Neuraxial analgesia is indicated to treat the pain of labor. In its 2019 Practice Bulletin, Obstetric Analgesia and Anesthesia , the American College of Obstetricians and Gynecologists (ACOG) reaffirmed an earlier opinion jointly published by the American Society of Anesthesiologists (ASA) and ACOG, which stated that “in the absence of a medical contraindication, maternal request is a sufficient medical indication for pain relief during labor.” Furthermore, the ACOG has stated that “decisions regarding analgesia should be closely coordinated among the obstetrician-gynecologist or other obstetric care provider, the anesthesiologist, the patient, and skilled support personnel.” Neuraxial analgesia is an appropriate treatment for the pain of labor, including early labor (defined as regular uterine contractions that cause progressive effacement and dilation of the uterine cervix). Randomized controlled trials have confirmed that initiation of neuraxial analgesia in early labor does not increase the risk for cesarean delivery (see later discussion).

Neuraxial analgesia may facilitate an atraumatic vaginal breech delivery, the vaginal delivery of twin infants, and vaginal delivery of a preterm infant (see Chapters 33 and 34 ). By providing effective pain relief, neuraxial analgesia facilitates blood pressure control in women with preeclampsia (see Chapter 35 ). Neuraxial analgesia also blunts the hemodynamic effects of uterine contractions (e.g., sudden increase in cardiac preload) and the associated pain response (tachycardia, increased systemic vascular resistance, hypertension, hyperventilation) in patients with other medical comorbidities (e.g., mitral stenosis, spinal cord injury, intracranial neurovascular disease, asthma; see Chapters 41 , 47 , and 51 ).

Box 24.1 lists the contraindications to administration of epidural or spinal analgesia. Some anesthesia providers have suggested that systemic maternal infection, preexisting neurologic disease, or severe stenotic heart lesions are relative contraindications to neuraxial analgesia. However, most cases of systemic infection (especially if properly treated), or neurologic or cardiac disease, do not contraindicate the administration of neuraxial analgesia (see Chapters 36 , 41 , and 47 ). It is controversial whether mild or isolated abnormalities in tests of blood coagulation preclude the use of neuraxial analgesia. The dose and timing of administration of drugs administered for thromboprophylaxis must also be considered (see Chapter44 ). The anesthesia provider should consider the risks and benefits of neuraxial analgesia for each patient individually.

Thorough preparation for neuraxial labor analgesia involves several steps ( Box 24.2 ). These include (1) a review of the parturient’s obstetric history; (2) a focused preanesthetic evaluation that includes maternal obstetric, anesthetic, and health history; and (3) a brief physical examination (i.e., vital signs, airway, heart, lungs, and back). Routine measurement of the platelet count and other laboratory measurements are not necessary, except in selected patients. Similarly, routine intrapartum blood typing and screening or cross-matching is not necessary in healthy parturients, although consideration should be given to sending a blood sample to the blood bank (to facilitate the rapid availability of blood products in case of emergency need). For parturients at increased risk for hemorrhage and for those with antenatal anemia (see Chapter 44 ), intrapartum typing and screening or cross-matching should be performed. Fetal well-being should be assessed by a skilled provider, and equipment (including resuscitation equipment) should be checked by the anesthesia provider (see Box 12.1 ). Informed consent should be obtained (see Chapters 12 and 32 ). Early and ongoing communication among the obstetric and anesthesia providers, nursing staff, and other members of the multidisciplinary team is encouraged.

The technical aspects of neuraxial analgesic/anesthetic techniques are discussed in detail in Chapter 12 . These techniques include continuous epidural, combined spinal-epidural (CSE), dural-puncture epidural (DPE), and occasionally, continuous or single-shot spinal analgesia or caudal analgesia. There are advantages and disadvantages to each technique ( Table 24.1 ).

Informed consent is an important aspect of preparation for neuraxial labor analgesia (see Chapters 12 and 32 ). The preanesthetic evaluation and informed consent process allow the anesthesia provider to allay the parturient’s concerns and to demonstrate a commitment to her care. Most laboring women understand the need for informed consent and appreciate the opportunity to participate in decisions about their care.

Resuscitation equipment, drugs, and supplies must be immediately available for the management of serious complications of neuraxial analgesia (e.g., hypotension, total spinal anesthesia, LAST) (see Box 12.1 ). Emergency airway equipment should be checked before the administration of neuraxial analgesia.

During the initiation of neuraxial analgesia, the parturient’s oxygen saturation should be measured continuously and the blood pressure should be assessed every 2 to 3 minutes for 15 to 20 minutes after the neuraxial anesthetic administration, or until the mother is hemodynamically stable (see Chapter 12 ). The fetal heart rate (FHR) should be monitored before and after the initiation of neuraxial analgesia; it may be difficult to monitor the FHR during the actual procedure. During maintenance of neuraxial analgesia, maternal blood pressure should be measured every 15 to 30 minutes, or more frequently if hypotension ensues. The sensory level of analgesia and the intensity of motor block ( Box 24.3 ) should be assessed after the administration of the test and therapeutic doses of local anesthetics. Subsequently, sensory level, motor block, and pain control should be assessed at regular intervals.

Before the initiation of neuraxial analgesia, ultrasonographic imaging of the back may be helpful, especially in parturients whose landmarks are difficult to palpate (see Chapter 12 ).

Placement of an intravenous catheter (preferably 18-gauge or larger) and correction of hypovolemia with intravenous hydration are necessary before the initiation of neuraxial analgesia to mitigate hypotension that can result from sympathetic blockade. Data from small studies are conflicting as to whether a fluid bolus administered immediately before the initiation of analgesia decreases the risk for nonreassuring FHR patterns. The ASA Task Force on Obstetric Anesthesia is silent on intravenous fluid management, although many anesthesia providers administer approximately 500 mL of lactated Ringer’s solution (without dextrose) immediately before or during the initiation of analgesia. Severe hypotension is less likely with the contemporary practice of administering a dilute solution of local anesthetic for epidural analgesia or an intrathecal opioid for spinal analgesia.

Studies of intravenous hydration and spinal anesthesia for cesarean delivery suggest that there is no advantage to administering the fluid before the initiation of anesthesia (preload) compared with administering the fluid at the time of initiation of anesthesia (coload). Fluid administration should be judicious in parturients at risk for pulmonary edema (e.g., women with preeclampsia with severe features, heart disease). Anesthesia and obstetric providers should avoid the bolus administration of dextrose-containing solutions in laboring women.

Either the lateral decubitus or the sitting position can be used during initiation of neuraxial analgesia (see Chapter 12 ). Factors to consider when positioning the parturient for the procedure include patient comfort, avoidance of aortocaval compression, ability to monitor the FHR, provider comfort and experience, and optimal positioning of the spine and palpation of landmarks. Patient position relative to the baricity of the anesthetic solution should be considered during initiation of spinal analgesia/anesthesia. There is no evidence that patient position during an epidural catheter insertion and the initial bolus injection of anesthetic solution influences the extent of neuroblockade. After completion of the procedure, parturients should be monitored for the first 15 to 30 minutes, usually in the lateral position to minimize aortocaval compression during the onset of neuraxial labor analgesia. Patient position generally does not influence sensory block distribution if bolus maintenance techniques are used (see later discussion). However, if analgesia is maintained with a continuous infusion technique, sensory block may become more extensive or dense on the dependent side over time. Regular changes in maternal position are encouraged to avoid development of one-sided sensory blockade and compression injury.

The purpose of the test dose is to help identify unintentional cannulation of a vein or the subarachnoid space. The test dose should contain a dose of local anesthetic and/or another marker sufficient to allow the recognition of intravenous or subarachnoid injection but not so large as to cause LAST or total spinal anesthesia. The most common intravascular test dose contains epinephrine (adrenaline) (see Chapter 12 ).

The use of the epinephrine test dose in obstetrics is not without detractors. Some anesthesia providers fear that intravenous injection of epinephrine may decrease uteroplacental perfusion and precipitate fetal compromise. However, there has been no report of adverse neonatal outcome after intravenous injection of an epinephrine-containing test dose. Another argument against routine use of a test dose is that aspiration of multiorifice catheters is 98% sensitive in identifying their intravascular location. (The sensitivity of aspiration is significantly lower for single-orifice catheters.) The epinephrine test dose is less specific in laboring women because cyclic changes in the maternal heart rate complicate the interpretation of its effects. For this reason, if used, the test dose should be given immediately after a uterine contraction so there is less confusion as to whether tachycardia is caused by pain or intravenous epinephrine. In some cases (e.g., hypertensive crisis, critical aortic stenosis), a test dose containing epinephrine is best avoided. Other methods of detecting intravascular injection are discussed in Chapter 12 .

The local anesthetic component of the test dose tests for unintended intrathecal catheter placement. Because modern epidural labor analgesia involves the infusion of low-concentration local anesthetic solution, unintentional intravascular or intrathecal administration is not likely to result in cardiovascular collapse or total spinal anesthesia.

Proponents of using a test dose argue that it still has a role in obstetric anesthesia practice. Large volumes of concentrated local anesthetic solution are still routinely administered for emergency cesarean delivery. Although not a safety issue, it is easier for the parturient and anesthesia provider to identify a misplaced catheter at the time of initial placement and to replace the catheter at that time rather than identify the misplaced catheter after the sterile field has been breached and the parturient repositioned. No matter whether a formal test dose is used or not, it is imperative for the anesthesia provider to take the time to look for evidence of unintentional intrathecal or intravascular injection of local anesthetic. Finally, every anesthesia provider should remember that no single test dose regimen can exclude every case of unintentional intravenous or subarachnoid injection. Box12.3 summarizes steps that may be taken to decrease the risk for unintentional intravenous or subarachnoid injection of local anesthetic.

