Providing peripartum analgesia and anesthesia requires an understanding of the physiologic changes during pregnancy and labor; the effects of anesthetics on the mother, fetus, and neonate; and the benefits and risks associated with various anesthetic techniques. The course of labor and delivery and knowledge of high-risk maternal conditions must be clearly understood. These conditions require the ability to provide several analgesic and anesthetic techniques. Lastly, proper training and organization need to exist for potential obstetric emergencies and complications requiring immediate intervention, such as fetal distress and maternal hemorrhage.
Physiologic Changes in Pregnant Women
During pregnancy, labor, and delivery, women undergo significant changes in anatomy and physiology as a result of (1) altered hormonal activity; (2) biochemical changes associated with increasing metabolic demands of a growing fetus, placenta, and uterus; and (3) mechanical displacement by an enlarging uterus.
Cardiovascular System Changes
Changes in the cardiovascular system during pregnancy can be summarized as (1) an increase in intravascular fluid volume; (2) an increase in cardiac output; (3) a decrease in systemic vascular resistance; and (4) the presence of supine aortocaval compression ( Table 33.1 ).
|System Parameter||Value at Term Compared With Nonpregnant Value|
|Intravascular fluid volume||Increased 35%-45%|
|Plasma volume||Increased 45%-55%|
|Erythrocyte volume||Increased 20%-30%|
|Cardiac output||Increased 40%-50%|
|Stroke volume||Increased 25%-30%|
|Heart rate||Increased 15%-25%|
|Systemic vascular resistance||Decreased 20%|
|Pulmonary vascular resistance||Decreased 35%|
|Central venous pressure||No change|
|Pulmonary capillary wedge pressure||No change|
|Femoral venous pressure||Increased 15%-50%|
|Minute ventilation||Increased 45%-50%|
|Tidal volume||Increased 40%-45%|
|Breathing frequency||Increased 0-15%|
|Expiratory reserve volume||Decreased 20%-25%|
|Residual volume||Decreased 15%-20%|
|Functional residual capacity||Decreased 20%|
|Vital capacity||No change|
|Total lung capacity||Decreased 0-5%|
|Arterial blood gases and pH|
|Pa o 2||Normal or slightly increased|
|Pa co 2||Decreased 10 mm Hg|
|pH||No change or minimal alkalosis|
|Oxygen consumption||Increased 20%|
Intravascular Fluid and Hematology
Maternal intravascular fluid volume begins to increase in the first trimester. At term, plasma volume increases about 50% above the nonpregnant state, whereas the erythrocyte volume increases only about 25%. This disproportionate increase in plasma volume accounts for the relative anemia of pregnancy. Yet, the hemoglobin normally remains at 11 g/dL or more. This expanded intravascular fluid volume of 1000 to 1500 mL at term offsets the 300 to 500 mL blood loss that accompanies vaginal delivery and the average 800 to 1000 mL blood loss that accompanies cesarean delivery. In addition, the contracted uterus following delivery causes a form of autotransfusion , often in excess of 500 mL of blood.
The total plasma protein concentration is decreased as a result of the dilutional effect of the increased intravascular fluid volume. Pregnancy is a hypercoagulable state with concentration increases in factors I, VII, VIII, IX, X, and XII and decreases in factors XI, XIII, and antithrombin III. This results in an approximately 20% decrease in prothrombin time (PT) and partial thromboplastin time (PTT). Platelet count may remain normal or decrease 10% by term, and leukocytosis is common.
Cardiac output increases by about 35% by the end of the first trimester and increases to about 50% above baseline by the third trimester because of increases in both stroke volume (25% to 30%) and heart rate (15% to 25%). Additional increases of 10% to 25% in cardiac output occur with the onset of labor during the first stage and 40% in the second stage. The largest increase occurs immediately after delivery, when cardiac output is increased by as much as 80% above prelabor values. This presents a unique postpartum risk for patients with cardiac disease, such as fixed valvular stenosis. Cardiac output decreases within the first hours after delivery and reaches prelabor values about 48 hours postpartum. It then decreases substantially toward prepregnant values by 2 weeks postpartum.
Systemic Vascular Resistance
Although cardiac output and plasma volume increase, arterial blood pressure decreases in an uncomplicated pregnancy secondary to a 20% reduction in systemic vascular resistance at term. Systolic, mean, and diastolic blood pressure may all decrease 5% to 20% by 20 weeks of gestational age and gradually increase slightly toward prepregnant values as the pregnancy progresses further. There is no change in central venous pressure during pregnancy despite the increased plasma volume because of an increase in venous capacitance.
When supine, the gravid uterus can compress the aorta and vena cava. Compression of the vena cava can decrease preload, cardiac output, and systemic blood pressure ( Fig. 33.1 ). At term, the inferior vena cava is almost completely occluded in the supine position, with venous return of blood from the lower extremities through the epidural, azygos, and vertebral veins. In addition, significant aortoiliac artery compression occurs in 15% to 20% of pregnant women. Nearly 15% of pregnant women at term experience significant hypotension in the supine position. Diaphoresis, nausea, vomiting, and changes in cerebration often accompany the hypotension. This constellation of symptoms is termed supine hypotension syndrome . Vena cava compression decreases cardiac output 10% to 20% and may also contribute to lower extremity venous stasis and thereby result in ankle edema, varices, and increased risk of venous thrombosis.
There are significant changes in echocardiography during pregnancy. The heart is displaced anteriorly and leftward. Right-sided chambers increase in size by 20% and left-sided chambers increase in size by 10% to 12% with an associated left ventricular eccentric hypertrophy and increase in ejection fraction. Mitral, tricuspid, and pulmonary valve annuli diameters increase, but the aortic annulus remains the same. Tricuspid and pulmonary valve regurgitation is common, and about 1 in 4 women has mitral regurgitation. In addition, small insignificant pericardial effusions may be present during pregnancy.
