Systemic venous oxygen saturation after the Norwood procedure and childhood neurodevelopmental outcome.

Published

Journal Article

OBJECTIVE: Neonates with hypoplastic left heart syndrome have impaired systemic oxygen delivery and also have a high risk of hypoxic ischemic brain injury with resultant neurodevelopmental impairment. We hypothesized that decreased postoperative oxygen delivery, as measured on the basis of systemic venous oxyhemoglobin saturation, would be related to persistent neurodevelopmental abnormality assessed in childhood. METHODS: Early perioperative hemodynamic data, prospectively acquired from neonates undergoing staged palliation of hypoplastic left heart syndrome by using deep hypothermic circulatory arrest with uniform perioperative management, were tested for relationship to later neurodevelopmental outcome assessed at age 4 years. RESULTS: Complete hemodynamic and neurodevelopmental data were available in 13 patients aged 7 +/- 8 days at the time of the Norwood procedure and aged 4.5 +/- 0.7 years at follow-up assessment. The subjects scored significantly below the population mean for motor, visual-motor integration, and composite neurodevelopmental outcomes. The 5 (38%) patients with abnormal outcomes had significantly lower postoperative systemic venous oxygen saturation values than those with normal outcomes (46% +/- 8% vs 56% +/- 6%, P = .024). Standard hemodynamic parameters did not differentiate patient outcomes. The risk of abnormal outcome increased with increasing time at a systemic venous oxygen saturation of less than 40% (P < .001). A multivariate model of deep hypothermic circulatory arrest time, systemic venous oxygen saturation, blood pressure, and carbon dioxide tension accounted for 79% of the observed variance (P < .001). CONCLUSIONS: Decreased systemic oxygen delivery in the neonatal postoperative period is associated with hypoxic-ischemic brain injury and childhood neurodevelopmental abnormality. Measures of systemic oxygen delivery should be used to guide perioperative strategies to reduce the risk of hypoxic-ischemic brain injury.

Full Text

Cited Authors

  • Hoffman, GM; Mussatto, KA; Brosig, CL; Ghanayem, NS; Musa, N; Fedderly, RT; Jaquiss, RDB; Tweddell, JS

Published Date

  • October 2005

Published In

Volume / Issue

  • 130 / 4

Start / End Page

  • 1094 - 1100

PubMed ID

  • 16214525

Pubmed Central ID

  • 16214525

Electronic International Standard Serial Number (EISSN)

  • 1097-685X

International Standard Serial Number (ISSN)

  • 0022-5223

Digital Object Identifier (DOI)

  • 10.1016/j.jtcvs.2005.06.029

Language

  • eng