Uterine Contractility and Dystocia

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Chapter 11 Uterine Contractility and Dystocia

Richard A. Bashore, Dotun Ogunyemi, Robert H. Hayashi

Although the definition of dystocia is “difficult childbirth,” the term is used interchangeably with dysfunctional labor and characterizes labor that does not progress normally. The problem may be caused by (1) abnormalities of the “powers”: ineffective uterine expulsive forces; (2) abnormalities of the “passenger”: abnormal fetal lie, malpresentation, malposition, or fetal anatomic defects; or (3) abnormalities of the “passage”: maternal bony pelvic contractures, resulting in mechanical interference with the passage of the fetus through the birth canal. The cause or causes of abnormal labor should be determined as accurately as possible so that an effective and safe management plan can be developed.

Physiologic Changes of Labor

The pregnant uterus is a large smooth muscle organ consisting of billions of smooth muscle cells. Each smooth muscle cell becomes a contractile element when the intracellular ionic calcium concentration increases to trigger an enzymatic process that results in the formation of the actin-myosin element. Stimulation of oxytocin or prostaglandin receptors on the plasma membrane further activates the formation of the actin-myosin element.

Contractions occur in localized areas of the uterus during gestation, but during parturition, the entire uterus contracts in an organized way to empty itself. These coordinated smooth muscle contractions occur as a result of the involvement and action of special gap junction structures. Gap junctions are protein structures that form along the interface of two smooth muscle cell membranes and that act by promoting the movement of action potentials throughout the myometrium.

During labor, two distinct segments of the uterus are formed. The upper segment actively contracts and retracts to expel the fetus while the lower segment, along with the dilating cervix, becomes thinner and passive and is referred to as the lower uterine segment (LUS). A physiologic retraction ring forms at the interface between the two segments. With obstructed labor, the thinning of the LUS becomes very pronounced and is called the pathologic retraction ring of Bandl, and if the obstruction is not relieved, uterine rupture may occur.

The pregnant cervix contains collagen, smooth muscle, and ground substance and must be structurally altered from a firm, intact sphincter to a soft, pliable, dilatable structure through which the products of conception can pass at the appropriate time. These structural changes are the result of collagenolysis and increased hyaluronic acid, with a decrease in dermatan sulfate, which favors increased water content. These changes probably occur in response to an increase in the estrogen-to-progesterone ratio, prostaglandin E₂, and enzymatic remodeling of cervical tissue.

Normal Labor

Labor is diagnosed by regular, painful uterine contractions that increase in frequency and intensity with progressive cervical effacement or dilation.

The early part, or latent phase, of labor is involved with softening and effacement of the cervix with minimal dilation. This is followed by a more rapid rate of cervical dilation, known as the active phase of labor, which is further divided into the acceleration (maximal slope) and deceleration phases. The descent of the fetal presenting part usually begins during the active phase of labor, then progresses at a more rapid rate toward the end of the active phase and continues after the cervix is completely dilated. A useful method for assessing the progress of labor and detecting abnormalities in a timely manner is to plot the rate of cervical dilation and descent of the fetal presenting part (Figure 11-1).

FIGURE 11-1 Graphic plot of cervical dilation (green) and descent of the fetal presenting part (red) during labor.

(From Cohen WR, Friedman EA [eds]: Management of Labor. Gaithersburg, MD, Aspen Publishers, 1983, p 13.)

Normal cervical dilation and descent of the fetus take place in a progressive manner and occur within a well-defined time period. Dysfunctional labor occurs when rates of dilation and descent exceed these time limits. The phase of labor during which the abnormality occurs and the configuration of the abnormal labor curve may indicate the potential causes for the abnormal labor.

Abnormalities of the Latent Phase of Labor

The normal limits of the latent phase of labor extend up to 20 hours for nulliparous patients and up to 14 hours for multiparous patients. A latent phase that exceeds these limits is considered prolonged and may be caused by dysfunctional labor, premature or excessive use of sedatives or analgesics, fetal malpositions, or fetal size. A long, closed, firm cervix requires more time to efface and to undergo early dilation than does a soft, partially effaced cervix, but it is doubtful that a cervical factor alone causes a prolonged latent phase. Many patients who appear to be developing a prolonged latent phase are shown eventually to be in false labor or prelabor, with no progressive dilation of the cervix.

