First Stage of Labor

Pain experienced during the first stage of labor predominantly originates from afferents with peripheral terminals in the lower uterine segment and the cervix rather than the uterine body. In the absence of inflammation, uterine body afferents may be much less important in labor pain during uterine distention, as shown in laboratory animals (Bradshaw et al 1999), whereas manual cervical distention reproduces labor pain in humans (Javert and Hardy 1951). Furthermore, Bonica and Chadwick (1989) showed that patients undergoing cesarean section under a local anesthetic block did not experience pain from uterine distention but did from cervical distention, which resembled labor pain. Afferents innervating the lower uterine segment and endocervix have cell bodies in the thoracolumbar dorsal root ganglia and are different from those innervating the vaginal surface of the cervix and the vagina, which have cell bodies in the sacral dorsal root ganglia (Berkley et al 1993). Dilation of the endocervix in rats, resembling first-stage labor, leads to activation of afferents from the endocervix and lower uterine segment, thus suggesting significant roles for these afferents in first-stage labor pain (Papka et al 2002) (Fig. 55-2). However, afferents from the vaginal surface of the cervix and vagina are activated only during delivery, not during labor, and stimulation may result in antinociception or mating behavior in rats (Sandner-Kiesling et al 2002). From Cleland (1933), Berkley and colleagues (1993), and other investigators’ work we now know that first-stage labor pain is transmitted via visceral afferents with peripheral terminals in the lower uterine segment and cervix. They pass through the paracervical ganglion and the hypogastric nerve and plexus together with the lumbar sympathetic chain and enter the spinal cord in the T10–L1 region (Fig. 55-3). From the spinal cord, second-order cells send axons to supraspinal sites as discussed in Chapter 51. Visceral stimulation activates similar areas in the brain as somatic stimulation does (Strigo et al 2003). Interestingly, visceral stimulation is perceived to be more unpleasant than somatic stimulation of similar intensity. The diffuse localization of visceral pain in first-stage labor versus the precise location of somatic pain in second-stage labor helps clinicians determine the appropriate type of regional analgesia needed at these times (Pan and Eisenach 2010).

Second Stage of Labor

Second-stage labor begins with completed cervical dilation, at which time the pain tends to be sharp and well localized to the vagina and perineum as a result of distention, ischemia, and tissue injury. Second-stage labor pain includes pain transmitted by afferents as in the first stage of labor but also with additional somatic afferents innervating the vaginal surface of the cervix, vagina, and perineum. These afferents travel via the pudendal nerves to dorsal root ganglia located at the S2–4 levels and terminate in the superficial laminae of the dorsal horn with limited rostrocaudal extension. Of note, studies in animal and non-pregnant women have demonstrated an antinociceptive or minor analgesic effect of stimulation of the vaginal surface of the cervix. Its role in reduction of second-stage labor pain is unclear but suggests possible activation of endogenous analgesia during labor in the presence of noxious stimuli. In the late first stage and during the second stage of labor, aching, burning, and cramping discomfort may develop in the thighs, legs, and back in some parturients. This is probably due to painful stimulation from stretching and tension in the pelvic cavity, bladder, urethra, and rectum and from pressure on roots of the lumbosacral plexus, as in the case of an abnormal occiput posterior position of the fetus. Understanding the anatomic basis of pain during the various stages of labor allows an appropriate choice of different regional anesthesia techniques to relieve the labor pain. The visceral pain in first-stage labor can be relieved with a bilateral paracervical plexus or lumbar sympathetic block and second-stage somatic pain with a bilateral pudendal nerve block, whereas an epidural or intrathecal block and their variations can provide analgesia during both stages of labor with appropriate extension of the block (see Fig. 55-3).

Role of Peripheral Afferents

Sensitization of peripheral afferents may play a significant role in labor pain and its relief. Peripheral inflammation is common with acute and chronic pain, but peripheral synthesis and release of the inflammatory products (such as prostaglandin E₂ [PGE₂], cytokines, and growth factors) associated with labor and cervical ripening may play an important role in labor pain besides its role in preterm labor. Animal studies have demonstrated that PGE₂ induces peripheral sensitization by activation of protein kinase A (Aley and Levine 1999) and nitric oxide synthase (Aley et al 1998). These sensitizing substances can amplify the perception and severity of pain (Pan and Eisenach 2010). Furthermore, estrogen receptor signaling may modulate the response to pain by sensitizing mechanosensitive afferents, whereas long-term estrogen exposure increases the proportion of hypogastric afferents innervating the cervix that express transient receptor potential vanilloid 1 (TRPV1). TRPV1 receptor antagonists have been shown to reduce hypogastric afferent responses to cervical distention (Tong et al 2006, Yan et al 2007). Peripheral sensitization during labor may be responsible for the increase in labor pain associated with labor progression, as well as provide potential new targets specific for the relief of labor pain.

