Obstetric Anesthesia: Complications and Management
WHEC Practice Bulletin and Clinical Management Guidelines for healthcare providers. Educational grant provided by Women's Health and Education Center (WHEC).
During pregnancy, there are major alterations in nearly every maternal organ system. These changes are initiated by hormones secreted by the corpus luteum and placenta. The mechanical effects of the enlarging uterus and compression of surrounding structures play an increasing role in the second and third trimesters. This altered physiologic state had relevant implications for the anesthesiologist caring for the pregnant patient. Any drug that reaches the fetus undergoes metabolism and excretion. In this respect, fetus has an advantage over the new-born, in that it can excrete the drug back to the mother once the concentration gradient of the free drug across the placenta has been reversed. Most drugs, including anesthetic agents, readily cross the placenta. Several factors influence the placental transfer of drugs, including physiochemical characteristics of the drug itself, maternal drug concentrations in the plasma, properties of the placenta, and hemodynamic events within the feto-maternal unit. Pregnancy is associated with physiologic changes that 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. Maturation of the placenta can affect the rate of drug transfer to the fetus, as the thickness of the trophoblastic epithelium decreases from 25 to 2 mm at term. Uptake and biotransformation of anesthetic drugs by the placenta would decrease the amount transferred to the fetus.
The purpose of this document is to discuss anesthetic complications during labor and delivery. Well-conducted obstetric analgesia and anesthesia, in addition to relieving pain and anxiety, may benefit the mother. Placental drug uptake is limited, and there is no evidence to suggest that this organ metabolizes any of the agents commonly used in obstetric anesthesia. The idea that surgical anesthesia, although deemed necessary for the patient, might have detrimental effects on the growth and development of the human fetus has led to a great deal of investigation, both in-vitro and in experimental animals. Because a single exposure to anesthetic agents seems unlikely to result in fetal abnormalities, the selection of agent should be based on specific surgical requirements.
Summary of Physiologic Changes of Pregnancy:
Increased mineralocorticoid activity during pregnancy produces sodium retention and increased body water content. Thus, plasma volume and total blood volume begin to increase in early gestation, resulting in a final increase of 40 to 50% and 25 to 40%, respectively, at term. The summary of physiologic changes of pregnancy at term is listed below (1):
|Total blood volume||Increase||25-40%|
|Serum cholinesterase activity||Decrease||20-30%|
|Functional residual capacity||Decrease||20%|
|Arterial carbon dioxide tension||Decrease||10 mm Hg|
|Arterial oxygen tension||Increase||10 mm Hg|
|Minimum alveolar concentration||Decrease||32-40%|
Common Anesthetic Complications
With the use of local anesthetics, excretion of the drug back to the mother by fetus may occur, even though the total plasma concentration in the mother may exceed that in the fetus because there is lower protein binding in fetal plasma. There is only one drug, 2-chloroprocaine that is metabolized in the fetal blood so rapidly that even in acidosis, substantial accumulation in the fetus is avoided. In both the term and preterm newborn, the liver contains enzymes essential for the biotransformation of amide local anesthetics (2). Prolonged elimination half-lives in the newborn compared with the adult have been noted for other amide local anesthetics. The question remains whether the fetus and newborn are more sensitive than adults to the depressant and toxic effects of drugs. Laboratory investigations have shown that the newborn is, in fact, more sensitive to the depressant effects of opioids. Bupivacaine has been implicated as a possible cause of neonatal jaundice because of its high affinity for fetal erythrocyte membranes may lead to a decrease in filterability and deformability, rendering them more prone to hemolysis. However, a more recent study has failed to show increased bilirubin production in newborns whose mothers received bupivacaine for epidural anesthesia during labor and delivery (3). Finally, neuro-behavioral studies have revealed subtle changes in newborn neurologic and adaptive function. In the case of most anesthetic agents, these changes are minor and transient, lasting for only 24 to 48 hours.
