Sensory Innervation of the Genital Tract
Pain during the first stage of labor is generated largely from the uterus. Visceral sensory fibers from the uterus, cervix, and upper vagina traverse through the Frankenhäuser ganglion, which lies just lateral to the cervix, and enter into the pelvic plexus and then into the middle and superior internal iliac plexuses (Fig. 19-1). From there, the fibers travel in the lumbar and lower thoracic sympathetic chains to enter the spinal cord through the white rami communicantes associated with the T10 through T12 and L1 nerves. Early in labor, the pain of uterine contractions is transmitted predominantly through the T11 and T12 nerves.
Pathways of labor pain. Pain stimuli from the cervix and uterus travel through the paracervical region and the pelvic and hypogastric plexus to enter the lumbar sympathetic chain. Through the white rami communicantes of the T10, T11, T12, and L1 spinal nerves, they enter the dorsal horn of the spinal cord. Blockade at different levels along this path can alleviate the visceral component of labor pain. (Adapted from Eltzschig HK, Lieberman ES, and Camann WR: Medical progress: Regional anesthesia and analgesia for labor and delivery. N Engl J Med 348:319, with permission. Copyright © 2003 Massachusetts Medical Society. All rights reserved.)
The motor pathways to the uterus leave the spinal cord at the level of T7 and T8 vertebrae. Theoretically, any method of sensory block that does not also block motor pathways to the uterus can be used for analgesia during labor.
Lower Genital Tract Innervation
Pain with vaginal delivery arises from stimuli from the lower genital tract. These are transmitted primarily through the pudendal nerve, the peripheral branches of which provide sensory innervation to the perineum, anus, and the more medial and inferior parts of the vulva and clitoris. The pudendal nerve passes beneath the posterior surface of the sacrospinous ligament just as the ligament attaches to the ischial spine. As discussed in Chapter 2, Pudendal Nerve and Vessels, sensory nerve fibers of the pudendal nerve are derived from ventral branches of the S2 through S4 nerves.
Some of the more commonly used local anesthetics, along with their usual concentrations, doses, and durations of action, are summarized in Table 19-3. The dose of each agent varies widely and is dependent on the particular nerve block and physical status of the woman. The onset, duration, and quality of analgesia can be enhanced by increasing the dose. This can be done safely only by incrementally administering small-volume boluses of the agent and by carefully monitoring early warning signs of toxicity. Administration of these agents must be followed by appropriate monitoring for adverse reactions. Equipment and personnel to manage these reactions must be immediately available.
Table 19-3. Some Local Anesthetic Agents Used in Obstetrics |Favorite Table|Download (.pdf)
Table 19-3. Some Local Anesthetic Agents Used in Obstetrics
Usual Concentration (percent)
Usual Volume (mL)
Usual Dose (mg)
Average Duration (min)
Local or pudendal block
Epidural (not subarach-noid) for cesarean delivery
Low spinal block/6% glucosea
Spinal for cesarean delivery/5% glucosea
Local or pudendal block
Epidural for cesarean delivery
Spinal for cesarean or puerperal tubal ligation/7.5% glucosea
Spinal for vaginal delivery/7.5% glucosea
Epidural for cesarean delivery
Epidural for labor
Spinal for cesarean delivery/8.25% glucosea
Epidural for cesarean delivery
Epidural for labor
Most often, serious toxicity follows inadvertent intravenous injection. For this reason, when epidural analgesia is initiated, dilute epinephrine is sometimes added and given as a test dose. A sudden significant rise in the maternal heart rate or blood pressure immediately after administration suggests intravenous catheter placement. Personnel using these agents must be cognizant that these agents are manufactured in more than one concentration and ampule size, which increases the potential for dosing errors. Systemic toxicity from local anesthetics typically manifests in the central nervous and cardiovascular systems.
Central Nervous System Toxicity
Early symptoms are those of stimulation but, as serum levels increase, depression follows. Symptoms may include light-headedness, dizziness, tinnitus, metallic taste, and numbness of the tongue and mouth. Patients may show bizarre behavior, slurred speech, muscle fasciculation and excitation, and ultimately, generalized convulsions, followed by loss of consciousness. The convulsions should be controlled, an airway established, and oxygen delivered. Succinylcholine abolishes the peripheral manifestations of the convulsions and allows tracheal intubation. Thiopental or diazepam act centrally to inhibit convulsions. Magnesium sulfate, administered according to the regimen for eclampsia, also controls convulsions (see Chap. 34, Magnesium Sulfate to Control Convulsions). Abnormal fetal heart rate patterns such as late decelerations or persistent bradycardia may develop from maternal hypoxia and lactic acidosis induced by convulsions. With arrest of convulsions, administration of oxygen, and application of other supportive measures, the fetus usually recovers more quickly in utero than following immediate cesarean delivery. Moreover, the mother is better served if delivery is forestalled until the intensity of hypoxia and metabolic acidosis has diminished.
