Hypocapnia and other ventilation-related risk factors for cerebral palsy in low birth weight infants

Ventilatory management patterns in very low birth weight newborns, particul arly iatrogenic hypocapnia, have occasionally been implicated in perinatal brain damage. However, such relationships have not been explored in large r epresentative populations. To examine the risk of disabling cerebral palsy in mechanically ventilated very low birth weight infants in relation to hyp ocapnia and other ventilation-related variables, we conducted a population- based prospective cohort study of 1105 newborns with birth weights of 500-2 000 g born in New Jersey from mid-1984 through 1987, among whom 777 of 902 survivors (86%) had at least one neurodevelopmental assessment at age 2 y o r older. Six hundred fifty-seven of 777 assessed survivors (85%), of whom 4 00 had been mechanically ventilated, had blood gases obtained during the ne onatal period. Hypocapnia was defined as the highest quintile of cumulative exposure to arterial Pco(2) levels < 35 nun Hg during the neonatal period. Disabling cerebral palsy was diagnosed in six of 257 unventilated newborns (2.3%), 30 of 320 ventilated newborns without hypocapnia (9.4%), and 22 of 80 ventilated newborns with hypocapnia (27.5%). Two additional ventilatory risk factors for disabling cerebral palsy were found-hyperoxia and prolong ed duration of ventilation. In a multivariate analysis, each of the three v entilatory variables independently contributed a 2- to 3-fold increase in r isk of disabling cerebral palsy. These risks were additive. Although durati on of mechanical ventilation in very low birth weight newborns likely repre sents severity of illness, both hypocapnia and hyperoxia are largely contro lled by ventilatory practice. Avoidance of arterial Pco(2), levels <35 nun Hg and arterial Po-2 levels <greater than>60 mm Hg in mechanically ventilat ed very low birth weight infants would seem prudent.