Post-dural Puncture Headache (PDPH):
By virtue of gender, pregnant women are at a higher risk for developing post-dural puncture headache (PDPH). In addition, after delivery, the reduced epidural pressure increases the risk of cerebrospinal fluid leakage through the dural opening. The frequency of PDPH is related to the diameter of the dural puncture, ranging from in excess of 70% after use of 16-gauge needles to less than 1% with smaller 25- to 26-gauge spinal needles. The incidence of cephalalgia is reduced with the use of atraumatic pencil-point needles (Whitacre or Sprotte), which are believed to separate the dural fibers, rather than the diamond-shaped (Quincke) cutting needles (3)(4). Conservative treatment is indicated in the presence of mild to moderate discomfort, and includes bed rest, hydration, and simple analgesics. Caffeine (500 mg intravenously or 300 mg orally) or theophylline have also been used in the treatment of PDPH. Severe headache that does not respond to conservative measures is best treated with autologous blood patch. Using aseptic technique, 10 to 15 mL of the patient's blood is injected into the epidural space close to the site of dural puncture. This procedure may be repeated as necessary and is associated with excellent success rates. If an epidural catheter is in place after delivery, there is sufficient evidence to support the efficacy of injecting 15 to 20 mL of autologous blood may be injected through the catheter before removal.
PDPH should be managed conservatively with caffeine, theophylline, or sumatriptan in patients with human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS) (8). If these modalities fail, an epidural blood patch may be considered. There has been concern that an epidural blood patch, particularly if the viral load is high, may accelerate neurologic symptoms of the disease. In a more recent case series of six patients with HIV infection and PDPH requiring epidural blood patch, there was no evidence of acceleration of HIV symptoms (3).
Local Anesthetic-induced Seizures:
Unintended intravascular injection or drug accumulation after repeated epidural injection can result in high serum levels of local anesthetic. Rapid absorption of local anesthetic from highly vascular sites of injection may also occur after paracervical and pudendal blocks. Resuscitation equipment should always be available when any major nerve block is undertaken. Intravenous access, airway equipment, emergency drugs, and suction equipment should be immediately accessible. To avoid systemic toxicity of local anesthetic agents, strict adherence to recommended dosages, methods to detect misplaced needles and catheters, and fractional administration of the induction dose are essential. Despite these precautions, life-threatening convulsions and more rarely, cardiovascular collapse may occur. Seizure activity should be treated with intravenous thiopental 50 to 100 mg or diazepam 5 to 10 mg; larger doses may enhance local anesthetic-induced myocardial depression (3)(5). The maternal airway should be secured and oxygenation maintained. If cardiovascular collapse does occur, cesarean delivery may be required to relieve aortocaval compression and to ensure the efficiency of cardiac massage.
Neurologic sequelae of central neuraxial blockade, although rare, have been reported. Pressure exerted by a needle or catheter on spinal nerve roots produces immediate pain and requires repositioning. Infections such as epidural abscess or meningitis are rare and may be a manifestation of systemic sepsis. Epidural hematoma can also occur, usually in association with coagulation defects. Nerve root irritation may have a protracted recovery, lasting weeks or month. Peripheral nerve injury as a result of instrumentation, lithotomy position, or compression by the fetal head may occur even in the absence or neuraxial technique (6).
Total Spinal Anesthesia:
High or total spinal anesthesia is a rare complication of intrathecal injection that occurs after excessive cephalad spread of local anesthetic in the subarachnoid space. Unintentional intrathecal administration of epidural medication as a result of dural puncture or catheter migration may also result in this complication. Left uterine displacement, placement in the Trendelenburg position, and continued fluid and vasopressor administration may be necessary to achieve hemodynamic stability (5). Rapid control of the airway is essential, and endotracheal intubation may be necessary to ensure oxygenation without aspiration.
Regional anesthesia may be associated with hypotension. The risk of hypotension is lower in women who are in labor compared with non-laboring women. Maternal pre-hydration up to 20 mL/kg of lactated Ringer's solution before initiation of regional anesthesia and avoidance of aortocaval compression after induction may decrease the incidence of hypotension (5). It has been demonstrated that for effective prevention of hypotension, the blood volume increase from preloading must be sufficient to result in a significant increase in cardiac output. This was possible only with the administration of hetastarch, 0.5 to 1 L. Nonetheless, controversy exists regarding the efficacy of volume loading in the prevention of hypotension. If hypotension does occur despite pre-hydration, therapeutic measures include increased displacement of the uterus, rapid infusion of intravenous fluids, titration of intravenous ephedrine (5 to 10 mg) or phenylephrine (20 to 50 µg), oxygen administration, and placement of the patient in the Trendelenburg position. Continued vigilance and active management of hypotension can prevent serious sequelae in both mother and neonate.