The ideal analgesic drug for labor provides rapid onset of effective analgesia with minimal motor blockade, minimal risk for maternal toxicity, and has negligible effect on uterine activity and uteroplacental perfusion. It would undergo limited transplacental transfer and thus have minimal direct effect on the fetus. Finally, this ideal agent would have a long duration of action. Although this perfect analgesic drug does not exist, the combination of a local anesthetic with an opioid allows us to approach this goal.

Traditionally, local anesthetics were administered to block both the visceral pain of labor (lower uterine segment distention and cervical dilation) and the somatic pain (descent of the fetus in the birth canal). In 1976, investigators identified dense concentrations of opioid receptors in the dorsal horn of the spinal cord. The application of small doses of an opioid to these receptor sites generates a specific and profound opioid response. Intrathecal opioids effectively relieve the visceral pain of the early first stage of labor, although they must be combined with a local anesthetic to effectively relieve the somatic pain of the late first stage and the second stage of labor. The combination of a local anesthetic with a lipid-soluble opioid allows for the use of lower doses of each agent, thus minimizing undesirable side effects. For example, when used alone without an opioid, the local anesthetic dose required for effective epidural analgesia is associated with an unacceptably high incidence of motor blockade. Similarly, used alone, high doses of epidural opioid are required for satisfactory analgesia during early labor, and such doses are associated with significant systemic absorption and systemic side effects. The addition of an opioid to the local anesthetic also shortens latency, an important aspect of labor analgesia, especially with the use of long-acting local anesthetics that usually also have long latency. Thus, contemporary epidural labor analgesia practice most often incorporates low doses of a long-acting local anesthetic combined with a lipid-soluble opioid.

Opioids

Lipid-soluble opioids: fentanyl and sufentanil.

In contemporary practice, the lipid-soluble opioids play a central role alongside local anesthetics for the provision of neuraxial labor analgesia. The addition of lipid-soluble opioids to local anesthetics shortens latency and improves quality of analgesia. Permeability (of the dura-arachnoid) is not a rate-limiting factor; increasing the concentration gradient (by administration of a larger dose) facilitates faster entry into the spinal cord. The high lipid solubility of these agents also results in a shorter duration of action and greater systemic absorption than occurs with water-soluble drugs.

Some investigators have suggested that the improved analgesia results from a supraspinal action rather than a primary spinal action. However, several studies have refuted this, including studies of epidural opioid administration by bolus and continuous infusion. Vella et al. observed that the initiation of epidural analgesia with 0.25% bupivacaine with epidural fentanyl 80 µg resulted in more rapid, complete, and prolonged analgesia than intravenous fentanyl 80 µg, even though plasma fentanyl concentrations were higher in the intravenous group. Similarly, D’Angelo et al. demonstrated that a CEI but not an intravenous infusion of fentanyl reduced epidural bupivacaine requirements in laboring women. Polley et al. determined that the MLAC of epidural bupivacaine administered as a 20-mL bolus in laboring women was reduced from 0.064% to 0.034% when epidural rather than intravenous fentanyl was coadministered with bupivacaine. Ginosar et al. determined that the MLAC of bupivacaine administered by CEI during labor was lower by a factor of three when it was coadministered with an epidural (rather than intravenous) fentanyl infusion. Finally, in a volunteer study, lumbar epidural bolus administration of fentanyl resulted in tolerance of experimental pain at a lumbar but not a cranial dermatome, whereas lumbar epidural fentanyl infusion resulted in pain tolerance at both dermatomes, suggesting vascular absorption and a systemic effect of the fentanyl. Thus, the site(s) of action of fentanyl after epidural administration may depend on dose and mode of administration.

Pain and analgesic requirements are highly variable and depend on several factors, including parity, stage of labor, presence of ruptured membranes, and oxytocin augmentation. One study reported that the ED ₅₀ of epidural sufentanil was higher in women undergoing prostaglandin induction of labor than in women with spontaneous labor. Conell-Price et al. developed a model of labor pain in nulliparous women and found that the use of oxytocin was associated with 48% more pain at the start of labor.

The high doses of epidural fentanyl or sufentanil required to provide complete labor analgesia (administered alone without local anesthetic) are associated with significant adverse effects. Capogna et al. sought to determine the median effective analgesic dose (ED ₅₀ ) of epidural fentanyl and sufentanil alone (no local anesthetic) for the initiation of epidural analgesia in nulliparous women with a cervical dilation between 2 and 4 cm. The ED ₅₀ of fentanyl was 124 µg (95% CI, 118 to 131 µg), and the ED ₅₀ of sufentanil was 21 µg (95% CI, 20 to 22 µg), with a potency ratio of 5.9:1. Pruritus and sedation were common; side effects precluded significant dose escalation to establish the ED ₉₅ or to manage analgesia for more advanced labor.

Lipophilic opioids and local anesthetics have dose-sparing effects when combined. Indeed, even the lidocaine epidural test dose appears to augment the efficacy of a lipophilic opioid bolus to establish analgesia. In a study comparing sufentanil alone, sufentanil with bupivacaine, and bupivacaine alone, women randomly assigned to the sufentanil-alone (30 µg) group experienced satisfactory analgesia after the initial dose but not after subsequent doses. In this study, the initial dose was administered after an epidural test dose that contained lidocaine 60 mg. A second study compared the administration of epidural fentanyl or sufentanil immediately after a lidocaine 45-mg/epinephrine 15-µg test dose for the initiation of analgesia for women in early labor. There were no differences in analgesic onset, quality, or duration between women randomly assigned to receive either fentanyl 100 µg or sufentanil 20 µg, with both groups experiencing effective pain relief that lasted, on average, more than 2 hours. In a third study, when epidural fentanyl 100 µg was administered after a lidocaine and epinephrine test dose, the diluent volume (2 to 20 mL) did not affect the onset or duration of epidural labor analgesia, with analgesia lasting approximately 2 hours in all groups. This finding differs from local anesthetic solutions, where higher volumes of more dilute solutions have dose-sparing effects ( Table 24.3 ).

In clinical practice, either fentanyl or sufentanil is frequently combined with a low-concentration, long-acting amide local anesthetic to both initiate and maintain epidural labor analgesia. The addition of a lipid-soluble opioid to a local anesthetic for neuraxial labor analgesia decreases latency, prolongs the duration of analgesia, and improves the quality of analgesia. For example, 86% of women rated their analgesia as excellent after epidural analgesia was initiated with bupivacaine combined with sufentanil, compared with 50% of those who received bupivacaine without sufentanil. The percentage of women who experienced no or short periods of pain during the first stage of labor was 94% in women who received sufentanil and 76% in women who did not. After initiation of analgesia with 0.125% bupivacaine with epinephrine 1.25 µg/mL, 43% of women randomly assigned to receive epidural fentanyl 100 µg rated their analgesia as excellent, compared with 6% in a control group that did not receive fentanyl.

Epidural opioid administration allows the anesthesia provider to use a more dilute solution of local anesthetic to initiate epidural labor analgesia. Epidural fentanyl and sufentanil decrease epidural bupivacaine requirement during labor in a dose-dependent fashion ( Fig. 24.2 ). The reduction in MLAC by the addition of fentanyl or sufentanil is observed with levobupivacaine, ropivacaine, and 2-chloroprocaine as well as bupivacaine.

The effect of epidural fentanyl on the minimum local anesthetic concentration (defined as the effective concentration in 50% of subjects [EC ₅₀ ]) for epidural bupivacaine analgesia during labor. Data are expressed as median concentrations with 95% confidence intervals.

Data from Lyons G, Columb M, Hawthorne L, Dresner M. Extradural pain relief in labour: bupivacaine sparing by extradural fentanyl is dose dependent. Br J Anaesth . 1997;78:493–496.

The dose-sparing effects of fentanyl and sufentanil are also evident when the drugs are combined with a low-concentration solution of bupivacaine used for the maintenance of analgesia throughout labor. For example, in women randomly assigned to receive bupivacaine/epinephrine with or without fentanyl 100 µg, the total bupivacaine dose was 55 or 110 mg, respectively. The advantages of a lower total dose of local anesthetic include (1) decreased risk for LAST, (2) decreased risk for high- or total-spinal anesthesia, (3) decreased plasma concentrations of local anesthetic in the fetus and neonate, and (4) decreased intensity of motor blockade.

There are few rigorous dose-response studies of epidural fentanyl or sufentanil combined with bupivacaine for initiation of epidural labor analgesia. Herman et al. randomly assigned 100 laboring women with a cervical dilation of 5 cm or less to receive 0.125% bupivacaine 10 mL, combined with fentanyl 0 to 100 µg (in 25-µg increments) or sufentanil 0 to 25 µg (in 5-µg increments), injected after a negative epidural test dose (bupivacaine 7.5 mg with epinephrine 15 µg). Using probit analysis, these researchers calculated the effective dose in 95% of subjects (ED ₉₅ ) to be 50 µg for fentanyl and 8 µg for sufentanil; these figures equate to a sufentanil-to-fentanyl potency ratio of 6.3:1. Therefore, data suggest that the potency ratio of sufentanil to fentanyl administered into the epidural space is approximately 6:1, regardless of whether administered in the presence or absence of a local anesthetic solution.

