Friday, May 24, 2013

PATHOLOGY OF MATERNAL DISEASES

M&M Ch. 43: Obstetric Anesthesia

Key Concepts:
  • The most common morbidities encountered  in OB are severe hemorrhage  and severe preeclampsia
  • Regardless of time of last oral intake, all OB patients are full stomach and at risk for aspiration
  • Nearly all parenteral opioid analgesics and sedatives readily cross the placenta and can affect the fetus.  Regional techniques are preferred for management of labor pain.
  • Using a local anesthetic-opioid mixture for lumbar epidural anesthesia significantly reduces drug requirements, compared with using either agent alone.
  • Optimal analgesia for labor requires neural blockade at T10-L1 in first stage of labor and T10-S4 in the second stage.
  • Continuous lumbar epidural analgesia is the msot versatile and most commonly employed technique bc it can be used for pain relief for the first stage of labor as well as analgesia/anesthesia for subsequent vaginal delivery or c/s if necessary
  • When dilute mixtures of local anesthetic and opioid are used epidural analgesia has little if any effect on the progress of labor.
  • Even when aspiration does not yield blood or CSF, unintentional IV or intrathecal placement of an epidural needle or catheter is possible.
  • Hypotension is the most common side effect of regional anesthetic techniques and must be treated aggressively with ephedrine and IV fluid boluses to prevent fetal compromise.
  • CSE may benefit patients with severe pain early in labor and those who receive analgesia just prior to delivery
  • Regional is preferred to general anesthesia for c/s because regional is a/w lower maternal mortality.
  • Spinal for c/s is easier to perform and results in a more rapid and intense neural block than epidural anesthesia.  Epidural allows greater control over sensory levels and results in a more gradual fall in BP.
  • Systemic local anesthetic toxicity during epidural may be avoided by slowly administering dilute solutions for labor pain and fractionating the total dose for c/s into 5-ml increments.
  • In general anesthesia for c/s, if ETT intubation fails, the life of the mother takes priority over delivery of the fetus.
  • Maternal hemorrhage is the most common severe morbidities complicating OB anesthesia.  Causes include placenta previa, abruptio placentae, and uterine rupture.
  • Pregnancy-induced HTN describes one of 3 syndromes: preeclampsia, eclampsia, and the HELLP syndrome.
  • Common causes of postpartum hemorrhage include uterine atony, a retained placenta, obstetric lacerations, uterine inversion, and use of tocolytic agents prior to delivery.
  • Intrauterine asphyxia during labor is the most common cause of neonatal depression.  Fetal monitoring throughout labor is helpful in identifying which babies may be at risk, detecting fetal distress, and evaluating the effect of acute interventions.

Pregnancy-related Mortality
Higher for women >35 years, black patients, and patients without prenatal care.

Leading causes of death with a live birth: PE (21%), pregnancy-induced HTN (19%), other medical conditions (17%)

Major causes of death a/w a stillbirth: hemorrhage (21%), pregnancy-induced HTN (20%), sepsis (19%)

34% of patients died within 24 h of delivery, 55% died between 1-42 days, 11% died 43 days - 1 year.

Important additional causes of death: amniotic fluid embolism, intracranial hemorrhage

Morbidity
Risk factors: age > 34 y/o, nonwhite ethnic group, multiple pregnancy, history of HTN, previous postpoartum hemorrhage, emergency c/s

Most common causes of severe morbidity: severe hemorrhage, severe preeclampsia, HELLP syndrome, severe sepsis, eclampsia, uterine rupture, thromboembolic disease/events.

Anesthesia Mortality
Anesthesia accounts for 2-3% of maternal deaths. (GA > regional)
Most deaths occur during or after c/s.  Greater with emergency vs. elective c/s.

General Approach to the OB Patient
  • Pertinent historic items include age, parity, duration of pregnancy, and complicating factors.
  • Patients requiring anesthetic care should undergo focused preanesthetic eval: maternal health history, anestesia-related OB history, BP measurement, airway assessment, back exam for regional
  • All women in labor should have IV fluids (LR with dextrose) to prevent dehydration. 18 g IV
  • Blood sent for T&S in pts at high risk for hemorrhage.
  • Full stomach:
    • guidelines allow small amount of clear liquid for uncomplicated labor;
    • NPO at least 6 hr for elective c/s;
    • prophylactic admin of clear antacid (15-30 ml 0.3 M sodium citrate PO) every 3 h to maintain pH > 2.5 and decrease risk of aspiration pneumonitis
    • H2-blocker (ranitidine 100-150 mg PO or 50 mg IV) or reglan/metoclopramide 10 mg PO or IV should be given in high-risk patients and those expecting to receive G/A; H2 blockers reduce gastric volume and pH but have no effect on gastric contents already present.
    • Reglan accelerates gastric emptying, decreases gastric volume, increase LES tone
  • All patients should have a tocodynamic monitor and fetal heart rate monitor.
  • The supine position should be avoided unless a left uterine displacement device (> 15° wedge) is placed under the right hip. Uterine contractions can be directly measured via a catheter in patients with ruptured membranes, particularly those receiving oxytocin or those undergoing a trial of VBAC.
Anesthesia for Labor & Vaginal Delivery
Pain Pathways during Labor
The pain of labor arises from contraction of the myometrium against the resistance of the cervix and perineum, progressive dilatation of the cervix and lower uterine segment, as well as stretching and compression of pelvic and perineal structures.

First Stage
Pain during the first stage of labor is mostly visceral pain resulting from uterine contractions and cervical dilatation. It is usually initially confined to the T11–T12 dermatomes during the latent phase but eventually involves the T10–L1 dermatomes as the labor enters the active phase. The visceral afferent fibers responsible for labor pain travel with sympathetic nerve fibers first to the uterine and cervical plexuses, then through the hypogastric and aortic plexuses before entering the spinal cord with the T10–L1 nerve roots (see Chapter 18). The pain is primarily in the lower abdomen but may increasingly be referred to the lumbosacral area, gluteal region, and thighs as labor progresses. Pain intensity also increases with progressive cervical dilatation and the increasing intensity and frequency of uterine contractions. Nulliparous women and those with a history of dysmenorrhea appear to experience greater pain during the first stage of labor. Studies also suggest that women who experience more intense pain during the latent phase of labor have longer labors and are more likely to require cesarean section.

Second Stage
The onset of perineal pain at the end of the first stage signals the beginning of fetal descent and the second stage of labor. Stretching and compression of pelvic and perineal structures intensify the pain. Sensory innervation of the perineum is provided by the pudendal nerve (S2–4) so pain during the second stage of labor involves the T10–S4 dermatomes. Studies suggest that the more rapid fetal descent in multiparous women is associated with more intense pain than the more gradual fetal descent in nulliparous patients.

Psychological & Nonpharmacological Techniques
Psychological and nonpharmacological techniques are based on the premise that the pain of labor can be suppressed by reorganizing one's thoughts. Patient education and positive conditioning about the birthing process are central to such techniques. Pain during labor tends to be accentuated by fear of the unknown or previous unpleasant experiences. Techniques include those of Bradley, Dick-Read, Lamaze, Duola, and LeBoyer. The Lamaze technique, one of the most popular, coaches the parturient to take a deep breath at the beginning of each contraction followed by rapid shallow breathing for the duration of the contraction. The parturient also concentrates on an object in the room and attempts to focus her thoughts away from the pain. Less common nonpharmacological techniques include hypnosis, transcutaneous electrical nerve stimulation, biofeedback, and acupuncture (see Chapter 18). The success of all these techniques varies considerably from patient to patient, but most patients require additional forms of pain relief.

Parenteral Agents
Nearly all parenteral opioid analgesics and sedatives readily cross the placenta and can affect the fetus. Concern over fetal depression limits the use of these agents to the early stages of labor or to situations in which regional anesthetic techniques are not available. Central nervous system depression in the neonate may be manifested by a prolonged time to sustain respirations, respiratory acidosis, or an abnormal neurobehavioral examination. Moreover, loss of beat-to-beat variability in the fetal heart rate (seen with most central nervous system depressants) and decreased fetal movements (due to sedation of fetus) complicate the evaluation of fetal well-being during labor. Long-term fetal heart variability is affected more than short-term variability. The degree and significance of these effects depend on the specific agent, the dose, the time elapsed between its administration and delivery, and fetal maturity. Premature neonates exhibit the greatest sensitivity. In addition to maternal respiratory depression, opioids can also induce maternal nausea and vomiting and delay gastric emptying. Some clinicians have advocated use of opioids via patient-controlled analgesia devices early in labor because this technique appears to reduce total opioid requirements.

Meperidine, the most commonly used opioid, can be given in doses of 10–25 mg intravenously or 25–50 mg intramuscularly, usually up to a total of 100 mg. Maximal maternal and fetal respiratory depression is seen in 10–20 min following intravenous administration and in 1–3 h following intramuscular administration. Consequently, meperidine is usually administered early in labor when delivery is not expected for at least 4 h. Intravenous fentanyl, 25–100 g/h, has also been used for labor. Fentanyl in 25–100 g doses has a 3- to 10-min analgesic onset that initially lasts about 60 min, and lasts longer following multiple doses. However, maternal respiratory depression outlasts the analgesia. Lower doses of fentanyl may be associated with little or no neonatal respiratory depression and are reported to have no effect on Apgar scores. Morphine is not used because in equianalgesic doses it appears to cause greater respiratory depression in the fetus than meperidine and fentanyl. Agents with mixed agonist–antagonist activity (butorphanol 1–2 mg and nalbuphine 10–20 mg intravenously or intramuscularly) are effective and are associated with little or no cumulative respiratory depression (ceiling effect), but excessive sedation with repeat doses can be problematic.
Promethazine (25–50 mg intramuscularly) and hydroxyzine (50–100 mg intramuscularly) can be useful alone or in combination with meperidine. Both drugs reduce anxiety, opioid requirements, and the incidence of nausea but do not add appreciably to neonatal depression. A significant disadvantage of hydroxyzine is pain at the injection site following intramuscular administration. Nonsteroidal antiinflammatory agents, such as ketorolac, are not recommended because they suppress uterine contractions and promote closure of the fetal ductus arteriosus.

Benzodiazepines, particularly longer acting agents such as diazepam, are not used during labor because of their potential to cause prolonged neonatal depression. The amnestic properties of benzodiazepines make them undesirable agents for parturients because they usually want to remember the experience of delivery.
Low-dose intravenous ketamine is a powerful analgesic. In doses of 10–15 mg intravenously, good analgesia can be obtained in 2–5 min without loss of consciousness. Unfortunately, fetal depression with low Apgar scores is associated with doses greater than 1 mg/kg. Large boluses of ketamine (> 1 mg/kg) can be associated with hypertonic uterine contractions. Low-dose ketamine is most useful just prior to delivery or as an adjuvant to regional anesthesia. Some clinicians avoid use of ketamine because it may produce unpleasant psychotomimetic effects

Pudendal Nerve Block
Pudendal nerve blocks are often combined with perineal infiltration of local anesthetic to provide perineal anesthesia during the second stage of labor when other forms of anesthesia are not employed or prove to be inadequate. Paracervical plexus blocks are no longer used because of their association with a relatively high rate of fetal bradycardia; the close proximity of the injection site (paracervical plexus or Frankenhäuser's ganglia) to the uterine artery can result in uterine arterial vasoconstriction, uteroplacental insufficiency, and high levels of the local anesthetic in the fetal blood.

During a pudendal nerve block, a special needle (Koback) or guide (Iowa trumpet) is used to place the needle transvaginally underneath the ischial spine on each side; the needle is advanced 1–1.5 cm through the sacrospinous ligament, and 10 mL of 1% lidocaine or 2% chloroprocaine is injected following careful aspiration. The needle guide is used to limit the depth of injection and protect the fetus and vagina from the needle. Other potential complications include intravascular injection, retroperitoneal hematoma, and retropsoas or subgluteal abscess.

Regional Anesthetic Techniques
Regional techniques employing the epidural or intrathecal route, alone or in combination, are currently the most popular methods of pain relief during labor and delivery. They can provide excellent pain relief, yet allow the mother to be awake and cooperative during labor. Although spinal opioids or local anesthetics alone can provide satisfactory analgesia, techniques that combine the two have proved to be the most satisfactory in most parturients. Moreover, the apparent synergy between the two types of agents decreases dose requirements and provides excellent analgesia with few maternal side effects and little or no neonatal depression.

Spinal Opioids Alone
Preservative-free opioids may be given intraspinally as a single injection or intermittently via an epidural or intrathecal catheter (Table 43–2). Relatively high doses are required for analgesia during labor when spinal opioids are used alone. For example, the ED50 during labor is 124 g for epidural fentanyl and 21 g for epidural sufentanil. The higher doses may be associated with a high risk of side effects, most importantly respiratory depression. For that reason combinations of local anesthetics and opioids are most commonly used (see below). Pure opioid techniques are therefore most useful for high-risk patients who may not tolerate the functional sympathectomy associated with spinal or epidural anesthesia. This group includes patients with hypovolemia or significant cardiovascular disease such as aortic stenosis, tetralogy of Fallot, Eisenmenger's syndrome, or pulmonary hypertension. With the exception of meperidine, which has local anesthetic properties, spinal opioids alone do not produce motor blockade or maternal hypotension (sympathectomy). Thus, they do not impair the ability of the parturient to push the baby out. Disadvantages include less complete analgesia, lack of perineal relaxation, and side effects such as pruritus, nausea, vomiting, sedation, and respiratory depression. Side effects may improve with low doses of naloxone (0.1–0.2 mg/h intravenously).

