Chapter 20: Anesthesia for the Complicated Obstetric Patient

A thorough understanding of the nature of the parturient’s pain is the first aspect in providing optimal obstetric anesthetic care. Once the biology and pathophysiology of this special acute pain is discussed, the benefits of analgesia for this pain will appropriately follow. Pharmacology of local anesthetics and related drugs will be reviewed, with special emphasis on complications associated with their administration. A variety of techniques including epidural, subarachnoid, and other regional techniques will be discussed with benefits and complications reviewed. General anesthesia for cesarean section delivery will be outlined. A variety of special consideration patients will be addressed, including: (1) the preeclamptic patient, (2) preterm birth patient on tocolytics, (3) human immunodeficiency virus (HIV)–positive mothers, (4) coagulopathies, (5) cardiac disease, and (6) pulmonary disease.

The current concept of pain focuses on the peripheral nervous system relaying a stimulus to the central nervous system (CNS) for interpretive evaluation—the somatosensory system (Fig. 20-1). The peripheral system consists of afferent neurons that are embedded in body tissues awaiting nociceptive (painful) stimuli. These afferent neurons are termed Ad (A-delta) and C-fibers. These fibers transverse into the spinal segments and synapse at the dorsal spinal ganglion. Here, substance-P is released causing the painful effect to be initiated. From each spinal segment stimulated, these messages ascend through one of two pathways to the thalamus for further modulation: the lateral spinothalamic tract or the medial lemniscus tract. Once at the thalamus, adjustment and regulation from inherent emotional and psychological factors occur. The data support the emphasis on the importance of perceptual factors that influence a patient’s total pain experience (Table 20-1). The psychodynamics of prior experience, motivation, anxiety, anticipation of pain, attention, personality, and ethnic and cultural factors all influence the modulation of substance-P release, affecting the pain experience. From the thalamus, this information is synthesized in the sensory cortex for relay to the many effector sites that contribute to the pain response. Once pain has been perceived, there is an initiation of the pain response that has neuroendocrine, behavioral, and psychological implications.

In humans, there is a 300% to 600% increase in epinephrine and 200% to 400% increase in norepinephrine levels produced during severe pain experienced in active labor. There is a 200% to 300% increase in cortisol levels, as well as, increases in corticosteroid and adrenocortictropic hormone levels reaching their peaks at or after delivery. During labor, the cardiac output (CO) increase is 40% to 50% with a further 20% to 30% increase during painful contractions. The systolic and diastolic blood pressures also increase by 20 to 30 mm Hg. These increases in CO and systolic blood pressure (SBP) lead to a significant increase in left ventricular stroke work that may be harmful to patients with preeclampsia, hypertension, cardiac valvular disease, pulmonary hypertension, or severe anemia.

With the sympathetic-induced lipolytic metabolism, increases in free fatty acids and lactate produce relative maternal acidosis. Increased sympathetic activity increases metabolism and oxygen consumption, and decreases gastrointestinal and urinary bladder motility. Respiratory rate is increased with resultant respiratory alkalosis. The kidney compensates by excreting HCO₃^–. Diminished PaCO₂ levels below 25 to 27 mm Hg may result in increased uteroplacental resistance and reduced oxygen delivery to the fetus.

During peak contractions, there is a reduction in intervillous blood flow leading to a significant decrease in placental gas exchange. This exaggerates the already dramatic reduction in uterine blood flow, secondary to the increases in norepinephrine and cortisol (see Table 20-1).

By blocking nociceptive input, there is a reduction in the release of cathecholamines, adrenal corticotropic hormone, and cortisol in the parturient (Table 20-2). Effective analgesia significantly reduces pain-related hemodynamic changes. Maternal CO fluctuations are modulated and oxygen consumption is reduced. Gastric and bladder motility is not adversely affected by neuroblockade. Cautious epidural analgesia has been reported to provide a vasomotor blocking effect that increases intervillous blood flow and oxygen delivery to the fetus.