The range of fentanyl and sufentanil doses used for the initiation of epidural labor analgesia is shown in Table 24.2 . It is not clear whether higher doses of epidural lipophilic opioid (e.g., fentanyl 100 versus 50 µg) provide superior analgesia. Data are inconsistent, but overall suggest that higher doses result in more pruritus and neonatal depression (see later discussion). Current evidence supports the administration of epidural opioid doses at the lower end of the dose range, which are frequently sufficient for nulliparous women, for women in early labor, or when the opioid is coadministered with a local anesthetic. Fortunately, with a catheter-based epidural technique, relatively conservative initial doses may be augmented with additional local anesthetic and lipophilic opioid solution through the epidural catheter if satisfactory analgesia is not achieved with the initial bolus dose.

Other opioids.

Morphine was one of the first opioids used for labor analgesia. However, the inconsistent analgesia, long latency (30 to 60 minutes), along with the introduction of lipid-soluble opioids and epidural infusion pumps into clinical practice, have made the use of epidural morphine for continuous labor analgesia largely obsolete.

Several groups of investigators have reported the use of epidural hydromorphone for labor analgesia. The lipid solubility of hydromorphone lies between those of morphine and fentanyl, but is closer to that of morphine (see Table 13.3 ). In a large prospective observational study, effective labor analgesia was obtained by initiating analgesia with 0.25% bupivacaine (20 to 25 mg) with epinephrine (40 to 50 µg), followed by hydromorphone 100 µg. However, Mhyre observed that effective labor analgesia could not be provided by 0.035% bupivacaine (7 mg) with hydromorphone 100 to 110 µg. In another trial, parturients were randomly assigned to receive either epidural hydromorphone 300 µg or saline-control immediately after the initiation of analgesia with lidocaine 45 mg, epinephrine 15 µg, and fentanyl 100 µg. The duration of analgesia and side effects were similar in the two groups. At the current time, further investigation is required before hydromorphone can be recommended for epidural labor analgesia.

Meperidine may be used effectively alone (without a local anesthetic), in part because it possesses local anesthetic properties. When given during labor, epidural meperidine 100 mg provides analgesia similar to that provided by 0.25% bupivacaine, with less motor blockade. However, this dose of epidural meperidine produces more sedation, nausea, and pruritus than epidural bupivacaine. Handley and Perkins observed that the addition of meperidine 25 mg to 0.125%, 0.187%, or 0.25% bupivacaine (10 mL) provided adequate analgesia for the first stage of labor. Epidural administration of meperidine effectively prevents or treats the shivering that often occurs during labor. Massad et al. randomly allocated women to receive 0.1% bupivacaine with either meperidine 1 mg/mL or fentanyl 2 µg/mL. No differences were noted between groups in analgesic characteristics, except that women in the meperidine group had a higher incidence of nausea and vomiting. Currently there is no evidence that meperidine alone or in combination with bupivacaine has any advantages over a combination of a long-acting amide local anesthetic and a lipid-soluble opioid.

Several studies described the use of alfentanil with bupivacaine for labor analgesia. Alfentanil has lower lipid solubility than both fentanyl and sufentanil. Only a few small studies have compared alfentanil with other opioids for labor analgesia.

Butorphanol is a lipid-soluble opioid agonist-antagonist with weak µ-receptor and strong κ-receptor activity. Because κ-opioid receptors appear to be involved in the modulation of visceral pain, κ-receptor agonists may be useful agents for the relief of labor pain, which has a significant visceral component (see Chapter 21 ). Somnolence is the most prominent side effect of epidural butorphanol. The addition of butorphanol 1, 2, or 3 mg to 0.25% bupivacaine (25 mg) shortened latency and prolonged the duration of analgesia in comparison with epidural bupivacaine alone in one study. The investigators concluded that the optimal dose of butorphanol was 2 mg. Of concern was the observation of a transient sinusoidal FHR pattern in the 3-mg group that was not unlike that seen after the intravenous administration of butorphanol. However, there was no difference among groups in Apgar scores, umbilical cord blood gas and pH measurements, or neurobehavioral scores. Similarly, Abboud et al. observed that the addition of butorphanol 1 or 2 mg to 0.25% bupivacaine resulted in better quality and longer duration of analgesia than the epidural administration of bupivacaine alone, without maternal or neonatal side effects. However, some anesthesia providers have noted that the epidural administration of butorphanol results in somnolence and occasional dysphoria, which are side effects of κ-receptor stimulation.

Diamorphine (heroin) is available for epidural analgesia in the United Kingdom. Using isobolographic analysis, McLeod et al. concluded that the combination of diamorphine and levobupivacaine is additive when used for first-stage labor analgesia. Several studies from the United Kingdom have reported diamorphine doses between 250 and 500 µg/h (i.e., diamorphine 25 to 50 µg/mL combined with a low concentration of bupivacaine). Whether diamorphine offers any advantages over fentanyl or sufentanil has not been studied. It is not available for clinical administration in the United States.

Painful labor lasts several hours in most parturients; therefore, a single intrathecal or epidural injection of local anesthetic and/or opioid usually does not provide adequate analgesia for the duration of labor and supplemental doses are needed. Neuraxial analgesia is maintained with the intermittent or continuous administration of analgesics, usually a combination of a long-acting amide local anesthetic and a lipid-soluble opioid. By far the most common technique is administration of drugs via a catheter into the epidural space. It is occasionally advantageous to administer drugs via a catheter placed in the subarachnoid space.

Administration Techniques

Several techniques or combinations of techniques are used to maintain epidural labor analgesia. As epidural infusion pump technology has evolved, the role of clinician-administered boluses is increasingly restricted to the treatment of breakthrough pain. Modern epidural infusion pumps have multiple settings, including CEI, PCEA, and programmed intermittent epidural bolus (PIEB). The PCEA setting allows the patient to press a button to direct the infusion pump to administer a bolus dose. With PIEB, the pump is programmed to automatically deliver a bolus dose at a set interval. In modern practice, the two technologies are frequently combined (see later discussion).

Intermittent bolus.

Before the introduction of infusion pumps, epidural analgesia was routinely maintained by the intermittent administration of an additional therapeutic bolus dose of local anesthetic when analgesia began to wane. When the patient began to experience recurrent pain, the anesthesia provider assessed the pain relative to the stage of labor and the extent of sensory blockade and then administered another epidural bolus of local anesthetic. Analgesia was usually reestablished with the bolus injection of 8 to 12 mL of a local anesthetic/opioid solution.

The spread and quality of analgesia may change with repeated lumbar epidural injections of local anesthetic. After several injections, blockade of the sacral segments, intense motor blockade, or both may develop. The sensory level and the intensity of motor blockade should be assessed and recorded before and after each bolus injection of local anesthetic.

This intermittent bolus technique has several disadvantages, the most salient of which is that pain relief is constantly interrupted by the regression of analgesia. The patient must notify the labor nurse or midwife that she is again uncomfortable and request additional analgesia. In the United States, labor nurses are not allowed to administer additional epidural analgesic drugs ; therefore, the nurse must call the anesthesia provider, resulting in unavoidable delays in administration of additional analgesic drugs and additional pain for the patient.

Continuous infusion.

Administration of a CEI of a dilute solution of local anesthetic combined with an opioid for the maintenance of epidural labor analgesia reduces, but does not eliminate, the need for bolus doses of local anesthetic, compared with manual intermittent bolus administration. The continuous infusion technique lengthens the time between bolus injections and leads to greater patient satisfaction.

Most studies suggest that the CEI technique leads to the administration of a larger total dose of bupivacaine. The increased total bupivacaine dose does not seem to result in higher maternal venous or umbilical venous bupivacaine concentrations at delivery. Unfortunately, a prolonged epidural infusion of 0.125% bupivacaine at 10 to 14 mL/h may cause significant motor blockade. More dilute solutions of local anesthetic reduce the risk of significant motor blockade, but increase the likelihood of breakthrough pain. In vitro , animal, and human cadaveric data, along with clinical experience with modern drug delivery systems (see later discussion), suggest that distribution of the epidural solution in the epidural space may be limited when administered by infusion under low pressure.

Patient-controlled epidural analgesia.

The method of delivering the anesthetic solution into the epidural space influences the density of neuroblockade. Given the same concentration of local anesthetic, analgesia maintained by infusion results in greater drug use, a higher degree of motor blockade, and a higher incidence of operative vaginal delivery than intermittent boluses. However, intermittent manual bolus administration by the anesthesia provider results in more breakthrough pain, less patient satisfaction, and more work for the anesthesia provider. PCEA is a method of delivering anesthetic solution to the epidural space that overcomes these disadvantages. Since its first description in 1988 by Gambling et al., many studies have consistently found that the analgesia with PCEA is comparable to that with continuous infusion techniques.

Van der Vyver et al. reported a metaanalysis of nine randomized controlled trials ( n = 640) comparing PCEA (without a background infusion) with CEI analgesia. There were fewer anesthetic interventions in the PCEA group and the total bupivacaine dose was lower, as was the incidence of motor blockade. There were no differences in pain scores, patient satisfaction, and maternal and neonatal outcomes between groups.

Although patients can self-administer effective epidural labor analgesia using PCEA alone, the addition of a CEI allows for ongoing drug administration, which may be important for women who wish to sleep. Bupivacaine consumption is higher in PCEA with a background infusion than in a pure PCEA technique without a background infusion, but the addition of a background infusion provides better analgesia than pure PCEA. A 2015 metaanalysis that included seven studies identified a lower requirement for physician-administered rescue bolus doses in patients who receive a background infusion. There is no evidence that the higher local anesthetic dose associated with a background infusion has adverse effects on obstetric outcome when low-concentration infusion solutions are used.