Compensatory Responses and Risks
In the supine position, significant arterial hypotension is uncommon because the patient compensates for a decrease in preload by reflex increases in systemic vascular resistance. This compensatory increase in systemic vascular resistance is impaired by regional anesthetic techniques. Consequently, supine positioning is avoided during neuraxial anesthetic administration in the second and third trimesters. Significant lateral tilt is frequently used during labor analgesia and cesarean deliveries to reduce hypotension and preserve fetal circulation by displacing the gravid uterus leftward and off the inferior vena cava ( Fig. 33.2 ). Left uterine displacement can be accomplished by placing the patient in a left lateral position or by elevation of the right hip 10 to 15 cm with a blanket, wedge, or table tilt.
The gravid uterus can also compress the lower abdominal aorta. Arterial hypotension can then occur in the lower extremities, which accounts for systemic blood pressure measurements in the arms not reflective of this decrease. Aortocaval compression decreases uterine and placental blood flow. Even with a healthy uteroplacental unit, prolonged maternal hypotension (more than 25% decrease for an average patient) for longer than 10 to 15 minutes can significantly decrease uterine blood flow (UBF) and lead to progressive fetal acidosis.
The increased venous pressure distal to the level of vena caval compression serves to divert blood return from the lower half of the body via the paravertebral venous plexuses to the azygos vein. Flow from the azygos vein enters the superior vena cava, and cardiac venous return is maintained. Dilation of the epidural veins may increase the rate of unintentional intravascular placement of the epidural catheter. This could lead to accidental intravascular injection of the local anesthetic solution, which can have profound effects on the cardiovascular system and central nervous system (CNS) with potential for complete hemodynamic collapse, seizures, and death. A test dose is administered before dosing an epidural catheter in order to decrease the likelihood of an unintended intravascular placement before initiating neuraxial blockade. This technique is described later in the section “Epidural Analgesia” (also see Chapter 17 ).
Pulmonary System Changes
The most significant changes in the pulmonary system during pregnancy include alterations in (1) the upper airway, (2) minute ventilation, (3) arterial oxygenation, and (4) lung volumes (see Table 33.1 ).
Upper Airway (Also See Chapter 16 )
During pregnancy there is significant capillary engorgement of the mucosal lining of the upper respiratory tract and increased tissue friability. As a result, instrumentation of the upper airway is more likely to cause obstruction from tissue edema and bleeding. Additional care is needed during suctioning, placement of airways (avoid nasal instrumentation if possible), direct laryngoscopy, and intubation. It may be prudent to select a smaller cuffed tracheal tube (6.0 to 6.5 mm internal diameter) because the vocal cords and arytenoids are often edematous. The presence of preeclampsia, upper respiratory tract infections, and active pushing with associated increased venous pressure further exacerbate airway tissue edema making both endotracheal intubation and subsequent ventilation more challenging. In addition, the weight gain associated with pregnancy, particularly in women of short stature or with coexisting obesity (also see Chapter 29 ), can result in difficulty placing the laryngoscope because of a shorter neck and increased breast tissue.
Minute Ventilation and Oxygenation
Minute ventilation is increased about 50% above prepregnant levels during the first trimester and is maintained for the remainder of the pregnancy. This increased minute ventilation is achieved primarily by an increase in tidal volumes, with small increases in the respiratory rate (see Table 33.1 ). Increased circulating levels of progesterone and increased CO 2 production are the likely stimulus for the increased minute ventilation. Resting maternal Pa co 2 decreases from 40 mm Hg to approximately 30 mm Hg during the first trimester as a reflection of the increased minute ventilation. Arterial pH, however, remains only mildly alkalotic (7.42 to 7.44) because of increased renal excretion of bicarbonate ions (HCO 3− of approximately 20 to 21 mEq/L at term).
Early in gestation, maternal Pa o 2 while breathing room air is normally above 100 mm Hg because of the presence of hyperventilation and the associated decrease in alveolar CO 2 . Later, Pa o 2 becomes normal or even slightly decreased, most likely reflecting airway closure and intrapulmonary shunt. Maternal hemoglobin is shifted to the right with the P 50 increasing from 27 to approximately 30 mm Hg.
At term, oxygen consumption is increased by 20%. The added work of labor results in further increases in both minute ventilation and oxygen consumption. During labor, oxygen consumption increases above prelabor rates by 40% during the first stage and 75% during the second stage. The pain of labor can result in severe hyperventilation causing Pa co 2 to decrease below 20 mm Hg. This pain-associated hyperventilation and alkalosis can be attenuated by neuraxial analgesic techniques.
The expiratory reserve volume (ERV) and residual lung volume (RV), in contrast to the early appearance of increased minute ventilation, do not begin to change until about the third month of pregnancy (see Table 33.1 ). With increasing enlargement of the uterus, the diaphragm is forced cephalad, which is primarily responsible for the 20% decrease in functional residual capacity (FRC) present at term. This change is created by approximately equal decreases in the ERV and RV. As a result, FRC can be smaller than closing capacity for many small airways and may cause atelectasis in the supine position. Vital capacity is not significantly changed with pregnancy. The combination of increased minute ventilation and decreased FRC results in a more rapid rate at which changes in the alveolar concentration of inhaled anesthetics can be achieved. Respiratory measures of FEV 1 , FEV 1 /FVC (forced vital capacity), and closing capacity do not change significantly with pregnancy.
During induction of general anesthesia in a pregnant patient, Pa o 2 decreases much more rapidly than in a nonpregnant patient because of decreased oxygen reserve (decreased FRC) and increased oxygen uptake (increased metabolic rate). For these reasons, the administration of supplemental oxygen or preoxygenation prior to general anesthesia is especially critical for patient safety. The pregnant patient should breathe oxygen for 3 minutes before any period of anticipated apnea (such as induction of anesthesia) or take four maximal breaths over the 30 seconds just prior to induction of anesthesia if emergent general anesthesia is needed. In addition, the increased airway edema makes both ventilation and intubation more difficult and further increases the potential for complications and morbidity.
Gastrointestinal changes during pregnancy make women beyond 20 weeks gestation vulnerable to regurgitation, aspiration of gastric contents, and the development of acid pneumonitis. Displacement of the stomach and pylorus cephalad by the enlarged uterus repositions the intra-abdominal portion of the esophagus into the thorax and decreases the competence of the esophageal sphincter. Increased progesterone and estrogen levels of pregnancy further reduce esophageal sphincter tone. During vaginal delivery, gastric pressure is increased by both the gravid uterus and the lithotomy position. Gastrin, which is secreted by the placenta, stimulates gastric hydrogen ion secretion such that the pH of gastric fluid is predictably low in pregnant women. For these reasons, gastric fluid reflux into the esophagus with subsequent esophagitis (heartburn) is common and increases with the pregnancy gestational age. In addition, gastric emptying is delayed with the onset of labor or administration of opioids, further increasing the risk of aspiration.