Role of Inhibitory Receptors

Endogenous inhibitory receptors modulating pain responses are expressed in the peripheral afferent terminals, spinal cord, and supraspinal central nervous system to provide analgesia. Opioid receptor agonists, in particular, mu (μ) and kappa (κ) receptors, have been more commonly studied and used for analgesia. μ-Opioid receptor agonists produce antinociception in response to uterine cervical distention (UCD) through actions in the supraspinal central nervous system and the spinal cord but not in the peripheral afferent terminals (Sandner-Kiesling and Eisenach 2002) (Fig. 55-4). With somatic stimulation, tonic estrogen exposure reduces the supraspinal but not the spinal (intrathecal) analgesic effect of μ-opioid receptor agonists (Cicero et al 2002). κ-Opioid receptor agonists, which are unaffected by tonic estrogen exposure and have greater analgesic efficacy in women than in men, produce their antinociceptive effect through actions on visceral peripheral afferents and the supraspinal central nervous system (Cicero et al 2002) (see Fig. 55-4).

Role of the Spinal Cord

As a result of nociceptive stimuli, action potentials entering the spinal cord cause voltage-gated calcium channels to open and hence increased intracellular calcium concentrations, which in turn through a multistep process leads to the release of multiple excitatory neurotransmitters (amino acids such as glutamate and aspartate or peptides such as substance P, calcitonin gene–related peptide [CGRP], and neurokinin A) that interact with different receptors on spinal cord neurons (Ludwig et al 2002). Release of neurotransmitters at sensory afferent terminals is controlled by presynaptic receptors that mainly control the flux of intracellular calcium as action potentials arrive. Animal studies show that inhibition of calcium channels with gabapentin or related compounds provides antinociception in response to visceral stimulation by preventing the multistep process leading to the release of neurotransmitters (Feng et al 2003).

Sensitization and amplification of nociception can occur at the spinal cord level following repetitive nociceptor activation. Intensive noxious stimuli causing sustained release of the excitatory amino acid glutamate activates N-methyl-D-aspartate (NMDA) receptors, which leads to sustained depolarization and enhanced excitability of projection neurons (Headley and Grillner 1990). In 1933, Cleland had already reported skin hypersensitivity on dermatomes T11–12 in laboring women. This hypersensitivity, which is ablated by a paravertebral local anesthetic injection, is most likely due to enhanced sensitization of spinal cord neurons receiving ongoing nociceptive visceral input from the cervix and input from skin at these dermatomes. More recently, studies in rats have shown that UCD significantly increases spinal cord c-Fos immunoreactivity from T12–L2, which is a spinal cord neuronal activation pattern similar to that occurring with other noxious visceral stimuli. Furthermore, inhibition of c-Fos expression by prior lidocaine injection of the cervix or intrathecal ketorolac (cyclooxygenase inhibitor) suggests a role of spinal cyclooxygenase in UCD-evoked nociception and probably labor pain (Tong et al 2003). (For a summary of pain transmission in the spinal cord, see Chapter 51.)

Neuroendocrine Effects

The stress and pain of labor stimulate the sympathetic system, which results in an increase in plasma concentrations of epinephrine by 300–600%, norepinephrine by 200–400%, cortisol by 200–300%, and cardiac output, all of which reach peak values at or around delivery (Lederman et al 1977, Ohno et al 1986). These increases together with the reduced carbon dioxide tension associated with hyperventilation during labor result in a net reduction in uteroplacental perfusion in animal models (Bonica 1973, Shnider et al 1979). The β-adrenergic effects of epinephrine on the myometrium may result in dysfunctional labor, which may then become normal when labor analgesia is achieved.

Ferguson’s reflex involves neural input and results in enhanced release of oxytocin. However, even in women with disruption of this circuit, spontaneous labor and delivery are not abolished (Hingson and Hellman 1956). Papka and Shew (1993) suggested that afferent terminals in the lower uterine segment and cervix release stimulatory substances (substance P, glutamate, vasoactive intestine peptide) or inhibitory substances (CGRP, nitric oxide) that act on myometrial contraction and cervical dilatation when released locally into the cervix and lower uterine segment during afferent terminal depolarization as a result of the contraction-associated tissue distortion. Better understanding of how these released stimulatory and inhibitory substances affect the labor process and labor pain may provide opportunities for better management of labor and labor pain.