Table 43–2. Spinal Opioid Dosages for Labor and Delivery.
AgentIntrathecalEpidural
Morphine 0.25–0.5 mg5 mg
Meperidine 10–15 mg50–100 mg
Fentanyl 12.5–25 g50–150 g
Sufentanil 3–10 g10–20 g
Intrathecal Opioids
Intrathecal morphine in doses of 0.25–0.5 mg may produce satisfactory and prolonged (4–6 h) analgesia during the first stage of labor. Unfortunately, the onset of analgesia is slow (45–60 min), and these doses may not be sufficient in many patients. Higher doses are associated with a relatively high incidence of side effects. Morphine is therefore rarely used alone. The combination of morphine, 0.25 mg, and fentanyl, 12.5 g, (or sufentanil, 5 g) may result in a more rapid onset of analgesia (5 min). Intermittent boluses of 10–15 mg of meperidine, 12.5–25 g of fentanyl, or 3–10 g of sufentanil via an intrathecal catheter can also provide satisfactory analgesia for labor. Early reports of fetal bradycardia following intrathecal opioid injections (eg, sufentanil) are not supported by subsequent studies. Spinal meperidine has some weak local anesthetic properties and therefore can decrease blood pressure. Hypotension following intrathecal sufentanil for labor is likely related to the analgesia and decreased circulating catecholamine levels.

Epidural Opioids
Again relatively high doses ( 7.5 mg) of morphine are required for satisfactory analgesia during labor, but doses larger than 5 mg are not recommended because of the increased risk of delayed respiratory depression and because the analgesia is effective only in the early first stage of labor. The onset of analgesia may take 30–60 min but lasts up to 12–24 h (as will the risk of delayed respiratory depression). Epidural meperidine, 50–100 mg, provides consistently good but relatively brief analgesia (1–3 h). Epidural fentanyl, 50–150 g, or sufentanil, 10–20 g, usually produces analgesia within 5–10 min with few side effects, but it has a short duration (1–2 h). Although "single-shot" epidural opioids do not appear to cause significant neonatal depression, caution should be exercised following repeated administrations. Combinations of a lower dose of morphine, 2.5 mg, with fentanyl, 25–50 g (or sufentanil, 7.5–10 g), may result in a more rapid onset and prolongation of analgesia (4–5 h) with fewer side effects.

Local Anesthetic/Local Anesthetic–Opioid Mixtures
Epidural and spinal (intrathecal) analgesia more commonly utilizes local anesthetics either alone or with opioids for labor and delivery. Pain relief during the first stage of labor requires neural blockade at the T10–L1 sensory level, whereas pain relief during the second stage of labor requires neural blockade at T10–S4. Continuous lumbar epidural analgesia is the most versatile and most commonly employed technique, because it can be used for pain relief for the first stage of labor as well as analgesia/anesthesia for subsequent vaginal delivery or cesarean section, if necessary. "Single-shot" epidural, spinal, or combined spinal epidural analgesia may be appropriate when pain relief is initiated just prior to vaginal delivery (the second stage). Obstetric caudal injections have largely been abandoned because of less versatility (they are most effective for perineal analgesia/anesthesia), the need for large volumes of local anesthetic, early paralysis of the pelvic muscles that may interfere with normal rotation of the fetal head, and a small risk of accidental puncture of the fetus.

Absolute contraindications to regional anesthesia include infection over the injection site, coagulopathy, thrombocytopenia, marked hypovolemia, true allergies to local anesthetics, and the patient's refusal or inability to cooperate for regional anesthesia. Preexisting neurological disease, back disorders, and some forms of heart disease are relative contraindications. Neuraxial anesthesia is contraindicated in the setting of anticoagulation. The use of regional anesthesia in patients on "minidose" heparin is controversial, but an epidural should generally not be performed within 6–8 h of a subcutaneous minidose of unfractionated heparin or 12–24 h of low-molecular-weight heparin (LMWH). Concomitant administration of an antiplatelet agent increases the risk of spinal hematoma. A previous VBAC is not considered a contraindication to regional anesthesia during labor. Concern that the anesthesia masks the pain associated with uterine rupture may not be justified, because dehiscence of a lower segment scar frequently does not cause pain even without epidural anesthesia; moreover, changes in uterine tone and contraction pattern may be more reliable signs.

Before performing any regional block, appropriate equipment and supplies for resuscitation should be checked and made immediately available. Minimum supplies include oxygen, suction, a mask with a positive-pressure device for ventilation, a functioning laryngoscope, endotracheal tubes (6 or 6.5 mm), oral or nasal airways, intravenous fluids, ephedrine, atropine, thiopental (or propofol), and succinylcholine. The ability to frequently monitor blood pressure and heart rate is mandatory. A pulse oximeter and capnograph should also be readily available.

Lumbar Epidural Anaglesia
As discussed in Chapter 42, traditionally epidural analgesia for labor is administered only when labor is well established. However, recent studies suggest that when dilute mixtures of a local anesthetic and an opioid are used epidural analgesia has little if any effect on the progress of labor. Concerns about increasing the likelihood of an oxytocin augmentation, operative (eg, forceps) delivery, or cesarean sections appear to be unjustified. It is often advantageous to place an epidural catheter early, when the patient is comfortable and can be positioned easily. Moreover, should emergent cesarean section become necessary the presence of a well-functioning epidural catheter makes it possible to avoid general anesthesia.
Epidural analgesia should generally be initiated when the parturient wants it (on demand) and the obstetrician approves it. A more conservative approach is to wait until labor is well established. Although exact criteria vary, commonly accepted conservative criteria include no fetal distress; good regular contractions 3–4 min apart and lasting about 1 min; adequate cervical dilatation, ie, 3–4 cm; and engagement of the fetal head. Even with a conservative approach, epidural anesthesia is often administered earlier to parturients who are committed to labor, eg, ruptured membranes and receiving an oxytocin infusion once a good contraction pattern is achieved.

Technique
The technique of epidural analgesia/anesthesia is described in Chapter 16. Parturients may be positioned on their sides or in the sitting position for the block. The sitting position is often more useful for identifying the midline in obese patients. When epidural anesthesia is being given for vaginal delivery (second stage), the sitting position helps ensure good sacral spread.

Because the epidural space pressure may be positive in some parturients, correct identification of the epidural space may be difficult, and unintentional dural puncture can readily occur; the incidence of wet taps in obstetric patients is 0.25–9%, depending on clinician experience. Some clinicians advocate the midline approach, whereas others favor the paramedian approach. If air is used for detecting loss of resistance, the amount injected should be limited as much as possible; injection of excessive amounts of air (> 2–3 mL) in the epidural space has been associated with patchy or unilateral analgesia and headache. The average depth of the epidural space in obstetric patients is reported to be 5 cm from the skin. Placement of the epidural catheter at the L3–4 or L4–5 interspace is generally optimal for achieving a T10–S5 neural blockade. If unintentional dural puncture occurs, the anesthetist has two choices: (1) place the epidural catheter in the subarachnoid space for continuous spinal analgesia and anesthesia (see below), or (2) remove the needle and attempt placement at a higher spinal level.

Choice of Epidural Catheter
Many clinicians advocate use of a multiholed catheter instead of a single-holed catheter for obstetric anesthesia. Use of a multiholed catheter appears to be associated with fewer unilateral blocks, and greatly reduces the incidence of false-negative aspiration for intravascular catheter placement. Advancing a multiholed catheter 7–8 cm into the epidural space appears to be optimal for obtaining adequate sensory levels. A single-hole catheter need only be advanced 3–5 cm into the epidural space. Shorter insertion depths (< 5 cm), however, may favor dislodgment of the catheter out of the epidural space in obese patients following flexion/extension movements of the spine. Spiral wire-reinforced catheters are very resistant to kinking. A spiral or spring tip, particularly when used without a stylet, is associated with fewer, less intense paresthesias and may also be associated with a lower incidence of inadvertent intravascular insertion.

Choice of Local Anesthetic Solutions
The addition of opioids to local anesthetic solutions for epidural anesthesia has dramatically changed the practice of obstetric anesthesia. The synergy between epidural opioids and local anesthetic solutions appears to reflect separate sites of action, namely, opiate receptors and neuronal axons, respectively. When the two are combined, very low concentrations of both local anesthetic and opioid can be used. More importantly, the incidence of adverse side effects, such as hypotension and drug toxicity, is likely reduced. Although local anesthetics can be used alone, there is rarely a reason to do so. Moreover, when an opioid is omitted, the higher concentration of local anesthetic required (eg, bupivacaine 0.25% and ropivacaine 0.2%) can impair the parturient's ability to push effectively as the labor progresses. Bupivacaine or ropivacaine in concentrations of 0.0625–0.125% with either fentanyl 2–3 g/mL or sufentanil 0.3–0.5 g/mL is most often used. In general, the lower the concentration of the local anesthetic the higher the concentration of opioid that is required. Very dilute local anesthetic mixtures (0.0625%) generally do not produce motor blockade and may allow some patients to ambulate ("walking" or "mobile" epidural). The long duration of action of bupivacaine makes it a popular agent for labor. Ropivacaine may be preferable because of possibly less motor blockade and its reduced potential for cardiotoxicity. Systemic absorption of the opioid can decrease fetal heart rate variability due to transient sedation of the fetus.

The effect of epinephrine-containing solutions on the course of labor is somewhat controversial. Many clinicians use epinephrine-containing solutions only for intravascular test doses because of concern that the solutions may slow the progression of labor or adversely affect the fetus; others use only very dilute concentrations of epinephrine such as 1:800,000 or 1:400,000. Studies comparing these various agents have failed to find any differences in neonatal Apgar scores, acid–base status, or neurobehavioral evaluations.

Epidural Activation for the First Stage of Labor
Epidural injections may be done either before or after the catheter is placed. Activation through the needle can facilitate catheter placement, whereas activation through the catheter ensures proper function of the catheter. The following sequence is suggested for epidural activation:
1. Administer a 500- to 1000-mL intravenous bolus of lactated Ringer's injection while the epidural catheter is being placed. The value of crystalloid fluid boluses in preventing hypotension following activation has been questioned because of their modest efficacy (see below). Moreover, rapid infusion of intravenous fluids can transiently decrease uterine activity. Glucose-free intravenous fluid boluses are used to avoid maternal hyperglycemia and hypersecretion of insulin by the fetus. When placental transfer of glucose ceases abruptly following delivery, persistent high circulating levels of insulin in the neonate can result in transient hypoglycemia.
 
2. Test for unintentional subarachnoid or intravascular placement of the needle or catheter with a 3-mL test dose of a local anesthetic with 1:200,000 epinephrine (controversial; see the section on Prevention of Unintentional Intravascular and Intrathecal Injections). Many clinicians test with lidocaine 1.5% because of less toxicity following unintentional intravascular injection and a more rapid onset of spinal anesthesia than with bupivacaine and ropivacaine. The test dose should be injected between contractions to help reduce false positive signs of an intravascular injection, ie, tachycardia due to a painful contraction.
 
3. If after 5 min signs of intravascular or intrathecal injection are absent, with the patient supine and left uterine displacement, give 10 mL of the local anesthetic–opioid mixture in 5 mL increments, waiting 1–2 min between doses, to achieve a T10–L1 sensory level. The initial bolus is usually 0.1–0.2% of ropivacaine or 0.0625–0.125% of bupivacaine combined with either 50–100 g of fentanyl or 10–20 g of sufentanil.
 
4. Monitor with frequent blood pressure measurements for 20–30 min or until the patient is stable. Pulse oximetry should also be used. Oxygen is administered via face mask if there are any significant drops in blood pressure or oxygen saturation readings.
 
5. Repeat steps 3 and 4 when pain recurs until the first stage of labor is completed. Alternatively, a continuous epidural infusion technique may be employed using bupivacaine or ropivacaine in concentrations of 0.0625–0.125% with either fentanyl 1–5 g/mL or sufentanil 0.2–0.5 g/mL 10 mL/h, subsequently adjusted according to the patient's needs (range 5–15 mL/h). A third choice would be to use patient-controlled epidural analgesia (PCEA). Some studies suggest that total drug requirements may be less and patient satisfaction is greater with PCEA compared to other epidural techniques. PCEA settings are typically a 5 mL bolus dose with a 5–10 min lockout and 0–5 mL/h basal rate; a 1 h limit of 15–20 mL may used. Migration of the epidural catheter into a blood vessel during a continuous infusion technique may be heralded by loss of effective analgesia; a high index of suspicion is required because overt signs of systemic toxicity may be absent. Erosion of the catheter through the dura results in a slowly progressive motor blockade of the lower extremities and a rising sensory level.
Epidural Activation during the Second Stage of Labor
Activation for the second stage of labor extends the block to include the S2–4 dermatomes. Whether a catheter is already in place or epidural anesthesia is just being initiated, the following steps should be undertaken:
1. Give a 500- to 1000-mL intravenous bolus of lactated Ringer's injection.
 
2. If the patient does not already have a catheter in place, identify the epidural space while the patient is in a sitting position. A patient who already has an epidural catheter in place should be placed in a semiupright or sitting position prior to injection.
 
3. Give a 3-mL test dose of local anesthetic (eg, lidocaine 1.5%) with 1:200,000 epinephrine. Again the injection should be between contractions.
 