The first stage of labor refers to the beginning of cervical dilation and effacement until its completion. The second stage of labor extends from complete cervical dilation until delivery of the infant. The third stage is the delivery of the placenta (see Table 20-2).

Transmission of pain during the first stage of labor is from spinal segments (pain fibers) T₁₀, T₁₁, T₁₂, and L₁, and the second and third stage of labor is from S₂, S₃, and S₄ (Fig. 20-2). It is important for the care provider to understand the differences between the pain conduction (spinal levels) during the first stage of labor, as compared with the second and third stage, in order to provide appropriately directed analgesia. It is also important to consider that pain may also be due to the pathology of the gestation, such as abruptio placenta, infection, adnexal torsion, or appendicitis, and these may be masked if total neuroblockade is achieved from T₄ to S₅ at the onset of labor. Only segments necessary for the specific pain of labor should be blocked (Table 20-3). Relatively decreased fetal perfusion has been reported to occur both in the presence and absence of overt maternal hypotension secondary to a sympathectomy-mediated reduction in uterine blood flow.

The desired action of all local anesthetics is the reversible blockade of nerve conduction and, therefore, the cascade of events producing perception of pain. These drugs prevent the development of an action potential in a nerve by blocking sodium channels responsible for propagating a response in the nerve fiber (Fig. 20-3). Local anesthetics exist in both charged and uncharged form. The uncharged state of the drug crosses the lipid nerve membrane and enters the cell. Once in the cell, it reequilibrates into the charged form that is readily dissolved in water. This charged form now reaches the sodium channels and blocks them from inside (see Table 20-3).

Ionization

The capacity for an uncharged species to assume a charged form is the essential property of all local anesthetics. They are a combination of a weak base and a strong acid.

As a general principle, lowering the pH will increase the ionized percentage of the drug, and raising the pH will increase the uncharged form of the drug. Because the local anesthetics are usually supplied in an acidic medium, the addition of NaHCO₃ will increase the relative uncharged portion, allowing the drug to cross the nerve membrane more readily resulting in a quicker onset of block.

Usual Doses

0.1 cc NaHCO₃/10 cc bupivicaine

1.0 cc NaHCO₃/10 cc lidocaine

Precipitation of the local anesthetic will occur if too much NaHCO₃ is added. Comparative properties of lidocaine, ropivacaine, and bupivacaine are outlined in Table 20-4.

Protein Binding

Protein binding is another property important to understand. All local anesthetics bind to albumin and μ-1-acid glycoprotein (AAG). It is the free portion of the drug that is responsible for toxicity. In pregnancy, albumin levels are depressed, so AAG binding becomes most important. AAG is released in response to surgery, trauma, infection, and inflammation. Once AAG sites are saturated with local anesthetics, the free drug levels progressively increase. Protein binding also decreases with decreasing pH. Therefore, in an acidotic environment, a high proportion of free drug with the potential for cardiac or neurotoxicity should be anticipated.

Absorption

Absorption of local anesthetics refers to the movement of the drug from the site of injection to the bloodstream. Therefore, the more vascular the area and the larger the total dose of anesthetic used, the higher the resulting serum level of the drug. The addition of a vasoconstrictor (epinephrine) to the local anesthetic can decrease the absorption and, therefore, toxicity of the drug used (see Table 20-4).

Toxicity

Local anesthetic toxicity may manifest with CNS or cardiac effects. As the doses increase, disinhibition and CNS excitation occurs producing seizures. Local anesthetic bind and inhibit cardiac Na⁺, Ca²⁺, and K⁺ channels as concentrations increase causing cardiac arrest. Treatment of adverse reactions depends on the severity of their effects from spontaneous recovery, to supportive care with oxygen and maintaining the airway, to advanced cardiac life support (ACLS).