The outcome of a prolonged latent phase is generally favorable for both the mother and the fetus, provided that no other abnormalities of labor subsequently occur.

MANAGEMENT

A prolonged latent phase caused by premature or excessive use of sedation or analgesia usually resolves spontaneously after the effects of the medication have disappeared. Therapeutic rest with morphine sulfate or an equivalent drug has been shown to be effective in ruling out prelabor; women in true labor wake up in active labor, whereas those in prelabor stop contracting.

If a definite diagnosis of prolonged latent phase of labor is made or there are reasons to expedite delivery, augmentation of labor by oxytocin can be performed. This is accomplished by the addition of 10 U of oxytocin to 1000 mL of intravenous solution for a final concentration of 10 mU of oxytocin to each 1 mL of solution. A number of protocols have been suggested for the infusion of oxytocin. Oxytocin can be given as a low dose, in which the infusion is begun at a rate of 1 to 2 mU/minute and is increased in 1- to 2-mU/minute increments every 15 to 40 minutes until the desired frequency and intensity are obtained, or a maximum of 20 to 40 mU/minute is reached. The higher-dose infusion method is begun at a rate of 6 mU/minute, with incremental increases of 6 mU/minute every 15 to 40 minutes until uterine contractions of the desired frequency and intensity are obtained or a maximum of 40 mU/minute is reached.

Amniotomy or artificial rupture of the membranes may be considered as part of the management of the latent phase of labor. An associated risk is an increased incidence of chorioamnionitis.

Abnormalities of the Active Phase of Labor

When the cervix dilates to about 3 to 4 cm, the rate of dilation progresses more rapidly. Cervical dilation of less than 1.2 cm/hour in nulliparous women and 1.5 cm in multiparous women constitutes a protraction disorder of the active phase of labor. During the latter part of the active phase, the fetal presenting part also descends more rapidly through the pelvis and continues to descend through the second stage of labor. A rate of descent of the presenting part of less than 1 cm/hour in nulliparous women and 2 cm/hour in multiparous women is considered to be a protraction disorder of descent (Figure 11-2). If a period of 2 hours or more elapses during the active phase of labor without progress in cervical dilation, an arrest of dilation has occurred; a period of more than 1 hour without a change in station of the fetal presenting part is defined as an arrest of descent (Figure 11-3).

FIGURE 11-2 Normal dilation (green) and descent (red) curves of normal labor and curves depicting protracted dilation and descent abnormalities of labor.

(Modified from Friedman EA: Labor: Clinical Evaluation and Management, 2nd ed. New York, Appleton-Century-Crofts, 1978, p 65.)

FIGURE 11-3 Normal dilation (green) and descent (red) curves of normal labor and curves depicting arrest disorders of dilation and descent.

(Modified from Friedman EA: Labor: Clinical Evaluation and Management, 2nd ed. New York, Appleton-Century-Crofts, 1978, p 66.)

Etiology of active phase abnormalities include inadequate uterine activity, cephalopelvic disproportion, fetal malposition, or conduction anesthesia. The maternal pelvis should be evaluated, and the presenting fetal part should also be evaluated under these conditions.

MANAGEMENT

The American College of Obstetricians and Gynecologists (ACOG) recommends the use of oxytocin for all protraction and arrest disorders. Adequate labor (as assessed by intrauterine catheter) is defined as 200 Montevideo units (which is the sum of all the amplitudes of all the contractions in a 10-minute window) for at least 2 hours. Thus, a patient having four contractions in 10 minutes, each with an amplitude of 50 mm Hg, has adequate labor. Amniotomy should be performed if rupture of membranes has not occurred spontaneously.

