Increase in heart rate (15-25%) and cardiac output (up to 50%).

  Decrease in vascular resistance in the uterine, renal, and other vascular beds.

  Compression of the lower aorta in the supine position may further decrease uteroplacental perfusion and result in fetal asphyxia.

  For the above reason, significant hypotension is more likely to occur in the pregnant than in the nonpregnant woman having regional anesthesia, necessitating uterine displacement or lateral pelvic tilt maneuvers, intravascular preloading, and ready availability of vasopressors.

        From the second trimester, aortocaval compression by the enlarged uterus becomes progressively more important, reaching its maximum effect at 36-38 weeks, after which it may decrease as the fetal head descends into the pelvis.³ Cardiac output may decrease when patients are in the supine position but not in the lateral decubitus position. Venous occlusion by the growing fetus causes supine hypotensive syndrome in 10% of pregnant women and manifests as maternal tachycardia, arterial hypotension, faintness, and pallor.⁴ Compression of the lower aorta in this position may further decrease uteroplacental perfusion and result in fetal asphyxia. Uterine displacement or lateral pelvic tilt should be applied routinely during anesthetic management of the pregnant patient.

        Changes in the electrocardiogram are common in late pregnancy and consist of left axis deviation (caused by the upward displacement of the heart by the gravid uterus). There is also a tendency toward premature atrial contractions, sinus tachycardia, and paroxysmal supraventricular tachycardia.

Changes in the Respiratory System

Minute ventilation increases from the beginning of pregnancy to a maximum of 50% above normal by term.⁵ This is mostly a result of a 40% increase in tidal volume and a small increase in respiratory rate. Dead space does not change significantly during pregnancy; thus, alveolar ventilation is increased by 70% at term. After delivery, as blood progesterone levels decline, ventilation returns to normal within 1–3 weeks.⁶

        Elevation of the diaphragm occurs with increase in the size of the uterus. Expiratory reserve volume, residual volume, and functional residual capacity decrease by the third semester of pregnancy.⁵ However, because there is also an increase in inspiratory reserve volume, total lung capacity remains unchanged. A decreased functional residual capacity is typically asymptomatic in healthy parturients. Those with preexisting alterations in closing volume as a result of smoking, obesity, scoliosis, or other pulmonary disease may experience early airway closure with advancing pregnancy, leading to hypoxemia. The Trendelenburg and supine positions also exacerbate the abnormal relationship between closing volume and functional residual capacity. The residual volume and functional residual capacity return to normal shortly after delivery.

        Pregnant women often have difficulty with nasal breathing. Friability of the mucous membranes during pregnancy can cause severe bleeding, especially on airway instrumentation. These changes are caused by increase in extracellular fluid and vascular engorgement. It may also be difficult to perform a laryngoscopy in obese, short-necked parturients with enlarged breasts. Use of a short-handled laryngoscope has proved helpful.

Clinical Pearls

Metabolic Changes

Oxygen consumption increases during early pregnancy, with an overall increase of 20% by term. Regardless, increased alveolar ventilation occurring during pregnancy actually leads to a reduction in the partial pressure of carbon dioxide in arterial blood (Paco₂) to 32 mm Hg and an increase in the partial pressure of oxygen in arterial blood (Pao₂) to 106 mm Hg. The plasma buffer base decreases from 47 to 42 mEq; consequently, the pH remains practically unchanged. The maternal uptake and elimination of inhalational anesthetics are enhanced because of the increased alveolar ventilation and decreased FRC. However, the decreased functional residual capacity and increased metabolic rate predispose the mother to development of hypoxemia during periods of apnea/ hypoventilation.⁷

Changes in the Gastrointestinal System

Enhanced progesterone production causes decreased gastrointestinal motility and slower absorption of food. Gastric secretions are more acidic, lower esophageal sphincter one is decreased, and a delay in gastric emptying can be demonstrated by the end of the first trimester.⁸ Uterine growth leads to upward displacement and rotation of the stomach, with increased pressure and a further delay in gastric emptying. By the 34th week, evacuation of a watery meal may be prolonged by 60%.⁹ Pain, anxiety, and administration of opioids (systemic or neuraxial) and belladonna alkaloids may further exacerbate this delay.