Ropivacaine is a local anesthetic with similar characteristics to bupivicaine. This is produced solely as the S-enantiomer, whereas bupivicaine is a mixture of the S and R forms. This S-form has less ability to bind Na-channels in the myocardial conduction system. Therefore, there is less risk of cardiotoxicity with ropivacaine. As seen in Table 20-4, ropivacaine and bupivicaine have very similar physical properties except for the margin of safety, in ropivacaine, which produces less toxic side effects. There also appears to be less of a motor block compared to bupivicaine, which theorhetically should improve patient satisfaction during the laboring process. Caution has been used in administering this agent as it has several side effects that occur in a significantly high occurrence (>10% of patients). These include cardiovascular: hypotension (dose-related and age-related: 32%-69%), maternal bradycardia (6%-20%), gastrointestinal: nausea (11%-29%), vomiting (7%-14%), and neuromuscular and skeletal: back pain (7%-10%) of patients.

The pharmacologic treatment of local anesthetic systemic toxicity (LAST) is different from other cardiac arrest scenarios.

• Airway management—ventilate with 100% oxygen

• Seizure suppression with benzodiazepines avoiding propofol

• Use ACLS avoiding vasopressin, calcium channel blockers, β-blockers, or local anesthetics reducing epinephrine dose to less than 1 μg/kg

• 20% Intralipid 1.5 cc/kg bolus over 1 minute; start continuous infusion 0.25 cc/kg/min

Bolus may be repeated for persistent cardiac arrest and infusion rate may be doubled to 0.5 cc/kg/min; approximate upper limit is 10 cc/kg of the lipid emulsion.

Local anesthetic concentrations and maximum doses (approximate for 70-kg patient).

1. Lidocaine → 5 mg/kg

   • 1% lidocaine = 10 mg lidocaine/cc

     Maximum dose 35 cc

   • 2% lidocaine = 20 mg lidocaine/cc

     Maximum dose 17.5 cc

2. Lidocaine with epinephrine → 7 mg/kg

   • 

   • 

3. Marcaine with or without epinephrine → 2.5mg/kg

   • 

   • 

Epidural Analgesia/Anesthesia

Lumbar epidural block is the most common form of analgesia used to provide relief from the nociceptive pathways during the stages of labor. The epidural space is the interval superiorly bounded by the foramen magnum, inferiorly by the lower end of the dural sac, anteriorly by the posterior longitudinal ligament and posteriorly by the ligamentum flavum. The approach to the epidural space is posteriorly through the skin, subcutaneous fat, supraspinous ligament, interspinous ligament, ligamentum flavum, and into the epidural space (Fig. 20-4).

The size of the epidural space varies along its course with the largest diameter existing at the L₂ interspace with a range of 4 to 9 mm. A simple maneuver that helps open up the bony entrance to the epidural space is flexion of the lumbar spine (Fig. 20-5).

The contents of the epidural space include fat, vertebral venous plexus, lymphatics, arteries, and dural spinal nerve projections. In pregnancy, with the increase in intra-abdominal pressure, the venous plexus becomes distended. This phenomenon, and the accompaning increase in epidural fat that occurs during pregnancy, functions to reduce epidural volume substantially. Therefore, pregnant patients usually require less volume of local anesthetic, as compared to nonpregnant controls, to produce a similar level of blockade.

Once the epidural catheter is in place, local anesthetic is administered according to the appropriate pain pathway and corresponding stage of labor. In the first stage of labor, T₁₀ block is sufficient. In the late first stage and second stage of labor, the nerves to be blocked include the sacral area so the parturient should be dosed in the semi-Fowler position to allow downward spread of the local anesthetic. Finally, for predelivery and the third stage of labor, the parturient may be seated upright (with a vena cava tilt) to secure sacral root spread of the drug (Fig. 20-6). This blockade may be achieved by intermittent bolus injections or by continuous infusion of the drug with changes in patient positioning altering the level of blockade.

With the uppermost level of analgesia at T₁₀, the 5 lowermost vasomotor segments supplying the pelvis, lower trunk, and limbs are interrupted causing a decrease in total peripheral resistance, venous return, and CO. In normal parturients, this insult induces a reflex cardiovascular response directed toward maintaining systemic blood pressure. Coloading of an adequate intravenous crystalloid infusion, keeping the parturient on her side, and minimizing the dose of the local anesthetic all minimize the adverse decrease in blood flow to the pelvis and its structures.