Before deciding to proceed to cesarean delivery in the first stage of labor for abnormal labor progression, it should be ascertained that at least 4 hours of adequate contractions, as defined by 200 Montevideo units, has occurred. In a nullipara with dystocia, continuing labor for 6 to 8 hours is still associated with a high likelihood of vaginal delivery provided that the fetal heart rate is reassuring and there is some labor progress.

A cesarean delivery is indicated if cephalopelvic disproportion is diagnosed.

ACTIVE MANAGEMENT OF LABOR

Active management of labor has been proposed and used in the nulliparous patient as a strategy to lower the incidence of cesarean delivery for dystocia. This approach was initiated in the 1960s at the National Maternity Hospital in Dublin, where the rate of cesarean deliveries is relatively low. Published studies of this approach in institutions in the United States and Canada have been controversial with respect to the lowering of cesarean birth rates, but all studies have reported decreased length of labor in general when active management of labor is employed.

The criteria and components of this program are as follows: (1) nulliparous pregnant patient with spontaneous onset of labor and a singleton fetus in a cephalic presentation; (2) prenatal education classes and intrapartum reassurances to set realistic patient expectations and lower patient anxiety; (3) constant attendance during labor, usually by a labor nurse specialist or midwife; (4) peer review of all cesarean births; (5) nonadmittance to the labor unit without a clear diagnosis of labor (based not on the amount of cervical dilation but rather on the quality of contractions, which should be regular and painful with at least one of the following: complete cervical effacement, rupture of membranes, or bloody show); (6) performance of amniotomy on admission to the labor ward; (7) regular examination for progress in cervical dilation; (8) high-dose oxytocin if the patient fails to demonstrate cervical dilation at a rate of 1 cm/hour or more in the first stage of labor or if there is no descent of the fetal head for 1 hour in the second stage (most active management protocols use an initial infusion rate and increments of 4 to 6 mU/minute of oxytocin with only 15 minutes between increments to a maximum of 40 mU/minute); and (9) peer review of outcomes.

Many active management of labor programs have reported no compromise of perinatal outcomes and no cases of uterine rupture.

DYSTOCIA CAUSED BY ABNORMAL PRESENTATION AND POSITION

Presentations other than vertex and positions other than occipitoanterior (OA) are considered to be abnormal in the laboring patient. Disorders of the dilation and descent phases of labor occur with increased frequency in cases of abnormal presentation or position because of the altered relationship between the presenting part of the fetus and the maternal pelvis. Fetal malpresentations are discussed further in Chapter 13.

Persistent Occipitotransverse Position

The fetal head normally enters and engages in the maternal pelvis in an occipitotransverse (OT) position. It subsequently rotates to an OA position or, in a small percentage of cases, to an occipitoposterior position. This rotation occurs because the head flexes as the leading part of the vertex encounters the pelvic floor and then rotates to adjust to the shape of the gynecoid pelvis. In a small number of cases, the head fails to flex and rotate and persists in an OT position. This position may be caused by cephalopelvic disproportion; altered pelvic architecture, such as in a patient with a platypelloid or android pelvis; or a relaxed pelvic floor, brought about by epidural anesthesia or multiparity. The diagnosis of a persistent OT position may be difficult at times, owing to the obscuring of suture lines and fontanelles by the excessive molding and caput formation that often accompany this abnormal position.

A persistent OT position with arrest of descent for a period of 1 hour or more is known as transverse arrest. Arrest occurs because of the deflexion that accompanies the persistent OT position, resulting in the larger occipitofrontal diameter (11 cm) becoming the presenting diameter. Until the head undergoes flexion and rotation, further descent cannot take place. Transverse arrest commonly occurs with the vertex at a +1 to +2 station.

The management of transverse arrest at a +1 to +2 station is complex, in part, because at these stations the widest part of the fetal head is at or above the level of the ischial spines. If the midpelvis is compromised, cesarean delivery is indicated. If the pelvis is judged to be of normal size and the fetus is not macrosomic, oxytocic stimulation of labor may be appropriate if uterine contractions are inadequate.