        The risk of regurgitation on induction of general anesthesia depends, in part, on the gradient between the lower esophageal sphincter and intragastric pressures. In parturients with “heartburn,” the lower esophageal sphincter tone is greatly reduced.¹⁰ The efficacy of prophylactic nonparticulate antacids is diminished by inadequate mixing with gastric contents, improper timing of administration, and the tendency for antacids to increase gastric volume. Administration of histamine (H₂)-receptor antagonists, such as cimetidine and ranitidine, requires careful timing. A good case can be made for the administration of IV metoclopramide before elective cesarean section delivery. This dopamine antagonist hastens gastric emptying and increases resting lower esophageal sphincter tone in both nonpregnant and pregnant women.¹¹ However, conflicting reports have appeared on its efficacy and on the frequency of side effects, such as extrapyramidal reactions and transient neurologic dysfunction.^{12, 13} No routine prophylactic regimen can be recommended with certainty.

Endocrine Changes Influencing Plasma Volume, Blood Composition, & Glucose Metabolism

Plasma volume and total blood volume begin to increase in early gestation, resulting in an increase of 40-50% and 25-40% respectively, at term. These changes are due to an increased mineralocorticoid activity during pregnancy, which results in sodium retention and increased body water content.¹⁴ The relatively smaller increase in red blood cell volume (20%) accounts for a relative reduction in hemoglobin (to 11-12 g/L and hematocrit (to 35%); the platelet count, however, remains unchanged. Plasma fibrinogen concentrations increase during normal pregnancy by approximately 50%, whereas clotting factor activity is variable.¹⁵ Serum cholinesterase activity declines to a level of 20% below normal by term and reaches a nadir in the puerperium. The net effects of these changes in the serum cholinesterase is of negligible relevance to the metabolism of clinically used doses of succinylcholine or ester-type local anesthetics (2-choloroprocaine).^{16, 17} The albumin-globulin ratio declines because of the relatively greater reduction in albumin concentration. A decrease in serum protein concentration may be clinically significant in that the free fractions of protein-bound drugs can be expected to increase.

        Human placental lactogen and cortisol increase the tendency to hyperglycemia and ketosis, which may exacerbate preexisting diabetes mellitus. The patient–s ability to handle a glucose load is decreased, and the transplacental passage of glucose may stimulate fetal secretion of insulin, leading in turn to neonatal hypoglycemia in the immediate postpartum period.¹⁸

Altered Drug Responses in Pregnancy

Pregnancy results in a progesterone-mediated increase in neural sensitivity to local anesthetics.¹⁹ Lower doses oflocal anesthetic are needed per dermatomal segment of epidural or spinal block. This has been attributed to an increased spread of local anesthetic in the epidural and subarachnoid spaces as a result of epidural venous engorgement and enhanced sensitivity to local anesthetic block due to progesterone. The minimum alveolar concentration for inhalational agents is decreased by 8-12 weeks of gestation and may be related to an increase in progesterone levels.²⁰

Clinical Pearls

        PLACENTAL TRANSFER OF LOCAL ANESTHETICS

Local anesthetics readily cross the placenta by simple diffusion. Several factors influence the placental transfer of drugs, including the physicochemical characteristics of the drug itself, maternal drug concentrations in the plasma, properties of the placenta, and hemodynamic events within the fetomaternal unit.