4. If after 5 min signs of an intravascular or intrathecal injection are absent, give 10–15 mL of additional local anesthetic–opioid mixture at a rate not faster than 5 mL every 1–2 min.
 
5. Administer oxygen by face mask and lay the patient supine with left uterine displacement and monitor blood pressure every 1–2 min for the first 15 min, then every 5 min thereafter.
Prevention of Unintentional Intravascular and Intrathecal Injections
Safe administration of epidural anesthesia is critically dependent on avoiding unintentional intrathecal or intravascular injections. Unintentional intravascular or intrathecal placement of an epidural needle or catheter is possible even when aspiration fails to yield blood or cerebrospinal fluid (CSF). The incidence of unintentional intravascular or intrathecal placement of an epidural catheter is 5–15% and 0.5–2.5%, respectively. Even a properly placed catheter can subsequently erode into an epidural vein or an intrathecal position. This possibility should be excluded each time local anesthetic is injected through an epidural catheter.

Test doses of lidocaine, 45–60 mg, bupivacaine, 7.5–10 mg, ropivacaine, 6–8 mg, or chloroprocaine, 100 mg, can be given to exclude unintentional intrathecal placement. Signs of sensory and motor blockade usually become apparent within 2–3 min and 3–5 min, respectively, if the injection is intrathecal.
Test dose techniques for unintentional intravascular injections may not be reliable in parturients. The best method for detecting intravascular injections is controversial in obstetric anesthesia. In patients not receiving -adrenergic antagonists, the intravascular injection of a local anesthetic solution with 15–20 g of epinephrine consistently increases the heart rate by 20–30 beats/min within 30–60 s if the catheter (or epidural needle) is intravascular. This technique is not always reliable in parturients because they often have marked spontaneous baseline variations in heart rate with contractions. In fact, bradycardia has been reported in a parturient following intravenous injection of 15 g of epinephrine. Moreover, in animal studies, 15 g of epinephrine intravenously reduces uterine blood flow, and the dose has been associated with fetal distress in humans. Alternative methods of detecting unintentional intravascular catheter placement include eliciting tinnitus or perioral numbness following a 100-mg test dose of lidocaine, eliciting a chronotropic effect following injection of 5 g of isoproterenol, or injecting 1 mL of air while monitoring the patient with a precordial Doppler. With the possible exception of the precordial Doppler, false-negative responses may be encountered with all methods; false-positive responses can also be observed. The use of dilute local anesthetic solutions and slow injection rates of no more than 5 mL at a time may also enhance detection of unintentional intravascular injections before catastrophic complications develop.


Management of Complications
Hypotension
Generally defined as a 20–30% decrease in blood pressure or a systolic pressure less than 100 mm Hg, hypotension is the most common side effect of regional anesthesia. It is primarily due to decreased sympathetic tone and is greatly accentuated by aortocaval compression and an upright or semiupright position. Treatment should be aggressive in obstetric patients and consists of intravenous boluses of ephedrine (5–15 mg) or phenylephrine (25–50 g), supplemental oxygen, left uterine displacement, and an intravenous fluid bolus. Use of the head-down (Trendelenburg) position is controversial because of its potentially detrimental effects on pulmonary gas exchange.

Unintentional Intravascular Injections
Early recognition of intravascular injections, detected by the use of small incremental doses of local anesthetic, may prevent more serious local anesthetic toxicity, such as seizures or cardiovascular collapse. Intravascular injections of toxic doses of lidocaine or chloroprocaine usually present as seizures. Thiopental, 50–100 mg, will cease frank seizure activity. Small doses of propofol may also terminate seizures but experience with it is more limited for this purpose. Maintenance of a patent airway and adequate oxygenation are of paramount importance. Immediate endotracheal intubation with succinylcholine and cricoid pressure should be considered. Intravascular injections of bupivacaine can cause rapid and profound cardiovascular collapse as well as seizure activity. Cardiac resuscitation may be exceedingly difficult and is particularly aggravated by acidosis and hypoxia. Amiodarone appears to be particularly useful in reversing bupivacaine-induced decreases in the threshold for ventricular tachycardia.

Unintentional Intrathecal Injection
If dural puncture is recognized immediately after injection of local anesthetic, an attempt to aspirate the local anesthetic may be tried but is usually unsuccessful. The patient should be gently placed supine with left uterine displacement. Head elevation accentuates hypotension and should be avoided. The hypotension should be treated aggressively with ephedrine and intravenous fluids. A high spinal level can also result in diaphragmatic paralysis, which necessitates intubation and ventilation with 100% oxygen. Delayed onset of a very high and often patchy or unilateral block may be due to unrecognized subdural injection, which is managed similarly.

Postdural Puncture Headache (PDPH)
Headache frequently follows unintentional dural puncture in parturients. A self-limited headache may occur without dural puncture; in such instances injection of significant amounts of air into the epidural space during a loss of resistance technique may be responsible. PDPH is due to decreased intracranial pressure with compensatory cerebral vasodilatation.  Bed rest, hydration, oral analgesics, epidural saline injection (50 mL), and caffeine sodium benzoate (500 mg intravenously) may be effective in patients with mild headaches. Patients with moderate to severe headaches usually require an epidural blood patch (15–20 mL). Prophylactic epidural blood patches are generally not recommended; 25–50% of patients may not require a blood patch following dural puncture. Some clinicians believe that delaying a blood patch for 24 h increases its efficacy, but this practice is controversial. Subdural hematoma has been reported as a rare complication 1–6 weeks following unintentional dural puncture in obstetric patients.

Maternal Fever
Epidural analgesia for labor is associated with a higher incidence of temperature elevation in parturients compared with those delivering without the benefit of epidural analgesia. Maternal fever is often interpreted as chorioamnionitis and may trigger an invasive neonatal sepsis evaluation. There is no evidence, however, that neonatal sepsis is actually increased with epidural analgesia. This elevation in temperature may result from epidural-induced shivering or inhibition of sweating and hyperventilation; it is most commonly encountered in nulliparous women, who often have prolonged labor and are more likely to receive epidural analgesia.

Combined Spinal & Epidural (CSE) Analgesia
Techniques using CSE analgesia and anesthesia may particularly benefit patients with severe pain early in labor and those who receive analgesia/anesthesia just prior to delivery. Intrathecal opioid and local anesthetic are injected and an epidural catheter is left in place. The intrathecal drugs provide almost immediate pain control and have minimal effects on the early progress of labor, whereas the epidural catheter provides a route for subsequent analgesia for labor and delivery or anesthesia for cesarean section. Addition of small doses of local anesthetic agents to intrathecal opioid injection greatly potentiates their analgesia and can significantly reduce opioid requirements. Thus, many clinicians will inject 2.5 mg of preservative-free bupivacaine or 3–4 mg of ropivacaine with intrathecal opioids for analgesia in the first stage of labor. Intrathecal doses for CSE are fentanyl 4–5 g or sufentanil 2–3 g. Addition of 0.1 mg of epinephrine prolongs the analgesia with such mixtures but not for intrathecal opioids alone. Some studies suggest that CSE techniques may be associated with greater patient satisfaction than epidural analgesia alone. A 24- to 27-gauge pencil-point spinal needle (Whitacre, Sprotte, or Gertie Marx) is used to minimize the incidence of PDPH.

The spinal and epidural needles may be placed at different interspaces, but most clinicians use the same interspace. Use of saline for identification for the epidural space is best avoided because of potential confusion of saline for CSF. With the needle-through-needle technique, the epidural needle is placed in the epidural space and a long spinal needle is then introduced through it and advanced further into the subarachnoid space. A distinct pop is felt as the needle penetrates the dura. The needle-beside-needle technique typically employs a specially designed epidural needle that has a channel for the spinal needle. After the intrathecal injection and withdrawal of the spinal needle, the epidural catheter is threaded into position and the epidural needle is withdrawn. The risk of advancing the epidural catheter through the dural hole created by the spinal needle appears to be very small when a 25-gauge or smaller needle is used. The epidural catheter, however, should be aspirated carefully and local anesthetic should always be given slowly and in small increments to avoid unintentional intrathecal injections. Moreover, epidural drugs should be administered and titrated carefully because the dural hole may increase the flux of epidural drugs into CSF and enhance their effects. Some studies suggest that the incidence of dural puncture from an epidural needle is less with CSE than with an epidural technique alone.

Spinal Anesthesia
Spinal anesthesia given just prior to delivery—also known as saddle block—provides profound anesthesia for operative vaginal delivery. A 500- to 1000-mL fluid bolus is given prior to the procedure, which is performed with the patient in the sitting position. Use of a 22-gauge or smaller, pencil-point spinal needle (Whitacre, Sprotte, or Gertie Marx) decreases the likelihood of PDPH. Hyperbaric tetracaine (3–4 mg), bupivacaine (6–7 mg), or lidocaine (20–40 mg) usually provides excellent perineal anesthesia. Addition of fentanyl 12.5–25 g or sufentanil 5–7.5 g significantly potentiates the block. A T10 sensory level can be obtained with slightly larger amounts of local anesthetic. The intrathecal injection should be given slowly over 30 s and between contractions to minimize excessive cephalad spread. Three minutes after injection, the patient is placed in the lithotomy position with left uterine displacement.

General Anesthesia
Because of the increased risk of aspiration, general anesthesia for vaginal delivery is avoided except for a true emergency. If an epidural catheter is already in place and time permits, rapid-onset regional anesthesia can often be obtained with alkalinized lidocaine 2% or chloroprocaine 3%. Table 43–3 lists indications for general anesthesia during vaginal delivery. Many of these indications share the need for uterine relaxation. Intravenous nitroglycerin, 50–100 g, has been shown to be effective in inducing uterine relaxation and may obviate the need for general anesthesia in these cases.

Table 43–3. Possible Indications for General Anesthesia during Vaginal Delivery.
Fetal distress during the second stage
Tetanic uterine contractions
Breech extraction
Version and extraction
Manual removal of a retained placenta
Replacement of an inverted uterus
Psychiatric patients who become uncontrollable
Suggested Technique for Vaginal Delivery
1. Place a wedge under the right hip for left uterine displacement.
2. Preoxygenate the patient for 3–5 min as monitors are applied. Defasciculation with a nondepolarizing muscle relaxant is usually not necessary, because most pregnant patients do not fasciculate following succinylcholine. Moreover, fasciculations do not appear to promote regurgitation, because any increase in intragastric pressure is matched by a similar increase in the lower esophageal sphincter.
3. Once all monitors are applied and the obstetrician is ready, proceed with a rapid-sequence induction while cricoid pressure is applied and intubate with a 6- to 6.5-mm endotracheal tube. Propofol, 2 mg/kg, or thiopental, 4 mg/kg, and succinylcholine, 1.5 mg/kg, are most commonly used unless the patient is hypovolemic or hypotensive, in which case ketamine, 1 mg/kg, is used as the induction agent.
4. After successful intubation, use 1–2 minimum alveolar concentration (MAC) of any potent volatile inhalational agent in 100% oxygen while carefully monitoring blood pressure.
5. If skeletal muscle relaxation is necessary, a short- to intermediate-acting, nondepolarizing muscle relaxant (eg, mivacurium or atracurium) is used.
6. Once the fetus and placenta are delivered, the volatile agent is decreased to less than 0.5 MAC or discontinued, an oxytocin infusion is started (20–40 U/L of intravenous fluid), and a nitrous oxide–opioid technique or propofol infusion can be used to avoid recall.
7. An attempt to aspirate gastric contents may be made via an orogastric tube to decrease the likelihood of pulmonary aspiration on emergence.
8. At the end of the procedure, the skeletal nondepolarizing muscle relaxant is reversed, the gastric tube (if placed) is removed, and the patient is extubated while awake.
Anesthesia for Cesarean Section
Common indications for cesarean section are listed in Table 43–4. The choice of anesthesia for cesarean section is determined by multiple factors, including the indication for operating, its urgency, patient and obstetrician preferences, and the skills of the anesthetist. Cesarean section rates between institutions generally vary between 15 and 25%. In the United States approximately 80–90% are performed under regional anesthesia, nearly evenly split between spinal and epidural anesthesia. Regional anesthesia has become the preferred technique because general anesthesia has been associated with higher maternal mortality. Deaths associated with general anesthesia are generally related to airway problems, such as inability to intubate, inability to ventilate, or aspiration pneumonitis, whereas deaths associated with regional anesthesia are generally related to excessively high neural blockade or local anesthetic toxicity.