Manual rotation using the fingers of the examiner’s hand or forceps rotation using Kielland forceps may be indicated if the pelvis is of normal size and shape. Forceps rotation and delivery of a persistent OT position at a +1 to +2 station is now referred to as a low forceps procedure. However, because of the marked degree of molding and caput formation that usually occurs in this circumstance, the bony part of the fetal vertex may be at a +1 station even though the scalp may be visible at the introitus. Thus, what appears to be an uncomplicated low forceps operation may actually be a more difficult midforceps procedure. One method for avoiding this problem is to clinically evaluate the relationship between the fetal head and the sacrum. If the fetal head fills the hollow of the sacrum, the biparietal diameter is usually at or below the spines, and an attempt at forceps delivery can be considered.

Persistent Occipitoposterior Position

The head generally rotates from OT to OA during the descent through the maternal pelvis. Even if the head initially rotates to an occipitoposterior position, most fetuses will eventually rotate spontaneously during labor to OA, leaving only a small percentage (5% to 15%) of fetuses with a persistent OP position.

The course of labor in the presence of a persistent OP position is usually normal except for a tendency for the second stage to be prolonged (>2 hours). It is also associated with considerably more discomfort. As with the persistent OT position, the fetal head may become markedly molded with extensive caput formation, which may cause difficulty in diagnosing its correct station and position. Observation of a prolonged second stage of labor is appropriate, provided that labor continues to be progressive, and the fetal heart rate is normal.

Delivery of the head may occur spontaneously in the OP position, but if the perineum provides undue resistance to delivery, a low forceps-assisted delivery may be required (e.g., using Simpson’s forceps). In the past a Kielland forceps rotation was usually performed, but because of a lack of experience and training, fetuses in the OP position are usually now delivered without rotation. Use of a vacuum extractor with a cup designed for a safe and secure posterior application may be performed. Sometimes the head will rotate, but it will usually deliver in the OP position. A wide mediolateral episiotomy may be required to lessen the resistance of the outlet to the delivery of the fetal head.

DYSTOCIA CAUSED BY ABNORMALITIES OF FETAL STRUCTURE

Macrosomia and Shoulder Dystocia

The ACOG defines macrosomia as a fetus weighing 4500 g or more. Large for gestational age is defined as birth weight equal to or above the 90th percentile of fetal weight for a given gestational age. Macrosomia is associated with genetic determinants, maternal diabetes, prepregnancy weight, weight gain during pregnancy, multiparity, male sex, gestational age greater than 40 weeks, ethnicity, maternal birth weight, maternal height, and maternal age. Maternal morbidity associated with macrosomia includes labor dystocia, shoulder dystocia, and genital trauma, with a corresponding increase in the cesarean delivery rate. There is also an increase in postpartum hemorrhage and puerperal infection. There is increased perinatal morbidity resulting from dystocia and birth trauma, especially shoulder dystocia.

An accurate estimate of fetal weight is elusive. Errors in the estimation of macrosomia by ultrasound may be up to 50%. Prospective studies have shown that clinical estimates by physicians or patients are as inaccurate as ultrasonic assessments. Suspected macrosomia alone is not an indication for cesarean delivery or induction of labor. Induction of labor has not been shown to improve fetal or maternal outcome. Because the risk for shoulder dystocia and possible fetal injury increases significantly as the upper extremes of fetal weight are reached, however, ACOG recommends cesarean delivery for an estimated fetal weight of 5000 g or more in women without diabetes, and 4500 g or more in women with diabetes.

Although the mean duration of labor is prolonged for excessively large fetuses, it is not unusual to encounter unexpected shoulder dystocia after a labor that has been entirely normal up to the moment of delivery.

Shoulder dystocia means difficult delivery of the shoulder. It has been defined as delivery of the shoulder requiring the use of procedures in addition to gentle downward traction on the fetal head or a prolonged head-to-body delivery interval of more than 60 seconds.

Shoulder dystocia depends on the size of the maternal pelvis in relation to the size of the fetus and occurs from impaction of the shoulder on the pubic symphysis anteriorly or the sacral promontory posteriorly. The most important risk factors for shoulder dystocia are fetal macrosomia and maternal diabetes. Others include obesity, multiparity, post-term gestation, short stature, previous history of macrosomic birth, and previous history of shoulder dystocia. During labor, risk factors include labor induction, epidural analgesia, prolonged labor, and operative vaginal delivery.