A typical background infusion provides one-third to one-half of the total hourly dose. Sng et al. described a PCEA system in which they used a computer-integrated infusion pump to modify the background infusion rate based on the previous hour’s requirement for patient-administered bolus doses. Future pump technology will likely incorporate machine learning to tailor the administered anesthetic dose more closely to patient need.

A wide variety of PCEA regimens have been described ( Table 24.6 ). The anesthesia provider can manipulate the infusion solution (local anesthetic/opioid concentration), patient-controlled bolus volume, lockout interval, background infusion rate, and maximum allowable dose per hour. Patient-controlled bolus doses from 2 to 20 mL and lockout intervals from 5 to 30 minutes have been reported ; most studies have evaluated patient-controlled bolus volumes of 5 to 12 mL.

Table 24.6

Examples of Patient-Controlled Epidural Analgesia (PCEA) Settings a

PCEA Technique	Basal Infusion Rate (mL/h)	Bolus Dose (mL)	Lockout Interval (min)
Without background infusion	0	8–12	10–20
With background infusion	4–8	5–8	10–15

Evidence suggests that a larger patient-controlled bolus volume is superior to a smaller volume. In a randomized controlled trial using bupivacaine 0.125% with sufentanil, a low-volume patient-controlled bolus (4 mL, 8-minute lockout) was compared with a high-volume bolus (12 mL, 25-minute lockout). The high-volume group had lower pain scores at 6- and 9-cm cervical dilation, greater patient satisfaction with analgesia, and no differences in obstetric outcomes. In the first of a pair of experiments, Roofthooft et al. compared maintenance analgesia with PCEA alone (5-mL bolus, 12-minute lockout interval, no background infusion) with PIEB plus PCEA (PIEB, 10-mL bolus every hour; PCEA, 5-mL bolus, 20-minute lockout interval). Analgesia was superior with the PIEB technique (less breakthrough pain, less motor block). In the second study by the same research team, PCEA with a larger bolus volume and longer lockout interval (10-mL bolus, 30-minute lockout interval, no background infusion) was compared with the same PIEB technique. In contrast to the findings of the first study, breakthrough pain and motor block were not different between the groups. These studies suggest that larger patient-controlled bolus volumes (approximately 10 mL) are more efficacious than smaller bolus volumes (approximately 5 mL), even when total medication administration is similar. An experiment in a swine model confirmed that the epidural solution spread in the epidural space improves with a bolus administration compared with continuous infusion, and with larger bolus volumes. The investigators administered radiopaque dye, either as a 10-mL/h CEI, a 2-mL bolus every 12 minutes (total 10 mL), or a single 10-mL bolus. The spread of the solution averaged 5.6, 7.9, and 10.4 spinal levels, respectively.

Various local anesthetic concentrations also have been studied. No studies have reported any differences in analgesia efficacy. The use of more-concentrated local anesthetic solutions results in higher local anesthetic consumption and greater motor blockade than the use of less-concentrated solutions. Thus, as with continuous infusion epidural analgesia, administration of a dilute local anesthetic solution combined with an opioid results in less local anesthetic consumption and motor blockade without a reduction in analgesia efficacy.

In summary, solutions used for PCEA are identical to those used for CEI analgesia (see Table 24.5 ). It is suggested that larger bolus volumes be used if PCEA is administered without a background infusion. Early PCEA studies investigated higher-concentration local anesthetic solutions (i.e., 0.125% to 0.25% bupivacaine), smaller bolus volumes (≤5 mL), and low background infusion rates (3 to 5 mL/h). Given the more recent data supporting the efficacy of epidural administration of higher volumes of more dilute solutions of local anesthetic, it appears reasonable to apply this principle to PCEA. The safety of large-volume boluses (>10 mL) has not been determined.

Programmed intermittent epidural bolus injection.

Bolus administration of a large volume of epidural solution into the epidural space results in better analgesia than CEI or administration of small bolus volumes. However, both provider-administered bolus dosing and PCEA are associated with inconsistent analgesia as pain relief wanes and is then reestablished with a bolus dose. PIEB may overcome this disadvantage.

Wong et al. randomly assigned patients to receive either a CEI of a dilute bupivacaine/fentanyl solution at 12 mL/h or 6 mL of the same solution delivered as a programmed bolus every 30 minutes. All patients in both studies were allowed PCEA for the treatment of breakthrough pain. The total dose of local anesthetic was smaller, breakthrough pain was less, and patient satisfaction was greater in the PIEB group than in the continuous infusion groups.

A 2023 systematic review of 18 randomized studies and 4590 women comparing PIEB with continuous infusion suggested that PIEB (5 to 10 mL every 30 to 60 minutes) administered via a programmable pump results in improved patient satisfaction, less drug use, longer duration of analgesia, and less breakthrough pain. Data were insufficient to determine if the incidences of operative vaginal (RR, 0.85; 95% CI, 0.71 to 1.01) and cesarean delivery (RR, 0.85; 95% CI, 0.69 to 1.06) were different between the groups.

Studies of the PIEB technique have attempted to ascertain the optimal bolus volume and administration interval. Wong et al. randomized nulliparous women to receive 1 of 3 PIEB regimens: 10-mL bolus every 60 minutes, 5-mL bolus every 30 minutes, 2.5-mL bolus every 15 minutes. The epidural solution was 0.0625% bupivacaine with fentanyl 2 µg/mL and all patients had access to PCEA. Although analgesia was not different between groups, local anesthetic consumption was lowest in the group that received a 10-mL bolus every 60 minutes. Using the same bupivacaine/fentanyl solution administered at 40-minute intervals, Zakus et al. reported an effective analgesia volume in 90% of women (defined as no breakthrough pain requiring a patient-controlled or clinician-administered bolus) of 10.7 mL (95% CI, 10.3 to 11.0 mL). In a network metaanalysis that included 30 trials, a PIEB volume of 10 mL every 60 minutes was ranked higher than 5 mL every 30 minutes for the outcome of total local anesthetic dose and incidence of motor block. The authors concluded that future research should focus on PIEB volume of 5 mL or greater and an administration interval of 30 minutes or greater.

Investigators have studied the optimal bolus delivery interval using a fixed volume of local anesthetic/opioid solution. Using a biased-coin up-and-down sequential allocation trial design with bupivacaine 0.0625% and fentanyl 2 µg/mL, Epsztein Kanczuk et al. found an interval of 42.6 minutes (95% CI, 38.9 to 46.4 minutes) provided effective analgesia in 90% of women (defined as no breakthrough pain requiring a patient-controlled or clinician-administered bolus). Yao et al., using ropivacaine 0.1% and sufentanil 0.5 µg/mL, found an effective interval in 90% of patients of 37.0 minutes (95% CI, 28.4 to 40.9 minutes).

Finally, using an innovative mathematical modeling tool, response surface methodology, Munro et al. aimed to estimate the optimal PIEB next bolus interval (interval between initiation bolus and first pump-administered bolus), the PIEB interval, and the PIEB volume that maximizes patient-centered outcomes (patient satisfaction, the number of clinician-administered boluses, and patient-administered boluses). The study solution was ropivacaine 0.1% with fentanyl 2 µg/mL. The suggested PIEB parameters to maximize these outcomes were next bolus 29.4 minutes, PIEB interval 59.8 minutes, and PIEB volume 6.2 mL. Overall, these trials suggest that the optimal interval ranges from 30 to 60 minutes and the optimal volume from 6 to 10 mL. The optimal values likely vary depending on the local anesthetic and opioid concentrations of the maintenance solution, and on individual patient preference, whether to minimize the need for PCEA demand doses (e.g., to facilitate sleep), or to allow for more control and analgesic titration using PCEA.

The design of the distal end of the epidural catheter and the infusion/bolus rate may influence the distribution of anesthetic solution in the epidural space (see Chapter 12 ). At low infusion rates, the epidural solution exits only the most proximal hole of a multiorifice catheter; thus, the multiorifice catheters behave like single-orifice catheters. In an in vitro study, an infusion rate > 300 mL/h was necessary to engage all three orifices of a multiorifice catheter. Higher infusion rates, such as those used with PIEB, will more consistently use all three orifices, depending on flow rate. The catheter design and infusion rate may also influence the “distance traveled” of the epidural solution as well as the pressure generated during a bolus injection. Most commercial epidural pumps administer bolus doses (PCEA or PIEB) at a default infusion rate 200 to 250 mL/h, although some pump manufacturers allow this rate to be manipulated by the user.

Using single-orifice epidural catheters, Lange et al. randomized nulliparous women to PIEB maintenance analgesia with a bolus delivery rate of 100 mL/h or 300 mL/h and found no differences in analgesic outcomes between group. In contrast, in a study of PIEB using a high bolus delivery rate (480 mL/h), women randomized to single-orifice epidural catheters had better analgesia and sacral coverage with fewer PCEA boluses and less local anesthetic consumption compared with women randomized to multiorifice catheters. Additional studies are needed with the PIEB technique to fully delineate the influence of catheter type and bolus delivery rate on analgesia characteristics.

A schematic diagram demonstrating the use of PIEB is shown in Fig. 24.5 , and examples of PIEB pump parameters are shown in Table 24.7 .

Programmed Intermittent Epidural Bolus (PIEB) Schematic Diagrams. The PIEB pump is programmed with the following parameters: initiation interval = 45 min (time from initial clinician-administered neuraxial analgesia loading dose to first PIEB dose), PIEB interval = 30 min (interval between each PIEB dose), patient-controlled epidural analgesia (PCEA) lockout interval = 15 min (interval after PIEB dose or PCEA dose during which a bolus request by the patient or a PIEB dose will not be administered by the pump). On figure time line, A: Clinician-administered initial neuraxial (epidural/spinal) analgesia loading dose, B: First PIEB dose administered, C: Second PIEB dose administered 30 min later, D: PCEA dose is requested, but the dose is not administered because it is within the 15-min lockout interval of the PIEB dose at Time C, E: PCEA requested and administered, F: PIEB dose delayed because it was programmed to occur within the 15-min lockout interval of the PCEA dose administered at Time E, G: Delayed PIEB dose is administered 15 min after the PCEA dose (Time E) at end of 15-min lockout interval.