Table 43–4. Major Indications for Cesarean Section.
Labor unsafe for mother and fetus 
  Increased risk of uterine rupture
    Previous classic cesarean section
    Previous extensive myomectomy or uterine reconstruction
  Increased risk of maternal hemorrhage
    Central or partial placenta previa
    Abruptio placentae
    Previous vaginal reconstruction
Dystocia 
  Abnormal fetopelvic relations
    Fetopelvic disproportion
    Abnormal fetal presentation
       Transverse or oblique lie
       Breech presentation
  Dysfunctional uterine activity
Immediate or emergent delivery necessary 
  Fetal distress
  Umbilical cord prolapse
  Maternal hemorrhage
  Amnionitis
  Genital herpes with ruptured membranes
  Impending maternal death
Other advantages of regional anesthesia include (1) less neonatal exposure to potentially depressant drugs, (2) a decreased risk of maternal pulmonary aspiration, (3) an awake mother at the birth of her child, with the father also present if desired, and (4) the option of using spinal opioids for postoperative pain relief. The choice between spinal and epidural anesthesia is often based on physician preferences. Epidural anesthesia is preferred over spinal anesthesia by some clinicians because of the more gradual decrease in blood pressure associated with epidural anesthesia. Continuous epidural anesthesia also allows better control over the sensory level. Conversely, spinal anesthesia is easier to perform, has a more rapid, predictable onset, may produce a more intense (complete) block, and does not have the potential for serious systemic drug toxicity (because of the smaller dose of local anesthetic employed). Regardless of the regional technique chosen, the ability to administer a general anesthetic at any time during the procedure is mandatory. Moreover, administration of a nonparticulate antacid 1 h prior to surgery should also be considered.
General anesthesia offers (1) a very rapid and reliable onset, (2) control over the airway and ventilation, and (3) potentially less hypotension than regional anesthesia. General anesthesia also facilitates management in the event of severe hemorrhagic complications such as placenta accreta. Its principal disadvantages are the risk of pulmonary aspiration, the potential inability to intubate or ventilate the patient, and drug-induced fetal depression. Present anesthetic techniques, however, limit the dose of intravenous agents such that fetal depression is usually not clinically significant with general anesthesia when delivery occurs within 10 min of induction of anesthesia. Regardless of the type of anesthesia, neonates delivered more than 3 min after uterine incision have lower Apgar scores and acidotic blood gases.

Regional Anesthesia
Cesarean section requires a T4 sensory level. Because of the associated high sympathetic blockade, all patients should receive a 1000- to 1500-mL bolus of lactated Ringer's injection prior to neural blockade. Crystalloid boluses do not consistently prevent hypotension but can be helpful in some patients. Smaller volumes (250–500 mL) of colloid solutions, such as albumin or hetastarch, are more effective. After injection of the anesthetic, the patient is placed supine with left uterine displacement; supplemental oxygen (40–50%) is given; blood pressure is measured every 1–2 min until it stabilizes. Intravenous ephedrine, 10 mg, should be used to maintain systolic blood pressure > 100 mm Hg. Small intravenous doses of phenylephrine, 25–100 g, or an infusion up to 100 g/min may also be used safely. Some studies suggest less neonatal acidosis with phenylephrine compared to ephedrine. Prophylactic administration of ephedrine (5 mg intravenous or 25 mg intramuscular) has been advocated by some clinicians for spinal anesthesia, as precipitous hypotension may be seen but is not recommended for most patients because of a risk of inducing excessive hypertension. Hypotension following epidural anesthesia typically has a slower onset. Slight Trendelenburg positioning facilitates achieving a T4 sensory level and may also help prevent severe hypotension. Extreme degrees of Trendelenburg may interfere with pulmonary gas exchange.

Spinal Anesthesia
The patient is usually placed in the lateral decubitus or sitting position, and a hyperbaric solution of tetracaine (7–10 mg), lidocaine (50–60 mg), or bupivacaine (10–15 mg) is injected. Epinephrine 0.1 mg can enhance the quality of the block and may prolong its duration of tetracaine and bupivacaine. Use of a 22-gauge or smaller, pencil-point spinal needle (Whitacre, Sprotte, or Gertie Marx) decreases the incidence of PDPH. Adding 12.5–25 g of fentanyl or 5–10 g of sufentanil to the local anesthetic solution enhances the intensity of the block and prolongs its duration without adversely affecting neonatal outcome. Addition of preservative-free morphine, 0.2–0.3 mg, can prolong postoperative analgesia up to 24 h but requires special monitoring for delayed postoperative respiratory depression. Regardless of the anesthetic agents used, considerable variability in the maximum sensory level should be expected.
Continuous spinal anesthesia is also a reasonable option following unintentional dural puncture while placing an epidural catheter for cesarean section. After the catheter is advanced 2–2.5 cm into the lumbar subarachnoid space and secured, it can be used to inject anesthetic agents; moreover, it allows later supplementation of the anesthesia if necessary.

Epidural Anesthesia
Epidural anesthesia for cesarean section is generally most satisfactory when an epidural catheter is used. The catheter facilitates achieving an initial T4 sensory level, allows supplementation if necessary, and provides an excellent route for postoperative opioid administration. After a negative test dose, a total of 15–25 mL of local anesthetic is injected slowly in 5-mL increments. Lidocaine 2% (with or without 1:200,000 epinephrine) or chloroprocaine 3% is most commonly used. Addition of fentanyl, 50–100 g, or sufentanil, 10–20 g, greatly enhances the intensity of the block and prolongs its duration without adversely affecting neonatal outcome. Some practitioners also add sodium bicarbonate (7.5% or 8.4% solution) to local anesthetic solutions (1 mEq/10 mL of lidocaine and 0.05 mEq/10 mL of bupivacaine or ropivacaine) to increase the concentration of the nonionized free base and produce a faster onset and more rapid spread of epidural anesthesia. If pain develops as the sensory level recedes, additional local anesthetic is given in 5-mL increments to maintain a T4 sensory level. "Patchy" anesthesia prior to delivery of the baby can be treated with 10–20 mg of intravenous ketamine or 30% nitrous oxide. After delivery, intravenous opioid supplementation may also be used, provided excessive sedation and loss of consciousness are avoided. Pain that remains intolerable in spite of a seemingly adequate sensory level and that proves unresponsive to these measures necessitates general anesthesia with endotracheal intubation. Nausea can be treated intravenously with ondansetron 4 mg or metoclopramide 10 mg.

Epidural morphine, 5 mg, at the end of surgery provides good to excellent pain relief postoperatively for 6–24 h. An increased incidence (3.5–30%) of recurrent herpes simplex labialis infection has been reported 2–5 days following epidural morphine in some studies. Postoperative analgesia can also be provided by continuous epidural infusions of fentanyl, 25–75 g/h, or sufentanil, 5–10 g/h, at a volume rate of approximately 10 mL/h. Epidural butorphanol, 2 mg, can also provide effective postoperative pain relief, but marked somnolence is often a troublesome side effect.

CSE Anesthesia
The technique for CSE is described in the above section on combined spinal epidural analgesia. For cesarean section, it combines the benefit of rapid, reliable, intense blockade of spinal anesthesia with the flexibility of an epidural catheter. The catheter also allows supplementation of anesthesia and can be used for postoperative analgesia. As mentioned previously, drugs given epidurally should be administered and titrated carefully because the dural hole created by the spinal needle increases the flux of epidural drugs into CSF and enhances their effects.

General Anesthesia
Pulmonary aspiration of gastric contents (incidence: 1:500–400 for obstetric patients versus 1:2000 for all patients) and failed endotracheal intubation (incidence: 1:300 versus 1:2000 for all patients) during general anesthesia are the major causes of maternal morbidity and mortality. Every effort should be made to ensure optimal conditions prior to the start of anesthesia and to follow measures aimed at preventing these complications.

All patients should possibly receive prophylaxis against severe nonparticulate aspiration pneumonia with 30 mL of 0.3 M sodium citrate 30–45 min prior to induction. Patients with additional risk factors predisposing them to aspiration should also receive intravenous ranitidine, 50 mg, and/or metoclopramide, 10 mg, 1–2 h prior to induction; such factors include morbid obesity, symptoms of gastroesophageal reflux, a potentially difficult airway, or emergent surgical delivery without an elective fasting period. Premedication with oral omeprazole, 40 mg, at night and in the morning also appears to be highly effective in high-risk patients undergoing elective cesarean section. Although anticholinergics theoretically may reduce lower esophageal sphincter tone, premedication with a small dose of glycopyrrolate (0.1 mg) helps reduce airway secretions and should be considered in patients with a potentially difficult airway.

Anticipation of a difficult endotracheal intubation may help reduce the incidence of failed intubations. Examination of the neck, mandible, dentition, and oropharynx often helps predict which patients may have problems. Useful predictors of a difficult intubation include Mallampati classification, short neck, receding mandible, and prominent maxillary incisors. The higher incidence of failed intubations in pregnant patients compared with nonpregnant surgical patients may be due to airway edema, a full dentition, or large breasts that can obstruct the handle of the laryngoscope in patients with short necks. Proper positioning of the head and neck may facilitate endotracheal intubation in obese patients: elevation of the shoulders, flexion of the cervical spine, and extension of the atlantooccipital joint (Figure 43–3). A variety of laryngoscope blades, a short laryngoscope handle, at least one extra styletted endotracheal tube (6 mm), Magill forceps (for nasal intubation), a laryngeal mask airway (LMA), an intubating LMA (Fastrach), a fiberoptic bronchoscope, the capability for transtracheal jet ventilation, and possibly an esophageal-tracheal Combitube should be readily available. When difficulty in securing the airway is suspected, alternatives to the standard rapid-sequence induction, such as regional anesthesia or awake fiberoptic techniques, should be considered. Moreover, a clear plan should be formulated for a failed endotracheal intubation following induction of anesthesia (Figure 43–4). Note that the life of the mother takes priority over delivery of the fetus. In the absence of fetal distress, the patient should be awakened, and an awake intubation, with regional or local (infiltration) anesthesia, may be tried. In the presence of fetal distress, if spontaneous or positive ventilation (by mask or LMA) with cricoid pressure is possible, delivery of the fetus may be attempted. In such instances, a potent volatile agent in oxygen is employed for anesthesia, but once the fetus is delivered, nitrous oxide can be added to reduce the concentration of the volatile agent; sevoflurane may be the best volatile agent because it may be least likely to depress ventilation. The inability to ventilate the patient at any time mandates immediate cricothyrotomy or tracheostomy.

Suggested Technique for Cesarean Section
1. The patient is placed supine with a wedge under the right hip for left uterine displacement.
2. Preoxygenation is accomplished with 100% oxygen for 3–5 min while monitors are applied. Defasciculation is generally not necessary (see the section on Suggested Technique for Vaginal Delivery).
3. The patient is prepared and draped for surgery.
4. When the surgeons are ready, a rapid-sequence induction with cricoid pressure is performed using propofol, 2 mg/kg (or thiopental 4 mg/kg) and succinylcholine, 1.5 mg/kg. Ketamine, 1 mg/kg, is used instead of thiopental in hypovolemic or asthmatic patients. Other agents, including methohexital, etomidate, and midazolam, offer little benefit in obstetric patients. In fact, midazolam may be more likely to produce maternal hypotension and neonatal depression.
5. Surgery is begun only after proper placement of the endotracheal tube is confirmed by capnography. Excessive hyperventilation (PaCO2, 25 mm Hg) should be avoided because it can reduce uterine blood flow and has been associated with fetal acidosis.
6. Fifty percent nitrous oxide in oxygen with up to 0.75 MAC of a low concentration of a volatile agent (eg, 1% sevoflurane, 0.75% isoflurane, or 3% desflurane) is used for maintenance. The low dose of volatile agent helps ensure amnesia but is generally not enough to cause excessive uterine relaxation or prevent uterine contraction following oxytocin. A muscle relaxant of intermediate duration (mivacurium, atracurium, cisatracurium, or rocuronium) is used for relaxation.
7. After the neonate and placenta are delivered, 20–30 U of oxytocin is added to each liter of intravenous fluid. The nitrous oxide concentration may then be increased to 70% and/or additional intravenous agents, such as additional propofol, an opioid or benzodiazepine, can be given to ensure amnesia.
8. If the uterus does not contract readily, an opioid should be given, and the halogenated agent should be discontinued. Methylergonovine (Methergine), 0.2 mg intramuscularly, may also be given but can increase arterial blood pressure. 15-Methylprostaglandin F2 (Hemabate), 0.25 mg intramuscularly, may also be used.
9. An attempt to aspirate gastric contents may be made via an oral gastric tube to decrease the likelihood of pulmonary aspiration on emergence.
10. At the end of surgery, muscle relaxants are completely reversed, the gastric tube (if placed) is removed, and the patient is extubated while awake to reduce the risk of aspiration.
Anesthesia for Emergency Cesarean Section
Indications for emergency cesarean section include massive bleeding (placenta previa or accreta, abruptio placentae, or uterine rupture), umbilical cord prolapse, and severe fetal distress. A distinction must be made between a true emergency requiring immediate delivery (previous referred to as "crash") and one in which some delay is possible. Close communication with the obstetrician is necessary to determine whether fetus, mother, or both are in immediate jeopardy requiring general anesthesia or there is time to safely administer regional anesthesia. In the first instance, even if the patient has an epidural catheter in place, the delay in establishing adequate epidural anesthesia may prohibit its use. Moreover, regional anesthesia is contraindicated in severely hypovolemic or hypotensive patients. Adequate preoxygenation may be achieved rapidly with four maximal breaths of 100% oxygen while monitors are being applied. Ketamine, 1 mg/kg, should be substituted for thiopental in hypotensive or hypovolemic patients.

Table 43–5 lists commonly accepted signs of fetal distress, an imprecise and poorly defined term. In most instances the diagnosis is primarily based on monitoring of fetal heart rate (see below). Because worrisome fetal heart rate patterns have a relatively high incidence of false-positive results, careful interpretation of other parameters, such as fetal scalp pH or fetal pulse oximetry, may also be necessary. Moreover, continuation of fetal monitoring in the operating room may help avoid unnecessary induction of general anesthesia for fetal distress when additional time for use of regional anesthesia is possible. In selected instances where immediate delivery is not absolutely mandatory, epidural anesthesia (with 3% chloroprocaine or alkalinized 2% lidocaine) or spinal anesthesia may be appropriate.