The major neonatal complication is the occurrence of Erb’s palsy, which can be caused by excessive traction on the brachial plexus by the delivery attendant. This is an important cause of malpractice in obstetrics. If Erb’s palsy occurs on the posterior shoulder, the damage could not have been caused by excessive traction, but was most likely caused by abnormalities of the sacral promontory applying pressure on the brachial plexus before delivery. Other neonatal complications include Klumpke’s palsy, clavicular fracture, humeral fracture, hypoxia, brain injury, and death. Maternal complications include genital tract lacerations and postpartum hemorrhage.

Shoulder dystocia is recognized at delivery by retraction of the fetal head, which is called the turtle sign. Shoulder dystocia is not overcome by traction on the fetal head but, instead, by one or more maneuvers designed to displace the anterior shoulder from behind the symphysis pubis. An initial maneuver is suprapubic pressure, which involves lateral pressure only with the hand over the maternal suprapubic region in an effort to guide the anterior shoulder under or away from the symphysis pubis. McRoberts’ maneuver may also be employed as an initial or second procedure. In McRoberts’ maneuver, the maternal thighs are sharply flexed against the maternal abdomen to reduce the angle between the sacrum and spine, thus freeing the impacted shoulder. If this is not successful, pressure is applied with the operator’s fingers against the scapula of the posterior shoulder in an attempt to rotate (corkscrew, Woods maneuver) the posterior shoulder upward until it becomes the anterior shoulder. If this maneuver does not correct the problem, a hand is inserted into the vagina, and the posterior arm is grasped and pulled across the chest, resulting in delivery of the posterior shoulder and displacement of the anterior shoulder from behind the symphysis pubis. Fracture of the humerus may result from this maneuver, but the bone heals quickly in the neonate. Putting the patient on all fours (knee-chest position) may also be considered because the downward pull of gravity may disimpact the shoulder. If none of these maneuvers is successful, one or both clavicles must be fractured, preferably by pressure on the clavicle directed away from the pleural cavity to prevent traumatic puncture of the lungs.

A maneuver has been described, attributed to Zavanelli, to manage shoulder dystocia that is not corrected successfully by the methods already described. In this last-resort procedure, the fetal head is manually returned to its prerestitution position, and then slowly replaced into the vagina by steady upward pressure against the head. Delivery is subsequently accomplished by cesarean birth. A uterine relaxant may be required to carry out this procedure.

Developmental Abnormalities

Localized abnormalities of fetal anatomy may lead to dystocia. Internal hydrocephalus may cause enlargement of the fetal head to the extent that vaginal delivery is not possible. The diagnosis is usually made by ultrasonography performed because of the clinical suspicion, or it may appear as an unexpected finding on ultrasonography performed for other indications.

Several options are available for the delivery of the fetus with hydrocephalus. Excessive cerebrospinal fluid may be removed by inserting a needle directly into the ventricular space through the dilated cervix during labor, or transabdominally under ultrasonic guidance before or during labor. Alternatively, the fetus may be delivered by cesarean birth to avoid the risk for infection, which can result from transvaginal or transabdominal drainage.

Intrauterine shunting of the fetal ventricular system into the amniotic fluid compartment is an experimental procedure that has not been shown to have the long-term benefits to justify its performance.

The accumulation of ascites in the fetal abdomen or enlargement of fetal organs, such as the bladder or liver, may result in unexpected dystocia (due to an enlarged fetal abdomen) after the fetal head has been delivered. Ascites usually occurs as part of hydrops, which is defined as fetal fluid retention in two of the following sites: skin, abdomen, pericardial cavity, or pleural cavity. Immune hydrops is usually caused by Rhesus disease, while nonimmune hydrops may be caused by congenital infections, chromosomal abnormalities, or fetal arrhythmias. If any of the above conditions is present, careful ultrasonic evaluation before or during labor should be performed to identify excessive enlargement of the fetal abdomen. Ascitic fluid or urine from a massively enlarged bladder may be removed by transabdominal drainage with a needle before vaginal delivery. Cesarean delivery may be indicated if the fetal abdomen cannot be sufficiently decompressed.