Illustration by Naveen Nathan, M.D., NorthShore University HealthSystem, University of Chicago Pritzker School of Medicine, Evanston, IL.

Table 24.7

Examples of Programmed Intermittent Epidural Bolus (PIEB) Settings a

PIEB initial bolus time b	15–45 min
PIEB bolus volume	5–10 mL
PIEB bolus interval	30–60 min
PCEA bolus volume	5–10 mL
PCEA lockout interval	10–15 min

PCEA , Patient-controlled epidural analgesia.

The placement of a catheter in the subarachnoid space allows the anesthesia provider to administer continuous spinal analgesia by intermittent bolus injection or continuous infusion of a local anesthetic combined with an opioid. Continuous spinal analgesia is an option when unintentional dural puncture has occurred (see later discussion). The technique has also been described for use in patients in whom placement of an epidural catheter is difficult (e.g., in patients with morbid obesity or abnormal vertebral anatomy, such as kyphoscoliosis, or in patients with severe cardiac disease who require careful titration of analgesia).

Reports of this technique usually describe the use of a standard epidural catheter placed through an 18- or 19-gauge epidural needle. Over 30 years ago, to reduce the incidence of post–dural puncture headache, very small (e.g., 28- to 32-gauge) catheters were developed for insertion through small (e.g., 22- to 26-gauge) spinal needles. Unfortunately, several cases of cauda equina syndrome (associated with the use of spinal microcatheters during surgery in nonpregnant patients) prompted the US FDA to remove these microcatheters from the market in 1992. The etiology of these neurologic deficits is unclear. Some authors have suggested that neurologic injury may result from the maldistribution of local anesthetic within the subarachnoid space. The very slow rate of injection through a caudally directed microcatheter may lead to the pooling of local anesthetic solution in the terminal part of the dural sac. If the local anesthetic solution is hyperbaric, the neighboring elements of the cauda equina experience prolonged exposure to a high concentration of local anesthetic and a hyperglycemic, hyperosmotic (e.g., 550 to 800 mOsm/L) marinade. Permanent neural damage may occur from the combination of tissue dehydration and a toxic concentration of local anesthetic. It is unclear whether this complication is unique to the use of microcatheters.

Arkoosh et al. reported a randomized multicenter study that compared continuous spinal labor analgesia (via a 28-gauge catheter) with continuous epidural analgesia. The incidence of neurologic complications was not different between the two groups, and patients in the spinal group had better early analgesia, less motor blockade, and better patient satisfaction. The study was underpowered to determine if the incidence of post–dural puncture headache differed between the two groups. The spinal catheter was associated with a higher incidence of technical difficulties and catheter failures.

A 23-gauge, FDA-approved, spinal catheter is now available in the United States. The catheter is inserted using a “catheter-over-needle” technique. Initial observational study found that this catheter may have clinical utility ; however, similar to the Arkoosh et al. study, the study was not large enough to assess the risk for complications. Several commercial spinal catheters are available in Europe.

Continuous spinal analgesia can be initiated with the same drug combination and dose used to initiate CSE analgesia (see Table 24.2 ). For maintenance of analgesia, my colleagues and I administer our standard epidural solution (0.08% bupivacaine with fentanyl 2 µg/mL) at an initial rate of 2 mL/h. The infusion is then titrated to patient needs. We prefer to use our standard PCEA pumps for the continuous infusion, with the PCEA function disabled. A separate “recipe” for continuous spinal analgesia is preprogrammed in the pump. This approach allows the anesthesia provider to administer a small (1 to 3 mL) bolus from the infusion bag without disconnecting the spinal catheter from the infusion tubing. Alternatively, the infusion pump can be programmed to administer 1-mL patient-controlled bolus doses. The catheter and pump should be clearly labeled so that all care providers know that the catheter is a spinal, not an epidural, catheter.

Continuous spinal analgesia with opioids has also been described for patients with obstructive cardiac lesions. If intrathecal local anesthetics are used for intrapartum analgesia, the sensory level and the intensity of motor blockade should be monitored. Moreover, the anesthesia provider must be prepared to treat hypotension and other complications associated with high spinal anesthesia.

The term “walking” or “mobile” epidural analgesia was first coined to describe low-dose CSE opioid analgesia because motor function was maintained and the ability to walk was not impaired. However, the term is more accurately applied to any neuraxial analgesic technique that allows safe ambulation. Initial studies using clinical testing to assess sensory and motor impairment and dorsal column function produced conflicting results. After initiation of epidural analgesia with 15 mL of 0.1% bupivacaine/fentanyl 2 µg/mL, Buggy et al. demonstrated that 66% of women had altered proprioception and 38% had impaired vibration sense. In contrast, Parry et al. found that dorsal column function was impaired in only 7% of laboring women who received low-dose epidural or CSE analgesia. The same group of investigators then used computerized dynamic posturography to assess balance in nonpregnant women, term pregnant women not in labor, and laboring women after initiation of CSE analgesia with bupivacaine 2.5 mg and fentanyl 5 µg. Pregnancy significantly affected balance function, but initiation of CSE analgesia did not further impair function. However, further supplementation of analgesia with the epidural injection of 10 mL of 0.1% bupivacaine/fentanyl 2 µg/mL in a subgroup of patients resulted in impaired balance function. The investigators concluded that the results supported the safety of allowing ambulation after low-dose CSE analgesia, but further studies are required to understand the relative contributions of dorsal column function, proprioception, and lower limb motor strength to overall balance and ability to ambulate.

Several studies have shown that an epidural test dose containing lidocaine 45 mg and epinephrine 15 µg adversely affects the ability to ambulate after initiation of CSE or low-dose epidural analgesia.

The concept of the “walking epidural” is popular in the lay press; however, many women, once comfortable, prefer to rest rather than ambulate. The ability to walk to the toilet or sit in a chair at the bedside, however, remains desirable to many laboring women. In a small study, the ability to walk to the toilet to void resulted in lower postvoid residual volume than voiding on a bedpan. Although ambulation per se has not been shown to affect the progress or outcome of labor positively or negatively, dense motor blockade may adversely affect the spontaneous vaginal delivery rate (see later discussion). Thus, the intent of the “walking epidural”—minimization of motor blockade—should be the goal of the anesthesia provider, whether or not the patient wishes to ambulate.

Safe ambulation during labor requires several safeguards ( Box 24.5 ). Before ambulation, orthostatic blood pressure and heart rate should be measured, and motor function and balance must be assessed. The patient should not ambulate alone.

Neuraxial anesthesia–induced sympathetic blockade leads to peripheral vasodilation and increased venous capacitance. Hypotension that occurs after extensive neuroblockade primarily reflects decreased systemic vascular resistance. Hypotension is often defined as a 20% to 30% decrease in systolic blood pressure (compared with baseline) or a systolic blood pressure < 90 to 100 mm Hg. Modest hypotension rarely has adverse consequences in young, nonpregnant patients. However, placental circulation has limited autoregulation; thus, maintenance of uteroplacental perfusion largely depends on maintenance of maternal blood pressure (see Chapter 3 ). Uncorrected hypotension results in decreased uteroplacental perfusion. If hypotension is severe and prolonged, hypoxia and acidosis will develop in the fetus. Blood pressure should be monitored frequently (every 2 to 3 minutes) after initiation of analgesia, until stable blood pressure is ascertained.

The incidence of hypotension after initiation of neuraxial analgesia during labor is approximately 14%. Kinsella and Black reported that maternal position and the position of the blood pressure cuff markedly influence the measured blood pressure. With laboring patients in the full lateral position, the mean difference in systolic blood pressure between the dependent and upper arm was 10 mm Hg; the mean difference in diastolic pressure was 14 mm Hg.

A metaanalysis of studies comparing low-dose epidural analgesia with CSE analgesia found no difference in the incidence of hypotension between the two techniques.

The prevention of hypotension includes avoidance of aortocaval compression. Preston et al. noted a higher incidence of severe FHR decelerations in women placed in the supine-lateral tilt position than in those in the full lateral position after initiation of epidural analgesia. In contrast, Beilin et al. found no difference in maternal blood pressure and FHR decelerations between the two positions.

Traditionally, intravenous “preload” (also known as “prehydration”) with 0.5 to 1.5 L of crystalloid solution was used to reduce the incidence and severity of hypotension after the initiation of neuraxial labor analgesia. However, several randomized controlled trials have shown that the incidence of hypotension after preload with 0.5 to 1.0 L of fluid is no lower than that after no preload. In women undergoing spinal anesthesia for cesarean delivery, there is no difference in the incidence of hypotension when crystalloid is administered as a rapid bolus before the initiation of neuroblockade (preload) compared with administration concurrently with the initiation of anesthesia (coload). Data are inconsistent as to whether a fluid bolus decreases the risk for nonreassuring FHR changes associated with the initiation of neuraxial analgesia (see earlier discussion). Many anesthesia providers omit a fluid bolus, especially in patients at risk for pulmonary edema (e.g., women with preeclampsia), or in women who have maintained hydration with clear liquid oral intake during labor. In our practice, my colleagues and I usually administer approximately 500 mL of intravenous crystalloid (coload) at the time of initiation of neuraxial labor analgesia.

