Variations in Criteria for Eligibility Determination for Early Intervention Services with a Focus on Eligibility for Children with Neonatal Complications.

OBJECTIVE: The purpose of this policy review is to describe data on eligibility determination practices for early intervention (EI) services across the United States as they particularly relate to eligibility determination for children seen in neonatal follow-up clinics. METHOD: Policy information was gathered from posted information on state EI websites and confirmed through follow-up phone calls. Information collected included definition of delay, approved measures for developmental assessment, and inclusion criteria for medically at-risk status based on birth weight, prematurity, and/or neonatal abstinence syndrome/prenatal exposure. RESULTS: States varied widely across enrollment practices and policies. Forty percent of states defined eligibility based on percent delay (vs SD). Thirty-five states had criteria for enrollment based on birth weight and/or prematurity, and 19 states specifically allowed enrollment for an infant with neonatal abstinence syndrome. CONCLUSION: Providers working in neonatal follow-up clinics should be carefully educated about the eligibility criteria and approved tests for assessing development in the states in which they practice, recognizing that there is obvious and significant variability across states.

High Altitude Reduces NO-Dependent Myometrial Artery Vasodilator Response During Pregnancy.

The chronic hypoxia of high-altitude (HA) residence reduces uterine artery blood flow during pregnancy, likely contributing to an increased frequency of preeclampsia and intrauterine growth restriction. We hypothesized that this lesser pregnancy blood flow rise was due, in part, to reduced vasodilation of myometrial arteries (MAs). Here, we assessed MA vasoreactivity in healthy residents of high (2902±39 m) or low altitude (LA; 1669±10 m). MA contractile responses to potassium chloride, phenylephrine, or the thromboxane A2 agonist U46619 did not differ between LA and HA women. Acetylcholine vasodilated phenylephrine or U466119 preconstricted MAs at LA, yet had no effect on HA MAs. In contrast, another vasodilator, bradykinin, relaxed MAs from both altitudes similarly. At LA, the NO synthase inhibitor L-NG-nitroarginine methyl ester decreased both acetylcholine and bradykinin vasodilation by 56% and 33%, respectively. L-NG-nitroarginine methyl ester plus the COX (cyclooxygenase) inhibitor indomethacin had similar effects on acetylcholine and bradykinin vasodilation (68% and 42% reduction, respectively) as did removing the endothelium (78% and 50% decrease, respectively), suggesting a predominantly NO-dependent vasodilation at LA. However, at HA, L-NG-nitroarginine methyl ester did not change bradykinin vasodilation, whereas indomethacin or endothelium removal decreased it by 28% and 72%, respectively, indicating impaired NO signaling at HA. Suggesting that the impairment was downstream of eNOS (endothelial NO synthase), HA attenuated the vasodilation elicited by the NO donor sodium nitroprusside. We concluded that reduced NO-dependent MA vasodilation likely contributes to diminished uteroplacental perfusion in HA pregnancies.