When the diagnosis of IUGR has been established, it is helpful to determine a specific etiology. Therapy may be nonspecific but should try to address the underlying cause. Many infants thought to be growth-retarded are, in retrospect, found to be constitutionally small. The key management issues are the gestational age of the pregnancy at the time of diagnosis and the urgency to expedite delivery. Most fetal deaths involving IUGR occur after 36 weeks of gestation and before labor begins. 1 The clinician must balance the risk of delivering a premature infant against the potential for intrauterine demise.
Infection and inflammation : This process involves microglial (brain macrophage) cell activation and cytokine release , which causes damage to a specific cell type in the developing brain called the oligodendrocyte. The oligodendrocytes are a type of supportive brain cell that wraps around neurons to form the myelin sheath, which is essential for white matter development. Intrauterine infections activate the fetal immune system, which produces cytokines (., interferon γ and TNF-α) that are toxic to premyelinating oligodendrocytes. Infections also activate microglial cells, which release free radicals. Premyelinating oligodendrocytes have immature defences against reactive oxygen species (., low production of glutathione , an important antioxidant). IVH is hypothesized to cause PVL because iron-rich blood causes iron-mediated conversion of hydrogen peroxide to hydroxyl radical, contributing to oxidative damage.
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