Table 43–5. Signs of Fetal Distress.
Nonreassuring fetal heart rate pattern
  Repetitive late decelerations
  Loss of fetal beat-to-beat variability associated with late or deep decelerations
  Sustained fetal heart rate < 80 beats/min
Fetal scalp pH < 7.20
Meconium-stained amniotic fluid
Oligohydramnios
Intrauterine growth restriction
Anesthesia for the Complicated Pregnancy
Umbilical Cord Prolapse
Prolapse of the umbilical cord complicates 0.2–0.6% of deliveries. Umbilical cord compression following prolapse can rapidly lead to fetal asphyxia. Predisposing factors include excessive cord length, malpresentation, low birth weight, grand parity (more than five pregnancies), multiple gestations, and artificial rupture of membranes. The diagnosis is suspected after sudden fetal bradycardia or profound decelerations and is confirmed by physical examination. Treatment includes immediate steep Trendelenburg or knee-chest position and manual pushing of the presenting fetal part back up into the pelvis until immediate cesarean section under general anesthesia. If the fetus is not viable, vaginal delivery is allowed to continue.

Dystocia & Abnormal Fetal Presentations & Positions
Dystocia, or difficult labor, may be due to ineffective uterine contractions; abnormal lie, position, or presentation; or cephalopelvic disproportion that is either due to a large fetus or a small maternal pelvis. Abnormal fetal positions and presentations increase maternal and fetal morbidity and mortality. They also increase the likelihood that anesthesia will be required.

The fetus may lie longitudinally, transversely, or obliquely in the uterus. Fetal presentation refers to the body part that overlies the pelvic inlet. Spontaneous vaginal delivery can occur only with a longitudinal lie, in which either the head (vertex) or buttocks or legs (breech) descend first. The posture (attitude) of the fetus is normally flexion but may be extension. A vertex presentation with flexion together with rotation of the head into an occiput anterior position allows for optimal passage of the fetal skull through the pelvis.

Primary Dysfunctional Labor
Failure of labor to progress normally (see Chapter 42) may be due to inadequate or ineffective uterine contractions, referred to as primary dysfunctional labor. Although in most instances abnormal uterine contractility is responsible, anatomic abnormalities may also play a major role (see the section on Abnormal Vertex Presentations).

A prolonged latent phase by definition exceeds 20 h in a nulliparous parturient and 14 h in a multiparous patient. The cervix usually remains at 4 cm or less but is completely effaced. The etiology is likely ineffective contractions without a dominant myometrial pacemaker. Arrest of dilatation is present when the cervix undergoes no further change after 2 h in the active phase of labor. A protracted active phase refers to slower than normal cervical dilatation, defined as < 1.2 cm/h in a nulliparous patient and < 1.5 cm/h in a multiparous parturient. A prolonged deceleration phase occurs when cervical dilatation slows markedly after 8 cm. The cervix becomes very edematous and appears to lose effacement. A prolonged second stage (disorder of descent) is defined as a descent of less than 1 cm/h and 2 cm/h in nulliparous and multiparous parturients, respectively. Failure of the head to descend 1 cm in station after adequate pushing is referred to as arrest of descent.

Oxytocin (see Chapter 42) is generally the treatment of choice for uterine contractile abnormalities. The drug is given intravenously at 1–6 mU/min and increased in increments of 1–6 mU/min every 15–40 min, depending on the protocol. Use of amniotomy is controversial. Treatment is usually expectant management, as long as the fetus and mother are tolerating the prolonged labor. When a trial of oxytocin is unsuccessful or when malpresentation or cephalopelvic disproportion is also present, operative vaginal delivery or cesarean section is indicated.

Breech Presentation
Breech presentations complicate 3–4% of deliveries and significantly increase both maternal and fetal morbidity and mortality rates. The most common cause is prematurity. Breech presentations increase neonatal mortality more than 5-fold. The incidence of cord prolapse is up to 10%. External cephalic version may be attempted after 36–38 weeks gestation and prior to the onset of labor; the procedure attempts to reverse the fetal lie and guide the head into the pelvis. Some obstetricians may also administer a tocolytic agent at the same time. In some centers, epidural anesthesia is used; the epidural catheter can then be used for analgesia after induction of labor. Although an external version is successful in 75% of patients it can cause placental abruption and umbilical cord compression necessitating immediate cesarean section.
Because the shoulders or head can become trapped after vaginal delivery of the body, some obstetricians employ cesarean section for all breech presentations. The cesarean section rate for breech is 80–100%. Manual or forceps-assisted partial breech extraction is usually necessary with vaginal delivery. The need for breech extraction does not appear to be increased when epidural anesthesia is used for labor—if labor is well established prior to epidural activation. Moreover, epidural anesthesia may decrease the likelihood of a trapped head, because the former relaxes the perineum. Nonetheless, the fetal head can become trapped in the uterus even during cesarean section under regional anesthesia; rapid induction of general endotracheal anesthesia and administration of a volatile agent are necessary in such instances to relax the uterus. Alternatively, nitroglycerin 50–100 g intravenously can be tried.

Abnormal Vertex Presentations
When the fetal occiput fails to spontaneously rotate anteriorly, a persistent occiput posterior presentation results in a more prolonged and painful labor. Manual, vacuum, or forceps rotation is usually necessary but increases the likelihood of maternal and fetal injuries. Regional anesthesia can be used to provide perineal analgesia and pelvic relaxation, allowing manual or forceps rotation followed by forceps delivery.
A face presentation occurs when the fetal head is hyperextended and generally requires cesarean section. Vaginal delivery of a face presentation is possible only if the chin is directed anteriorly (mentum anterior). Persistent mentum posterior requires cesarean section. Brow presentation is often associated with prolonged and dysfunctional labor. Vaginal delivery can occur only if the head extends into a face presentation or flexes into a normal vertex presentation. Shoulder presentations occur with an oblique lie or transverse lie. Vaginal delivery is impossible. It typically leads to dysfunctional labor and predisposes to cord prolapse when the membranes rupture. Delivery requires cesarean section. A compound presentation occurs when an extremity enters the pelvis along with either the head or the buttocks. Vaginal delivery is usually still possible as the extremity often withdraws as the labor progresses.
Impaction of a shoulder against the pubic symphysis, or shoulder dystocia, complicates 0.2–2% of deliveries and is one of the major causes of birth injuries. The most important risk factor is fetal macrosomia. Shoulder dystocias are often difficult to predict. Several obstetric maneuvers can be used to relieve it, but a prolonged delay in the delivery could result in fetal asphyxia. Induction of general anesthesia may be necessary, if an epidural catheter is not already in place.

Multiple Gestations
Multiple gestations account for 1 birth in 90 and are commonly associated with two complications: breech presentation and prematurity. Anesthesia may be necessary for version, extraction, or cesarean section. The second baby (and any subsequent ones) is often more depressed and asphyxiated than the first. Regional anesthesia provides effective pain relief during labor, minimizes the need for central nervous system depressants, and may shorten the interval between the birth of the first and second baby. Some studies suggest that the acid–base status of the second twin is better when epidural anesthesia is used. Patients with multiple gestations, however, are more prone to develop hypotension from aortocaval compression, particularly after regional anesthesia. Left lateral uterine displacement and intravenous fluid loading are mandatory prior to regional anesthesia. Either regional or general anesthesia may be used for cesarean section; regional anesthesia may be associated with less neonatal depression.

Partum Hemorrhage
Maternal hemorrhage is one of the most common severe morbidities complicating obstetric anesthesia. Causes include placenta previa, abruptio placentae, and uterine rupture.

Placenta Previa
The incidence of placenta previa is 0.5% of pregnancies. Placenta previa often occurs in patients who have had a previous cesarean section or uterine myomectomy; other risk factors include multiparity, advanced maternal age, and a large placenta. The placenta may completely cover the internal cervical os (central or complete placenta previa), may partially cover the os (partial placenta previa), or may be close to the internal cervical os without extending beyond its edge (low-lying or marginal placenta). An anterior lying placenta previa increases the risk of excessive bleeding for cesarean section.

Placenta previa usually presents as painless vaginal bleeding. Although the bleeding often stops spontaneously, severe hemorrhage can occur at any time. When the gestation is less than 37 weeks in duration and the bleeding is mild to moderate, the patient is usually treated with bed rest and observation. After 37 weeks of gestation, delivery is usually accomplished via cesarean section. Patients with low-lying placenta may be allowed—although rarely—to deliver vaginally if the bleeding is mild.

All parturients with vaginal bleeding are assumed to have placenta previa until proved otherwise. An abdominal ultrasound examination can localize the placenta and establishes the diagnosis. If the patient is stable and fluid resuscitation has already taken place, regional anesthesia may be considered. Active bleeding or an unstable patient requires immediate cesarean section under general anesthesia. The patient should have two large-bore intravenous catheters in place, intravascular volume deficits must be vigorously replaced, and blood must be available for transfusion. A central venous line may be useful in monitoring and provides excellent access for rapid transfusion. The bleeding can continue after delivery because the placental implantation site in the lower uterine segment often does not contract well as does the rest of the uterus.

A history of a previous placenta previa or cesarean section increases the risk of placenta accreta, placenta increta, and placenta percreta in subsequent pregnancies. In these conditions, the placenta becomes adherent to the surface, invades the muscle, or completely penetrates the myometrium and surrounding tissues, respectively. The placenta becomes difficult or impossible to separate from the uterus. Moreover, these conditions regularly produce life-threatening maternal hemorrhage. Hysterectomy after delivery of the fetus is usually required to control profuse bleeding following separation of the placenta. Coagulopathy is common and requires correction with blood components.

Abruptio Placentae
Premature separation of a normal placenta complicates approximately 1–2% of pregnancies; it is said to be the most common cause of intrapartum fetal death. Bleeding into the basal layers of the decidua causes placental separation. Expansion of the hematoma can progressively extend the separation. The blood occasionally may extend into the myometrium (Couvelaire uterus). Most abruptions are mild (grade I), but up to 25% are severe (grade III). Risk factors include hypertension, trauma, a short umbilical cord, multiparity, a prolonged premature rupture of membranes, alcohol abuse, cocaine use, and an abnormal uterus. Patients usually experience painful vaginal bleeding with uterine contraction and tenderness. The diagnosis is made by excluding placenta previa on abdominal ultrasound. Amniotic fluid is port wine colored. Mild to moderate abruptions may be managed with vaginal delivery if the fetus is over 37 weeks of gestational age, but immediate cesarean section should be carried out after any signs of fetal distress. The choice between regional and general anesthesia must factor in the urgency for delivery, maternal hemodynamic stability, and any coagulopathy. The bleeding may remain concealed inside the uterus and cause underestimation of blood loss. Severe abruptio placentae can cause coagulopathy, particularly following fetal demise. Fibrinogen levels are mildly reduced (150–250 mg/dL) with moderate abruptions but are typically less than 150 mg/dL with fetal demise. The coagulopathy is thought to be due to activation of circulating plasminogen (fibrinolysis) and the release of tissue thromboplastins that precipitate disseminated intravascular coagulation (DIC). Platelet count and factors V and VIII are low, and fibrin split products are elevated. Severe abruption is a life-threatening emergency that necessitates a crash emergency cesarean section under general anesthesia. Massive blood transfusion, including replacement of coagulation factors and platelets, is necessary.

Uterine Rupture
Uterine rupture is relatively uncommon (1:1000–3000 deliveries) but can occur during labor as a result of (1) dehiscence of a scar from a previous (usually classic) cesarean section (VBAC), extensive myomectomy, or uterine reconstruction; (2) intrauterine manipulations or use of forceps (iatrogenic); or (3) spontaneous rupture following prolonged labor in patients with hypertonic contractions (particularly with oxytocin infusions), fetopelvic disproportion, or a very large, thin, and weakened uterus. Uterine rupture can present as frank hemorrhage, fetal distress, loss of uterine tone, and/or hypotension with occult bleeding into the abdomen. Even when epidural anesthesia is employed for labor, uterine rupture is often heralded by the abrupt onset of continuous abdominal pain and hypotension. The use of dilute concentrations of local anesthetics for epidural anesthesia during labor may facilitate early recognition. Treatment requires volume resuscitation and immediate laparotomy under general anesthesia. Ligation of the internal iliac (hypogastric) arteries, with or without hysterectomy, may be necessary to control intraoperative bleeding.

Premature Rupture of Membranes & Chorioamnionitis
Premature rupture of membranes (PROM) is present when leakage of amniotic fluid occurs before the onset of labor. The pH of amniotic fluid causes nitrazine paper to change color from blue to yellow. PROM complicates 10% of all pregnancies and up to 35% of premature deliveries. Predisposing factors include a short cervix, prior history of PROM or preterm delivery, infection, multiple gestations, polyhydramnios, and smoking. Spontaneous labor commences within 24 h of ruptured membranes in 90% of patients. Management of PROM balances the risk of infection with the risk of fetal prematurity. Delivery is usually indicated sometime after 34 weeks gestation. Patients with a gestation of less than 34 weeks can be managed expectantly with prophylactic antibiotics and tocolytics for 5–7 days to allow some additional maturation of fetal organs. The longer the interval between rupture and the onset of labor, the higher the incidence of chorioamnionitis. PROM also predisposes to placental abruption and postpartum endometritis.
Chorioamnionitis represents infection of the chorionic and amnionic membranes, and may involve the placenta, uterus, umbilical cord, and fetus. It complicates up to 1–2% of pregnancies and is usually but not always associated with ruptured membranes. The contents of the amniotic cavity are normally sterile, but become vulnerable to ascending bacterial infection from the vagina when the cervix dilates or the membranes rupture. Intraamniotic infections are less commonly caused by hematogenous spread of bacteria or retrograde seeding through the fallopian tubes. The principal maternal complications of chorioamnionitis are dysfunctional labor, often leading to cesarean section, intraabdominal infection, septicemia, and postpartum hemorrhage. Fetal complications include premature labor, acidosis, hypoxia, and septicemia.
Diagnosis of chorioamnionitis requires a high index of suspicion. Clinical signs include fever (> 38°C), maternal and fetal tachycardia, uterine tenderness, and foul smelling or purulent amniotic fluid. Blood leukocyte count is useful only if markedly elevated because it normally increases during labor (normal average 15,000/L). C-reactive protein levels are usually elevated (> 2 mg/dL). Gram stain of amniotic fluid obtained by amniocentesis is helpful in ruling out infection.