These manifestations generally develop later than those from cerebral toxicity, but may not develop at all because they are induced by higher serum drug levels. The notable exception is bupivacaine, which is associated with the development of neurotoxicity and cardiotoxicity at virtually identical levels (Mulroy, 2002). Because of this risk of systemic toxicity, use of 0.75-percent solution of bupivacaine for epidural injection was proscribed by the Food and Drug Administration in 1984. Similar to neurotoxicity, cardiovascular toxicity is characterized first by stimulation and then by depression. Accordingly, there is hypertension and tachycardia, which soon is followed by hypotension, cardiac arrhythmias, and impaired uteroplacental perfusion.
Hypotension is managed initially by turning the woman onto either side to avoid aortocaval compression. A crystalloid solution is infused rapidly along with intravenously administered ephedrine. Emergency cesarean delivery should be considered if maternal vital signs have not been restored within 5 minutes of cardiac arrest (see Chap. 42, Cardiopulmonary Resuscitation). As with convulsions, however, the fetus is likely to recover more quickly in utero once maternal cardiac output is reestablished.
This block is a relatively safe and simple method of providing analgesia for spontaneous delivery. As shown in Figure 19-2, a tubular introducer that allows 1.0 to 1.5 cm of a 15-cm 22-gauge needle to protrude beyond its tip is used to guide the needle into position over the pudendal nerve. The end of the introducer is placed against the vaginal mucosa just beneath the tip of the ischial spine. The needle is pushed beyond the tip of the director into the mucosa and a mucosal wheal is made with 1 mL of 1-percent lidocaine solution or an equivalent dose of another local anesthetic (Table 19-3). To guard against intravascular infusion, aspiration is attempted before this and all subsequent injections. The needle is then advanced until it touches the sacrospinous ligament, which is infiltrated with 3 mL of lidocaine. The needle is advanced farther through the ligament, and as it pierces the loose areolar tissue behind the ligament, the resistance of the plunger decreases. Another 3 mL of solution is injected into this region. Next, the needle is withdrawn into the introducer, which is moved to just above the ischial spine. The needle is inserted through the mucosa and 3 more mL is deposited. The procedure is then repeated on the other side.
Local infiltration of the pudendal nerve. Transvaginal technique showing the needle extended beyond the needle guard and passing through the sacrospinous ligament to reach the pudendal nerve.
Within 3 to 4 minutes of injection, the successful pudendal block will allow pinching of the lower vagina and posterior vulva bilaterally without pain. If delivery occurs before the pudendal block becomes effective and an episiotomy is indicated, then the fourchette, perineum, and adjacent vagina can be infiltrated with 5 to 10 mL of 1-percent lidocaine solution directly at the site where the episiotomy is to be made. By the time of the repair, the pudendal block usually has become effective.
Pudendal block usually does not provide adequate analgesia when delivery requires extensive obstetrical manipulation. Moreover, such analgesia is usually inadequate for women in whom complete visualization of the cervix and upper vagina or manual exploration of the uterine cavity is indicated.
This block usually provides satisfactory pain relief during the first stage of labor. We do not use it routinely in our institutions. Because the pudendal nerves are not blocked, however, additional analgesia is required for delivery. For paracervical blockade, usually lidocaine or chloroprocaine, 5 to 10 mL of a 1-percent solution, is injected into the cervix laterally at 3 and 9 o'clock. Bupivacaine is contraindicated because of an increased risk of cardiotoxicity (American Academy of Pediatrics and American College of Obstetricians and Gynecologists, 2007; Rosen, 2002b). Because these anesthetics are relatively short acting, paracervical block may have to be repeated during labor.
Fetal bradycardia is a worrisome complication that occurs in approximately 15 percent of paracervical blocks (Rosen, 2002b). Bradycardia usually develops within 10 minutes and may last up to 30 minutes. Doppler studies have shown an increase in the pulsatility index of the uterine arteries following paracervical blockade (see Chap. 16, Uterine Artery). These observations support the hypothesis of drug-induced arterial vasospasm as a cause of fetal bradycardia (Manninen and co-workers, 2000). For these reasons, paracervical block should not be used in situations of potential fetal compromise.
Spinal (Subarachnoid) Block
Introduction of a local anesthetic into the subarachnoid space to effect analgesia has long been used for delivery. Advantages include a short procedure time, rapid onset of blockade, and high success rate. Because of the smaller subarachnoid space during pregnancy, likely the consequence of engorgement of the internal vertebral venous plexus, the same amount of anesthetic agent in the same volume of solution produces a much higher blockade in parturients than in nonpregnant women.
Low spinal block can be used for forceps or vacuum delivery. The level of analgesia should extend to the T10 dermatome, which corresponds to the level of the umbilicus. Blockade to this level provides excellent relief from the pain of uterine contractions (see Fig. 19-1).