Regardless of the time interval since the ingestion of food, women in labor must be treated as having a full stomach and an increased risk for pulmonary aspiration of gastric contents. This includes the routine use of nonparticulate antacids, rapid sequence induction, cricoid pressure, and cuffed endotracheal intubation as part of the general anesthesia induction sequence in a pregnant woman after approximately 20 weeks gestational age. Pain, anxiety, and opioids administered during labor can further slow gastric emptying beyond an already prolonged transit time. Epidural analgesia using local anesthetics does not delay gastric emptying, but using epidural boluses of fentanyl does. The low pH of aspirated gastric fluid is important in the production and severity of acid pneumonitis and is the basis for the administration of antacids to pregnant women before induction of anesthesia. Current American Society of Anesthesiologists (ASA) guidelines recommend the “timely administration of oral nonparticulate antacids, intravenous (IV) H 2 -receptor antagonists, and/or metoclopramide for aspiration prophylaxis” prior to the induction of anesthesia in pregnant women. Nonparticulate antacids such as sodium citrate (30 mL) work rapidly. Metoclopramide can significantly decrease gastric volume in as little as 15 minutes, although gastric hypomotility associated with prior opioid administration reduces the effectiveness of metoclopramide. H 2 -receptor antagonists increase gastric fluid pH in pregnant women approximately 1 hour after administration without producing adverse effects. Antacids plus H 2 -antagonists are better than antacids alone in decreasing gastric acidity.
Nervous System Changes
Volatile anesthetic requirements (minimum alveolar concentration, or MAC) decrease up to 40% during pregnancy in animal studies and 28% in humans within the first trimester of pregnancy. However, an electroencephalographic monitoring study illustrated that the anesthetic effects of sevoflurane on the brain are similar in pregnant and nonpregnant women. Consequently the magnitude and mechanism of the decreased anesthetic requirement remains uncertain. A clinical implication of this decreased MAC is that alveolar anesthetic concentrations that would not routinely produce unconsciousness may approximate anesthetizing concentrations in pregnant women. Judicious administration of anesthetics that depress the CNS is required to prevent unintended impairment of upper airway reflexes and add to the already increased risk of aspiration of gastric contents.
Pregnant patients are more sensitive to the local anesthetics used during neuraxial blockade. There is a decrease in local anesthetic dose needed for epidural or spinal anesthesia in pregnant women at term. The observation of decreased neuraxial local anesthetic doses as early as the first trimester suggests a role for both anatomic and biochemical changes. This decreased requirement is occurring before significant aortocaval compression and decreases in the volume of the epidural space from dilated veins. Although this increased sensitivity is likely based on hormonal changes, mechanical changes may also be involved. Engorgement of epidural veins as intra-abdominal pressure increases with progressive enlargement of the uterus results in a decrease in both the size of the epidural space and volume of cerebrospinal fluid (CSF) in the subarachnoid space. The decreased volume of these spaces facilitates the spread of local anesthetics. Yet, the CSF pressure itself does not increase with pregnancy.
Renal blood flow and the glomerular filtration rate are increased about 50% to 60% by the third month of pregnancy and do not return to prepregnant levels until 3 months postpartum. Therefore, the normal upper limits in blood urea nitrogen and serum creatinine concentrations are decreased about 50% in pregnant women. There is decreased tubular resorption of both protein and glucose, and excretion of them in the urine is common. In a 24-hour urine collection, findings of less than 300 mg protein or 10 g glucose are considered the upper limits of normal in pregnancy.
Liver blood flow does not change significantly with pregnancy. Plasma protein concentrations are reduced during pregnancy, and decreased serum albumin levels can increase free blood levels of highly protein-bound drugs. Slightly increased liver function tests are common in the third trimester. Plasma cholinesterase (pseudocholinesterase) activity is decreased about 25% to 30% from the tenth week of gestation up to 6 weeks postpartum. Yet, this decreased activity is likely not sufficient to prolong the neuromuscular blockade of succinylcholine. In addition, incomplete gallbladder emptying and changes in bile composition increase the risk of gallbladder disease during pregnancy. Even without underlying pathologic abnormality, alkaline phosphatase levels double during pregnancy from placental production.
Physiology of the Uteroplacental Circulation
The placenta is the interface of maternal and fetal tissue for the purpose of physiologic exchange. Maternal blood is delivered to the uterus and placenta by two uterine arteries. Nutrient-rich and waste-free blood is transferred from the placenta to the fetus through a single umbilical vein and fetal blood returns to interface with the maternal circulation via two umbilical arteries.
Uterine Blood Flow
UBF increases throughout gestation from about 100 mL/min before pregnancy to 700 mL/min (about 10% of cardiac output) at term gestation. About 80% of the UBF perfuses the intervillous space (placenta) and 20% supports the myometrium. The uterine vasculature has limited autoregulation and remains essentially maximally dilated under normal pregnancy conditions. UBF decreases because of either reduced uterine perfusion pressure or increased umbilical arterial resistance. Decreased perfusion pressure can result from systemic hypotension secondary to hypovolemia, aortocaval compression, or decreased systemic resistance from either general or neuraxial anesthesia. UBF also decreases with increased uterine venous pressure. This can result from vena caval compression (supine position), prolonged or frequent uterine contractions, or significant abdominal musculature contraction (Valsalva maneuver during pushing). Additionally, extreme hypocapnia (Pa co 2 < 20 mm Hg) associated with hyperventilation secondary to labor pain can reduce UBF to the point of fetal hypoxemia and acidosis.