The primary clinical risk factor for developing a fever after epidural analgesia is duration of exposure to the epidural itself. As a result, the risk of epidural fever is largely confined to nulliparous patients. Most multiparous patients deliver shortly after receiving epidural analgesia, and as a result do not have a significantly increased risk of fever. In fact, randomized trials have shown only 4% of multiparas on epidural analgesia develop fever, versus 3% in controls. The mechanism for fever is not known. Theories include thermoregulation and chorioamnionitis. More recent research suggests a non-infectious inflammatory cause. Investigators have correlated epidural analgesia in labor with higher levels of interleukin-6, a marker for maternal inflammation. Although we do not understand the mechanism of this cascade, the time course of the response (within 1 hour) suggests that susceptible women are different from women who remain afebrile, and that these differences are present at the time of epidural placement. Several lines of evidence suggest that women with a propensity toward an exaggerated inflammatory response are more likely to develop intrapartum fever (6).
At this time there are no effective and safe ways to prevent epidural fever in nulliparous patients. Several prophylactic strategies have been attempted. Acetaminophen, 650 mg, given rectally every 4 hours, has no effect on rates of fever or temperature following epidural analgesia. Similarly, antibiotic prophylaxis for group B streptococcus does not decrease the rate of subsequent intrapartum fever. However, methylprednisolone (100 mg IV every 4 hours) started immediately prior to catheter placement reduces the rate of maternal fever by more than 90%. In addition, maternal steroids at this dose significantly reduce intrauterine exposure to fetal inflammation as measured by cord blood interleukin-6 levels. Prophylactic treatment with maternal corticosteroids is seen to be accompanied by a significant increase in symptomatic neonatal bacteremia. Due to this safety concern, there is no recommended maternal treatment to prevent fetal exposure to hyperthermia and inflammation.
Obstetrical Anesthesia and Cesarean Delivery Rates:
Neuraxial analgesia techniques (epidural, spinal, and combined spinal-epidural) are the most effective and least depressant treatments for labor pain (2). Early studies generated concern that the benefits of neuraxial analgesia may be offset by an associated increase in the risk of cesarean delivery. Recent studies, however, have determined that when compared with intravenous systemic opioid analgesia, the initiation of early neuraxial analgesia does not increase the risk of cesarean delivery (9). Furthermore, certain studies demonstrated an even greater association between epidural analgesia and cesarean delivery in women who receive received their epidurals before reaching cervical dilatation of 5 cm. In 2002, an evaluation of cesarean delivery sponsored by the American College of the Obstetricians and Gynecologists (ACOG) concluded: there is considerable evidence suggesting that there is in fact an association between the use of epidural analgesia for pain relief during labor and the risk of cesarean delivery. Since the last Committee Opinion on analgesia and cesarean delivery, additional studies have addressed the issue of neuraxial analgesia and its association with cesarean delivery. Three recent meta-analyses systematically and independently reviewed the previous literature, and all concluded that epidural analgesia does not increase the rates of cesarean delivery (odds ratio 1.00-1.04; 95% confidence interval, 0.17-1.48). In addition, three recent randomized controlled trials clearly demonstrated no difference in rate of cesarean deliveries between women who had received epidurals and women who had received only intravenous analgesia. Furthermore, a randomized trial comparing epidurals done early in labor versus epidurals done later in labor demonstrated no difference in the incidence of cesarean delivery (17.8% versus 20.7%). The use of intrathecal analgesia and the concentration of the local anesthetic used in an epidural also have no impact on the rate of cesarean delivery (7).
Therefore, ACOG reaffirms the opinion it published jointly with the American Society of Anesthesiologists, in which the following statement was articulated: "Labor causes severe pain for many women. There is no other circumstance where it is considered acceptable for an individual to experience untreated severe pain, amenable to safe intervention, while under a physician's care. In the absence of a medical contraindication, maternal request is a sufficient medical indication for pain relief during labor. The fear of unnecessary cesarean delivery should not influence the method of pain relief that women can choose during labor". ACOG recognizes that many techniques are available for analgesia in laboring patients. None of the techniques appears to be associated with an increased risk of cesarean delivery. The choice of technique, agent, and dosage is based on many factors, including patient preference, medical status, and contraindications (10)(11)(12).
The risk of inhalation of gastric contents is increased in pregnant women, as discussed previously, particularly if difficulty is encountered establishing the airway. Measures to decrease the risks of aspiration include comprehensive airway evaluation, prophylactic administration of non-particulate antacids, and preferred use of regional anesthesia. Occasionally, general anesthesia may be unavoidable in obstetric anesthesia practice, and therefore, awake intubation may be indicated in women in whom airway difficulties are anticipated.