Several local anesthetic agents have been used for spinal analgesia. Addition of glucose to any of these agents creates a hyperbaric solution, which is heavier and denser than cerebrospinal fluid. A sitting position causes a hyperbaric solution to settle caudally, whereas a lateral position will have a greater effect on the dependent side. Lidocaine given in a hyperbaric solution produces excellent analgesia and has the advantage of a rapid onset and relatively short duration. Bupivacaine in an 8.25-percent dextrose solution provides satisfactory anesthesia to the lower vagina and the perineum for more than 1 hour. Neither is administered until the cervix is fully dilated and all other criteria for safe forceps delivery have been fulfilled (see Chap. 23, Prerequisites for Forceps Application). Preanalgesic intravenous hydration with 1 L of crystalloid solution will prevent or minimize hypotension in many cases.
A level of sensory blockade extending to the T4 dermatome is desired for cesarean delivery (see Fig. 19-3). Depending on maternal size, 10 to 12 mg of bupivacaine in a hyperbaric solution or 50 to 75 mg of lidocaine hyperbaric solution are administered. The addition of 20 to 25 mg of fentanyl increases the rapidity of blockade onset and reduces shivering. The addition of 0.2 mg of morphine improves pain control during delivery and postoperatively.
Complications of Regional Analgesia
Shown in Table 19-4 are some of the more common complications associated with regional analgesia. The estimated incidences were derived from 19 studies published between 1987 and 2000, as well as data from the Maternal-Fetal Medicine Units (MFMU) Network, which included more than 37,000 women undergoing cesarean delivery (Bloom and colleagues, 2005). Importantly, obese women have significantly impaired ventilation and thus close clinical monitoring is imperative (von Ungern-Sternberg and associates, 2004).
Table 19-4. Complications of Regional Analgesia Techniques |Favorite Table|Download (.pdf)
Table 19-4. Complications of Regional Analgesia Techniques
Incidence (percent) from ACOGa
Incidence (percent) from MFMUb
Spinal (n = N/A)
Epidural (n = N/A)
Combinedc (n = N/A)
Spinal (n = 14,797)
Epidural (n = 15,443)
Combinedc (n = 4375)
Postdural puncture headache
Failed regional blockade (need for GETA)
High spinal blockade
Chemical meningitis or epidural abscess or hematoma
This common complication may develop soon after injection of the local anesthetic agent. It is the consequence of vasodilatation from sympathetic blockade and is compounded by obstructed venous return due to uterine compression of the great vessels. In the supine position, even in the absence of maternal hypotension measured in the brachial artery, placental blood flow may still be significantly reduced. Treatment includes uterine displacement by left lateral positioning of the patient, intravenous hydration, and intravenous bolus injections of ephedrine or phenylephrine.
Ephedrine is a sympathomimetic drug that binds to alpha- and beta-receptors but also indirectly enhances norepinephrine release. It raises blood pressure by increasing heart rate and cardiac output and by variably elevating peripheral vascular resistance. In animal studies, ephedrine preserves uteroplacental blood flow during pregnancy compared with alpha1-receptor agonists. For this reason, it is a preferred vasopressor for obstetric use. Phenylephrine is a pure alpha agonist and raises blood pressure solely through vasoconstriction. A meta-analysis of seven randomized trials by Lee and colleagues (2002b) suggests that the safety profiles of ephedrine and phenylephrine are comparable.
In a randomized trial at Parkland Hospital, Morgan and colleagues (2000) found that from the standpoint of umbilical artery pH at birth, epinephrine used as needed to maintain blood pressure during spinal injection was superior to prophylactic ephedrine. Mean pH in the former group was 7.26 and in the latter 7.12. Following their systematic review of 14 reports, Lee and colleagues (2002a) question whether routine prophylactic ephedrine is needed for elective cesarean delivery. Ngan Kee and associates (2004) have used prophylactic phenylephrine infusion without the fetal acidemia reported with prophylactic ephedrine use.
Most often, complete spinal blockade follows administration of an excessive dose of local anesthetic agent. This is certainly not always the case, because accidental total spinal block has even occurred following an epidural test dose (Palkar and associates, 1992). With complete spinal block, hypotension and apnea promptly develop and must be immediately treated to prevent cardiac arrest. In the undelivered woman: (1) the uterus is immediately displaced laterally to minimize aortocaval compression, (2) effective ventilation is established, preferably with tracheal intubation, and (3) intravenous fluids and ephedrine are given to correct hypotension.
Spinal (Postdural Puncture) Headache
Leakage of cerebrospinal fluid from the site of puncture of the meninges can lead to spinal headache. Presumably, when the woman sits or stands, the diminished volume of cerebrospinal fluid creates traction on pain-sensitive central nervous system structures. Rates of this complication can be reduced by using a small-gauge spinal needle and avoiding multiple punctures. In a prospective, randomized study of five different spinal needles, Vallejo and colleagues (2000) concluded that Sprotte and Whitacre needles had the lowest risks of postdural puncture headaches. In a recent study by Sprigge and Harper (2008), the incidence of postdural puncture headache was 1 percent in more than 5000 women undergoing spinal analgesia.