Epidural or spinal anesthesia does not alter UBF as long as maternal hypotension is avoided. Endogenous catecholamines induced by stress or pain and exogenous vasopressors have the capability of increasing uterine arterial resistance and decreasing UBF. The use of phenylephrine (α-adrenergic agonist) to correct maternal hypotension does not influence fetal well-being. Although ephedrine is safe to use to correct maternal hypotension, phenylephrine administration results in less fetal acidosis and base deficit as shown in clinical trials. Although further work is needed to confirm the safety and efficacy of norepinephrine as a vasopressor in obstetric patients before routine clinical use, a 2015 study comparing norepinephrine and phenylephrine for arterial blood pressure maintenance during cesarean delivery noted norepinephrine was associated with a more rapid maternal heart rate and increased cardiac output.
Transfer of oxygen from the mother to the fetus is dependent on a variety of factors including the ratio of maternal UBF to fetal umbilical blood flow, the oxygen partial pressure gradient, the respective hemoglobin concentrations and affinities, the placental diffusing capacity, and the acid-base status of the fetal and maternal blood (Bohr effect). The fetal oxyhemoglobin dissociation curve is left-shifted (greater oxygen affinity) whereas the maternal hemoglobin binding curve is right-shifted (decreased oxygen affinity), resulting in facilitated oxygen transfer to the fetus. The fetal Pa o 2 is normally 40 mm Hg and never more than 60 mm Hg even if the mother is breathing 100% oxygen. This is because the placental exchange to the fetus from the mother represents venous rather than arterial blood. Carbon dioxide readily crosses the placenta and is not limited by diffusion but rather flow.
Placental exchange of most drugs and other substances less than 1000 Da occurs principally by diffusion from the maternal circulation to the fetus and vice versa. Diffusion of a substance across the placenta to the fetus depends on maternal-to-fetal concentration gradients, maternal protein binding, molecular weight, lipid solubility, and the degree of ionization of that substance. Minimizing the maternal blood concentration of a drug is the most important method of limiting the amount that ultimately reaches the fetus.
The large molecular weight and poor lipid solubility of nondepolarizing neuromuscular blocking drugs result in the limited ability of these drugs to cross the placenta (also see Chapter 11 ). Succinylcholine has a low molecular weight but is highly ionized and therefore does not readily cross the placenta. Thus, during administration of a general anesthetic for cesarean delivery, the fetus/neonate is not paralyzed. Additionally, both heparin and glycopyrrolate have significantly limited placental transfer. Placental transfer of barbiturates, local anesthetics, and opioids is facilitated by the relatively low molecular weights of these substances. In general, drugs that readily cross the blood-brain barrier also cross the placenta.
Fetal uptake of a substance that crosses the placenta is affected by the lower pH (0.1 unit) of fetal blood compared to maternal. The lower fetal pH means that weakly basic drugs (local anesthetics, opioids) that cross the placenta in the nonionized form will become ionized in the fetal circulation. Because an ionized drug cannot readily cross the placenta and return to the maternal circulation, this drug will accumulate in the fetal blood against a concentration gradient. Therefore, in an acidotic fetus, larger concentrations of local anesthetic can accumulate (ion trapping), especially during periods of fetal distress. Increased concentrations of local anesthetics in the fetus can result in decreased neonatal neuromuscular tone. If direct maternal intravascular local anesthetic injection occurs, significant fetal toxicity can result in bradycardia, ventricular arrhythmia, acidosis, and severe cardiac depression. Placental transfer and fetal uptake of specific analgesic and anesthetic drugs are detailed in the upcoming sections on “Methods of Labor Analgesia” and “Anesthesia for Cesarean Delivery.”
Characteristics of the Fetal Circulation
The fetal circulation helps protect vital fetal organs from exposure to large concentrations of drugs initially present in umbilical venous blood. For example, about 75% of umbilical venous blood initially passes through the fetal liver, such that significant portions of many drugs are metabolized before reaching the fetal arterial circulation for delivery to the heart and brain. Despite decreased liver enzyme activity in comparison to adults, fetal/neonatal enzyme systems still can metabolize most drugs. Moreover, drugs in the portion of umbilical venous blood that enter the inferior vena cava via the ductus venosus will be diluted by drug-free blood returning from the lower extremities and pelvic viscera of the fetus. These circulatory characteristics decrease the fetal plasma drug concentrations compared to maternal following an IV drug bolus.
Stages of Labor
It is important to understand the stages of labor and when labor can become dysfunctional, resulting in more intervention from the obstetrician. Obstetrics can be predictably unpredictable. A patient may adopt a particular birth plan only to have it change at the outset of labor or after many hours. Labor can occur spontaneously or be induced based on maternal or fetal indications. What constitutes normal labor progress has been more precisely defined. Ideally these changes will prevent cesarean deliveries in the first stage of labor (active stage arrest) when the woman is not yet in active labor.
Labor is a continuous process divided into three stages. The first stage refers to the onset of labor until the cervix is fully dilated. The first stage is further divided into two phases: latent phase and active phase. The latent phase can persist for many hours and in some cases days. Active phase begins at the point when the rate of cervical dilation increases. This usually occurs between 5 to 6 cm dilation. The second stage of labor begins when the cervix is fully dilated and ends when the neonate is born. This stage is referred to as the “pushing and expulsion” stage. Once the neonate is delivered the third and final stage begins and is completed when the placenta is delivered. If progression of labor through the stages is halted or delayed, there is concern for dysfunctional labor and potential for obstetric intervention.
If a woman’s cervix fails to dilate or dilates slowly in the active phase (first stage of labor) despite pharmacologic interventions, this is considered an active phase arrest and will result in a cesarean delivery. Arrest of descent occurs during the second stage of labor, when the neonate is unable to deliver vaginally. The mode of delivery depends on what pelvic level the arrest of descent occurs and the position of the neonatal head. If the neonate is low enough in the pelvis, the obstetrician can perform an instrumented vaginal delivery (also known as an operative vaginal delivery ) via vacuum or forceps. If the neonate remains too high in the pelvis, then the woman will need to undergo a cesarean delivery. In addition, the fetal condition can dictate a change in labor course and delivery mode based on the fetal heart rate (FHR) tracing.
The anesthesia provider can be consulted at any time throughout the labor to aid in a safe delivery. The labor course, mode of delivery, and maternal comorbid conditions should all be considered in determining which analgesic or anesthetic technique is most appropriate.
