholamine-resistant hypotension if their greatest inotrope score was >15. RESULTS: Of 95 infants enrolled, 43 (45%) developed hypotension and 14 (15%) developed catecholamine-resistant hypotension. Low postoperative cortisol levels were not associated with the overall incidence of hypotension after ligation. However, low cortisol levels were associated with the refractoriness of the hypotension to catecholamine treatment. In a multivariate analysis: the OR for developing catecholamine-resistant hypotension was OR 36.6, 95% CI 2.8-476, P = .006. Low cortisol levels (in infants with catecholamine-resistant hypotension) were not attributable to adrenal immaturity or impairment; their cortisol precursor concentrations were either low or unchanged, and their response to cosyntropin was similar to infants without catecholamine-resistant hypotension. CONCLUSION: Infants with low cortisol concentrations after PDA ligation are likely to develop postoperative catecholamine-resistant hypotension. We speculate that decreased adrenal stimulation, rather than an impaired adrenal response to stimulation, may account for the decreased production.
OBJECTIVE: To test the hypothesis that an impaired adrenal response to stress might play a role in the hypotension that follows patent ductus arteriosus (PDA) ligation. STUDY DESIGN: We performed a multicenter study of infants born at <32 weeks' gestation who were about to undergo PDA ligation. Serum adrenal steroids were measured 3 times: before and after a cosyntropin (1.0 μg/kg) stimulation test (performed before the ligation), and at 10-12 hours after the ligation. A standardized approach for diagnosis and treatment of postoperative hypotension was followed at each site. A modified inotrope score (1 × dopamine [μg/kg/min] + 1 × dobutamine) was used to monitor the catecholamine support an infant received. Infants were considered to have catecholamine-resistant hypotension if their greatest inotrope score was >15. RESULTS: Of 95 infants enrolled, 43 (45%) developed hypotension and 14 (15%) developed catecholamine-resistant hypotension. Low postoperative cortisol levels were not associated with the overall incidence of hypotension after ligation. However, low cortisol levels were associated with the refractoriness of the hypotension to catecholamine treatment. In a multivariate analysis: the OR for developing catecholamine-resistant hypotension was OR 36.6, 95% CI 2.8-476, P = .006. Low cortisol levels (in infants with catecholamine-resistant hypotension) were not attributable to adrenal immaturity or impairment; their cortisol precursor concentrations were either low or unchanged, and their response to cosyntropin was similar to infants without catecholamine-resistant hypotension. CONCLUSION:Infants with low cortisol concentrations after PDA ligation are likely to develop postoperative catecholamine-resistant hypotension. We speculate that decreased adrenal stimulation, rather than an impaired adrenal response to stimulation, may account for the decreased production.
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Authors: Sydney R Rooney; Elaine L Shelton; Ida Aka; Christian M Shaffer; Ronald I Clyman; John M Dagle; Kelli Ryckman; Tamorah R Lewis; Jeff Reese; Sara L Van Driest; Prince J Kannankeril Journal: Pharmacogenomics Date: 2019-08 Impact factor: 2.533
Authors: S Noori; P McNamara; A Jain; P M Lavoie; A Wickremasinghe; T A Merritt; T Solomon; K Sekar; J T Attridge; J R Swanson; M Gillam-Krakauer; J Reese; B B Poindexter; M Brook; R J Auchus; R I Clyman Journal: J Perinatol Date: 2014-08-14 Impact factor: 2.521
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