Uterine muscle malfunction can result from uterine overdistention, obstructed labor, or both. Thus, infective labor is generaly accepted as a possible warning sign of etopelvic disproportion.
Although artificial separation of labor abnormalities into pure uterine dysfunction andetopelvic disproportion simplifies classification, it is an incomplete characterization because these two abnormalities are closely interlinked. Indeed, the bony pelvis rarely limits vaginal delivery. In the absence of objective means of precisely distinguishing these two causes of labor failure, clinicians must rely on a trial of labor to determine if labor can be successful in efecting vaginal delivery.
Cervical dilation as well as propulsion and expulsion of the fetus are brought about by uterine contractions. During second-stage labor, these contractions are then reinforced by voluntary or involuntary muscular action of the abdominal wall-"pushing." The diagnosis of uterine dysfunction in the latent phase is diicult and sometimes can be made only in retrospect. Women who are not yet in active labor commonly are erroneously treated for this dysfunction.
Beginning in the 1960s, at least three significant advances have aided treatment of uterine dysfunction. First is the realization that undue labor prolongation may contribute to maternal and perinatal morbidity and mortality rates. Second, dilute intravenous infusion of oxytocin is administered to treat certain types of uterine dysfunction. Last, cesarean delivery is selected rather than diicult midforceps delivery when oxytocin fails or its use is inappropriate.
• Types of Uterine Dysfunction
Reynolds and coworkers (1948) emphasized that uterine contractions of normal labor are characterized by a gradient of myometrial activity. These forces are greatest and last longest at the fundus-considered fundal dominance-and they diminish toward the cervix. Caldeyro-Barcia and colleagues (1950) from Montevideo, Uruguay, inserted small balloons into the myometrium at various levels (Chap. 24, p. 478). hey reported that in addition to a gradient of activity, the onset of the contractions difered in the fundus, midzone, and lower uterine segments. Larks (1960) described the stimulus as starting in one cornu and then several milliseconds later in the other. he excitation waves then join and sweep over the fundus and down the uterus. Normal spontaneous contractions often exert pressures approximating 60 mm Hg (Hendricks, 1959). Even so, the Montevideo group ascertained that the lower limit of contraction pressure required to dilate the cervix is 15 mm Hg.
From these observations, two physiological types of uterine dysfunction are defined. In the more common hypotonic uterine dyunction, there is no basal hypertonus, and uterine contractions have a normal gradient pattern (synchronous). However, pressure during a contraction is insuicient to dilate the cervix.
In the second type, hypertonic uterine dysunction or incoordinate uterine dyunction, either basal tone is elevated appreciably or the pressure gradient is distorted. Gradient distortion may result from more forceful contraction of the uterine midsegment than the fundus, from complete asynchrony of the impulses originating in each cornu, or from a combination of these two.
hese just-described types of uterine dysfunction can in turn lead to labor abnormalities (Table 23-2). First, the latent phase may be prolonged, which is defined as exceeding 20 hours in the nullipara and 14 hours in the multipara. In some, uterine contractions cease, suggesting false labor. In the remainder, an abnormally long latent phase persists and is often treated with oxytocin stimulation.