The hypotension associated with neuraxial analgesia is usually easily treated. Treatment includes the administration of additional intravenous crystalloid, placement of the mother in the full lateral position, and administration of an intravenous vasopressor. Traditionally, ephedrine 5 to 10 mg has been administered; however, studies in women undergoing spinal anesthesia for elective cesarean delivery have shown that phenylephrine is equally or more efficacious in restoring blood pressure and is associated with higher umbilical arterial blood pH measurements at birth. No differences in neonatal outcome have been noted. Because there is no evidence that the choice of vasopressor influences maternal or neonatal outcome, the use of either drug is acceptable. The FHR should be monitored continuously, and treatment should be more aggressive if nonreassuring FHR patterns are noted or if the mother is symptomatic (e.g., presence of presyncope or nausea). Ephedrine crosses the placenta and may increase both FHR and FHR variability (e.g., saltatory FHR pattern).

Pruritus is the most common side effect of epidural or intrathecal opioid administration (see Chapter 27 ). Intrathecal opioid administration is associated with a higher incidence and severity of pruritus than epidural opioid administration. The incidence of pruritus after intrathecal opioid administration is close to 100% in some studies, although the need for treatment is much lower. The incidence and severity of pruritus are dose dependent for both epidural and spinal opioid administration. The coadministration of local anesthetic decreases the incidence of pruritus, whereas the coadministration of epinephrine may worsen pruritus.

The cause of the neuraxial opioid–induced pruritus is incompletely understood. In contrast to peripheral morphine administration, mast cell degranulation and release of histamine likely do not play a role. Current evidence suggests that neuraxial morphine causes sensitization of central itch-signaling pathways, leading to an enhanced response to peripheral stimulation. Neuraxial opioids may cause itching through the inhibition of inhibitory neurons in the dorsal horn of the spinal cord as a result of dysregulation of opioid-sensitive pathways involving µ- and κ-opioid receptor signaling.

Few studies have addressed the treatment of established pruritus (see Chapter 27 ). Most studies have addressed pruritus after intrathecal morphine, not lipid-soluble opioids such as fentanyl and sufentanil. The most effective treatment is a centrally acting µ-opioid antagonist (e.g., naloxone or naltrexone ) or a partial agonist-antagonist, such as nalbuphine ( Table 24.8 ). However, the use of these agents in a bolus or continuous infusion may reverse the analgesia. Antihistamines (e.g., diphenhydramine), low-dose propofol, 5-HT ₃ receptor antagonists (e.g., ondansetron), pentazocine (a κ-opioid and partial µ-opioid receptor agonist), and dopamine-2 receptor antagonists have been studied for the treatment of pruritus after spinal morphine, but not the lipid-soluble opioids fentanyl and sufentanil. Results of published studies are inconsistent and these drugs are not considered first-line treatment of neuraxial opioid–induced pruritus.

Several drugs have been investigated for prophylaxis against neuraxial opioid–induced pruritus, primarily coincident with neuraxial morphine administration. A 2016 metaanalysis included six randomized controlled trials of prophylactic ondansetron for prevention of intrathecal fentanyl- or sufentanil-induced pruritus in both obstetric and nonobstetric patients. Ondansetron 8 mg did not decrease the incidence of pruritus. A single trial in obstetric patients who received ondansetron 4 or 8 mg before intrathecal fentanyl 25 µg found no benefit compared with a placebo.

We do not routinely administer prophylaxis for the pruritus associated with neuraxial administration of opioids for labor analgesia. The pruritus is typically self-limiting; the severity of pruritus usually diminishes markedly in the first hour after opioid administration, and most women do not require treatment. For moderate to severe pruritus that requires treatment, we usually administer nalbuphine 2.5 mg and repeat the dose in 10 to 15 minutes if no improvement is noted. The advantage of nalbuphine is that it is less likely to reverse the intrathecal or epidural opioid analgesia than a pure µ-opioid receptor agonist.

Nausea and vomiting occur frequently during labor. It is difficult to determine the incidence of nausea and vomiting directly related to epidural and intrathecal opioid administration. Nausea and vomiting may also be secondary to neuraxial analgesia–induced hypotension. Maternal blood pressure should be measured when the patient complains of nausea in the presence of neuroblockade. Other causes of nausea and vomiting during labor are pregnancy itself, pain, opioid-induced delay of gastric emptying (see later discussion), and systemic opioids, which are sometimes administered before intrathecal or epidural opioids. In one study, the incidences of nausea (7% versus 44%) and vomiting (2% versus 17%) were significantly lower in women randomly assigned to receive intrathecal fentanyl than in those assigned to receive systemic hydromorphone analgesia in early labor.

The etiology of neuraxial opioid–associated nausea is unclear, but it may be caused by the modulation of afferent input at the area postrema (i.e., the chemoreceptor trigger zone) or at the nucleus of the tractus solitarius, which is a key relay station in the visceral sensory network. Of interest, nausea is less common after epidural or intrathecal opioid administration during labor than after the administration of the same drugs for post–cesarean delivery analgesia. Norris et al. noted that women who received epidural or intrathecal opioid analgesia during labor had an incidence of nausea of only 1.0% and 2.4%, respectively.

Although the incidence of nausea is low, treatment should be available. No studies, however, have specifically addressed the treatment of neuraxial analgesia–associated nausea and vomiting during labor. We do not routinely administer prophylactic antiemetics before the administration of neuraxial lipid-soluble opioids for labor analgesia.

Both observational and randomized controlled trials have consistently noted a gradual rise in core temperature over several hours in a subset of laboring women receiving epidural analgesia that is not observed in women receiving no analgesia, inhaled nitrous oxide, or parenteral opioids. The mean increase in core temperature is typically small (<1.0°C); however, women with epidural analgesia are more likely to have clinical fever (usually defined as core temperature ≥38°C) than those without epidural analgesia (odds ratio [OR], 4.17; 95% CI, 2.93 to 5.94). The incidence epidural-related maternal fever (ERMF) ranges from 15% to 25%. The variability may be attributed to differences in study design, study populations, and the definition of fever.

In the subset of women who eventually develop clinical fever, core temperature begins to rise within 1 hour of initiation of epidural analgesia at a rate of approximately 0.18°C/h. For these women, the development of fever is likely directly related to the duration of epidural analgesia. Others do not demonstrate this hourly increase in temperature ( Fig. 24.6 ). It is unclear why some women receiving epidural analgesia develop a fever, whereas most do not. Genetic factors (polymorphisms in genes that produce proteins controlling the immune response) may play a role, but further research is needed to explore this hypothesis. ERMF is not observed in nonlaboring women undergoing cesarean delivery with epidural anesthesia, nor is it observed in nonpregnant patients receiving epidural anesthesia for nonobstetric surgery. This suggests that there is something unique about the physiologic state of labor and its interaction with epidural analgesia and maternal genetics or other unidentified risk factors that leads to fever.

Maternal tympanic temperature in the 4 h immediately after initiation of epidural analgesia, stratified by ultimate intrapartum fever status (temperature ≥ 38.0°C or <38°C). * P <.001; ^† P <.05; ^‡ P <.01 (repeated measures analysis, febrile versus afebrile); ** P =.26 (repeated measures analysis, afebrile group temperature change over time).

Modified from Goetzl L, Rivers J, Zighelboim I, et al. Intrapartum epidural analgesia and maternal temperature regulation. Obstet Gynecol . 2007;109:687–690.

The neuraxial technique, specific local anesthetic agents, and inclusion of opioids used to initiate and maintain analgesia have not been shown to influence the risk for ERMF. The incidence of fever does not differ in women who receive epidural compared with CSE analgesia, in early compared with late labor initiation of neuraxial analgesia, or with bupivacaine epidural analgesia with and without fentanyl. Likewise, delayed initiation of the epidural infusion does not affect the incidence of fever.

Two mechanisms are proposed to explain ERMF: (1) epidural analgesia influences maternal immunomodulation, the so-called sterile inflammation hypothesis ; and (2) epidural analgesia, via sympathetic nervous system blockade, inhibits heat dissipation in laboring parturients, the so-called thermoregulation hypothesis . Sterile inflammation is a state of noninfectious inflammation—labor itself is a state of sterile inflammation. Concentrations of both pro- and antiinflammatory cytokines increase during labor. The prophylactic administration of glucocorticoids inhibits this rise in proinflammatory cytokines and lowers the incidence of ERMF. There is evidence of an inhibitory effect of bupivacaine on the release of the antipyrogenic factor IL-1 receptor antagonist (IL-1ra) from circulating leukocytes by reducing the activation of caspase-1. This finding supports the theory that epidural analgesia may cause fever by disrupting leukocyte immune function, and proinflammatory cytokines may cause fever if the release of the antipyrogenic IL-1ra is inhibited.

During labor, heat production is increased. The thermoregulatory hypothesis suggests that epidural labor analgesia may reduce heat loss by several mechanisms, including decreased sweating (cholinergic blockade), increased thermoregulatory vasoconstriction, baroreceptor-mediated reflex vasoconstriction (physiologic response to a decrease in blood pressure), an elevated vasoconstriction set point, blockade of active cutaneous vasodilation, decreased heat-dissipating activities such as hyperventilation, and a reduced shivering threshold. The current preponderance of evidence suggests that sterile inflammation is the most likely explanation of ERMF.