A defect in the fetal lumbosacral vertebrae may result in the protrusion of a meningeal sac (meningocele) or a sac containing spinal cord (meningomyelocele). These defects are usually detected as a result of abnormal serum or amniotic fluid alpha-fetoprotein values or by ultrasonography. If the sac is large, abdominal delivery is advisable to avoid dystocia or rupture of the sac and potential infection. If the sac is small and is covered by fetal skin, as reflected by a normal alpha-fetoprotein value, vaginal delivery may be appropriate.

Other potential causes of fetal dystocia include a very large fetal sacrococcygeal teratoma, conjoined twins, and locked preterm twins when twin A is breech and twin B is vertex and they enter the pelvis at the same time.

DYSTOCIA CAUSED BY MATERNAL PELVIC ABNORMALITIES

Cephalopelvic disproportion (CPD) exists if the maternal bony pelvis is not of sufficient size and of appropriate shape to allow the passage of the fetal head. This problem may occur as a result of contraction of one of the planes of the pelvis. Relative CPD may exist with a normal pelvis, if the fetal head is excessively large or if it is in an abnormal position. Contraction of the maternal pelvis may occur at the level of the inlet or midpelvis, but contraction of the outlet is extremely unusual unless it is found in association with a midpelvic contraction (see Chapter 8).

Cephalopelvic disproportion at the level of the pelvic inlet causes a failure of descent and engagement of the head. The finding of an unengaged head in a nulliparous patient at the start of labor indicates an increased likelihood of CPD at the pelvic inlet, but an unengaged fetal head in a multiparous patient in labor is not an unusual occurrence. Relative CPD can occur in the multiparous patient (the “multip trap”), however, and should be kept in mind.

The management of a nulliparous patient with an unengaged fetal head in labor should begin with a careful clinical evaluation of the maternal pelvis. If the pelvis is clinically adequate, expectant management with observation of the labor pattern is appropriate. If uterine contractions are ineffective, oxytocic stimulation of labor may be considered.

The occurrence of CPD at the level of the midpelvis occurs more frequently than inlet dystocia because the capacity of the midpelvis is smaller than that of the inlet and also because deflection or positional abnormalities of the fetal head are more likely to occur at that level. The occurrence of bony dystocia at the level of the midpelvis is usually indicated by an arrest of descent of the head at a +1 to +2 station. With CPD and arrest of descent, application of the head to the cervix is poor, resulting in the loss of part of the force needed for cervical dilation. Thus, CPD may be associated with a protracted or expected rate of cervical dilation before an arrest of descent is apparent.

DYSTOCIA CAUSED BY CONDUCTION ANESTHESIA

The use of epidural anesthesia for pain control during the first stage of labor has gained wide acceptance. Refinement of the epidural technique has allowed a segmental block and titratable continuous infusion of narcotics and local anesthetics to better tailor pain control, with less interference with the process of labor (see Chapter 8).

Current evidence suggests that epidural analgesia does not increase the primary cesarean delivery rate, but it may be associated with increased need for oxytocin augmentation, prolonged first and second stages of labor, and operative vaginal delivery.

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Uterine Contractility and Dystocia

MANAGEMENT

MANAGEMENT

ACTIVE MANAGEMENT OF LABOR

DYSTOCIA CAUSED BY ABNORMAL PRESENTATION AND POSITION

Persistent Occipitotransverse Position

Persistent Occipitoposterior Position

DYSTOCIA CAUSED BY ABNORMALITIES OF FETAL STRUCTURE

Macrosomia and Shoulder Dystocia

Developmental Abnormalities

DYSTOCIA CAUSED BY MATERNAL PELVIC ABNORMALITIES

DYSTOCIA CAUSED BY CONDUCTION ANESTHESIA

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