Anatomy of Labor Pain
Contraction of the uterus, dilatation of the cervix, and distention of the perineum cause pain during labor and delivery. Somatic and visceral afferent sensory fibers from the uterus and cervix travel with sympathetic nerve fibers to the spinal cord ( Fig. 33.3 ). During the first stage of labor (cervical dilation), the majority of painful stimuli are the result of afferent nerve impulses from the lower uterine segment and cervix, with contributions from the uterine body causing visceral pain (poorly localized, diffused, and usually described as a dull but intense aching). These fibers pass through the paracervical tissue and course with the hypogastric nerves and the sympathetic chain to the dorsal root ganglia of levels T10 to L1. During the second stage of labor (pushing and expulsion), afferents innervating the vagina and perineum cause somatic pain (well localized and described as sharp). These somatic impulses travel primarily via the pudendal nerve to dorsal root ganglia of levels S2 to S4. Pain during this stage is also caused by distention and tissue ischemia of the vagina, perineum, and pelvic floor muscles. Pain is associated with descent of the fetus into the pelvis and delivery. Neuraxial analgesic techniques that block levels T10 to L1 during the first stage of labor must be extended to include S2 to S4 for efficacy during the second stage of labor.
Labor pain can have significant physiologic effects on the mother, fetus, and the course of labor. Pain stimulates the sympathetic nervous system, increases plasma catecholamine levels, creates reflex maternal tachycardia and hypertension, and can reduce UBF. In addition, changes in uterine activity can occur with the rapid decrease in plasma epinephrine concentrations associated with onset of neuraxial analgesia. Oscillations in epinephrine can cause many uterine effects ranging from a transient period of uterine tachysystole (extremely frequent uterine contractions) to a period of uterine quiescence. Alternatively, these epinephrine changes can convert dysfunctional uterine activity patterns associated with poorly progressive cervical dilation to more regular patterns associated with normal cervical dilation.
Methods of Labor Analgesia
A variety of nonpharmacologic techniques for labor analgesia exist. Although data are limited, acupuncture, acupressure, transcutaneous electrical nerve stimulation, relaxation, and massage all demonstrate a modest analgesic benefit. Other techniques such as hypnosis and intradermal water injections do not show significant benefit beyond control. Most nonpharmacologic techniques seem to reduce labor pain perception but lack the rigorous scientific methodology for useful comparison of these techniques to pharmacologic methods. A woman’s satisfaction with labor and delivery may not be directly associated with analgesic efficacy. A meta-analysis reviewing the effectiveness of a support individual (e.g., doula, family member) noted that women with a support individual used less pharmacologic analgesia, had a decreased length of labor, were more likely to have a vaginal birth, and were less likely to have negative feelings about childbirth.
Systemic analgesics are utilized on labor and delivery, but normally limited by bolus dose, dosing interval, and 24-hour cumulative dose. Although the use of systemic opioid analgesics is quite common, the use of sedatives, anxiolytics, and dissociative drugs is rare. The potential for maternal sedation, respiratory compromise, loss of airway protection, and proximity to time of delivery dictate judicious use of systemic opioids. For women who are in early spontaneous labor or beginning induction of labor, systemic opioid analgesia can be especially beneficial.
Opioids (Also See Chapter 9 )
Although there are individual differences among opioids, all readily cross the placental barrier and exert neonatal effects in typical clinical doses, including decreased FHR variability and dose-related neonatal respiratory depression. All opioids can have maternal side effects, including nausea, vomiting, pruritus, and decreased stomach emptying.
Meperidine is one of the most frequently used opioids worldwide likely secondary to cost, availability, and easy administration. It can be administered in doses of 12.5 to 25 mg IV or 25 to 50 mg intramuscularly. Maternal half-life of meperidine is 2 to 3 hours with half-life in the fetus and newborn significantly greater (13 to 23 hours) and more variable. In addition, meperidine is metabolized to an active metabolite (normeperidine) that can significantly accumulate after repeated doses. With increased dosing and shortened time interval between dose and delivery, neonatal risks of decreased Apgar scores, lowered oxygen saturation, and prolonged time to sustained respiration are more likely.
Morphine was used more frequently in the past, but currently is rarely used. Like meperidine it has an active metabolite (morphine-6-glucuronide) and a prolonged duration of analgesia; the half-life is longer in neonates compared to adults, and it produces significant maternal sedation. In latent labor, obstetric providers may use intramuscular morphine combined with phenergan for analgesia, sedation, and rest, termed morphine sleep . This produces analgesia for approximately 2.5 to 6 hours with an onset of 10 to 20 minutes and does not appear to affect maternal or neonatal morbidity.
Fentanyl is commonly used for labor analgesia. It has a short duration and no active metabolites. When given in small IV doses of 50 to 100 μg in an hour, there are no significant differences in neonatal Apgar scores and respiratory effort compared to newborns of mothers not receiving fentanyl.
Remifentanil patient-controlled analgesia (PCA) may be considered for women who have contraindications to neuraxial blockade. Although labor pain improved with remifentanil, a randomized controlled trial comparing epidural analgesia to remifentanil PCA had overall pain scores that were smaller in the epidural group. More sedation and hemoglobin desaturation were noted during remifentanil analgesia, but there was no difference between groups in fetal and neonatal outcomes. A more recent (2015) equivalence trial performed between remifentanil PCA and epidural analgesia found remifentanil was inferior to epidural analgesia for satisfaction of pain relief and pain relief scores. Because remifentanil has potential for significant maternal respiratory depression, its use should remain under close supervision of an anesthesiologist.
Inhaled nitrous oxide (N 2 O) has been used for decades for labor analgesia and recently has increased in use within the United States. Nitrous oxide is typically inhaled intermittently in a fixed mixture of 50% N 2 O with 50% oxygen. It provides satisfactory analgesia in some women but is inferior to epidural analgesia. The side effects are mild with nausea, dizziness, and drowsiness among the most common. Without coadministration of opioids, it is safe and does not result in hypoxia, unconsciousness, or loss of protective airway reflexes. Maternal cardiovascular and respiratory depression are minimal and uterine contractility is not affected. In addition, newborn Apgar scores from mothers using nitrous oxide in labor are similar to those from mothers using other labor pain management methods or no analgesia. When delivered with appropriate scavenging equipment there does not appear to be concern regarding occupational exposure. Despite its historical use, rigorous scientific studies are lacking to further assess its overall efficacy, safety, and long-term effects on the fetus and newborn.