The use of regional anesthesia in patients with chorioamnionitis is controversial because of the theoretical risk of promoting the development of meningitis or an epidural abscess. Available evidence suggests that this risk is very low and that concerns may be unjustified. Moreover, antepartum antibiotic therapy appears to reduce maternal and fetal morbidity. Nonetheless, concerns over hemodynamic stability following sympathectomy are justified, particularly in patients with chills, high fever, tachypnea, changes in mental status, or borderline hypotension. Therefore, in the absence of overt signs of septicemia, thrombocytopenia, or coagulopathy, most clinicians offer regional anesthesia to patients with chorioamnionitis following antibiotic therapy. When general anesthesia is being considered, the relative risks of failed intubation and aspiration must be weighed against those of a spinal infection following regional anesthesia.

Preterm Labor
Preterm labor by definition occurs between weeks 20 and 37 of gestation and is the most common complication of the third trimester. Approximately 8% of liveborn infants in the United States are delivered before term. Important contributory maternal factors include extremes of age, inadequate prenatal care, unusual body habitus, increased physical activity, infections, prior preterm labor, multiple gestation, and other medical illnesses or complications during pregnancy.

Because of their small size and incomplete development, preterm infants—particularly those under 30 weeks of gestational age or weighing less than 1500 g—experience a greater number of complications than term infants. Premature rupture of membranes complicates a third of premature deliveries; the combination of premature rupture of membranes and premature labor increases the likelihood of umbilical cord compression resulting in fetal hypoxemia and asphyxia. Preterm infants with a breech presentation are particularly prone to prolapse of the umbilical cord during labor. Moreover, inadequate production of pulmonary surfactant frequently leads to the idiopathic respiratory distress syndrome (hyaline membrane disease) after delivery. Surfactant levels are generally adequate only after week 35 of gestation. Lastly, a soft, poorly calcified cranium predisposes these neonates to intracranial hemorrhage during vaginal delivery.
When preterm labor occurs before 35 weeks of gestation, bed rest and tocolytic therapy are usually initiated. Treatment is successful in 75% of patients. Labor is inhibited until the lungs mature and sufficient pulmonary surfactant is produced, as judged by amniocentesis. The risk of respiratory distress syndrome is markedly reduced when the amniotic fluid lecithin/sphingomyelin ratio is greater than 2. Glucocorticoid (betamethasone) may be given to induce production of pulmonary surfactant, which requires a minimum of 24–48 h. Prophylactic antibiotics (penicillins) are given to patients until cultures for group B streptococcus are determined to be negative. The most commonly used tocolytics are 2-adrenergic agonists (ritodrine or terbutaline) and magnesium (6 g intravenously over 30 min followed by 2–4 g/h); intravenous alcohol is no longer used. Ritodrine (given intravenously as 100–350 g/min) and terbutaline (given orally as 2.5–5 mg every 4–6 h) also have some 1-adrenergic receptor activity, which accounts for some of their side effects. Maternal side effects include tachycardia, arrhythmias, myocardial ischemia, mild hypotension, hyperglycemia, hypokalemia, and, rarely, pulmonary edema. Other tocolytic agents include calcium channel blockers (nifedipine), prostaglandin synthetase inhibitors, oxytocin antagonists (atosiban), and possibly nitric oxide. Fetal ductal constriction can occur after 32 weeks gestation with nonsteroidal antiinflammatory drugs, such as indomethacin, but it is usually transient and resolves after discontinuation of the drug; renal impairment in the fetus may also cause oligohydramnios.

When tocolytic therapy fails to stop labor, anesthesia often becomes necessary. The goal during vaginal delivery of a preterm fetus is a slow controlled delivery with minimal pushing by the mother. A large episiotomy and low forceps are often employed. Spinal or epidural anesthesia allows complete pelvic relaxation. Cesarean section is performed for fetal distress, breech presentation, intrauterine growth retardation, or failure of labor to progress. Regional or general anesthesia may be employed, but because preterm infants may be more sensitive to all central nervous system depressants, regional anesthesia may be preferable. Residual effects from -adrenergic agonists may complicate general anesthesia. The half-life of ritodrine may be as long as 3 h. Halothane, pancuronium, ketamine, and ephedrine should be used cautiously (if at all). Hypokalemia is usually due to an intracellular uptake of potassium and rarely requires treatment; however, it may increase sensitivity to muscle relaxants. Magnesium therapy potentiates muscle relaxants and may predispose to hypotension (secondary to vasodilatation). Residual effects from tocolytics interfere with uterine contraction following delivery. Lastly, preterm newborns are often depressed at delivery and frequently need resuscitation. Preparations for resuscitation should be completed prior to delivery.

Pregnancy-Induced Hypertension
Hypertension during pregnancy can be classified as pregnancy-induced hypertension (PIH, often also referred to as preeclampsia), chronic hypertension that preceded pregnancy, or chronic hypertension with superimposed preeclampsia. PIH is usually defined as a systolic blood pressure greater than 140 mm Hg or diastolic pressure greater than 90 mm Hg, or, alternatively, as a consistent increase in systolic or diastolic pressure by 30 mm Hg and 15 mm Hg, respectively, above the patient's normal baseline. PIH more accurately describes one of three syndromes: preeclampsia, eclampsia, and the HELLP syndrome. Preeclampsia (or toxemia) refers to the triad of hypertension, proteinuria (> 500 mg/d), and edema (hand and face) occurring after week 20 of gestation and resolving within 48 h after delivery. When seizures occur, the syndrome is termed eclampsia. The HELLP syndrome describes PIH associated with hemolysis, elevated liver enzymes, and a low platelet count. In the United States, preeclampsia complicates approximately 7–10% of pregnancies; eclampsia is much more uncommon, occurring in one of 10,000–15,000 pregnancies. Severe PIH causes or contributes to 20–40% of maternal deaths and 20% of perinatal deaths. Maternal deaths are usually due to stroke, pulmonary edema, and hepatic necrosis or rupture.

Pathophysiology & Manifestations
PIH primarily affects primigravidas, but it can occur in multiparous women, particularly those with vascular disorders. Some evidence suggests that it may have an immunogenetic basis. The pathophysiology of this multisystem disease remains obscure but appears to be related to abnormal prostaglandin metabolism and endothelial dysfunction that lead to vascular hyperreactivity. Patients with PIH have elevated levels of thromboxane A2 (TXA2) production and decreased prostacyclin (PGI2) production. TXA2 is a potent vasoconstrictor and promoter of platelet aggregation, whereas PGI2 is a potent vasodilator and inhibitor of platelet aggregation. Endothelial dysfunction may reduce production of nitric oxide and increase production of endothelin-1. The latter is also a potent vasoconstrictor and activator of platelets. Abnormal regulation of oxygen-derived free radical and lipid peroxidation may also play an important role. Marked vascular reactivity and endothelial injury reduce placental perfusion and can lead to widespread systemic manifestations.


Other major manifestations of PIH include (1) generalized vasospasm, (2) reduced intravascular volume, (3) decreased glomerular filtration, and (4) generalized edema (Table 43–6). Severe PIH substantially increases both maternal and fetal morbidity and mortality and is defined by a blood pressure greater than 160/110 mm Hg, proteinuria in excess of 5 g/d, oliguria (< 500 mL/d), pulmonary edema, central nervous system manifestations (headache, visual disturbances, or seizures), hepatic tenderness, or the HELLP syndrome. Hepatic rupture may also occur in patients with the HELLP syndrome.

Table 43–6. Complications of Pregnancy-Induced Hypertension.
Neurological 
  Headache
  Visual disturbances
  Hyperexcitability
  Seizures
  Intracranial hemorrhage
  Cerebral edema
Pulmonary 
  Upper airway edema
  Pulmonary edema
Cardiovascular 
  Decreased intravascular volume
  Increased arteriolar resistance
  Hypertension
  Heart failure
Hepatic 
  Impaired function
  Elevated enzymes
  Hematoma
  Rupture
Renal 
  Proteinuria
  Sodium retention
  Decreased glomerular filtration
  Renal failure
Hematological 
  Coagulopathy
    Thrombocytopenia
    Platelet dysfunction
    Prolonged partial thromboplastin time
  Microangiopathic hemolysis

Patients with severe preeclampsia or eclampsia have widely differing hemodynamic profiles. Most patients have low-normal cardiac filling pressures with high systemic vascular resistance, but cardiac output may be low, normal, or high.

Treatment
Treatment consists of bed rest, sedation, antihypertensive drugs (usually labetalol 5–10 mg intravenously, hydralazine 5 mg intravenously, or methyldopa 250–500 mg orally), and magnesium sulfate (4 g intravenous loading, followed by 1–3 g/h) to treat hyperreflexia and prevent convulsions. Therapeutic magnesium levels are 4–6 mEq/L. Unlike labetalol, esmolol can have significant, potentially adverse fetal effects. Calcium channel blockers are generally not used because of their tocolytic action and potentiation of magnesium-induced circulatory depression.

Invasive arterial, central venous, and possibly pulmonary artery monitoring are probably indicated in patients with severe hypertension, pulmonary edema, or refractory oliguria; an intravenous vasodilator (nitroglycerin or nitroprusside) is often necessary. Nitroprusside in large doses (> 10 g/kg/min) or for prolonged periods increases the risk of cyanide toxicity in the fetus. Definitive treatment of PIH is delivery of the fetus and placenta.

Anesthetic Management
Patients with mild PIH generally require only extra caution during anesthesia; standard anesthetic practices may be used. Spinal and epidural anesthesia are associated with similar decreases in arterial blood pressure in these patients. Patients with severe disease, however, are critically ill and require stabilization prior to administration of any anesthetic. Hypertension should be controlled and hypovolemia corrected before anesthesia. In the absence of coagulopathy, continuous epidural anesthesia is the first choice for most patients with PIH during labor, vaginal delivery, and cesarean section. Moreover, continuous epidural anesthesia avoids the increased risk of a failed intubation due to severe edema of the upper airway.
A platelet count and coagulation profile should be checked prior to the institution of regional anesthesia in patients with severe PIH. It has been recommended that regional anesthesia be avoided if the platelet count is less than 100,000/L, but a platelet count as low as 70,000/L may be acceptable. Although some patients have a qualitative platelet defect, the usefulness of a bleeding time is questionable. Continuous epidural anesthesia has been shown to decrease catecholamine secretion and improve uteroplacental perfusion up to 75% in these patients, provided hypotension is avoided. Judicious colloid fluid boluses (250–500 mL) before epidural activation may be more effective than crystalloids in correcting the hypovolemia and preventing profound hypotension. A central venous line may be used to guide volume replacement; however, a pulmonary artery catheter should be used in severe cases (such as marked hypertension, refractory oliguria, hypoxemia, or frank pulmonary edema). Use of an epinephrine-containing test dose for epidural anesthesia is controversial because of questions about its reliability (see the above section on Prevention of Unintentional Intravascular and Intrathecal Injection) and the risk of exacerbating hypertension. Hypotension should be treated with small doses of vasopressors (ephedrine, 5 mg) because patients tend to be very sensitive to these agents.

Intraarterial blood pressure monitoring is indicated in patients with severe hypertension during both general and regional anesthesia. Intravenous nitroprusside, trimethaphan, or nitroglycerin is usually necessary to control blood pressure during general anesthesia. Intravenous labetalol (5–10 mg increments) can also be effective in controlling the hypertensive response to intubation and does not appear to alter placental blood flow. Because magnesium potentiates muscle relaxants, doses of nondepolarizing muscle relaxants should be reduced in patients receiving magnesium therapy and guided by a peripheral nerve stimulator.

Heart Disease
The marked cardiovascular changes associated with pregnancy, labor, and delivery often cause pregnant patients with heart disease (2% of parturients) to decompensate during this period. Although most patients have rheumatic heart disease, an increasing number of parturients are presenting with congenital heart lesions. Anesthetic management is directed toward employing techniques that minimize the added stresses of labor and delivery. Specific management of the various lesions is discussed elsewhere. Most patients can be divided into one of two groups. Patients in the first group include those with mitral valve disease, aortic insufficiency, or congenital lesions with left-to-right shunting. These patients benefit from regional techniques, particularly continuous epidural anesthesia. The induced sympathectomy reduces both preload and afterload, relieves pulmonary congestion, and in some cases increases forward flow (cardiac output).
Patients in the second group include those with aortic stenosis, congenital lesions with right-to-left or bidirectional shunting, or primary pulmonary hypertension. Regional anesthesia is generally detrimental in this group. Reductions in venous return (preload) or afterload are usually poorly tolerated. These patients are better managed with intraspinal opioids alone, systemic medications, pudendal nerve blocks, and, if necessary, general anesthesia.