There is no good evidence that placing a woman absolutely flat on her back for several hours is effective in preventing headache. Vigorous hydration may be of value, but compelling evidence to support its use is also lacking. The administration of caffeine, a cerebral vasoconstrictor, has been shown in randomized studies to afford temporary relief (Sechzer and Abel, 1978; Camann and colleagues, 1990).
With severe headache, an epidural blood patch is most effective. A few milliliters of autologous blood are obtained aseptically by venipuncture into a tube without anticoagulant. This blood is injected into the epidural space at the site of the dural puncture. Relief is immediate and complications uncommon. In a randomized trial of 64 women, Scavone and colleagues (2004) found that prophylactic blood patch did not decrease either the incidence of postdural puncture headache or the need for a subsequent therapeutic blood patch.
If a headache does not have the pathognomonic postural characteristics or persists despite treatment with a blood patch, other diagnoses should be considered. For example, Chisholm and Campbell (2001) described a case of superior sagittal sinus thrombosis that manifested as a postural headache. Chan and Paech (2004) have described persistent cerebrospinal fluid leak in three women. Smarkusky and colleagues (2006) described pneumocephalus, which caused immediate cephalgia. Finally, Dawley and Hendrix (2009) reported an intracranial subdural hematoma after spinal anesthesia.
In rare instances, postdural puncture cephalgia is associated with temporary blindness and convulsions. Shearer and colleagues (1995) described eight such cases associated with 19,000 regional analgesic procedures. It is presumed that these too are caused by cerebrospinal fluid hypotension. Immediate treatment of seizures and blood patch was effective in all cases.
With spinal analgesia, bladder sensation is likely to be obtunded and bladder emptying impaired for several hours after delivery. As a consequence, bladder distension is a frequent postpartum complication, especially if appreciable volumes of intravenous fluid are given.
Oxytocics and Hypertension
Paradoxically, hypertension from ergonovine or methylergonovine injections following delivery is more common in women who have received a spinal or epidural block.
Arachnoiditis and Meningitis
Local anesthetics are no longer preserved in alcohol, formalin, or other toxic solutes, and disposable equipment is used by most. These practices, coupled with aseptic technique, have made meningitis and arachnoiditis rare but have not eliminated them (Harding, 1994; Newton, 1994; Sandkovsky, 2009, and all their associates).
Contraindications to Spinal Analgesia
Shown in Table 19-5 are the absolute contraindications to regional analgesia according to the American College of Obstetricians and Gynecologists (2002). Obstetrical complications that are associated with maternal hypovolemia and hypotension—for example, severe hemorrhage—are contraindications to the use of spinal blockade. The additive cardiovascular effects of spinal blockade in the presence of acute blood loss in nonpregnant patients were documented by Kennedy and co-workers (1968).
Table 19-5. Absolute Contraindications to Regional Analgesia |Favorite Table|Download (.pdf)
Table 19-5. Absolute Contraindications to Regional Analgesia
- Refractory maternal hypotension
- Maternal coagulopathy
- Maternal use of once-daily dose of low-molecular-weight heparin within 12 hours
- Untreated maternal bacteremia
- Skin infection over site of needle placement
- Increased intracranial pressure caused by a mass lesion
Disorders of coagulation and defective hemostasis also preclude the use of spinal analgesia (see Chap. 47, Anticoagulation with Warfarins). Although there are no randomized studies to guide the management of anticoagulation at the time of delivery, consensus opinion suggests that women given subcutaneous unfractionated heparin or low-molecular-weight heparin should be instructed to stop therapy when labor begins (Krivak and Zorn, 2007). Subarachnoid puncture is also contraindicated if there is cellulitis at the site of needle entry. Neurological disorders are considered by many to be a contraindication, if for no other reason than that exacerbation of the neurological disease might be attributed without cause to the anesthetic agent. Other maternal conditions, such as significant aortic stenosis or pulmonary hypertension, are also relative contraindications to the use of spinal analgesia (see Chap. 44, Cardiovascular Disease: Introduction).
As with significant hemorrhage, severe preeclampsia is another complication in which markedly decreased blood pressure can be predicted when spinal analgesia is used. Gambling and Writer (1999) concluded that with severe preeclampsia, epidural analgesia is preferable to spinal blockade and especially preferable to a general anesthetic. Dyer and associates (2007), however, also concluded that single-dose spinal analgesia for cesarean delivery is safe.
As subsequently discussed, hypotension is also a risk with epidural analgesia and severe preeclampsia. Wallace and colleagues (1995) randomly assigned 80 women with severe preeclampsia undergoing cesarean delivery to receive general anesthesia or either epidural or combined spinal-epidural analgesia. There were no differences in maternal or neonatal outcomes. However, 30 percent of women given epidural analgesia and 22 percent of those given spinal-epidural blockade developed hypotension—the average reduction in mean arterial pressure was between 15 and 25 percent. In another randomized study of 100 women with severe preeclampsia, Visalyaputra and co-workers (2005) reported similar maternal and neonatal outcomes with spinal versus epidural analgesia given for cesarean delivery.