Cardiac, Respiratory, and Gastrointestinal Effects

Labor and labor pain exert stress on the cardiovascular and respiratory systems by increasing plasma catecholamines, which in turn elevate maternal cardiac output, blood pressure, and peripheral vascular resistance and reduce uteroplacental blood flow (Shnider et al 1979). Ueland and Hansen (1969) showed that maternal cardiac output increased throughout pregnancy when measured in the lateral position. The increase in cardiac output during pregnancy was due to an increased stroke volume and heart rate with the accompanying increase in blood volume. With the onset of labor, cardiac output further increased above the prelabor level by 15, 30, 45, and 65–80% during the early first stage, late first stage, second stage, and immediate after delivery, respectively (Hendricks and Quilligan 1956, Ueland and Hansen 1969) (Fig. 55-5). Return of the 250–300 mL of blood extruded from the uterus during contraction to the maternal venous circulation accounts for about half the increase in labor-associated maternal cardiac output, whereas the other half is due to sympathetic stimulation. Furthermore, maternal systolic and diastolic blood pressure can increase by 20–30 mm Hg with uterine contraction during labor without analgesia. The labor pain–associated changes in maternal hemodynamics and catecholamine concentrations, which may be deleterious to parturients with cardiovascular co-morbid conditions or uteroplacental insufficiency, can be lessened by half with complete analgesia, such as epidural or intrathecal analgesia (Shnider et al 1983, Walls and Melzack 1999).

Changes in lung volume during normal pregnancy are shown in Figure 55-6. The increased ventilation during pregnancy is due in part to an increase in CO₂ production (metabolism) and the hormonal effect of sensitizing the respiratory center to CO₂ as a direct respiratory stimulant (Pernoll et al 1975, Skatrud et al 1978). Labor pain is a powerful respiratory stimulus that results in a further increase in tidal volume, minute ventilation, and alveolar ventilation above the already increased values during pregnancy. During labor, maternal PaCO₂ can be reduced from 32 to as low as 16–20 mm Hg, which in combination with the elevated plasma catecholamine concentrations may result in decreases in cerebral and uterine blood flow. The persistent repetitive nature of labor pain also results in periods of hyperventilation during uterine contractions, followed by compensatory periods of hypoventilation between contractions, which in turn may lead to transient episodes of maternal and even fetal hypoxemia. Relief of labor pain, such as with neuraxial analgesia, reduces the increases in minute ventilation, oxygen consumption, catecholamine release, and lipolytic metabolism during the first stage of labor to levels comparable to pre-labor values. However, the expulsive effort of second-stage labor can result in a further increase in ventilation and metabolism even with neuraxial analgesia (Hägerdal 1983).

Labor pain, anxiety, and emotional stress increase gastrin release and inhibit the segmental and suprasegmental reflex of gastrointestinal and urinary motility (Marx and Greene 1964, Buchan 1980), which results in an increase in gastric acidity and volume and a delay in bladder emptying. These changes are further aggravated by recumbent positions, opioids, and depressant medications. Consequently, laboring parturients are at risk for pulmonary aspiration, especially during emergency induction of general anesthesia.

Non-pharmacological Methods

It is important to remember that labor pain is contextually unique with different meanings and significance to different parturients, depending on their culture, psychological state, experiences, expectations, support, and education. It is interesting to note that pain relief or the extent of pain relief in labor does not equate to overall satisfaction, which is correlated more with overall personal control, rapport, and participation in decision making. Despite the justifiable popularity and enthusiasm of neuraxial labor analgesia (now reaching 50–90% in developed countries), the majority of parturients around the world, especially in developing countries, may not have access to or the resources for neuraxial labor analgesia. Furthermore, some parturients prefer and treasure the experience of feeling the movement, rotations, and delivery of their baby through the birth canal. Various non-pharmacological methods, such as childbirth education, emotional and physical therapy support, psychoprophylaxis, hypnosis, hydrotherapy, transcutaneous electrical nerve stimulation (TENS), acupuncture, and intradermal water injection, are available to help parturients cope with labor pain. However, most of these non-pharmacological techniques have not been subjected to rigorous scientific testing and validation. Consequently, strong conclusive evidence of their efficacy in relieving labor pain is mostly not available.