        Highly lipid-soluble drugs, such as local anesthetics, cross biologic membranes more readily, and the degree of ionization is important because the nonionized moiety of a drug is more lipophilic than the ionized drug. Local anesthetics are weak bases, with a relatively low degree of ionization and considerable lipid solubility. The relative concentrations of drug existing in the nonionized and ionized forms can be estimated from the Henderson-Hasselbalch equation:

        The ratio of base to cation becomes particularly important with local anesthetics because the nonionized form penetrates tissue barriers, whereas the ionized form is pharmacologically active in blocking nerve conduction. The pKa is the pH at which the concentrations of free base and cation are equal. For the amide local anesthetics, the pKa values (7.7-8.1) are sufficiently close to physiologic pH so that changes in maternal or fetal biochemical status may significantly alter the proportion of ionized and nonionized drug (Figure 53–1). At steady state, the concentrations of nonionized local anesthetics in the fetal and maternal plasma are equal. With fetal acidosis, there is a greater tendency for drug to exist in the ionized form, which cannot diffuse back across the placenta. This causes a larger total amount oflocal anesthetic to accumulate in the fetal plasma and tissues. This is called ion trapping.²¹

Clinical Pearls

        The effects of maternal plasma protein binding on the rate and amount of local anesthetic accumulating in the fetus are inadequately understood. Animal studies have shown that the transfer rate is slower for drugs that are extensively bound to maternal plasma proteins such as bupivacaine.^22–23 However, with prolonged administration of highly proteinbound drugs such as bupivacaine, substantial accumulation of drug can occur in the fetus.²⁴

        The concentration gradient of free drug between the maternal and fetal blood is a significant factor. On the maternal side, the dose administered, the mode and site of administration, and the use of vasoconstrictors can influence fetal exposure. The rates of distribution, metabolism, and excretion of the drug, which may vary, are equally important. Higher doses result in higher maternal blood concentrations. The absorption rate can vary with the site of injection. For instance, an IV bolus results in the highest blood concentrations. It was believed that intrathecal administration resulted in negligible plasma concentrations oflocal anesthetics. However, we now know that spinal anesthesia induced with 75 mg lidocaine results in maternal plasma concentrations that are similar to those reported by others after epidural anesthesia.²⁵ Furthermore, significant levels of the drug can be found in the umbilical vein at birth.

        Repeated administration can result in high maternal blood concentrations, depending on the dose and frequency of reinjection, in addition to the kinetic characteristics of the drug. The half-life of amide local anesthetic agents is relatively long, so that repeated injection may lead to accumulation in the maternal plasma²⁶ (Figure 53–2). In contrast, 2-chloroprocaine, an ester local anesthetic, undergoes rapid enzymatic hydrolysis in the presence of pseudocholinesterase. After epidural injection, the mean half-life in the mother is approximately 3 minutes; after reinjection, 2-Chloroprocaine is the only drug that is metabolized in the fetal blood so quickly that even with acidosis, substantial exposure in the fetus is avoided.²⁷

Figure 53–1. Chemical structures of local anesthetics.

Figure 53–2. Increased maternal blood concentration after repeated doses of mepivacaine.

        Pregnancy is associated with physiologic changes, which also may influence maternal pharmacokinetics and the action of anesthetic drugs. These changes may be progressive during the course of gestation and are often difficult to predict. Nonetheless, the elimination half-life of bupivacaine after epidural injection has been shown to be similar in pregnant and nonpregnant women.²⁸

        Fetal regional blood flow changes can also affect the amount of drug taken up by individual organs. For example, during asphyxia and acidosis, a greater proportion of the fetal cardiac output perfuses the fetal brain, heart, and placenta. Infusion of lidocaine resulted in increased drug uptake in the heart, brain, and liver of asphyxiated baboon fetuses compared with nonasphyxiated control fetuses.²⁹

Risk of Drug Exposure: Fetus versus Newborn

The fetus can excrete local anesthetics back into the maternal circulation after the concentration gradient of the free drug across the placenta has been reversed. This may occur even if the total plasma drug concentration in the mother exceeds that in the fetus, because there is lower protein binding in fetal plasma.²³

        Term as well as preterm infants have the hepatic enzymes necessary for the biotransformation of amide local anesthetics. In a comparative study, pharmacokinetics of lidocaine among adult ewes and fetal/neonatal lambs indicated that the metabolic clearance in the newborn was similar to, and renal clearance greater than, that in the adult.³⁰ However, the half-life was longer in the newborn related to a greater volume of distribution and tissue uptake, so that at any given moment the neonate–s liver and kidneys are exposed to a smaller fraction of lidocaine accumulated in the body. Similar results have been reported in another study involving lidocaine administration to human infants in a neonatal intensive care unit.³¹