Neuraxial (Regional) Analgesia
Neuraxial analgesia (e.g., epidural, spinal, combined spinal-epidural [CSE]) is currently the most widely used method of labor analgesia in the United States. Placement of paracervical and pudendal blocks for analgesia is rare. Neuraxial analgesia typically involves the administration of local anesthetics, and often the coadministration of opioid analgesics. In addition, adjuvant drugs such as epinephrine and clonidine decrease the dose of local anesthetics or opioids required for analgesia. However, given that the FDA (Food and Drug Administration) issued a black box warning regarding the possibility of significant hypotension with neuraxial clonidine in obstetrics, caution should be used.
The ester-linked local anesthetics (e.g., 2-chloroprocaine, procaine, tetracaine) are rapidly metabolized by plasma cholinesterase, decreasing the risk of maternal toxicity and placental drug transfer. Amide-linked local anesthetics (e.g., lidocaine, bupivacaine, ropivacaine) are degraded by P-450 enzymes in the liver. Bupivacaine and ropivacaine are the most commonly used local anesthetics for labor analgesia, and both are extremely safe when appropriately dosed for epidural or intrathecal administration. An accidental, large intravascular dose of any local anesthetic can result in significant maternal morbidity (seizures, loss of consciousness, severe arrhythmias, and cardiovascular collapse) or fatality and the potential for fetal accumulation (ion trapping); see discussion under “Physiology of Uteroplacental Circulation.” Immediate recognition and treatment is essential (see “Systemic Toxicity and Excessive Blockade” ).
Neuraxial Opioids (Also See Chapter 9 )
Neuraxial opioids are commonly used in obstetric anesthesia. Lipid-soluble opioids such as fentanyl and sufentanil are frequently used to augment the neuraxial analgesia of local anesthetics. The administration of opioids alone in the epidural space can provide moderate analgesia, but they are not as effective as dilute solutions of local anesthetic. Intrathecal opioids are more potent than epidural or systemic administration but are of limited duration (<2 hours) and also less effective than using neuraxial local anesthetics. Coadministration of opioids with local anesthetics prolongs and improves the quality of analgesia and has local anesthetic-sparing effects. The addition of neuraxial opioids is associated with dose-related maternal side effects including pruritus, sedation, and nausea. In addition, administration of intrathecal opioids can result in fetal bradycardia independent of hypotension. The mechanism for fetal bradycardia is unclear but may result from uterine hyperactivity following the rapid onset of analgesia.
Neuraxial techniques represent the most effective form of labor analgesia and achieve the highest rates of maternal satisfaction. The patient remains awake and alert without sedative side effects, maternal catecholamine concentrations are reduced, hyperventilation is avoided, cooperation and capacity to participate actively during labor are facilitated, and excellent, predictable analgesia can be achieved, superior to the analgesia provided by all other techniques. However, a delay in providing neuraxial pain relief, inadequate analgesia, or poorly communicating information about neuraxial labor analgesia can contribute to a negative childbirth experience (also see Chapter 17 ).
Prior to initiation of any neuraxial blockade, anesthesia providers should assess the patient’s pregnancy and health history; perform a focused physical examination; discuss the risks, benefits, and alternatives; and obtain consent (also see Chapter 13 ). In otherwise healthy women, routine laboratory tests are not required. Resuscitation equipment and drugs must be immediately available to manage serious complications secondary to initiation of epidural or spinal blocks (see “Contraindications of Neuraxial Anesthesia” and “Complications of Regional Anesthesia” ). During initiation of the neuraxial blockade, mother and fetus are closely monitored (maternal vital signs and FHR monitoring). Current recommendations allow otherwise healthy laboring women to have modest amounts of clear liquids. However, in complicated labors (e.g., by morbid obesity, difficult airway, concerning fetal status), the decision to restrict oral intake should be determined by the individual anesthesia provider.
Timing and Placement of Epidural
The decision of when to place an epidural was previously controversial over the concern of adversely affecting the progress of labor. Current ASA and American College of Obstetricians and Gynecologists (ACOG) guidelines recommend that a maternal request for labor pain relief is sufficient justification for epidural placement, and the decision should not depend on an arbitrary cervical dilation. Randomized controlled clinical trials comparing patients receiving either systemic opioids or neuraxial analgesia in early labor (both spontaneous and induced) demonstrated no difference in rates of cesarean delivery. A Cochrane review based on studies dating up to 2011 that compared neuraxial and systemic opioid labor analgesia noted no difference in rates of cesarean delivery, but women with neuraxial analgesia did have an increased rate of instrumented vaginal delivery. Neuraxial analgesia is associated with a prolonged second stage of labor, and the mean duration of the second stage is approximately 20 minutes longer with epidural labor analgesia. A 2015 clinical trial found no difference between epidurals dosed with fentanyl alone versus local anesthetic suggesting a prolonged second stage is not a result of decreased pushing effort secondary to local analgesia. This increase in the second stage is not harmful to the infant or mother, and as long as the fetal status is reassuring and there is ongoing progress toward delivery, the duration of the second stage does not require intervention.