Childbirth education may help the parturient understand, prepare for, and cope with the labor process and should include participation of the support person. The psychoprophylactic method of analgesia (modification of the original Dick-Read method of “natural birth”) emphasizes patient control over the labor process and the belief that childbirth pain is a result of uterine tension secondary to fear and that childbirth itself is not inherently painful. The psychoprophylactic method was initially (in the 1950s) popularized in Russia and then modified by Lamaze (1956), who successfully introduced it into the United States about the same time as regional anesthesia was reintroduced. The technique incorporates various controlled muscle relaxation and breathing exercises, which are claimed to have a salutary effect on the pain experience. This technique demands close communication and coordination among the teacher, the patient, support persons, and the health care team to foster confidence in the parturient for pleasant fulfillment of the childbirth experience. The presence of a partner or friend can often provide emotional support to the parturient. Systematic reviews also suggest that laboring parturients who receive continuous labor support (defined here as non-medical support of the parturient by trained personnel such as a doula) have slightly shorter labor, fewer operative deliveries and analgesic interventions, and greater satisfaction without a significant influence on neonatal outcomes (Simkin and O’hara 2002, Hodnett et al 2007). However, results from North American studies of continuous labor support are less positive than those from Europe or Asia (Simkin and Bolding 2004).

The use of water at delivery and immersion in warm water to cover the lower half of the body up to the abdomen during labor (hydrotherapy) has been stated by some to provide relaxation to parturients and reportedly to have the potential to reduce labor pain and analgesic requirements according to systematic reviews (Simkin and O’Hara 2002, Cluett et al 2004). In general, parturients tend to be able to use coping skills from psychoprophylactic techniques during early labor, but as labor progresses, success becomes progressively lower, with less than a third of parturients being able to use the technique by the onset of second-stage labor. Furthermore, Melzack (1981) showed that more than 90% of nulliparas and 75% of multiparas who had prepared childbirth training still rated their labor pain as moderate to severe. It is important to note that childbirth education classes may sometimes create false expectations and even cause a sense of failure and inferiority and subsequent negative psychological reactions if the parturient does not enjoy the “natural” delivery or requires other forms of labor analgesia. The hypnotic technique, another form of non-pharmacological analgesia that has been used for labor analgesia, demands complete cooperation between the parturient and the hypnotizer and requires considerable time, concentration, and dedication to the technique, as well as belief in the patient’s own inner self and strength. In Bonica’s evaluation of the hypnotic method for labor analgesia, he found that only 5–10% experienced little or no pain, 15–20% had their pain and analgesic requirement decreased, and the rest had no decrease in pain but had less fear and anxiety (Bonica 1980).

Acupuncture, or stimulation at meridians, when applied to parturients according to the different stages of labor in several randomized controlled trials resulted in lower pain scores and less use of neuraxial or systemic analgesia than in women receiving placebo (Hantoushzadeh et al 2007, Borup et al 2009). Although acupuncture may hold some promise for labor analgesia, the need for trained personnel to perform the time-consuming procedure alone may limit its widespread use or attempts at intrapartum analgesia. TENS is the application of patient-controlled low-intensity, high-frequency electrical impulses via surface electrodes placed on paravertebral positions in the lower part of the back at the T10–L1 and S2–4 levels bilaterally. Theoretically, electrical stimulation produces antinociception as a result of activation of large afferent myelinated mechanosensory neurons, central release of endogenous endorphin, or an effect of distraction. Most studies of TENS have reported no, minimal, or inconsistent analgesic effect when used for intrapartum pain relief (Simkin and Bolding 2004, Dowswell et al 2009). However, Chao and co-authors (2007) reported that the application of TENS at specific acupuncture points resulted in decreased pain perception. On the other hand, intradermal or intracutaneous injection of water (0.1 mL sterile water) into the lower back region at four points defined by the sacral borders (so-called water block) is claimed to reduce severe lower back pain intensity for up to an average of 60–80 minutes during labor, but the requirement for other analgesics is not reduced (Simkin and Bolding 2004). Since the injection itself is quite painful and works only for a limited time, its use may be not appealing to most parturients.

Systemic Analgesia: Parenteral and Inhalational Analgesia

In early labor or with Braxton Hicks–type contractions, sedatives and hypnotics can be administered mostly to provide sedation, relieve anxiety, and improve disruptive sleep patterns before the onset of active labor. Some of the agents used commonly and their relative therapeutic effects are listed in Table 55-1. As labor progresses and pain worsens, two common forms of systemic analgesia are available: parenteral opioids and inhalational analgesia.