        Neonatal depression occurs at blood concentrations of mepivacaine or lidocaine that are approximately 50% less than those producing systemic toxicity in the adult. However, infants accidentally injected in utero with mepivacaine (intended for maternal caudal anesthesia) stopped convulsing when the mepivacaine level decreased below the threshold for convulsions in the adult.³² The relative central nervous toxicity and cardiorespiratory toxicity of local anesthetics have been studied in sheep.³³ The doses required to produce toxicity in the fetus and newborn lamb were greater than those required in the ewe. In the fetus, this difference was attributed to placental clearance of drug into the mother and better maintenance of blood gas tensions during convulsions, whereas in the newborn lamb, a larger volume of distribution was probably responsible for the higher doses needed to induce toxic effects.

        It has been suggested that bupivacaine may be implicated as a possible cause of neonatal jaundice because its high affinity for fetal erythrocyte membranes resulting in a decrease in filterability and deformability renders subjects more prone to hemolysis. However, a more recent study has failed to show demonstrable bilirubin production in newborns whose mothers were given bupivacaine for epidural anesthesia during labor and delivery.³⁴

        Neurobehavioral studies have revealed subtle changes in newborn neurologic and adaptive function with regional anesthesia. In the case of most anesthetic agents, these changes are minor and transient, lasting for only 24-48 hours.³⁵

        ANESTHESIA FOR LABOR & VAGINAL DELIVERY

In the first stage of labor, pain is caused by uterine contractions related to dilation of the cervix and distention of the lower uterine segment. Pain impulses are carried in visceral afferent type C fibers, which accompany the sympathetic nerves. In early labor, only the lower thoracic dermatomes (Tll-12) are affected. However, with progressive cervical dilation during the transition phase, adjacent dermatomes may be involved and pain referred from T10 to LI. During the second stage, additional pain impulses due to distention of the vaginal vault and perineum are carried in the pudendal nerve, which is composed of lower sacral fibers (S2-4).

        Regional analgesia may benefit the mother in other ways beyond relieving pain and anxiety. In animal studies, pain may cause maternal hypertension and reduced uterine blood flow.³⁶ Epidural analgesia blunts the increases in maternal cardiac output, heart rate, and blood pressure that occur with painful uterine contractions and “bearing-down” efforts.³⁷ By reducing maternal secretion of catecholamines, epidural analgesia may convert a previously dysfunctional labor pattern to a normal one.³⁸ Regional analgesia can benefit the fetus by eliminating maternal hyperventilation with pain, which often leads to a reduced fetal arterial oxygen tension owing to a leftward shift of the maternal oxygen-hemoglobin dissociation curve.³⁹

        The most frequently chosen methods for relieving the pain of parturition are psychoprophylaxis, systemic medication, and regional analgesia. Inhalational analgesia, conventional spinal analgesia, and paracervical blockade are less commonly used. General anesthesia is rarely necessary but may be indicated for uterine relaxation in some complicated deliveries.

Systemic Analgesia

The advantages of systemic analgesics include ease of administration and patient acceptability. However, the drug, dose, time, and method of administration must be chosen carefully to avoid maternal or neonatal depression. Drugs used for systemic analgesia are opioids, tranquilizers, and occasionally ketamine.