Relief of labor and childbirth pain, including cesarean delivery, can be accomplished by injection of a local anesthetic agent into the epidural or peridural space (Fig. 19-4). This potential space contains areolar tissue, fat, lymphatics, and the internal venous plexus. This plexus becomes engorged during pregnancy such that the volume of the epidural space is appreciably reduced. Entry for obstetrical analgesia is usually through a lumbar intervertebral space. Although only one injection may be given, usually an indwelling catheter is placed for repeat injections or continuous infusion using a volumetric pump.
Introduction of a catheter into the epidural space through a Tuohy needle.
Continuous Lumbar Epidural Block
Complete analgesia for the pain of labor and vaginal delivery necessitates a block from the T10 to the S5 dermatomes (Figs. 19-1 and 19-3). For cesarean delivery, a block extending from the T4 to the S1 dermatomes is desired. The spread of the anesthetic depends upon the location of the catheter tip; the dose, concentration, and volume of anesthetic agent used (see Table 19-3); and whether the mother is head-down, horizontal, or head-up (Setayesh and colleagues, 2001). Individual variations in anatomy or presence of synechiae may preclude a completely satisfactory block. Finally, the catheter tip may migrate from its original location during the course of labor.
One example of the sequential steps and techniques for performance of epidural analgesia is detailed in Table 19-6. Before injection of the local anesthetic agent's therapeutic dose, a test dose is given. The woman is observed for features of toxicity from intravascular injection and for signs of spinal blockade from subarachnoid injection. If these are absent, only then is a full dose given. Analgesia is maintained by intermittent boluses of similar volume, or small volumes of the drug are delivered continuously by infusion pump (Halpern and Carvalho, 2009). The addition of small doses of a short-acting narcotic—fentanyl or sufentanil—has been shown to improve analgesic efficacy while avoiding motor blockade (Chestnut and colleagues, 1988). Appropriate resuscitation equipment and drugs must be available during administration of epidural analgesia.
Table 19-6. Technique for Labor Epidural Analgesia |Favorite Table|Download (.pdf)
Table 19-6. Technique for Labor Epidural Analgesia
Informed consent is obtained, and the obstetrician consulted.
Monitoring includes the following:
- Blood pressure every 1 to 2 minutes for 15 minutes after giving a bolus of local anesthetic.
- Continuous maternal heart rate monitoring during analgesia induction.
- Continuous fetal heart rate monitoring.
- Continual verbal communication.
Hydration with 500 to 1000 mL of lactated Ringer solution.
The woman assumes a lateral decubitus or sitting position.
The epidural space is identified with a loss-of-resistance technique.
The epidural catheter is threaded 3 to 5 cm into the epidural space.
A test dose of 3 mL of 1.5% lidocaine with 1:200,000 epinephrine or 3 mL of 0.25% bupivacaine with 1:200,000 epinephrine is injected after careful aspiration to avert intravascular injection and after a uterine contraction. This minimizes the chance of confusing tachycardia that results from labor pain with that of tachycardia from intravenous injection of the test dose.
If the test dose is negative, one or two 5-mL doses of 0.25% bupivacaine are injected to achieve a sensory T10 level.
After 15 to 20 minutes, the block is assessed using loss of sensation to cold or pinprick. If no block is evident, the catheter is replaced. If the block is asymmetrical, the epidural catheter is withdrawn 0.5 to 1.0 cm and an additional 3 to 5 mL of 0.25% bupivacaine is injected. If the block remains inadequate, the catheter is replaced.
The woman is positioned in the lateral or semilateral position to avoid aortocaval compression.
Subsequently, maternal blood pressure is recorded every 5 to 15 minutes. The fetal heart rate is monitored continuously.
The level of analgesia and intensity of motor blockade are assessed at least hourly.
Epidural analgesia usually provides unparalleled relief from the pain of labor and delivery. That said, as shown in Table 19-4, there are certain problems inherent in its use. As with spinal blockade, it is imperative that close monitoring, including the level of analgesia, be performed by trained personnel.
Dural puncture with inadvertent subarachnoid injection may cause total spinal blockade. Sprigge and Harper (2008) cited an incidence of 0.91 percent recognized accidental dural punctures at the time of epidural analgesia in more than 18,000 women. Personnel and facilities must be immediately available to manage this complication as described in Spinal (Postdural Puncture) Headache.
