Authors: V. Kališ; Jakub Turek; A. Hudec; P. Rokyta; Z. Rokyta; B. Mejchar Authors‘ workplace: Gynek. -porod. klinika LF UK a FN Plzeň, přednosta doc. MUDr. Z. Rokyta, CSc. Published in: Ceska Gynekol 2001; (5): 363-368 Category:
Objective: A review of meconium pathophysiology and its contribution to the incidence of postnatal neurological handicap.Design: Reviewed article.Setting: Department of Gynaecology and Obstetrics, Charles University and Faculty Hospital Plzeò, Czech Republic.Subject and Method: Meconium can be a cause of infant neurological handicap. Two main pathogenetic pathways are mentioned. 1. Meconium (and its components: bile acids) may have a direct vesoconstrictive effect on umbilical and placental vessels. This way still remains controversial. 2. Meconium as a possible cause of intraamniotic infection results in a release of fetal cytokines (TNFa, IL-1b, IL-6), which can damage myelinogenesis in periventricular white matter.Results: Meconium in premature labour is a higher risk factor compared to term delivery. 41% of premature infants were diagnosed as having CP when meconium was present compared to 10% in the same group with clear amniotic fluid. The incidence in term pregnancy with meconium present is 0,4% compared to 0,3% in a population without any obstetrical risk.Conclusion: Ultrasonographically found periventricular leukomalacia is the most reliable sign of subsequent cerebral palsy or other neurological sequelae.
Key words: meconium, cerebral palsy, neonatal necephalopathy, cytokines, bile acids
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