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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study aimed to evaluate the role of hypocarbia as a risk factor for mortality and for cerebral palsy in extremely low birthweight infants. The records for 215 extremely low birthweight children were analysed, grouping the infants into those who died (n = 72), those who had a confirmed diagnosis of cerebral palsy (n = 27) and those without major neurological symptoms at the age of 2 y (n = 116). The analysed risk factors were: birthweight, gestational age, maternal diseases and toxaemia, multiple pregnancy, male gender, respiratory distress syndrome, abnormal neonatal cerebral ultrasound, occurrence of septic infection, and/or at least one episode of systemic hypotension and/or at least two episodes of hypocarbia (<3 kPa) during the neonatal period. The mortality rate was 31% and the rate of cerebral palsy was 17% in the survivors. Hypocarbia was found in 33% of children with cerebral palsy, in 10% of infants who died and in 19% of the healthy controls; the differences were statistically insignificant. Birthweight and gestational age, episodes of systemic hypotension and abnormal ultrasound emerged as risk factors for mortality. Abnormal cerebral ultrasound was the only significant risk factor for cerebral palsy. The role of hypocarbia in the pathogenesis of CP remained indistinct but the distribution of risk factors was different in infants with a mortal outcome and in infants with cerebral palsy.
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PMID:Does perinatal hypocarbia play a role in the pathogenesis of cerebral palsy? 1042 83

Decrease in the arterial partial pressure of carbon dioxide (PaCO(2)) causes a reduction in cerebral blood flow in humans and in most animal species; in adults as well as in newborns and even in fetal life. Severely decreased PaCO(2) increases cerebral lactate production, modifies spontaneous electric brain activity, and may decrease the metabolic rate of oxygen. A relation between very low PaCO(2) and brain injury, however, has not been shown in adult humans or full-term newborn infants, nor in perinatal animals. In contrast, an association between low PaCO(2) and cerebral palsy and white matter injury in preterm infants has been reported repeatedly. A cause-and-effect relation is suggested by data from the immature rat: brain damage induced by ligation of a carotid artery can be reduced by adding CO(2) to the inspired gas and hence avoiding the consequences of spontaneous hyperventilation. This may be relevant for the clinical care of preterm infants, since PaCO(2) to a large extent is a function of respiratory management. The questions to be addressed are whether hypocapnia sensitizes the brain to hypoxaemia, and also whether the escape mechanisms are less effective in the preterm human brain.
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PMID:Is periventricular leucomalacia a result of hypoxic-ischaemic injury? Hypocapnia and the preterm brain. 1127 50

Ventilatory management patterns in very low birth weight newborns, particularly iatrogenic hypocapnia, have occasionally been implicated in perinatal brain damage. However, such relationships have not been explored in large representative populations. To examine the risk of disabling cerebral palsy in mechanically ventilated very low birth weight infants in relation to hypocapnia and other ventilation-related variables, we conducted a population-based prospective cohort study of 1105 newborns with birth weights of 500-2000 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 or older. Six hundred fifty-seven of 777 assessed survivors (85%), of whom 400 had been mechanically ventilated, had blood gases obtained during the neonatal period. Hypocapnia was defined as the highest quintile of cumulative exposure to arterial PCO(2) levels <35 mm 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 prolonged duration of ventilation. In a multivariate analysis, each of the three ventilatory variables independently contributed a 2- to 3-fold increase in risk of disabling cerebral palsy. These risks were additive. Although duration of mechanical ventilation in very low birth weight newborns likely represents severity of illness, both hypocapnia and hyperoxia are largely controlled by ventilatory practice. Avoidance of arterial PCO(2) levels <35 mm Hg and arterial PO(2) levels >60 mm Hg in mechanically ventilated very low birth weight infants would seem prudent.
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PMID:Hypocapnia and other ventilation-related risk factors for cerebral palsy in low birth weight infants. 1172 29

The authors explored associations between blood gas abnormalities in more than 1,000 preterm infants during the first postnatal days and indicators of neonatal brain damage. During 2002-2004, women delivering infants before 28 weeks' gestation at one of 14 participating institutions in 5 US states were asked to enroll in the study. The authors compared infants with blood gas values in the highest or lowest quintile for gestational age and postnatal day (extreme value) on at least 1 of the first 3 postnatal days with the remainder of the subjects, with separate analyses for blood gas abnormalities on multiple days and for partial pressure of oxygen in the alveolar gas of <35. Outcomes analyzed were ventriculomegaly and an echolucent lesion on an ultrasound scan in the neonatal intensive care unit, and cerebral palsy, microcephaly, and a low score on a Bayley Scale of Infant Development at 24 months. Every blood gas derangement (hypoxemia, hyperoxemia, hypocapnia, hypercapnia, and acidosis) was associated with multiple indicators of brain damage. However, for some, the associations were seen with only 1 day of exposure; others were evident with 2 or more days' exposure. Findings suggest that individual blood gas derangements do not increase brain damage risk. Rather, the multiple derangements associated with indicators of brain damage might be indicators of immaturity/vulnerability and illness severity.
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PMID:Early blood gas abnormalities and the preterm brain. 2080 36