A study of anesthesia-related deaths in the United States between 1979 and 1990 revealed that the case fatality with general anesthesia was 16.7 times greater than that with regional anesthesia. Most anesthesia-related deaths were a result of cardiac arrest due to hypoxemia when difficulties securing the airway were encountered (3). Pregnancy-induced anatomic and physiologic changes, such as reduced functional residual capacity (FRC), increased oxygen consumption, and oropharyngeal edema, may expose the patient to serious risks of desaturation during periods of apnea and hypoventilation.
As oxygen consumption increases during pregnancy, the maternal cardiovascular system adapts to meet the metabolic demands of a growing fetus. Airway edema may be particularly severe in women with preeclampsia, in patients placed in Trendelenburg position for prolonged periods, or with concurrent use of tocolytic agents. A rapid-sequence induction of anesthesia, application of cricoids pressure, and intubation with a cuffed endotracheal tube are required for all pregnant women receiving general anesthesia after the first trimester. The driving force for placental drug transfer is the concentration gradient of free drug between the maternal and fetal blood. For cesarean section, the choice of anesthesia depends on the urgency of the procedure, in addition to the condition of the mother and child. The case fatality rate (maternal mortality) with general anesthesia is 16.7 times greater than that with regional anesthesia. By virtue of age and gender, as well as reduced epidural pressure after delivery, pregnant women are at a higher risk for developing post-dural puncture headache (PDPH).
Pregnancy and parturition are considered "high risk" when accompanied by conditions unfavorable to the well-being of the mother, fetus or both. Preeclampsia is classified as severe if it is associated with server hypertension, proteinuria or end-organ damage. Antepartum hemorrhage occurs most commonly in association with placenta previa. Heart disease during pregnancy is a leading non-obstetric cause of maternal mortality. Substance abuse with cocaine has the greatest implications for anesthetic management because it causes a heightened sympathetic state. Fetal asphyxia develops as a result of interference with maternal or fetal perfusion of the placenta. There is an increased incidence of adverse obstetric outcome, particularly after non-obstetric operations during the first trimester.
- Gordon M. Maternal physiology. In Obstetrics: Normal and Problem Pregnancies; 5th edition. Eds: Gabbe SG, Niebyl JR, Simpson JL. Publisher: Churchill Livingstone Elsevier; 2007
- Halpern SH, Muir H, Breen TW et al. A multi-center randomized controlled trial comparing patient-controlled epidural with intravenous analgesia for pain relief in labor. Anesth Analg 2004;99:1532-1536
- Santos AC, Braveman FR, Finster M. Obstetric anesthesia In Clinical Anesthesia. 5th edition; editors: Barash PG, Cullen BF, Stoeling. Publishers: Lippincott Williams & Wilkins. 2006
- Landon MB, Hauth JC, Leveno KJ et al. Maternal and perinatal outcomes associated with a trial of labor after prior cesarean delivery. N Engl J Med 2004;351(25):2581-2586
- Emmett RS, Cyna AM, Andrew M et al. Techniques for preventing hypotension during spinal anesthesia for cesarean delivery. Cochrane Database Syst Rev 2002;3:CD002251
- Cheney FW. Injuries associated with regional anesthesia in the 1980's and 1990's. Anesthesiology 2004;101:143-148
- ACOG Committee Opinion. Analgesia and cesarean delivery rates. Number 339, June 2006
- Hughes SC, Dailey PA, Landers et al. Parturients infected with human immunodeficiency virus and regional anesthesia: Clinical and immunologic response. Anesthesiology 2002;97:320-329
- Liu EHC, Sia ATH. Rates of cesarean section and instrumental vaginal delivery in nulliparous women after low concentration epidural infusions or opioid analgesia: systemic review. BMJ 2004;328:1410-1412
- Wong CA, Scavone BM, Peaceman AM et al. The risk of cesarean delivery with neuraxial analgesia given early vs late in labor. N Eng J Med 2005;352:655-665
- Mardirosoff C, Dumot K, Boulvain M et al. Fetal bradycardia due to intrathecal opioids for labor analgesia: a systemic review. BJOG 2002;109:274-281
- Abrao KC, Francisco RPV, Miyadahira S et al. Elevation of uterine basal tone and fetal heart rate abnormalities after labor analgesia. Obstet Gynecol 2009;113:41-47
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