Amniotic Fluid Embolism
Amniotic fluid embolism is a rare (1:20,000 deliveries) but potentially lethal complication (86% mortality rate in some series) that can occur during labor, delivery, cesarean section, or postpartum. The mortality exceeds 50% in the first hour. Entry of amniotic fluid into the maternal circulation can occur through any break in the uteroplacental membranes. Such breaks may occur during normal delivery or cesarean section or following placental abruption, placenta previa, or uterine rupture. In addition to desquamated fetal debris, amniotic fluid contains various prostaglandin and leukotrienes, which appear to play an important role in the genesis of this syndrome. The alternate term "anaphylactoid syndrome of pregnancy" has been suggested to emphasize the role of chemical mediators in this syndrome.

Patients typically present with sudden tachypnea, cyanosis, shock, and generalized bleeding. Three major pathophysiological manifestations are responsible: (1) acute pulmonary embolism, (2) DIC, and (3) uterine atony. Seizures and pulmonary edema may develop; the latter has both cardiogenic and noncardiogenic components. Acute left ventricular dysfunction appears to be a common feature. Although the diagnosis can be firmly established only by demonstrating fetal elements in the maternal circulation (usually at autopsy or less commonly by aspirating amniotic fluid from a central venous catheter), amniotic fluid embolism should always be suggested by sudden respiratory distress and circulatory collapse. The presentation may initially mimic acute pulmonary thromboembolism, venous air embolism, overwhelming septicemia, or hepatic rupture or cerebral hemorrhage in a patient with toxemia.

Treatment consists of aggressive cardiopulmonary resuscitation, stabilization, and supportive care. When cardiac arrest occurs prior to delivery of the fetus, the efficacy of closed-chest compressions appears to be marginal at best. Aortocaval compression impairs resuscitation in the supine position, whereas chest compressions are less effective in a lateral tilt position. Moreover, expeditious delivery appears to improve maternal and fetal outcome; immediate (cesarean) delivery should therefore be carried out. Once the patient is resuscitated, stabilization with mechanical ventilation, fluids, and inotropes is best carried out with full invasive hemodynamic monitoring. Uterine atony is treated with oxytocin, methylergonovine, and prostaglandin F2, whereas significant coagulopathies are treated with platelets and coagulation factors based on laboratory findings.

Postpartum Hemorrhage
Postpartum hemorrhage is usually considered present when the postpartum blood loss exceeds 500 mL. Up to 4% of parturients may experience postpartum hemorrhage, which is often associated with a prolonged third stage of labor, preeclampsia, multiple gestations, forceps delivery, and mediolateral episiotomy. Common causes include uterine atony, a retained placenta, obstetric lacerations, uterine inversion, and use of tocolytic agents prior to delivery. Atony is often associated with uterine overdistention (multiple gestation and polyhydramnios). Less commonly, a clotting defect may be responsible.

The anesthesiologist may be consulted to assist in venous access or fluid (and blood) resuscitation, as well as to provide anesthesia for careful examination of the vagina, cervix, and uterus. Perineal lacerations can usually be repaired with local infiltration of anesthetic or pudendal nerve blocks. Residual anesthesia from prior institution of epidural or spinal anesthesia facilitates examination of the patient; however, supplementation with an opioid, nitrous oxide, or both may be required. Induction of spinal or epidural anesthesia in the presence of hypovolemia is contraindicated. General anesthesia is usually required for bimanual massage of the uterus, manual extraction of a retained placenta, reversion of an inverted uterus, or repair of a major laceration. Uterine atony should be treated with oxytocin (20–30 U/L of intravenous fluid), methylergonovine (0.2 mg intramuscularly), and carboprost (0.25 mg intramuscularly). Emergency laparotomy and hysterectomy may be necessary in rare instances. Early ligation of the internal iliac (hypogastric) arteries may help avoid hysterectomy or reduce blood loss.


Fetal & Neonatal Resuscitation
Fetal Resuscitation
Resuscitation of the neonate starts during labor. Any compromise of the uteroplacental circulation readily produces fetal asphyxia. Intrauterine asphyxia during labor is the most common cause of neonatal depression. Fetal monitoring throughout labor is helpful in identifying which babies may be at risk, detecting fetal distress, and evaluating the effect of acute interventions. These include correcting hypotension with fluids or vasopressors, supplemental oxygen, and decreasing uterine contraction (stopping oxytocin or administering tocolytics). Some studies suggest that the normal fetus can compensate for up to 45 min of fetal hypoxia, a period termed "fetal stress"; the latter is associated with a marked redistribution of blood flow primarily to the heart, brain, and adrenal glands. With time, however, progressive lactic acidosis and asphyxia produce increasing fetal distress that necessitates immediate delivery.

Fetal Heart Rate Monitoring
Monitoring of fetal heart rate (FHR) is presently the most useful technique in assessing fetal well being. Alone it has a 35–50% false-positive rate of predicting fetal compromise. Because of this, the term "fetal distress" in the context of FHR monitoring has been largely replaced with "nonreassuring" FHR. Correct interpretation of heart rate patterns is crucial. Three parameters are evaluated: baseline heart rate, baseline variability, and the relationship to uterine contractions (deceleration patterns). Monitoring of heart rate is most accurate when fetal scalp electrodes are used, but this may require rupture of the membranes and is not without complications (ie, amnionitis or fetal injury).

Baseline Heart Rate
The mature fetus normally has a baseline heart rate of 110–160 beats/min. An increased baseline heart rate may be due to prematurity, mild fetal hypoxia, chorioamnionitis, maternal fever, maternally administered drugs (anticholinergics or -agonists), or, rarely, hyperthyroidism. A decreased baseline heart rate may be due to a postterm pregnancy, fetal heart block, or fetal asphyxia.

Baseline Variability
The healthy mature fetus normally displays a baseline beat-to-beat (R wave to R wave) variability that can be classified as minimal (< 5 beats/min), moderate (6–25 beats/min), or marked (> 25 beats/min). Baseline variability, which is best assessed with scalp electrodes, has become an important sign of fetal well-being and represents a normally functioning autonomic system. Sustained decreased baseline variability is a prominent sign of fetal asphyxia. Central nervous system depressants (opioids, barbiturates, benzodiazepines, or magnesium sulfate) and parasympatholytics (atropine) also decrease baseline variability, as do prematurity, fetal dysrhythmias, and anencephaly. A sinusoidal pattern that resembles a smooth sine wave is associated with fetal depression (hypoxia, drugs, and anemia secondary to Rh isoimmunization).

Accelerations
Accelerations of FHR are defined as increases of 15 beats/min or more lasting for more than 15 s. Periodic accelerations in FHR reflect normal oxygenation and are usually related to fetal movements and responses to uterine pressure. Such accelerations are generally considered reassuring. By 32 weeks, fetuses display periodic increases in baseline heart rate that are associated with fetal movements. Normal fetuses have 15–40 accelerations/h. The mechanism is thought to be increases in catecholamine secretion with decreases in vagal tone. Accelerations diminish with fetal sleep, some drugs (opioids, magnesium, and atropine), as well as fetal hypoxia. Accelerations to fetal scalp or vibroacoustic stimulation are considered a reassuring sign of fetal well-being. The absence of both baseline variability and accelerations is "nonreassuring" and may be important signs of fetal compromise.

Deceleration Patterns
Early (Type I) Decelerations
Early deceleration (usually 10–40 beats/min) (Figure 43–5A) is thought to be a vagal response to compression of the fetal head or stretching of the neck during uterine contractions. The heart rate forms a smooth mirror image of the contraction. Early decelerations are generally not associated with fetal distress and occur during descent of the head.


Late (Type II) Decelerations
Late decelerations (Figure 43–5B) are associated with fetal compromise and are characterized by a decrease in heart rate at or following the peak of uterine contractions. Late decelerations may be as few as 5 beats/min and are thought to be due to the effect of a decrease in arterial oxygen tension on chemoreceptors or the sinoatrial node. Late decelerations with normal variability may be observed following acute insults (maternal hypotension or hypoxemia) and are usually reversible with treatment. Late decelerations with decreased variability are associated with prolonged asphyxia and may be an indication for fetal scalp sampling (see the section below on Other Monitoring). Complete abolition of variability in this setting is an ominous sign signifying severe decompensation and the need for immediate delivery.

Variable (Type III) Decelerations
The most common type of decelerations are of the variable type (Figure 43–5C). These decelerations are variable in onset, duration, and magnitude (often > 30 beats/min). They are typically abrupt in onset and are thought to be related to umbilical cord compression and acute intermittent decreases in umbilical blood flow. Variable decelerations are typically associated with fetal asphyxia when they are greater than 60 beats/min, last more than 60 s, or occur in a pattern that persists for more than 30 min.

Other Monitoring
Other less commonly used monitors include fetal scalp pH measurements, scalp lactate concentration, fetal pulse oximetry, and fetal ST-segment analysis. Experience is limited with all except fetal scalp pH measurements. Unfortunately the latter is associated with a small but significant incidence of false negatives and false positives. Fetal blood can be obtained and analyzed via a small scalp puncture once the membranes are ruptured. A fetal scalp pH higher than 7.20 is usually associated with a vigorous neonate, whereas a pH less than 7.20 is often but not always associated with a depressed neonate. Because of wide overlap, fetal blood sampling can be interpreted correctly only in conjunction with heart rate monitoring.

Treatment of the Fetus
Aggressive treatment of intrauterine fetal asphyxia is necessary to prevent fetal demise or permanent neurological damage. All interventions are directed at restoring an adequate uteroplacental circulation. Aortocaval compression, maternal hypoxemia or hypotension, or excessive uterine activity (during oxytocin infusions) must be corrected. Changes in maternal position, supplemental oxygen, and intravenous ephedrine or fluid, or adjustments in an oxytocin infusion often correct the problem. Failure to relieve fetal stress as well as progressive acidosis and asphyxia necessitate immediate delivery.

Neonatal Resuscitation
General Care of the Neonate
One person whose sole responsibility is to care for the neonate and is capable of providing resuscitation should attend every delivery. As the head is delivered, the nose, mouth, and pharynx are suctioned with a bulb syringe. After the remainder of the body is delivered, the skin is dried with a sterile towel. Once the umbilical cord stops pulsating or breathing is initiated, the cord is then clamped and the neonate is placed in a radiant warmer with the bed tilted in a slight Trendelenburg position.

Evaluation and treatment are carried out simultaneously (Figure 43–6). If the neonate is obviously depressed, the cord is clamped early and resuscitation is initiated immediately. Breathing normally begins within 30 s and is sustained within 90 s. Respirations should be 30–60 breaths/min and the heart rate 120–160 beats/min. Respirations are assessed by auscultation of the chest, whereas heart rate is determined by palpation of the pulse at the base of the umbilical cord or auscultation of the precordium. It is critically important to keep the neonate warm.

In addition to respirations and heart rate, color, tone, and reflex irritability should be evaluated. The Apgar score (Table 43–7), recorded at 1 min and again at 5 min after delivery, remains the most valuable assessment of the neonate. The 1-min score correlates with survival, whereas the 5-min score is related to neurological outcome.


Table 43–7. Apgar Score.
 Points
Sign012
Heart rate (beats/min)Absent< 100> 100
Respiratory effortAbsentSlow, irregularGood, crying
Muscle toneFlaccidSome flexionActive motion
Reflex irritabilityNo responseGrimaceCrying
ColorBlue or paleBody pink, extremities blueAll pink

Neonates with Apgar scores of 8–10 are vigorous and may require only gentle stimulation (flicking the foot, rubbing the back, and additional drying). A catheter should first be gently passed through each nostril to rule out choanal atresia, and then through the mouth to suction the stomach and rule out esophageal atresia.

Meconium-Stained Neonates
The presence or absence of meconium in the amniotic fluid (about 10–12% of deliveries) dictates the immediate management of the neonate at birth. Fetal distress, particularly after 42 weeks of gestation, is often associated with release of thick meconium into the fluid. Fetal gasping during stress results in entry of a large amount of meconium-tainted amniotic fluid into the lungs. When the neonate initiates respiration at birth, the meconium moves from the trachea and large airways down toward the periphery of the lung. Thick or particulate meconium obstructs small airways and causes severe respiratory distress in 15% of meconium-stained neonates. Moreover, these infants can develop persistent fetal circulation (see Chapter 42). Amnioinfusion prior to delivery can reduce the severity of meconium aspiration syndrome.
Unless the neonate has absent or depressed respirations, thin watery meconium does not require suctioning beyond careful bulb suctioning of the oropharynx when the head emerges from the perineum (or from the uterus at cesarean section). When thick (pea soup) meconium is present in the amniotic fluid, however, some clinicians intubate and suction the trachea immediately after delivery but before the first breath is taken. If the baby is not vigorous, tracheal suctioning is recommended when meconium is present. Tracheal suctioning of the thick meconium is accomplished by a special suctioning device attached to the endotracheal tube as the tube is withdrawn. If meconium is aspirated from the trachea, the procedure should be repeated until no meconium is obtained—but no more than three times, after which it is usually of no further benefit. The infant should then be given supplemental oxygen by face mask and observed closely. The stomach should also be suctioned to prevent passive regurgitation of any meconium. Newborns with meconium aspiration have an increased incidence of pneumothorax (10% compared with 1% for all vaginal deliveries).