Using currently popular continuous epidural infusion regimens such as 0.125-percent bupivacaine with 2-mg/mL fentanyl, 90 percent of women rate their pain relief as good to excellent (Sharma and colleagues, 1997). Alternatively, a few women find epidural analgesia to be inadequate for labor. In a study of almost 2000 parturients, Hess and associates (2001) found that approximately 12 percent complained of three or more episodes of pain or pressure. Risk factors for such breakthrough pain included nulliparity, heavier fetal weights, and epidural catheter placement at an earlier cervical dilatation. Dresner and colleagues (2006) reported that epidural analgesia was more likely to fail as body mass index increased. If the epidural analgesia is allowed to dissipate before another injection of anesthetic drug, subsequent pain relief may be delayed, incomplete, or both.
In some women, epidural analgesia is not sufficient for cesarean delivery. For example, in the MFMU Network study cited earlier, 4 percent of women initially given epidural analgesia required a general anesthetic for cesarean delivery (Bloom and colleagues, 2005). Also, at times, perineal analgesia for delivery is difficult to obtain, especially with the lumbar epidural technique. When this situation is encountered, pudendal block or systemic analgesia or rarely general anesthesia may be added.
Sympathetic blockade from epidurally injected analgesic agents may cause hypotension and decreased cardiac output. In normal pregnant women, hypotension induced by epidural analgesia usually can be prevented by rapid infusion of 500 to 1000 mL of crystalloid solution as described for spinal analgesia. Danilenko-Dixon and associates (1996) showed that maintaining a lateral position minimized hypotension compared with the supine position. Despite these precautions, hypotension is the most common side effect and is severe enough to require treatment in a third of women (Sharma and colleagues, 1997).
Central Nervous Stimulation
Convulsions are an uncommon but serious complication, the immediate management of which was described previously. Also cited was the case described by Smarkusky and co-workers (2006) of acute onset of intrapartum headache due to a postdural pneumocephalus.
Since the observation by Fusi and associates (1989) that the mean temperature increased in laboring women given epidural analgesia, a number of randomized and retrospective cohort studies have confirmed that some women develop intrapartum fever following this procedure. Many studies are limited by inability to control for other risk factors, such as length of labor, duration of ruptured membranes, and number of vaginal examinations (Yancey and co-workers, 2001a). With this in mind, the frequency of intrapartum fever associated with epidural analgesia was found by Lieberman and O'Donoghue (2002) to be 10 to 15 percent above the baseline rate.
The two general theories concerning the etiology of maternal hyperthermia are maternal-fetal infection or dysregulation of body temperature. Dashe and co-workers (1999) studied placental histopathology in laboring women given epidural analgesia and identified intrapartum fever only when there was placental inflammation. This suggests that fever is due to infection. The other proposed mechanisms include alteration of the hypothalamic thermoregulatory set point, impairment of peripheral thermoreceptor input to the central nervous system with selective blockage of warm stimuli, or imbalance between heat production and heat loss (Yancey and co-workers, 2001a). To support this theory, Goetzl and colleagues (2007) reported that hyperthermia is seen in a minority of women and that it develops soon after epidural injection. Whatever the mechanism, women with persistent fever are usually treated with antimicrobials for presumed chorioamnionitis.
An association between epidural analgesia and back pain has been reported by some, but not all (Breen, 1994; Howell, 2001; MacArthur, 1997, and all their colleagues). In a prospective cohort study, Butler and Fuller (1998) reported that back pain after delivery was common with epidural analgesia, however, persistent pain was uncommon. Based on their systematic review, Lieberman and O'Donoghue (2002) concluded that available data do not support an association between epidural analgesia and development of de novo, long-term backache.
A spinal or epidural hematoma rarely complicates placement of an epidural catheter (Grant, 2007). Epidural abscesses are equally rare (Darouiche, 2006). Uncommonly, the plastic epidural catheter is sheared off (Noblett and co-workers, 2007).
Most studies, including the combined five randomized trials from Parkland Hospital shown in Table 19-7, report that epidural analgesia prolongs labor and increases the use of oxytocin stimulation. Alexander and associates (2002) examined the effects of epidural analgesia on the Friedman (1955) labor curve described in Chapter 17, Active-Phase Abnormalities. There were 459 nulliparas randomly assigned to patient-controlled epidural analgesia or patient-controlled intravenous meperidine. Compared with Friedman's original criteria, epidural analgesia prolonged the active phase of labor by 1 hour. As shown in Table 19-7, epidural analgesia also increases the need for operative vaginal instrumented delivery because of prolonged second-stage labor, but importantly, without adverse neonatal effects (Chestnut, 1999; Thorp and Breedlove, 1996). A more contemporaneous concern is perineal trauma associated with instrumented delivery. This relationship is discussed in detail in Chapter 17, Laceration Risks and Morbidity and Chapter 23, Lacerations and Episiotomy.