Epidural analgesia is a catheter-based technique used to provide continuous pain relief during labor (also see Chapter 17 ). The technique involves insertion of a specialized needle (Tuohy) between vertebral spinous processes in the back, into the epidural space ( Fig. 33.4 ). This needle has a slightly curved blunt tip to minimize dural puncture. The woman can either be in the sitting or lateral position based on both the experience of the anesthetic provider and optimal exposure to critical anatomic landmarks. Based on ASA task force recommendations regarding neuraxial infectious complications, aseptic techniques should always be used during placement of neuraxial needles and catheters, including (1) removal of jewelry (e.g., rings and watches), handwashing, and wearing of caps, masks, and sterile gloves; (2) use of individual packets of antiseptics for skin preparation; (3) use of chlorhexidine (preferred) or povidone-iodine (preferably with alcohol) for skin preparation, allowing for adequate drying time; (4) sterile draping of the patient; and (5) use of sterile occlusive dressings at the catheter insertion site. The needle is normally inserted between L2 and L4. The needle traverses the skin and subcutaneous tissues, supraspinous ligament, interspinous ligament, and the ligamentum flavum and is advanced into the epidural space ( Fig. 33.5 ). The tip of the Tuohy needle should not penetrate the dura, which forms the boundary between the intrathecal or subarachnoid space and the epidural space. To locate the epidural space, a tactile technique called loss of resistance is used. The tactile resistance noted with pressure on the plunger of an air- or saline-filled syringe dramatically decreases as the tip of the needle is advanced through the ligamentum flavum (dense resistance) into the epidural space (no resistance), which has an average depth of approximately 5 cm from the skin. Once the needle is properly positioned, a catheter is inserted through the needle. The catheter remains in the epidural space, and the needle is removed. The catheter is secure and used for intermittent or continuous injections. Once the catheter is in place, analgesia is achieved by administration of local anesthetics, or opioids, or both (see earlier discussion), and maintained throughout the course of labor and delivery. The catheter can also be used for instrumented or cesarean delivery as well as administration of morphine for postoperative analgesia, when necessary.
Combined Spinal-Epidural Technique
The CSE technique follows the epidural technique as described, but after the loss of resistance a spinal needle (24- to 27-gauge, pencil-point needle) is inserted into the epidural needle, using a needle through needle procedure. Once CSF is visualized, an intrathecal dose of local anesthetic and opioid is administered. The spinal needle is removed and the epidural catheter is threaded as described with the epidural technique. The benefits of the CSE include quicker onset of analgesia and no motor blockade if opioids alone are placed intrathecally. A systematic review of CSE versus epidural literature found no major difference in maternal benefit or fetal risks but an increased rate of analgesia onset and maternal pruritus with the CSE technique.
Epidural and Combined Spinal-Epidural Dosing and Delivery Techniques
During labor, an epidural catheter allows continuous infusion of local anesthetic with or without opioid drugs. In addition, anesthesia providers can bolus the catheter with either the same or a more concentrated solution of local anesthetic. Programmable infusion pumps allow a patient-controlled epidural analgesia (PCEA) method of delivering the chosen anesthetic mixture with or without a background infusion. Compared to a continuous infusion alone, a PCEA method of delivery allows for fewer medical personnel, decreased motor block, improved patient satisfaction, and lower local anesthetic consumption. Adding a background infusion to PCEA further improves labor analgesia, reduces the need for clinician boluses, and does not increase maternal or neonatal adverse events. However, there is not enough current evidence to determine if adding a continuous background infusion to a PCEA affects the length of labor and need for operative delivery. Programmed intermittent epidural bolus (PIEB) is a more recent method of administering automated fixed epidural boluses at scheduled intervals. PIEB can be used alone or with a PCEA technique. Use of PIEB may slightly reduce local anesthetic usage, improve maternal satisfaction, and decrease the need for rescue boluses. Concentrations of labor epidural local anesthetics have decreased over time because dense motor blockade may adversely affect vaginal delivery rate. Typical maintenance infusion concentrations for epidural bupivacaine (0.04% to 0.125%) or ropivacaine (0.0625% to 0.2%) are both effective. Opioids such as fentanyl (2 μg/mL) or sufentanil (0.2 μg/mL) may be added to the infusion mixture to augment analgesia and decrease local anesthetic requirements, but they increase the side effects of pruritus, nausea, and sedation in a dose-dependent manner. Bolus administration of opioids can also be administered through the epidural catheter with typical doses of fentanyl 50 to 100 μg or sufentanil 5 to 10 μg to improve analgesia. Dilute concentrations of epinephrine (1:300,000 to 1:800,000) can also be added to the epidural mixture to augment analgesia.
For CSEs the initial intrathecal dose can include an opioid, local anesthetic, or a combination of the two. Typical intrathecal doses for opioids are fentanyl (10 to 20 μg) or sufentanil (1.5 to 5 μg), and local anesthetic doses include bupivacaine (1.25 to 3.5 mg) and ropivacaine (2 to 5 mg). Use of large-dose opioids (e.g., sufentanil 7.5 μg) is associated with increased risk of fetal bradycardia and severe pruritus even without the presence of hypotension. Prior to initiation of the epidural, a test dose should be performed to evaluate the possibility of unintended IV or intrathecal catheter placement. Commonly, 3 mL of 1.5% lidocaine containing 1:200,000 epinephrine is used. Increases in heart rate and arterial blood pressure more than 20% above baseline (intravascular placement) or rapid analgesia and lower extremity motor block (intrathecal placement) indicate epidural catheter misplacement. Whenever a bolus is administered in the epidural for initiation or breakthrough pain, it is recommended to administer the anesthetic mixture incrementally through the epidural catheter while monitoring maternal arterial blood pressure and FHR continuously.
Instrumented vaginal delivery may become necessary for arrest of descent and fetal indications. Use of forceps often requires a denser block with perineal anesthesia. Supplementation with 5 to 10 mL of epidural lidocaine (1% to 2%) or 2-chloroprocaine (2% to 3%) may be needed.
Spinal Labor Analgesia
Spinal analgesia can be administered just before vaginal delivery. This technique is useful for advanced second-stage analgesia, instrumented (forceps/vacuum) delivery, evaluation/evacuation of retained placenta, or repair of high-degree perineal lacerations. Placement of spinal block (3 to 5 mg bupivacaine with or without 10 to 20 μg of fentanyl) allows the rapid onset of analgesia. This dose is significantly less than that needed for a cesarean delivery. The duration of this type of spinal analgesia is approximately 60 to 90 minutes. A 24- to 27-gauge pencil-point spinal needle is selected to reduce the risk of post–dural puncture headache. If anesthesia is primarily needed for perineal laceration repair, the patient may be left in the sitting position for a few additional minutes following use of hyperbaric local anesthetic in order to concentrate the sensory block in the perineal region (saddle block). A true saddle block anesthetic does not produce complete uterine pain relief because the afferent fibers (extending to T10) from the uterus are not blocked.