The significance of ERMF during labor is unclear. At issue is the diagnosis of ERMF and its differentiation from chorioamnionitis. Currently, there is no reliable intrapartum method for differentiating the two entities. The ACOG defines three categories of maternal fever: (1) isolated maternal fever (single oral maternal temperature of 39°C or greater, or sustained oral temperature between 38°C and 38.9°C when rechecked after 30 minutes); (2) suspected intraamniotic infection; and (3) confirmed intraamniotic infection. Suspected chorioamnionitis is defined as maternal fever and the presence of one or more of the following criteria: leukocytosis, purulent cervical discharge, and/or fetal tachycardia. Confirmed diagnosis requires positive amniotic fluid evidence of infection or placental histopathologic diagnosis. The ACOG recommends intrapartum antibiotic therapy for suspected or confirmed chorioamnionitis.

Studies have found that epidural analgesia is associated with increased intrapartum antibiotic use. Given that ERMF does not have an infectious etiology, it is likely that women with ERMF (and their fetuses) are being unnecessarily exposed to antibiotics. Inflammation and fever are associated with abnormal labor curves, fetal intolerance to labor, and an increased rate of operative vaginal delivery. It is not clear whether these adverse outcomes are associated with all types of inflammation and fever (i.e., including ERMF) or are limited to infectious fever.

Fetal and neonatal outcomes are also of concern. The US Centers for Disease Control and the American Academy of Pediatrics recommend laboratory studies and empiric antibiotic therapy for neonates whose mothers have suspected or confirmed chorioamnionitis. Similar to maternal antibiotic therapy, these measures are unnecessary if ERMF is misdiagnosed as chorioamnionitis. At a minimum, this care is stressful for parents and neonates, separates neonates from their parents shortly after birth, and adds unnecessary healthcare costs. More worrisome is the finding that maternal fever in the presence of fetal acidosis is associated with a markedly increased risk for neonatal encephalopathy, suggesting that fever may lower the threshold for fetal hypoxic brain injury. Greenwell et al. demonstrated that women with epidural analgesia who developed intrapartum fever had increased risk for adverse neonatal outcomes (including assisted ventilation, lower Apgar scores, and early onset seizures) compared with women who did not develop a fever. Again, because of the difficulty in diagnosing ERMF, it is not clear whether fever, per se , is the culprit, or infectious or noninfectious inflammation interact to play a role in adverse neonatal outcome.

Several factors, including hormonal factors, likely influence thermoregulatory response during labor and delivery. Shivering is frequently observed during labor and may occur more commonly after administration of epidural analgesia, although its incidence and intensity are less than during cesarean delivery with epidural anesthesia. Panzer et al. performed an observational study of shivering during labor. Before delivery, 18% of women shivered, and 15% of these episodes were associated with normothermia and vasodilation, suggesting a nonthermoregulatory cause of the shivering. After delivery, shivering was observed in 16% of women, and in 28% of them it was nonthermoregulatory. There was no difference in the incidence of shivering between women who chose epidural (bupivacaine/fentanyl) analgesia and those who chose systemic meperidine analgesia. The addition of an opioid to the local anesthetic solution may affect the shivering response. At least one study has suggested that the epidural administration of epinephrine increases shivering ; the etiology of this response is unknown.

Urinary retention is a troublesome side effect of neuraxial anesthesia/analgesia. The bladder and urethral sphincters receive sympathetic innervation from the low thoracic/high lumbar sympathetic fibers and parasympathetic innervation from the sacral fibers. Neuraxial local anesthetics cause urinary retention through blockade of sacral nerve roots. Efferent and afferent nerve traffic via the S2, S3, and S4 nerve roots controls the detrusor muscle (responsible for urine storage and micturition) and internal and external sphincter function. Intrathecal opioids cause dose-dependent suppression of detrusor muscle contractility and decreased urge sensation via inhibition of sacral parasympathetic nervous system outflow. The onset of urinary retention appears to parallel the onset of analgesia.

It is difficult to determine the magnitude of this problem during labor because parturients often require catheterization for other reasons. Postpartum bladder dysfunction was observed in 14% of women who had a normal spontaneous vaginal delivery and in 38% of women who underwent operative vaginal delivery, all without epidural analgesia.

Several observational studies suggest that there is a higher risk for intrapartum and postpartum urinary retention in women who receive epidural labor analgesia than in those who receive nonepidural or no analgesia. Similarly, a metaanalysis of four small randomized controlled trials that compared neuraxial with systemic opioid analgesia, in which urinary retention was reported as a secondary outcome, also identified this association. Whether this higher risk reflects a cause-and-effect relationship or patient selection bias is not clear. Wilson et al. found that women randomized to receive neuraxial labor analgesia with low-concentration bupivacaine with opioid more often retained the ability to void spontaneously than women who received epidural analgesia with 0.25% bupivacaine (approximately 31% versus 11%), which suggests a dose-response relationship.

Any difference in bladder function appears to be short-lived; differences between groups in one study had resolved by postpartum day 1. In two studies, patients were randomly assigned to receive epidural analgesia with or without an opioid; there was no difference between groups in the incidence of intrapartum or postpartum urinary retention.

Parturients should be regularly observed during labor for evidence of bladder distention, especially if they complain of suprapubic pain during contractions. The differential diagnosis of breakthrough pain during neuraxial labor analgesia should include bladder distention. Personal observation suggests that many women can void in the presence of low-dose neuroblockade if placed on a bedpan or escorted to the toilet, even if they do not perceive a full bladder. The inability to void and bladder distention should prompt catheterization to empty the bladder.

The common cold sore or fever blister is a manifestation of the reactivation of latent herpes simplex virus (HSV) infection. Reactivation can occur after exposure to ultraviolet light, fever, immunosuppression, or trauma. Prospective randomized studies have demonstrated a higher incidence of postpartum oral HSV reactivation in women randomly assigned to receive neuraxial morphine than among women assigned to receive systemic morphine for post–cesarean delivery analgesia. We are unaware of any study that has investigated whether epidural or intrathecal opioid administration during labor increases the incidence of recurrent oral HSV infection after vaginal delivery. Therefore, we do not withhold neuraxial opioids during labor in women with a history of oral herpes.

Labor may result in delayed gastric emptying, which may be exacerbated by opioid administration (see Chapter 28 ). Intravenous or intramuscular opioid administration results in delayed gastric emptying in laboring women. Data are inconsistent on whether neuraxial opioids delay gastric emptying. Early studies assessed gastric emptying using acetaminophen absorption. Several studies suggest that epidural fentanyl combined with bupivacaine and administered as part of a CEI does not result in delayed gastric emptying compared with infusion of bupivacaine alone ; however, a third study found a small delay in gastric emptying following the infusion of epidural fentanyl after a cumulative fentanyl dose > 100 µg (after approximately 4 hours of infusion). Two studies found delayed gastric emptying with epidural fentanyl administered as a bolus (50 to 100 µg) with bupivacaine. In another study, intrathecal fentanyl 25 µg resulted in delayed gastric emptying compared with epidural fentanyl 50 µg plus bupivacaine or bupivacaine alone.

In a study using gastric ultrasonography and measurement of antral cross-sectional area (CSA) in women who received epidural labor analgesia with ropivacaine and sufentanil, median CSA decreased between the preepidural initiation assessment and assessment at full cervical dilation (the median interval between the measurements was 188 minutes). Another study using gastric ultrasonography identified solid food in the stomach of 9 of 10 laboring parturients without epidural analgesia fed a light meal; in contrast, only 3 of 10 parturients with epidural analgesia (ropivacaine with sufentanil) had solid food in the stomach. Finally, a study comparing low (<100 µg) to high (>100 µg) cumulative fentanyl dose 2 hours after initiation of epidural analgesia with ropivacaine found no difference in antral CSA between the two groups. Overall, these data do not suggest a clinically significant delay in gastric emptying when neuraxial local anesthetics are combined with opioids for labor analgesia.

In one of the early studies of intrathecal opioid administration during labor, Cohen et al. observed decreased sensation to cold and pinprick in women who received intrathecal sufentanil. Subsequent studies have demonstrated that these sensory changes do not result from a local anesthetic effect of sufentanil. Sensory changes do not predict the quality or duration of analgesia or the extent of hemodynamic change. Further, intrathecal sufentanil does not cause a sympathectomy. Intrathecal opioids do not affect the efferent limb of the nervous system and so do not impair motor function. Thus, affected patients should be reassured that respiratory efforts are not compromised and that the symptoms will subside in 30 to 60 minutes.

In addition to sensory changes, case reports have described mental status changes, aphasia, and automatisms after theintrathecal injection of fentanyl and sufentanil. These symptoms seem to be related to an opioid effect. In one case, the symptoms were partially reversed by naloxone.

The reported failure rate for neuraxial analgesia varies according to the definition of “failure.” In survey studies, the rate of epidural catheter replacement has ranged from 5% to 13%. Successful siting of the epidural space is not always possible, and satisfactory analgesia does not always occur, even when the epidural space has been identified correctly. Factors such as patient age and weight, the specific technique, the type of epidural catheter, and the skill of the anesthesia provider are associated with the rate of failure of neuraxial analgesia. Failure to provide adequate analgesia not only results in a dissatisfying experience for the patient but also may lead to litigation. The risk for failed anesthesia and the potential need to place a second epidural catheter should be discussed with the patient during the preanesthetic evaluation, before placement of the first epidural catheter.