Table 19-7. Selected Labor Events in 2703 Nulliparous Women Randomized to Epidural Analgesia or Intravenous Meperidine Analgesia |Favorite Table|Download (.pdf)
Table 19-7. Selected Labor Events in 2703 Nulliparous Women Randomized to Epidural Analgesia or Intravenous Meperidine Analgesia
Epidural Analgesia (n = 1339)
Intravenous Meperidine (n = 1364)
First-stage duration (hr)b
8.1 ± 5
7.5 ± 5
Second-stage duration (min)
60 ± 56
47 ± 57
Oxytocin after analgesia
Type of delivery
Hill and colleagues (2003) examined the effects of epidural analgesia with 0.25-percent bupivacaine on fetal heart rate patterns. Compared with intravenous meperidine, no deleterious effects were identified. In fact, reduced beat-to-beat variability and fewer accelerations were more common in fetuses whose mothers received meperidine (see Chap. 18, Cardiac Arrhythmia). Based on their systematic review of eight studies, Reynolds and co-workers (2002) reported that epidural analgesia was associated with improved neonatal acid-base status compared with meperidine.
A more contentious issue in the past was whether epidural analgesia increased the risk for cesarean delivery. Evidence that it did was from the era when dense blocks of local anesthetic agents were used that impaired motor function and therefore likely contributed to increased rates of cesarean delivery. As techniques were refined, many investigators were of the opinion that epidural administration of dilute anesthetic solutions did not increase cesarean delivery rates (Chestnut, 1997; Thompson and colleagues, 1998). Several studies conducted at Parkland Hospital were designed to answer this and related questions. From 1995 to 2002, a total of 2703 nulliparous women at term and in spontaneous labor were enrolled in five trials to evaluate epidural analgesia techniques compared with methods for administration of intravenous meperidine. The results from these are summarized in Figure 19-5 and show that epidural analgesia does not significantly increase cesarean delivery rates.
Results of five studies comparing the incidence of cesarean delivery in women given either epidural analgesia or intravenous meperidine. The individual odds ratios (ORs) with 95-percent confidence intervals (CIs) for each randomized study, as well as overall crude and adjusted ORs with 95-percent CIs, are shown. An OR of less than 1.0 favored epidural over meperidine analgesia. (From Sharma and associates, 2004, with permission.)
Yancey and co-workers (1999) described the effects of an on-demand labor epidural analgesia service at Tripler Army Hospital in Hawaii. This followed a policy change in military medical centers. As a result, the incidence of labor epidural analgesia increased from 1 percent before the policy to 60 percent within 2 years. The primary cesarean delivery rate was 13.4 percent before and 13.2 percent after this dramatic change. In a follow-up study, Yancey and co-workers (2001b) reported that fetal malpresentations at vaginal delivery were not more common after epidural usage increased. The only significant difference that they found was an increased duration of second-stage labor of approximately 25 minutes (Zhang and co-workers, 2001).
Based on these randomized studies and a meta-analysis of 14 such trials, Sharma and Leveno (2003) and Leighton and Halpern (2002) concluded that epidural analgesia is not associated with an increased rate of cesarean deliveries.
Timing of Epidural Placement
In several retrospective studies, epidural placement in early labor was linked to an increased risk of cesarean delivery (Lieberman, 1996; Rogers, 1999; Seyb, 1999, and all their co-workers). These observations prompted at least five randomized trials, which showed that timing of epidural placement has no effect on the risk of cesarean birth, forceps delivery, or fetal malposition (Chestnut, 1994a, b; Luxman, 1998; Ohel, 2006; Wong, 2005, 2009, and all their associates). Thus, withholding epidural placement until some arbitrary cervical dilation has been reached is unsupportable and serves only to deny women maximal labor pain relief.
The relative safety of epidural analgesia is attested to by the extraordinary experiences reported by Crawford (1985) from the Birmingham Maternity Hospital in England. From 1968 through 1985, more than 26,000 women were given epidural analgesia for labor, and there were no maternal deaths. The nine potentially life-threatening complications followed either inadvertent intravenous or intrathecal injection of lidocaine, bupivacaine, or both. Similarly, according to the Confidential Enquiries into Maternal Deaths in the United Kingdom between 2003 and 2005, there were only a few anesthesia-related deaths associated with epidural use (Lewis, 2007).
There were no anesthesia-related maternal deaths among nearly 20,000 women who received epidural analgesia in the MFMU Network study cited earlier (Bloom and colleagues, 2005). And finally, Ruppen and associates (2006) reviewed data from 27 studies involving 1.4 million pregnant women who received epidural analgesia. They calculated risks of 1:145,000 for deep epidural infection, 1:168,000 for epidural hematoma, and 1:240,000 for persistent neurological injury.
As with spinal analgesia, contraindications to epidural analgesia include actual or anticipated serious maternal hemorrhage, infection at or near the sites for puncture, and suspicion of neurological disease (see Table 19-5).
Although low platelet counts are intuitively worrisome, the level at which epidural bleeding might develop is unknown according to the American Society of Anesthesiologists Task Force on Obstetrical Anesthesia (2007). Epidural hematomas are extremely rare, and incidence of nerve damage from a hematoma is estimated to be 1 in 150,000 (Grant, 2007). The American College of Obstetricians and Gynecologists (2002) has concluded that women with a platelet count of 50,000 to 100,000/μL may be candidates for regional analgesia.