Contraindications of Neuraxial Anesthesia
Certain conditions contraindicate neuraxial procedures. They include (1) patient refusal, (2) infection at the needle insertion site, (3) significant coagulopathy, (4) hypovolemic shock, (5) increased intracranial pressure from mass lesion, and (6) inadequate resources or provider expertise. Other conditions such as systemic infection, neurologic disease, and mild coagulopathies are relative contraindications that should be evaluated on a case-by-case basis using current guidelines. Human immunodeficiency virus (HIV) and hepatitis infection are not contraindications to neuraxial technique in pregnant women.
Complications of Regional Anesthesia
The retrospective rates of inadequate epidural analgesia or inadequate CSE analgesia requiring catheter replacement were 7% and 3%, respectively, at a U.S. academic center. The rate of accidental dural puncture during epidural catheter placement is approximately 1% to 2%, and about half of these punctures result in a severe headache, which is typically managed with analgesics, hydration, rest, caffeine, or blood patch if necessary. Other potential side effects from neuraxial blockade include pruritus, nausea, shivering, urinary retention, motor weakness, low back soreness, and a prolonged block. More serious complications of meningitis, epidural hematoma, and nerve or spinal cord injury are extremely rare. A 2014 multicenter database analysis of 257,000 obstetric patients examined rates of serious neurologic events. The rate of epidural abscess or meningitis was 1:63,000, epidural hematoma was 1:251,000, and high neuraxial block 1:4300. A 2006 meta-analysis of 1.37 million women receiving labor epidurals noted rates of deep epidural infections 1:145,000, epidural hematoma 1:168,000, and persistent neurologic injury remaining longer than 1 year at 1:240,000 (also see Chapter 17 ).
Systemic Toxicity and Excessive Blockade
Infrequent but occasionally life-threatening complications can result from administration of neuraxial anesthesia. The most serious complications are from accidental IV or intrathecal injections of local anesthetics. An unintended bolus of IV local anesthetic causes dose-dependent consequences ranging from minor side effects (e.g., tinnitus, perioral tingling, mild arterial blood pressure, and heart rate changes) to major complications (seizures, loss of consciousness, severe arrhythmias, cardiovascular collapse). The severity depends on the dose, type of local anesthetic, and preexisting condition of the patient. Bupivacaine has greater affinity for sodium channels than lidocaine and dissociates more slowly. In addition, its high protein affinity makes cardiac resuscitation more difficult and prolonged. Measures that minimize the likelihood of accidental intravascular injection include careful aspiration of the catheter before injection, test dosing, and incremental administration of therapeutic doses. Successful resuscitation and support of the mother will reestablish UBF. This will provide adequate fetal oxygenation and allow time for excretion of local anesthetic from the fetus. The neonate has an extremely limited ability to metabolize local anesthetics and may have prolonged convulsions if emergent delivery is required.
A high spinal (total spinal) block can result from an unrecognized epidural catheter placed subdural, migration of the catheter during its use, or an overdose of local anesthetic in the epidural space (i.e., high epidural). Both high spinal blocks and high epidural blocks can result in severe maternal hypotension, bradycardia, loss of consciousness, and blockade of the motor nerves to the respiratory muscles.
Treatment of complications resulting from both intravascular injection and high spinal block are directed at restoring maternal and fetal oxygenation, ventilation, and circulation. Intubation, vasopressors, fluids, and advanced cardiac life support (ACLS) algorithms are often required. Changes to ACLS guidelines for pregnancy include use of manual left uterine displacement (rather than tilt) to relieve aortocaval compression, avoidance of lower extremity vessels for drug delivery, and no modifications to pharmacologic or defibrillation protocol except removal of fetal and uterine monitors prior to shock, unless it would delay the intervention. If a local anesthetic overdose occurs, consider use of a 20% IV lipid emulsion to bind the drug and decrease toxicity. In any situation of maternal cardiac arrest with unsuccessful return of spontaneous circulation, the fetus should be emergently delivered if the mother is not resuscitated within 4 minutes of the arrest. This guideline for emergent cesarean delivery increases the chances of survival for both the mother and neonate. In addition, the use of checklists and simulation can improve performance during the rare but critical events.
Hypotension (decrease in systolic blood pressure > 20%) secondary to sympathetic blockade is the most common complication of neuraxial blockade for labor analgesia with rates of approximately 14%. Prophylactic measures include left uterine displacement and hydration. Although a standard for timing, amount, and hydration fluid remains controversial, all agree dehydration should be avoided. Prehydration with up to 1 L IV crystalloid does not appear to significantly decrease rates of hypotension from small-dose labor epidurals. Although IV fluid preloading may be used to reduce the frequency of maternal hypotension after spinal anesthesia, there is no consistently significant difference in hypotension following spinal anesthesia if a preload or co-load of either IV crystalloid or colloid is administered. Treatment of hypotension consists of further uterine displacement, IV fluids, and vasopressor administration. Either phenylephrine or ephedrine can be used to treat hypotension. Although ephedrine (primarily β-adrenergic) was historically used, more recent data confirm that (1) a phenylephrine (primarily α-adrenergic) infusion at the time of spinal placement is effective at preventing hypotension; (2) compared with ephedrine, phenylephrine is associated with less placental transfer and fetal acidosis; and (3) phenylephrine is now widely considered the vasopressor of choice for treating maternal hypotension. However, significant decreases in maternal heart rate below baseline signify a decrease in cardiac output, and consequently both heart rate and arterial blood pressure should be considered when choosing vasopressor drugs to manage maternal hypotension. If treated promptly, transient maternal hypotension does not lead to fetal depression or neonatal morbidity.
Increased Core Temperature
An increase in core maternal body temperature and fever are associated with labor epidural analgesia (also see Chapter 20 ). Only about 20% of women who receive epidural labor analgesia develop a fever and the remaining 80% have no increase in core body temperature. Although the cause of the maternal temperature rise remains uncertain, an association with noninfectious inflammation mediated by proinflammatory cytokines is a likely cause. This increase in maternal temperature is not associated with a change in white blood cell count or with an infectious process, and treatment is not necessary. In addition, the fever associated with epidural labor analgesia does not increase the incidence of neonatal sepsis and need not affect neonatal septic workup. Although some studies note no effect on fetal well-being, other studies suggest maternal temperatures greater than 38° C are associated with adverse neonatal outcomes including seizures, hypotonia, and need for a period of assisted ventilation.