Systemic Opioids

In the past, meperidine was the most commonly used systemic analgesic to ameliorate pain during the first stage of labor. It can be administered by IV injection (effective analgesia in 5-10 minutes) or intramuscularly (peak effect in 40-50 minutes). It was also commonly used for postoperative pain in the general population. But with the popularity of its administration, disturbing side effects began to emerge. One of the most serious side effects was the occurrence of seizures both from the primary drug effect and from its metabolite, normeperidine. In the pregnant patient at risk for seizures—that is, with pregnancy-induced hypertension or preeclampsia—confusing the picture by the administration of a drug known to cause seizures complicates patient care.^{40, 41} Other side effects are nausea and vomiting, doserelated depression of ventilation, orthostatic hypotension, the potential for neonatal depression, and euphoria out of proportion to the analgesic effect, leading to misuse of the drug.⁴² Meperidine may also cause transient alterations of the fetal heart rate, such as decreased beat-to-beat variability and tachycardia. Among other factors, the risk of neonatal depression is related to the interval from the last drug injection to delivery.⁴³ The placental transfer of an active metabolite, normeperidine, which has a long elimination half-life in the neonate (62 hours), has also been implicated in contributing to neonatal depression and subtle neonatal neurobehavioral dysfunction. Consequently, the use of meperidine has fallen out of favor as an analgesic for labor.

        Experience with the newer synthetic opioids, such as fentanyl and alfentanil, has been limited. Although they are potent, their use during labor is restricted by their short duration of action. For example, a single IV injection of fentanyl, up to 1 mcg/kg, results in prompt pain relief without severe neonatal depression.⁴⁴ These drugs offer an advantage when analgesia of rapid onset but short duration is necessary (eg, with forceps application). For more prolonged analgesia, fentanyl can be administered with patient-controlled delivery devices.⁴⁵ More commonly, fentanyl (15-25 meg) and sufentanil (5-10 meg) have been used with local anesthetics in an initial spinal dose with a local anesthetic during the placement of a continuous spinal-epidural for labor with excellent relief of pain.^46–47

        Remifentanil is an opioid that is rapidly metabolized by serum and tissue cholinesterases, and consequently, has a short (3-minute), context-sensitive half-time.⁴⁸ When used in bolus dosing (0.3-0.8 mcg/kg per bolus), remifentanil has been found to have an acceptable level of maternal side effects and minimal effect on the neonate. Remifentanil crosses the placenta and appears to be either rapidly metabolized or redistributed in the neonate.⁴⁹ In one study, Apgar and neurobehavioral scores were good in neonates whose mothers were given an intravenous infusion of remifentanil, 0.1 mcg- kg/min during cesarean section delivery under epidural anesthesia.⁵⁰ When administered by patient-controlled analgesia, remifentanil has been found to provide better pain relief, equivalent hemodynamic stability, less sedation, and a lesser degree of oxygen desaturation when compared with meperidine.^{49, 51} In countries outside the United States, intermittent nitrous oxide has been used for labor analgesia. When comparing remifentanil with nitrous oxide, remifentanil was found to provide better pain relief with fewer side effects.⁵²

        Opioid agonists-antagonists, such as butorphanol and nalbuphine, have also been used for obstetric analgesia. These drugs have the proposed benefits of a lower incidence of nausea, vomiting, and dysphoria, as well as a “ceiling effect” on depression of ventilation.⁵³ Butorphanol is probably the most popular; unlike meperidine, it is biotransformed into inactive metabolites and has a ceiling effect on depression of ventilation in doses exceeding 2 mg. A potential disadvantage is a high incidence of maternal sedation. The recommended dose is 1-2 mg by IV or IM injection. Nalbuphine 10 mg IV or IM is an alternative to butorphanol.

        Naloxone, a pure opioid antagonist, should not be administered to the mother shortly before delivery to prevent neonatal ventilatory depression because it reverses maternal analgesia at a time when it is most needed. In some instances, naloxone has been reported to cause maternal pulmonary edema and even cardiac arrest. If necessary, the drug should be given directly to the newborn IM (0.1 mg/kg.

Ketamine

Ketamine is a potent analgesic. However, it may also induce unacceptable amnesia that may interfere with the mother–s recollection of the birth. Nonetheless, ketamine is a useful adjuvant to incomplete regional analgesia during vaginal delivery or for obstetric manipulations. In low doses (0.2-0.4 mg/kg), ketamine provides adequate analgesia without causing neonatal depression.