Regional Analgesia

A variety of regional analgesia techniques can be used individually or in combination to provide optimal and effective labor analgesia with fewer drug-induced maternal and fetal side effects than seen with systemic analgesics. Among the various regional techniques, neuraxial labor analgesia is the most commonly used and is the most effective and complete labor analgesia, whereas lumbar sympathetic block is performed much less frequently and paracervical, pudendal, and local perineal infiltration techniques are performed occasionally by obstetricians, sometimes as a supplement to inadequate neuraxial analgesia or sometimes as sole labor analgesia. The techniques for pudendal and paracervical block are illustrated in Figures 55-8 and 55-9. About one-third of parturients in the United Kingdom chose neuraxial labor analgesia according to the U.K. National Health Service Maternity Statistics of 2005–2006 (National Health Service 2005). In the last major obstetric workforce survey performed in U.S. hospitals, about 77% of parturients in hospitals with 1500 or more deliveries received some form of neuraxial labor analgesia, and many hospitals with a larger number of deliveries may have a neuraxial labor analgesia rate as high as 80–90% (Bucklin et al 2005). Among the types of neuraxial labor analgesia, the continuous lumbar epidural technique is most commonly used, but the combined spinal epidural (CSE) technique has been gaining popularity over recent decades. Single-shot techniques and caudal analgesia remain uncommon as a result of limited duration and the requirement for a large amount of local anesthetic, respectively. Continuous spinal analgesia is not commonly used because of the lack of appropriate and approved equipment such as small-gauge spinal introducer needles and intrathecal catheters. Occasionally and despite the risk for post–dural puncture headache (PDPH), an intrathecal catheter is inserted either intentionally or unintentionally with the epidural needle puncturing the dura. Not only does continuous (epidural or intrathecal) catheter-based neuraxial analgesia provide excellent labor analgesia, but such catheters also allow rapid conversion of neuraxial analgesia to anesthesia for cesarean delivery and minimize the need for general anesthesia and manipulation of the airway. Recent findings of potential apoptotic neurodegeneration in developing brains and long-term behavioral consequences in juvenile animals exposed to drugs involving NMDA and/or γ-aminobutyric acid (GABA) receptors (which include almost all sedative–hypnotics and inhalational anesthetics) have prompted in a joint statement from the American Society of Anesthesiologists, Society of Pediatric Anesthesia, American Academy of Pediatrics, and Food and Drug Administration in 2011 encouraging research to more fully evaluate these potential neurological changes. Even though prospective human data are lacking and the applicability of animal data to clinical practice is uncertain, these current findings remain a theoretical reason to consider regional analgesia/anesthesia over systemic analgesia for relief of labor pain or for general anesthesia for cesarean delivery or maternal surgery during pregnancy (Loepke and Soriano 2008).

