A Perinatal Pathology View of Preterm Labor

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Pathophysiologic Mechanisms of Spontaneous Prematurity

The actual physiologic mechanism that initiates preterm labor has not been clearly identified but has been shown to be influenced by such factors as prostaglandin synthesis, oxytocin release, hormonal ratios (decline in progesterone level, rise in estradiol level), mechanical stretch of the uterine tissues, and changes in uterine blood flow. In order to develop effectively directed interventions in cases of women at high risk of preterm delivery, the pathophysiology of the cascade of events that precede the actual onset of labor must be better elucidated. Cases of so-called idiopathic spontaneous prematurity differ from cases of indicated prematurity involving fetal or maternal complications, and investigation should be targeted at these cases, as they may be preventable.

In a study of 50 women who gave birth between 23 and 36 weeks and failed tocolysis,[13] faulty placentation, intrauterine infection, and immunologic factors were the 3 groups of factors most often identified, with 50%, 38%, and 30%, respectively, of the patients having these indicators of abnormal placental environment. Of the 50 patients, 29 (58%) had 2 or more possible factors, 19 (38%) had 1 factor, and only 2 (4%) had no placental factor identified. Therefore, in 96% (48/50) of the patients, at least 1 possible placental basis of preterm labor and delivery was identified. Of the 19 patients with only 1 possible factor, 7 had faulty placentation (1 placenta previa, 6 abruptio placentae), and 6 had an intrauterine infection. Of the 29 patients with 2 or more possible factors identified, faulty placentation and immunologic factors were found together in 7 (24%), and cervical incompetence was concomitant with intrauterine infection in 6 (21%).

Some cases of spontaneous prematurity, especially those seemingly either caused or exacerbated by chronic psychosocial factors, are difficult to characterize as treatable during an ongoing pregnancy. For instance, low socioeconomic status, low prepregnancy weight, poor nutrition, stress, inadequate weight gain during pregnancy, and a negative perception of the current pregnancy have been shown to be associated with increased risk of prematurity. Early detection and intervention may not significantly decrease risk in these cases.

Pathologic studies have shown, however, that some cases of spontaneous prematurity may manifest pathologic symptoms subclinically in the uteroplacental tissues and membranes, probably significantly earlier than any clinical presentation. A state of prolonged intrauterine compromise resulting in nutritional deprivation of the fetus may cause intrauterine growth restriction and the initiation of preterm labor. Subclinical and chronic placental pathologic conditions may accompany apparently acute situations, such as spontaneous preterm labor or premature rupture of membranes, and indicate an underlying chronic compromise of potential long-term significance to the infant.[14]

A placental examination can document the presence of lesions associated with inflammation, abnormal coagulation, and abnormalities of the uteroplacental blood vessels. The most well-characterized lesions associated with prematurity are those secondary to acute ascending infection. Data suggest that the etiology of a great proportion of spontaneous prematurity cases are more complex, however, and may also involve chronic villous and uteroplacental vascular disease[14] in addition to or instead of lesions of acute inflammation. Placental infarction, chronic villitis, and lesions of the uteroplacental vessels (abruption, thrombosis, failure of physiologic change) have previously been shown to be associated with preterm births characterized by decreased fetal growth.

A study comparing clinical and pathologic findings of women with preterm labor or premature rupture of membranes found that patients with preterm labor or premature rupture of membranes who have infection are delivered earlier, have smaller babies, have more severe morbidity, and have greater mortality than patients with preterm labor or premature rupture of membranes who do not have infection and have maternal placental vascular abnormalities.[15] (This observation, since confirmed in other populations, identified and characterized 2 distinct mechanistic subgroups of patients with preterm labor or premature rupture of membranes, giving support to the theory of overlapping mechanisms between the etiologically heterogeneous modes of preterm delivery. Now, back to the case studies.

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