Chronic Fetal Distress and Placental Insufficiency (Part 1 of 3)

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Abstract
Infants born malnourished and retarded in growth, have presumably gone through a prolonged period of intrauterine deprivation. This contributes materially to perinatal morbidity and mortality. Chronic fetal distress has a duration of weeks, subacute distress extends over days, and acute perinatal distress usually begins hours before birth (or death in utero). For statistical purposes, chronic fetal distress was arbitrarily defined as the result of deprivation lasting sufficiently long to produce a deficit of birth weight of at least mean minus 2 standard deviations for the respective gestational age. Among births at 33 to 40 weeks, this occurs in 3% of surviving infants, and 24% of perinatal deaths. In subacute fetal distress, there is wasting but no significant growth retardation. This phase includes most of the malnourished postmature infants. Placental insufficiency which presumably causes much of the chronic and subacute fetal distress, is the result of interaction of many factors, normal as well as abnormal. No given type and extent of pathologic change is uniformly associated with a certain form and degree of effect on the fetus. If pregnancy terminates at approximately 36 to 41 weeks, placental lesions are frequently present when the fetus shows signs of deprivation. Very small size of the placenta, and gross lesions account for a small number of cases of insufficiency. Minute lesions include numerous microinfarcts, and groups of avascular villi frequently associated with occlusion of vessels in small villous stems. In prolonged pregnancy, significant lesions are usually absent when the infant is born malnourished; the deficiency is presumably a relative one. There are suggestions that permanent reduction of body growth, and cerebral defects may be caused by chronic fetal distress; long term follow-up studies of pertinent cases are needed.

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