Neuraxial Analgesia

Lumbar Epidural Analgesia

Lumbar epidural analgesia is a safe and effective method of providing a T10–L1 sensory block for analgesia during first-stage labor and has the flexibility of extending the block for sacral (S2–4) analgesia during second-stage labor or converting to epidural anesthesia for operative delivery, if needed. Over the past 2 decades, modification of techniques and new drugs and adjuvants have provided effective analgesia with minimal motor block and minimal maternal and fetal/neonatal side effects. Typically, labor lumbar epidural analgesia is administered sterilely with a 17- or 18-gauge Tuohy epidural needle, through which a 19- or 20-gauge flexible single- or multi-orifice catheter is inserted epidurally for continuous or intermittent bolus administration of epidural drugs. After an appropriate test dose or doses to exclude inadvertent intrathecal or intravenous catheter insertion, an initial loading dose of epidural drug is administered to initiate analgesia and confirm that the epidural catheter is functioning appropriately to provide a bilateral sensory block as intended. Continual epidural analgesia is then maintained, often with continuous epidural infusion (CEI) with or without PCEA boluses or scheduled/programmed intermittent epidural boluses (PIEBs) and, less commonly, clinician-administered intermittent boluses (CAIEBs) at patient demand (without PCEA or CEI). If breakthrough pain occurs and is not relieved with PCEA boluses, top-up boluses can be administered commonly by anesthesia providers (in some institutions by trained labor nurses). When comparing CEI and CAIEB on demand (without PCEA or CEI), CEI resulted in higher total local anesthetic consumption, fewer clinician-administered boluses, and higher patient satisfaction but greater motor block and potentially increased risk for instrumental vaginal delivery (Bogod et al 1987). These results suggest that some form of continual delivery of epidural drugs, whether by CEI, PCEA, PIEB, or their combinations, would be appropriate to reduce the frequency of clinician top-ups and therefore workload. Other studies have explored which mode of delivery would be best to provide continual delivery of epidural drugs for optimal analgesia with the least need for clinician intervention, least motor block, and lowest total drug consumption. A meta-analysis by van der Vyver and co-workers (2002) showed that PCEA (without background basal CEI) seemed to be more favorable and resulted in less clinician intervention (top-ups), less total local anesthetic consumption, and less motor blockade than occurred with CEI without PCEA. The next logical questions seem to be (1) whether background infusion should be used with PCEA and, (2) if so, should the background be administered as CEI or PIEB. Various studies exploring the first question of whether background CEI is needed for PCEA seemed to show inconsistent results. Boseli and colleagues (2004) compared basal CEI rates of 0, 3, 6, and 9 mL/hr, all with PCEA, and found that patient satisfaction, clinician intervention, and analgesia were all similar with or without any of the basal CEI rates with PCEA but that total drug consumption was higher only when a basal CEI rate of 6 or 9 mL/hr was used. Bremerich and associates (2005) compared PCEA with or without background CEI and reported that periods with visual analog scale scores higher than 40 mm were significantly (P < 0.001) more frequent with PCEA without background CEI (22.4%) than with PCEA with background CEI (7.5%) in treating labor pain without increasing total drug consumption. Halpern and Carvalho (2009) recently reviewed studies comparing PCEA with or without basal CEI and concluded that when using a dilute concentration of local anesthetic for maintenance of epidural analgesia, the use of basal CEI with PCEA improved analgesia and decreased clinician interventions (especially with a long duration of labor) and that a larger bolus (>5 mL) seemed to provide better analgesia than smaller boluses with PCEA. If some form of background delivery for PCEA is favorable, should the background infusion be delivered by CEI or PIEB? Fettes and colleagues (2006), in comparing 10-mL/hr CEI versus PIEB of 10 mL every hour, both without PCEA, in 40 parturients after receiving epidural (not CSE) analgesia in a randomized, controlled trial, showed fewer supplemental injections, lower total drug consumption, and longer time to the first rescue bolus with PIEB than with CEI. Similarly, other authors have compared PIEB and CEI with or without PCEA for maintenance of epidural analgesia after initiation with CSE intrathecal analgesia in randomized clinical trials (Lim et al 2005, Wong et al 2006). These studies showed mostly similar results. That is, PIEB provided lower total local anesthetic consumption per hour, a smaller percentage of patients required rescue boluses (top-ups) by a clinician, and/or patient satisfaction was higher (Lim et al 2005, Wong et al 2006, 2011), as well as less motor block (Capogna et al 2011). However, one study using 6 mL of dilute local anesthetic with PIEB every 30 minutes versus CEI each after initial CSE analgesia and with PCEA indicated that among parturients with a duration of labor (from analgesia to delivery) shorter than about 3 hours (median of the groups), the differences (number of rescue boluses required and hourly local anesthetic consumption) observed between groups diminished to insignificant (Wong et al 2006). Another study reported that PIEB, 2.5 mL every 15 minutes, was not different from CEI, 10 mL/hr (Lim et al 2010). Collectively, these studies suggest that PIEB may be more favorable (less drug, less rescue, higher patient satisfaction), especially for longer labor, than CEI, each with or without PCEA, but the optimal volume and frequency of the boluses administered via PIEB remained to be determined.

The traditional technique of continuous epidural analgesia using CEI and the extent and intensity of the analgesia during the first and second stages of labor and for delivery are summarized in Figure 55-11. Commonly used epidural regimens (local anesthetic and adjuvants) for initiation, continuous infusion, and PCEA are listed in Table 55-3. Opioid (fentanyl or sufentanil), with its local anesthetic-sparing effect, is commonly added to the epidural local anesthetic solution to provide synergistic analgesia, to reduce the concentration and total amount of local anesthetic needed for analgesia, and to decrease the amount of motor block. Other less commonly used adjuvants, such as neostigmine, clonidine, and epinephrine, have been attempted. Varying degrees of success and associated side effects limit some of these adjuvants from more popular use. During the second stage of labor, forceps delivery or episiotomy and supplement epidural doses with a higher concentration of local anesthetic (e.g., 5–10 mL of 1–2% lidocaine or 2–3% 2-chloroprocaine) may be required in some patients for sacral analgesia to block the pain from distention and pressure on the perineum, vagina, and pelvic floor.