Care of the Depressed Neonate
Approximately 6% of newborns, most of whom weigh less than 1500 g, require some form of advanced life support. Resuscitation of the depressed neonate requires two or more persons—one to manage the airway and ventilation and another to perform chest compressions, if necessary. A third person greatly facilitates the placement of intravascular catheters and the administration of fluids or drugs. The anesthesiologist caring for the mother can render only brief assistance and only when it does not jeopardize the mother; other personnel are, therefore, generally responsible for neonatal resuscitation.

Because the most common cause of neonatal depression is intrauterine asphyxia, the emphasis in resuscitation is on respiration. Hypovolemia is also a contributing factor in a significant number of neonates. Factors associated with hypovolemia include early clamping of the umbilical cord, holding the neonate above the introitus prior to clamping, prematurity, maternal hemorrhage, placental transection during cesarean section, sepsis, and twin-to-twin transfusion.

Failure of the neonate to quickly respond to respiratory resuscitative efforts mandates vascular access and blood gas analysis; pneumothorax (1% incidence) and congenital anomalies of the airway, including tracheoesophageal fistula (1:3000–5000 live births), and congenital diaphragmatic hernia (1:2000–4000) should also be considered.

Grouping by the 1-min Apgar score greatly facilitates resuscitation: (1) mildly asphyxiated neonates (Apgar score of 5–7) usually need only stimulation while 100% oxygen is blown across the face; (2) moderately asphyxiated neonates (Apgar score of 3–4) require temporary assisted positive-pressure ventilation with mask and bag; and (3) severely depressed neonates (Apgar score of 0–2) should be immediately intubated, and chest compressions may be required.

Guidelines for Ventilation
Indications for positive-pressure ventilation include (1) apnea, (2) gasping respirations, (3) persistent central cyanosis with 100% oxygen, and (4) heart rate less than 100 beats/min. Excessive flexion or extension of the neck can cause airway obstruction. A 1-in.-high towel under the shoulders may be helpful in maintaining proper head position. Assisted ventilation by bag and mask should be at a rate of 30–60 breaths/min with 100% oxygen. Initial breaths may require peak pressures of up to 40 cm H2O, but pressures should not exceed 30 cm H2O subsequently. Adequacy of ventilation should be checked by auscultation and chest excursions. Gastric decompression with an 8F tube often facilitates ventilation. If after 30 s the heart rate is over 100 beats/min and spontaneous ventilations become adequate, assisted ventilation is no longer necessary. If the heart rate is less than 60 beats/min or is 60–80 beats/min and not rising, the neonate is intubated and chest compressions are started. If the heart rate is 60–80 beats/min and rising, assisted ventilation is continued and the neonate is observed. Failure of the heart rate to rise above 80 beats/min is an indication for chest compressions. Indications for endotracheal intubation include ineffective ventilation, prolonged mask ventilation, and the need to administer medications.

Intubation (Figure 43–7) is performed with a Miller 00, 0, or 1 laryngoscope blade, using a 2.5-, 3-, or 3.5-mm endotracheal tube (for neonates < 1 kg, 1–2 kg, and > 2 kg, respectively). Correct endotracheal tube size is indicated by a small leak with 20 cm H2O pressure. Right endobronchial intubation should be excluded by chest auscultation. The correct depth of the endotracheal tube ("tip to lip") is usually 6 cm plus the weight in kilograms. Oxygen saturation can usually be measured by a pulse oximeter probe applied to the palm. Capnography is also very useful in confirming endotracheal intubation. Transcutaneous oxygen sensors are useful for measuring tissue oxygenation but unfortunately require time for initial equilibration. Use of a laryngeal mask airway (LMA#1) has been reported in neonates > 2.5 kg and may be useful if endotracheal intubation is difficult (eg, Pierre Robin syndrome).

Figure 43–7.Add to 'My Saved Images'

 Intubation of the neonate. The head is placed in a neutral position, and the laryngoscope handle is held with the thumb and index finger as the chin is supported with the remaining fingers. Pressure applied over the hyoid bone with the little finger will bring the larynx into view. A straight blade such as a Miller 0 or 1 usually provides the best view.

Guidelines for Chest Compressions
Indications for chest compressions are a heart rate that is less than 60 beats/min or 60–80 beats/min and not rising after 30 s of adequate ventilation with 100% oxygen.
Cardiac compressions should be provided at a rate of 120/min. The two thumb-encircling hands (Figure 43–8) technique is generally preferred because it appears to generate higher peak systolic and coronary perfusion pressures. Alternatively, the two-finger technique can be used (Figure 43–9). The depth of compressions should be approximately one-third of the anterior–posterior diameter of the chest and enough to generate a palpable pulse.

Figure 43–8.Add to 'My Saved Images'

 Chest compressions in the neonate. The neonate is held with both hands as each thumb is placed just beneath a line connecting the nipples and the remaining fingers encircle the chest. The sternum is compressed ⅓ to ¾ in. (1 cm) at a rate of 120/min.
Figure 43–9.Add to 'My Saved Images'

 The alternative technique for neonatal chest compressions: two fingers are placed on the lower third of the sternum at right angles to the chest. The chest is compressed approximately 1 cm at a rate of 120/min.
Compressions should be interposed with ventilation in a 3:1 ratio, such that 90 compressions and 30 ventilations are given per minute. The heart rate should be checked periodically. Chest compressions should be stopped when the spontaneous heart rate exceeds 80 beats/min.

Vascular Access
Cannulation of the umbilical vein with a 3.5F or 5F umbilical catheter is easiest and the preferred technique. The tip of the catheter should be just below skin level and allow free backflow of blood; further advancement may result in infusion of hypertonic solutions directly into the liver. A peripheral vein or even the endotracheal tube can be used as an alternate route for drug administration.
Cannulation of one of the two umbilical arteries allows measurement of blood pressure and facilitates blood gas measurements but may be more difficult. Specially designed umbilical artery catheters allow continuous PaO2 or oxygen saturation monitoring as well as blood pressure. Care must be taken not to introduce any air into either the artery or the vein.

Volume Resuscitation
Some neonates at term and nearly two-thirds of premature infants requiring resuscitation are hypovolemic at birth. Diagnosis is based on physical examination (low blood pressure and pallor) and a poor response to resuscitation. Neonatal blood pressure generally correlates with intravascular volume, and should therefore routinely be measured. Normal blood pressure depends on birth weight and varies from 50/25 mm Hg for neonates weighing 1–2 kg to 70/40 mm Hg for those weighing over 3 kg. A low blood pressure suggests hypovolemia. Volume expansion may be accomplished with 10 mL/kg of either lactated Ringer's injection, normal saline, or type O-negative blood cross-matched with maternal blood. Less common causes of hypotension include hypocalcemia, hypermagnesemia, and hypoglycemia.

Drug Therapy
Epinephrine
Epinephrine, 0.01–0.03 mg/kg (0.1–0.3 mL/kg of a 1:10,000 solution), should be given for asystole or a spontaneous heart rate of less than 60 beats/min in spite of adequate ventilation and chest compressions. It may be repeated every 3–5 min. Epinephrine may be given in 1 mL of saline down the endotracheal tube if venous access is not available.

Naloxone
Naloxone, 0.1 mg/kg intravenously or 0.2 mg/kg intramuscularly, is given to reverse the respiratory depressant effect of opioids given to the mother in the last 4 h of labor. Withdrawal symptoms may be precipitated in babies of opioid addicts.

Other Drugs
Other drugs may be indicated only in specific settings. Sodium bicarbonate (2 mEq/kg of a 0.5 mEq/mL 4.2% solution) should generally be given only for a severe metabolic acidosis documented by blood gas measurements and when ventilation is adequate. It may also be administered during prolonged resuscitation (> 5 min)—particularly if blood gas measurements are not readily available. The infusion rate should not exceed 1 mEq/kg/min to avoid hypertonicity and intracranial hemorrhage. Moreover, to prevent hypertonicity-induced hepatic injury, the catheter tip should not be in the liver. Calcium gluconate 100 mg/kg (CaCl2, 30 mg/kg) should be given only to neonates with documented hypocalcemia or those with suspected magnesium intoxication (from maternal magnesium therapy); these neonates are usually hypotensive, hypotonic, and appear vasodilated. Glucose (8 mg/kg/min of a 10% solution) is given only for documented hypoglycemia because hyperglycemia worsens hypoxic neurological deficits. Blood glucose should be measured because up to 10% of neonates may have hypoglycemia (glucose < 35 mg/dL), particularly those delivered by cesarean section. Dopamine may be started at 5 g/kg/min to support arterial blood pressure. Lastly, surfactant may be given through the endotracheal tube to premature neonates with respiratory distress syndrome.

Case Discussion: Appendicitis in a Pregnant Woman
A 31-year-old woman with a 24-week gestation presents for an appendectomy.

How Does Pregnancy Complicate the Management of This Patient?
Nearly 1–2% of pregnant patients require surgery during their pregnancy. The most common procedure during the first trimester is laparoscopy; appendectomy (1:1500 pregnancies) and cholecystectomy (1:2000–10,000 pregnancies) are the most commonly performed open abdominal procedures. Cervical cerclage may be necessary in some patients for cervical incompetence. The physiological effects of pregnancy can alter the manifestations of the disease process and make diagnosis difficult. Patients may therefore present with advanced or complicated disease. The physiological changes associated with pregnancy (see Chapter 42) further predispose the patient to increased morbidity and mortality. Moreover, both the surgery and the anesthesia can adversely affect the fetus.

What Are the Potentially Detrimental Effects of Surgery and Anesthesia on the Fetus?
The procedure can have both immediate and long-term undesirable effects on the fetus. Hypotension, hypovolemia, severe anemia, hypoxemia, and marked increases in sympathetic tone can seriously compromise the transfer of oxygen and other nutrients across the uteroplacental circulation and promote intrauterine fetal asphyxia. The stress of the procedure and the underlying process may also precipitate preterm labor, which often follows intraabdominal surgery near the uterus. Laparoscopy may be safely performed but the CO2 insufflation has the potential to cause fetal respiratory acidosis. Mild to moderate maternal hyperventilation and limiting both insufflation pressure and duration of the procedure limit the degree of acidosis. Long-term detrimental effects relate to possible teratogenic effects on the developing fetus.

When Is the Fetus Most Sensitive to Teratogenic Influences?
Three stages of susceptibility are generally recognized. In the first 2 weeks of intrauterine life, teratogens have either a lethal effect or no effect on the embryo. The third to eighth weeks are the most critical period, when organogenesis takes place; drug exposure during this period can produce major developmental abnormalities. From the eighth week onward, organogenesis is complete, and organ growth takes place. Teratogen exposure during this last period usually results in only minor morphological abnormalities but can produce significant physiological abnormalities and growth retardation. Although the teratogenic influences of anesthetic agents have been extensively studied in animals, retrospective human studies have been inconclusive. Past concerns about possible teratogenic effects of nitrous oxide and benzodiazepines do not appear to be justified. Nonetheless, as with all drugs, exposure to anesthetic agents should be kept to a minimum in terms of the number of agents, dosage, and duration of exposure.

What Would Be the Ideal Anesthetic Technique in This Patient?
Toward the end of the second trimester (after 20–24 weeks gestation), most of the physiological changes associated with pregnancy have taken place. Regional anesthesia is preferable to general anesthesia to decrease the risks of pulmonary aspiration and failed intubation and to minimize drug exposure to the fetus. The patient should be transported and maintained with left lateral uterine displacement when supine. Drug exposure is least (probably negligible) with spinal anesthesia. Moreover, spinal anesthesia may be preferable to epidural anesthesia because it is not associated with unintentional intravascular injections or potentially large intrathecal doses of local anesthetic. On the other hand, general anesthesia guarantees patient comfort and, when a volatile agent is used, may even suppress preterm labor (see Chapter 42). Nitrous oxide without concomitant administration of a halogenated anesthetic is reported to reduce uterine blood flow.
Although regional anesthesia is preferable in most instances, the choice between regional and general anesthesia must be individualized according to the patient, the anesthesiologist, and the type of surgery. Spinal anesthesia is usually satisfactory for appendectomies, whereas general anesthesia is more satisfactory for cholecystectomies. The same techniques and doses used for the parturient should be followed.

Are Any Special Monitors Indicated Perioperatively?
In addition to standard monitors, fetal heart rate and uterine activity should be monitored with a Doppler and tocodynamometer during induction of anesthesia, emergence, and recovery, and, whenever possible, during surgery in a woman who is 24 weeks or more pregnant. When regular organized uterine activity is detected, early treatment with a -adrenergic agonist such as ritodrine usually aborts the preterm labor. Magnesium sulfate and oral or rectal indomethacin may also be used as tocolytics.

When Should Elective Operations Be Performed during Pregnancy?
All elective operations should be postponed until 6 weeks after delivery. Only emergency procedures that pose an immediate threat to the mother or fetus should be routinely performed. The timing of semielective procedures, such as those for cancer, valvular heart disease, or intracranial aneurysms, must be individualized and must balance the threat to maternal health versus fetal well-being. Controlled (deliberate) hypotensive anesthesia may be necessary to reduce blood loss during extensive cancer operations; nitroprusside, nitroglycerin, and hydralazine have been used during pregnancy without apparent fetal compromise. Nonetheless, large doses and prolonged infusions of nitroprusside should be avoided because the immature liver of the fetus may have a limited ability to metabolize the cyanide breakdown product. Cardiopulmonary bypass has been employed in pregnant patients successfully without adverse fetal outcome, but should probably be carried out only with continuous fetal echocardiography. Circulatory arrest during pregnancy is not recommended.