Pan et al. used quality assurance data to retrospectively assess the failure rate among more than 12,000 neuraxial procedures performed for labor analgesia over a 3-year period ( Table 24.9 ). The overall failure rate of 12% included procedures that resulted in no or inadequate analgesia, unintentional dural puncture with an epidural needle or catheter, intravenous cannulation with the epidural catheter, or replacement of the catheter for any reason. The rate of failed analgesia was significantly lower after CSE than after epidural analgesia (10% versus 14%, respectively; P <.001). In a follow-up study from the same group of investigators, the rate of epidural catheter failure was 6.6% after CSE analgesia and 11.6% after epidural analgesia ( P =.001). Other studies have also found a higher epidural catheter failure rate when analgesia is initiated with a traditional epidural approach compared with a CSE technique. Of note, these studies were performed in academic institutions where the neuraxial procedures were performed primarily by trainees. In a randomized trial comparing CSE with epidural analgesia in a large maternity hospital staffed by private practice anesthesiologists, the epidural catheter replacement rate was lower and there was no difference between CSE and epidural analgesia (2% and 1.2% incidence, respectively; 95% CI of difference, −3.3% to 1.8%).

Typically, failed analgesia after injection of intrathecal or epidural anesthetics results in no neuroblockade, unilateral or asymmetric blockade, missed segments, or inadequate density of neuroblockade. Patient complaints of pain should prompt timely evaluation and treatment ( Box 24.7 ). The progress of labor should be assessed, and the patient should be queried as to the nature of the pain. Typically, pain becomes more intense as labor progresses; for example, an epidural block that was adequate at 4-cm cervical dilation may not be adequate at 8-cm cervical dilation. Expectations and treatment may be different for women in latent versus active or second-stage labor. The bladder should be checked and emptied if distended. The position of the epidural catheter at the skin should be assessed to exclude the possibility of catheter migration out of the epidural space. Inadequate analgesia may also result from migration of the epidural catheter into a vein or movement of the catheter outside the epidural space. Before giving a large bolus dose of local anesthetic, the anesthesia provider should give a test dose to exclude intravenous migration of the catheter.

The extent of neuroblockade should be assessed with a cold or sharp stimulus that starts over the lateral thighs (the dermatomal level at which the tip of the epidural catheter is sited) and moves both cephalad and caudad on both sides. Inexperienced anesthesia providers often fail to check for the presence of a sacral blockade. In the case of no sensory blockade, the epidural catheter should be replaced. If the extent of neuroblockade is inadequate (in either the cephalad or caudad direction), or if there is unilateral blockade or missed segments, the injection of a large volume (10 to 15 mL) of a dilute local anesthetic solution (e.g., 0.0625% to 0.125% bupivacaine) may result in satisfactory analgesia. An advantage of using a more dilute solution of local anesthetic is the ability to increase the administered volume to ensure adequate spread of analgesia.

Some anesthesia providers advocate withdrawing the epidural catheter 1 to 2 cm out of the epidural space before administering the bolus injection. However, flexible epidural catheters begin to coil after being inserted into the epidural space. A study in young male patients used fluoroscopy to track the advancement of lumbar epidural catheters ; only 13% of catheters were threaded 4 cm beyond the tip of the epidural needle without coiling. Therefore, unless the epidural catheter is threaded deeply into the epidural space (e.g., beyond 6 to 8 cm), pulling the epidural catheter back 1 to 2 cm likely pulls out the coil, but does not change the location of the tip of the epidural catheter.

Some women appear to have pain despite adequate distribution of sensory blockade. These women may require more dense analgesia; a larger dose of local anesthetic (10- to 15-mL bolus of 0.125% bupivacaine or a 5- to 10-mL bolus of 0.25% bupivacaine) often successfully reestablishes analgesia. Alternatively, a lipid-soluble opioid (e.g., fentanyl 50 µg) may be added to the solution. Reynolds and O’Sullivan showed that epidural bupivacaine 10 mg combined with fentanyl 100 µg was more effective for the treatment of breakthrough pain and had a faster onset and longer duration of action than either bupivacaine 25 mg or fentanyl 100 µg administered alone. The opioid is especially helpful if the parturient is experiencing back pain because the fetus is in the occiput posterior position. Epidural clonidine (75 µg) may be used to treat breakthrough pain that occurs during/after epidural administration of the standard local anesthetic-opioid solution.

Although available data are inconsistent, it appears that maternal position has little effect on the development of an asymmetric block after a bolus dose of anesthetic solution into the epidural space. It is likely that the position of the epidural catheter in relation to other epidural space structures (e.g., connective tissue, fatty tissue, blood vessels) affects the spread and quality of analgesia to a greater extent than maternal position. Anatomic barriers (e.g., a longitudinal connective tissue band between the dura and ligamentum flavum) or placement of the catheter tip in the anterior epidural space or paravertebral space may explain some cases of single nerve root, unilateral, or asymmetric blockade.

The response to the bolus dose should be assessed in a timely fashion, and the epidural catheter should be replaced (with the patient’s consent) if satisfactory analgesia is not obtained.

In a metaanalysis of 13 studies that involved more than 300,000 obstetric patients, Choi et al. determined that the rate of unintentional dural puncture with an epidural needle or catheter was 1.5% (95% CI, 1.5% to 1.5%) (see Chapter30 ). Dural puncture may be detected at the time of insertion of the epidural needle or after placement of the catheter. If dural puncture is detected with the epidural needle, it is best to replace the stylet to stop the loss of CSF while considering next steps. The anesthesia provider has two primary options. The epidural needle may be withdrawn, and an epidural catheter may be sited at another interspace (intrathecal analgesia may be initiated by injecting a spinal analgesic dose through the epidural needle before it is removed and resited at a different interspace). Alternatively, the anesthesia provider may place a catheter in the subarachnoid space through the “epidural” needle and administer continuous spinal analgesia for labor and delivery. This latter technique is particularly advantageous for patients at high risk for repeat dural puncture on a second attempt or in cases in which it may be difficult to enter either the epidural or subarachnoid space successfully at an alternative interspace (e.g., in obese women or in patients with abnormal anatomy of the lumbar spine). It is very important to append a label that clearly identifies the catheter as a spinal catheter to decrease the risk for injecting an epidural dose of local anesthetic into the subarachnoid space. The parturient and all providers on the obstetric unit, including nurses, midwives, and other anesthesia providers, must be made aware of the intrathecal catheter, and this information must be communicated during any hand-off of care to another provider. Particular care must be taken if the catheter is used to extend the block for cesarean delivery.

Resiting the epidural catheter in a different interspace eliminates the problem of mistaking an intrathecal catheter for an epidural catheter. However, local anesthetic or opioid injected through the epidural catheter may pass through the dural puncture site and into the subarachnoid space, resulting in an unexpectedly high neuroblockade. This complication is more likely to occur with the bolus injection of local anesthetic than with an epidural infusion of local anesthetic.

If dural puncture is not recognized until CSF is aspirated from the catheter, or if administration of the test dose results in spinal anesthesia, the anesthesia provider has the following two options: (1) replace the epidural catheter at an alternative interspace or (2) provide continuous spinal analgesia through the existing catheter.

The administration of opioids by any route entails a risk for respiratory depression. Factors that affect the risk for respiratory depression after neuraxial opioid administration include the choice and dose of drug and its interaction with systemically administered opioids and other central nervous system depressants. The most important factor affecting the onset of respiratory depression is the lipid solubility of the drug. In general, if respiratory depression is going to occur, it will do so within 2 hours of the injection of a lipid-soluble opioid such as fentanyl or sufentanil. When a lipid-soluble opioid gains access to the CSF, it is quickly absorbed by lipophilic body tissues. Subsequent clearance and elimination are similar to those associated with intravenous injection of the same drug. Thus, with a spinal or epidural injection of a lipid-soluble opioid, the “time window” for respiratory depression is short. Conversely, with a hydrophilic drug such as morphine, the onset of respiratory depression is delayed. Once a hydrophilic drug such as morphine enters the CSF, it tends to stay in the CSF. Rostral migration and absorption into the respiratory centers occur over several hours, so respiratory depression may not occur until 6 to 12 hours after injection of the drug (see Fig. 13.12 ).

A risk factor for respiratory depression is previous parenteral opioid administration. Several reports have implicated prior intravenous opioid administration as a contributing factor to the respiratory arrest that occurred after intrathecal sufentanil 10 µg administration in laboring women. (This dose is higher than the currently recommended intrathecal dose range.) For this reason, we refrain from administering a bolus dose of epidural or spinal opioid to women who have recently received systemic opioid analgesia.

The incidence of fatal LAST appears to have declined since initial reports in the early 1980s. In a prospective audit from the United Kingdom of more than 145,000 obstetric epidural procedures (1987 to 2003), the incidence of intravascular injection was 1 in 5000 ( Table 24.10 ). Bupivacaine 0.75% is no longer used for epidural anesthesia in obstetric patients. In the United States, lidocaine or 2-chloroprocaine is most often used when a high-concentration local anesthetic is required for operative epidural anesthesia, but in other countries bupivacaine 0.5%, levobupivacaine 0.5%, and ropivacaine 0.75% are often used; low concentrations of local anesthetic are now routinely used for labor analgesia. Nonetheless, LAST remains a serious potential complication during the administration of epidural anesthesia in obstetric patients. Steps to decrease the risk of LAST are outlined in Box 12.3 .

Table 24.10

Incidence of Unintentional Intravascular, Intrathecal, and Subdural Injections During Attempted Epidural Labor Analgesia a

Modified from Jenkins JG. Some immediate serious complications of obstetric analgesia and anaesthesia: a prospective study of 145,550 epidurals. Int J Obstet Anesth . 2005;14:37–42.

Event	Incidence	Rate (%) b
Intravascular injection	1:5000	0.020 (0.014 to 0.029)
Intrathecal injection	1:2900	0.035 (0.027 to 0.046)
Subdural injection	1:4200	0.025 (0.017 to 0.033)
High/total spinal anesthesia	1:16,200	0.006 (0.003 to 0.012)

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