Combined Spinal and Epidural Labor Analgesia

The first crude CSE approach was described in the 1930s, but it was not until a couple of decades ago that CSE re-emerged to gradually gain popularity for neuraxial labor analgesia. With CSE, a small amount of opioid with or without a small amount of local anesthetic is administered intrathecally via a 25- or 27-gauge pencil-point spinal needle inserted 12–15 mm through the tip of a standard 18- or 17-gauge epidural needle after the epidural space is identified. After removal of the spinal needle, the epidural catheter is inserted and used in the standard manner. Advantages of CSE labor analgesia are a faster onset (2–5 minutes with CSE versus 5–20 minutes with an epidural) of an excellent quality of analgesia that lasts about 90–180 minutes, less motor and sympathetic blockade, and even potentially faster speed of cervical dilatation (Tsen et al 1999) than with the traditional epidural technique (Simmons et al 2007). Local anesthetic (usually bupivacaine) is commonly added to the intrathecal opioid (usually fentanyl or sufentanil) to prolong the duration of analgesia with intrathecal opioid alone and also to provide an earlier onset of more complete sacral analgesia than can be achieved with an epidural technique alone, especially during advanced stages of labor. Therefore, CSE labor analgesia is often administered during advanced stages of labor and in multiparous women expecting fast labor. However, it is reasonable to consider its use even in nulliparous women not in an advanced stage of labor if the patient is already in severe labor pain and/or prefers more control of motor function or ambulation. After analgesia established by the intrathecal drug or drugs in the CSE technique, an epidural test dose is commonly administered via the epidural catheter to exclude intrathecal and intravenous catheter placement, and then maintenance of continual epidural analgesia is usually initiated immediately afterward with either CEI or PIEB, each with or without PCEA, in the same manner as with the epidural technique alone.

Commonly cited disadvantages of CSE are dural puncture, dose-dependent opioid-induced pruritus (Simmons et al 2007), potentially increased risk for fetal bradycardia (Clarke et al 1994), and untested epidural catheter function. The overall incidence of PDPH resulting from CSE is not different from that with the epidural technique alone. Insertion of the spinal needle during the CSE procedure may guide or prevent inadvertent dural puncture by the Tuohy needle, especially in cases with poorly defined loss of resistance to the suspected epidural space, thus balancing the small risk for PDPH associated with dural puncture by the small-gauge spinal needle. Therefore, the overall risk for PDPH after CSE does not seem to be increased over that with the standard epidural technique alone. Pruritus occurs in a dose-dependent manner much more frequently with intrathecal opioid (almost 100%) than with epidural opioid and is probably mediated via a central μ-opioid receptor, central inhibitory neurotransmitter, central 5-hydroxytryptamine (5-HT₃) receptor, or their combination (Scott and Fischer 1982, Ganesh and Maxwell 2007). The symptoms are usually worse during the initial 30 minutes, but the need for treatment is relatively low and the symptoms can be treated effectively with nalbuphine (2.5–5 mg) or naloxone (40–120 μg) if needed. Fetal bradycardia occurring shortly after CSE is thought to be related to the precipitous decrease in maternal plasma epinephrine in relation to norepinephrine, which can lead to uterine hypertonicity, hypoperfusion, and ultimately, if persistent, fetal bradycardia (Clark et al 1994). Fetal bradycardia and uterine hypertonicity can occur 15–45 minutes after the initiation of either epidural or CSE analgesia (Shnider et al 1983). A systematic review conducted by Mardirosoff and colleagues (2002) showed that the use of intrathecal opioid analgesia may result in an increased risk for fetal bradycardia when compared with non-opioid intrathecal analgesia. Van de Velde and co-authors (2004) reported a dose-dependent increase in the incidence of fetal bradycardia with intrathecal sufentanil, but no difference in operative delivery. However, Nielsen and colleagues (1996) did not report any difference in fetal heart rate abnormalities (including bradycardia) when comparing parturients receiving intrathecal sufentanil versus epidural bupivacaine. Fortunately, these episodes of fetal bradycardia are usually transient and self-limited and do not alter overall obstetric and neonate outcomes, such as the cesarean delivery rate. Treatment consists of exclusion of other causes and supportive treatment, such as discontinuing any exogenous uterotonic agents, maintaining normal hemodynamics, uterine displacement, administration of supplemental oxygen, and administration of a short-acting uterine muscle relaxant such as nitroglycerin or terbutaline if the uterine hypertonus and fetal bradycardia persist.