Regional Analgesia Techniques

Regional techniques provide excellent analgesia with minimal depressant effects in mother and fetus. The techniques most commonly used for labor anesthesia include central neuraxial blocks (spinal, epidural, and combined spinal/epidural), paracervical, and pudendal blocks, and, less frequently, lumbar sympathetic blocks. Hypotension resulting from sympathectomy is the most common complication that occurs with central neuraxial blockade. Therefore, maternal blood pressure must be monitored at regular intervals, typically every 2-5 minutes for approximately 15-20 minutes after the initiation of the block and at routine intervals thereafter. Regional analgesia may be contraindicated in the presence of severe coagulopathy, acute hypovolemia, or infection at the site of needle insertion. Chorioamnionitis without sepsis, is not a contraindication to central neuraxial blockade.

Epidural Analgesia

Effective analgesia for the first stage of labor is achieved by blocking the T10-L1 dermatomes with a low concentrations of local anesthetic, often in combination with a lipid-soluble opioid. For the second stage of labor and delivery, because of pain due to vaginal distention and perineal pressure, the block should be extended to include the pudendal segments, S2-4 (Figures 53-3 and 53-4).

Figure 53–3. Pain pathways in a parturient.

        There has been concern that early initiation of epidural analgesia during the latent phase of labor (2-4 cm cervical dilation) may result in prolongation of the first stage of labor and a higher incidence of dystocia and cesarean section delivery, particularly in nulliparous women.^54–57 Generally speaking, the first stage of labor is not prolonged by epidural analgesia, provided that aortocaval compression is avoided.^54-56-58,59 Chestnut et al.^{58, 59} demonstrated that the incidence of cesarean section delivery was no different in nulliparous women having epidural analgesia initiated during the latent phase (at 4 cm dilation) compared with women whose analgesia was initiated during the active phase. Others have shown that epidural analgesia is not associated with an increased incidence of cesarean section delivery compared with IV patient-controlled analgesia in nulliparous women.^55–56 However, a prolongation of the second stage of labor has been reported in nulliparous women, possibly owing to a decrease in expulsive forces or malposition of the vertex.^{54, 59} Thus, with use of epidural analgesia, the American College of Obstetricians and Gynecologists (AC.OG) has defined an abnormally prolonged second stage of labor as longer than 3 hours in nulliparous and 2 hours in multiparous women.⁶⁰ A longer second stage of labor may be minimized by the use of an ultra-dilute local anesthetic solution in combination with opioid.⁶¹ Long-acting amides such as bupivacaine, ropiva- caine, and levobupivacaine are most frequently used because they produce excellent sensory analgesia while sparing motor function, particularly at the low concentrations used for epidural analgesia.

Clinical Pearls

        Analgesia for the first stage of labor may be achieved with 5-10 mL of bupivacaine, ropivacaine, or levobupivacaine (0.125-0.25%) followed by a continuous infusion (8-12 mL/h) of 0.0625% bupivacaine or levobupivacaine, or 0.1% ropivacaine. Fentanyl 1-2 mcg/mL or sufentanil 0.3-0.5 mcg/mL may be added. During the actual delivery, the perineum may be blocked with 10 mL of 0.5% bupivacaine, 1% lidocaine, or, if a rapid effect is required, 2% chloroprocaine in the semirecumbent position.

        There is controversy regarding the need for a test dose when using a dilute solution oflocal anesthetic.^{62, 63} Catheter aspiration alone is not always diagnostic. For that reason, some authors believe that a test dose should be administered to improve detection of an intrathecally or intravascularly placed epidural catheter. If injected into a blood vessel, 15 meg epinephrine results in a change in heart rate of 20-30 bpm with a slight increase in blood pressure within 30 seconds of administration. The duration is approximately 30 seconds. The anesthesiologist should observe the tachometer during the first minute after injection to determine whether an accidental intravascular injection has occurred. Other subtle signs of intravascular injection may include a feeling of apprehension, unease, or palpitations. It is important to fractionate the total dose of local anesthetic and observe the patient at 1-minute intervals.