Women receiving anticoagulation therapy who are given regional analgesia are at increased risk for spinal cord hematoma and compression (see Chap. 47, Anticoagulation with Warfarins). The American College of Obstetricians and Gynecologists (2002) has concluded the following:
Women receiving unfractionated heparin therapy should be able to receive regional analgesia if they have a normal activated partial thromboplastin time (aPTT)
Women receiving prophylactic doses of unfractionated heparin or low-dose aspirin are not at increased risk and can be offered regional analgesia
For women receiving once-daily low-dose low-molecular-weight heparin, regional analgesia should not be placed until 12 hours after the last injection
Low-molecular-weight heparin should be withheld for at least 2 hours after the removal of an epidural catheter
The safety of regional analgesia in women receiving twice-daily low-molecular-weight heparin has not been studied sufficiently. It is not known whether delaying regional analgesia for 24 hours after the last injection is adequate.
Potential concerns with epidural analgesia in those with severe preeclampsia include hypotension as well as hypertension from pressor agents given to correct hypotension. Additionally, there is the potential for pulmonary edema following infusion of large volumes of crystalloid. These are outweighed by disadvantages of general anesthesia. Tracheal intubation may be difficult because of upper airway edema. Moreover, general anesthesia can lead to severe, sudden hypertension that can cause pulmonary or cerebral edema or intracranial hemorrhage.
With improved techniques for infusion of dilute local anesthetics into the epidural space, most obstetricians and obstetrical anesthesiologists have come to favor epidural blockade for labor and delivery in women with severe preeclampsia (Cheek and Samuels, 1991; Gambling and Writer, 1999; Gutsche, 1986). There seems to be no argument that epidural analgesia for women with severe preeclampsia-eclampsia can be safely used when specially trained anesthesiologists and obstetricians are responsible for the woman and her fetus (American College of Obstetricians and Gynecologists, 2002; Cunningham and Leveno, 1995). In a study from Parkland Hospital, Lucas and colleagues (2001) randomly assigned 738 women with hypertension to epidural analgesia or patient-controlled intravenous analgesia during labor. A standardized protocol for prehydration, incremental epidural administration, and ephedrine use was employed. They concluded that labor epidural analgesia was safe in women with hypertensive disorders. In a similar study from the University of Alabama at Birmingham, Head and colleagues (2002) randomly assigned 116 women with severe preeclampsia to receive either intrapartum epidural or patient-controlled intravenous opioid analgesia. Epidural analgesia provided superior pain relief without a significant increase in maternal or neonatal complications.
Intravenous Fluid Preload
Women with severe preeclampsia have remarkably diminished intravascular volume compared with normal pregnancy (Zeeman and colleagues, 2009). Conversely, total body water is increased because of the capillary leak caused by endothelial cell activation (see Chap. 34, Endothelial Cell Activation). This imbalance is manifested as pathological peripheral edema, proteinuria, ascites, and total lung water. For all of these reasons, aggressive volume replacement increases the risk for pulmonary edema, especially in the first 72 hours postpartum (Clark and colleagues, 1985; Cotton and associates, 1986). In one study, Hogg and associates (1999) reported that 3.5 percent of women with severe preeclampsia developed pulmonary edema when preloaded without a protocol limitation to volume. Importantly, this risk can be reduced or obviated with judicious prehydration—usually with 500 to 1000 mL of crystalloid solution. Specifically, in the study by Lucas and colleagues (2001) cited earlier, there were no instances of pulmonary edema among the women in whom crystalloid preload was limited to 500 mL. Moreover, vasodilation produced by epidural blockade is less abrupt if the analgesia level is achieved slowly with dilute solutions of local anesthetic agents. This allows maintenance of blood pressure while simultaneously avoiding infusion of large volumes of crystalloid.
With vigorous intravenous crystalloid therapy, there is also concern about development of cerebral edema (see Chap. 34, Cerebral Edema). Moreover, Heller and co-workers (1983) demonstrated that most cases of pharyngolaryngeal edema were related to aggressive volume therapy.
Epidural Opiate Analgesia
Injection of opiates into the epidural space to relieve pain from labor has become popular. Their mechanism of action derives from interaction with specific receptors in the dorsal horn and dorsal roots. Opiates alone usually will not provide adequate analgesia, and they most often are given with a local anesthetic agent such as bupivacaine. The major advantages of using such a combination are the rapid onset of pain relief, a decrease in shivering, and less dense motor blockade (Meister and colleagues, 2000). Side effects are common and include pruritus and urinary retention. Immediate or delayed respiratory depression is worrisome (Ackerman and colleagues, 1992). Naloxone, given intravenously, will abolish these symptoms without affecting the analgesic action.