The other disadvantage of CSE is the untested catheter since the function of the epidural catheter is not completely known or tested until the spinal analgesia of CSE wears off. Therefore, it is common for clinicians to not use CSE analgesia in patients with increased risk or anticipated airway difficulty for operative delivery, for which a functioning epidural catheter that allows rapid institution of epidural anesthesia is critical to avoid the risks associated with general anesthesia. However, even with the conventional epidural technique, the epidural catheter may still have the potential to fail at any time during labor or operative delivery. Various retrospective reviews and quality assurance data suggest that the incidence of epidural catheter failure requiring replacement during the course of labor ranges from 5–13% (Eappen et al 1998, Eisenach 2002). In a retrospective review of more than 12,000 neuraxial labor analgesia procedures, Pan and co-authors (2004) reported a 6.8% catheter replacement rate during the course of labor even after the initial analgesia provided from the epidural catheter is adequate. However, the use of CSE was not associated with an increase in epidural catheter failure during labor or when needed for operative delivery over that with the traditional epidural technique.

Failure of the spinal analgesia portion of CSE has reportedly ranged from 0.5–15% (Rigler et al 1991, Grondin et al 2009). A commonly cited reason for failure is deviation of needle placement from the midline resulting in no return of spinal fluid when the spinal needle is inserted through the epidural needle after the epidural space is identified. Figure 55-12 shows some of the common reasons for failure of the CSE procedure. Grondin and co-authors (2009) also reported that if there was no return of spinal fluid through the spinal needle during the CSE procedure, subsequent insertion of the epidural catheter was associated with a significantly higher catheter replacement rate (28.6%) because of subsequent inadequate epidural analgesia during the course of labor than in those with initial fluid return (4.1%; P < 0.03).

Continuous Spinal Labor Analgesia

Continuous spinal analgesia requires the insertion of a catheter into the low lumbar subarachnoid space, through which spinal medication can be administered intermittently or continuously. In the early 1990s, a series of cases of cauda equina syndrome in non-pregnant patients was reported in association with the administration of continuous spinal anesthesia via 32-gauge spinal microcatheters (Rigler et al 1991). Subsequently, the spinal microcatheter was removed from clinical use by the U.S. Food and Drug Administration. The reason for neurological injury is not fully understood but is thought to be due to subarachnoid maldistribution of a relatively high concentration of agents (local anesthetic and/or dextrose) (Rigler and Drasner 1991). More recently, a randomized controlled trial comparing conventional continuous epidural labor analgesia with continuous spinal labor analgesia via a 28-gauge spinal catheter showed no statistically significant difference in neurological complications or incidence of PDPH between groups (spinal, 9%; epidural, 4%) (Arkoosh et al 2008). However, the authors reported a higher incidence of technical difficulty and catheter failure in the continuous spinal group and also indicated that safe use of the spinal catheter needed to be confirmed with larger studies. Subsequently, the manufacturer did not market the spinal catheter. Because of the lack of an appropriate small spinal introducer needle and spinal catheter, continuous spinal labor analgesia is usually performed by puncturing the dura with the standard epidural needle and inserting the standard epidural catheter as a spinal catheter. Besides the risk for PDPH with a large spinal catheter and its large introducer needle, the risk for neurological injury and complications (high spinal or total spinal block, accidental administration of the epidural dose through the spinal catheter, which is actually the usual epidural catheter) is probably increased. When these complications develop in the relatively uncontrolled setting of the labor and delivery suite, there is a further increase in risk for lethal catastrophic outcomes. Therefore, continuous spinal labor analgesia is uncommonly performed and should be reserved only for selected cases with extra special precautions. Examples of such cases are intentional or unintentional dural puncture with the epidural needle in patients in whom epidural catheter placement has proved difficult or not possible (e.g., scoliosis, morbid obesity). For initiation of spinal analgesia, a typical CSE dose, such as 1.5–2.5 mg bupivacaine with 10–20 μg fentanyl, can be used. Maintenance of continuous spinal analgesia can be provided by the continuous infusion or intermittent bolus method (Table 55-4). If operative delivery is needed, analgesia can be converted to surgical anesthesia quickly. The maintenance medication can be the standard epidural solution, such as 0.1% bupivacaine with 2 μg/mL fentanyl running at 1–2 mL/hr and then titrated to effect. A standard PCEA pump may be used to deliver the spinal medication either by continuous infusion or by provider-administered intermittent boluses without risking contamination from repeated opening of the spinal catheter connector for each bolus administration. However, special labeling of the catheter (and the PCEA pump if used) and clear communication to make all providers aware of the spinal catheter (not the epidural catheter), meticulous sterile technique, and careful frequent assessment of the patient are essential for the safe use of continuous spinal labor analgesia.

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