        Patient-controlled epidural analgesia is a safe and effective alternative to conventional bolus or infusion techniques.⁶⁴ Maternal acceptance is excellent, and demands on anesthesia manpower may be reduced. Initial analgesia is achieved with bolus doses of local anesthetic. Once the mother is comfortable, patient-controlled epidural analgesia may then be started with a maintenance infusion (4-8 mL/h)of local anesthetic (bupivacaine, levobupivacaine, ropivacaine 0.0625-0.125%) with or without opioid (fentanyl 1-2 mcg/mL; sufentanil 0.3-0.5 mcg/mL). The machine may be programmed to administer an epidural demand bolus of 4 mL with a lockout period of 10 minutes between doses.⁶⁴ The caudal rather than the lumbar approach may result in a faster onset of perineal analgesia and therefore may be preferable to the lumbar epidural approach when an imminent vaginal delivery is anticipated. However, caudal analgesia is no longer popular because of occasionally painful needle placement, a high failure rate, potential contamination at the injection site, and risks of accidental fetal injection. Before caudal injection, a digital rectal examination must be performed to exclude needle placement in the fetal presenting part. Low spinal “saddle block” has virtually eliminated the need for caudal anesthesia in modern practice.

Figure 53–4. Dermatomal level of the lower abdomen, perineal area, hip, and thighs.

Spinal Analgesia

A single intrathecal injection for labor analgesia has the benefits of a reliable and rapid onset of neural blockade. However, repeated intrathecal injections may be required for a long labor, thus increasing the risk of postdural puncture headache. In addition, motor block may be uncomfortable for some women and may prolong the second stage of labor.

        Microcatheters were introduced for continuous spinal anesthesia in the 1980s. They were subsequently withdrawn when found to be associated with neurologic deficits, possibly related to maldistribution oflocal anesthetic in the cauda equina region.⁶⁵ Fortunately, in a recent multi-institutional study, no cases of neurologic symptoms occurred after the use of 28-gauge microcatheters for continuous spinal analgesia in laboring women.⁶⁶ Spinal anesthesia is also a safe and effective alternative to general anesthesia for instrumental delivery.

Combined Spinal-Epidural Analgesia

Combined spinal-epidural analgesia is an ideal analgesic technique for use during labor. It combines the rapid, reliable onset of profound analgesia resulting from spinal injection with the flexibility and longer duration of epidural techniques.

Technique

After identification of the epidural space using a conventional (or specialized) epidural needle, a longer (127-mm), pencil-point spinal needle is advanced into the subarachnoid space through the epidural needle (more detail on this technique can be found in Chapter 16). After intrathecal injection, the spinal needle is removed and an epidural catheter inserted. Intrathecal injection of fentanyl 10-25 meg or sufentanil 2.5-5 meg, alone or in combination with 1 mL of isobaric bupivacaine 0.25%, produces profound analgesia lasting for 60-120 minutes with minimal motor block.⁶⁷ Opioid alone may provide sufficient relief for the early latent phase, but almost always the addition of bupivacaine is necessary for satisfactory analgesia during advanced labor. An epidural infusion of bupivacaine 0.03-0.0625% with opioid may be started within 10 minutes of spinal injection. Alternatively, the epidural component may be activated when necessary. Women with hemodynamic stability and preserved motor function who do not require continuous fetal monitoring may ambulate with assistance.^{68, 69} Before ambulation, women should be observed for 30 minutes after intrathecal or epidural drug administration to assess maternal and fetal well-being. A recent study indicated that early administration of combined spinal-epidural analgesia to nulliparous women did not increase the cesarean section delivery rate.⁷⁰

Clinical Pearls

Related posts:

Regional Anesthesia in the Patient with Preexisting Neurologic Disease. The History of Local Anesthesia. Stimulating Catheters. Ultrasound-Assisted Nerve Blocks in Adults. Cutaneous Blocks for the Upper Extremity. Cervical Plexus Block.

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