High epidural anesthesia that extends to T₄-S₅ is associated with a significant interruption of vasomotor segments, resulting in significant hypotension. Again, fluid coload and lateral tilt of the parturient can augment the reflex corrective responses of the cardiovascular system in this situation. Extending the epidural blockade above spinal level T₁₀ is unnecessary and counterproductive for the normal laboring patient. If epidural analgesia needs to be changed to anesthesia for a cesarian section, these risks are necessary and measures to prevent them should be instituted. In addition, Neo-Synephrine is the best vasopressor to augment blood pressure without reducing blood supply to the uterus. Studies suggest there is improved fetal acid-base status and Apgar scores with prophylactic Neosynephrine boluses and infusion as compared to ephedrine as was previously used.

Contraindications to lumbar epidural analgesia/anesthesia are reviewed in Table 20-5. The advantages and disadvantages of regional analgesia/anesthesia are outlined in Table 20-6.

A combined spinal/epidural analgesia technique provides rapid onset of spinal opioid analgesia, plus the flexibility of the epidural blockade. Sufentanil 10 μg or fentanyl 25 μg injected spinally, when the epidural catheter is inserted, can reliably give several hours of analgesia to patients in the early first stage of labor (<5 cm dilation). The continuous infusion of a weak local anesthetic (0.125%/0.0625% bupivicaine or 0.2%/0.1% ropivacaine) with a low-dose narcotic (sufentanil 1-2 μg/cc or fentanyl 5-10 μg/cc) can provide good perineal analgesia for later stages of labor. If needed, higher concentrations of bupivacaine or lidocaine can be bolused for more complete nerve blockade. Less motor blockade, less hypotension, less local anesthetic administered with inherent toxicity risk, and faster onset of analgesia are all benefits of this combined technique.

The side effects of intrathecal opioids and corresponding treatment are listed in Table 20-7.

Fetal Bradycardia in Epidural Analgesia and Combined Spinal/Epidural Techniques

Fetal bradycardia is a nonreassuring fetal heart rate after induction of neuraxial anesthesia that may be due to maternal hypotension or uterine hyperactivity. It is mostly associated with the combined spinal/epidural technique but can be seen with any technique that produces profound analgesia.

The placental circulation is dependent on the maternal SBP, and with a sudden onset sympathetic block from the local anesthetic, this can decrease placental perfusion and therefore cause fetal bradycardia. Local decreases in perfusion can occur without ever ascertaining a drop in the maternal SBP.

Another proposed explanation is that the fetal bradycardia is due to intrathecal opioid-induced uterine hypertonus. The uterine tetany is thought to be due to rapid onset of analgesia, which causes a sudden decrease in maternal plasma epinephrine and subsequent withdrawal of epinephrine’s β-sympathomimetic relaxant effects on the myometrium. This is followed with decreased placental blood flow, fetal asphyxia, and fetal bradycardia.

Preanalgesic adequate hydration of the patient must be achieved with coloading using crystalloids, as well as, the prevention of overdosing with high blocks beyond that necessary to achieve analgesia for the nerve roots involved with the labor pains. With this physiological understanding of the dynamics occurring, treatment is based on relaxing the uterus. Uterine hypertonus may be reversed with 1 or 2 doses of intravenous nitroglycerin (60-90 μg). The hypotension that results is treated with phenylephrine (40-80 μg). Persistent hypertonus can be treated with another dose of nitroglycerin or a β-agonist, such as terbutaline 0.25 mg intravenously; however, terbutaline results in an extended period of uterine relaxation and maternal tachycardia.

There are 2 important techniques to discuss that may be used by the obstetric care provider to provide analgesia when obstetric anesthesia coverage is unavailable. Although these techniques are relatively easy to execute, a thorough knowledge of the anatomy, physiology, and effects of local anesthetics on mother and fetus is paramount.

Bilateral Pudendal Nerve Block

This block is an effective blockade for the second and third stages of labor, blocking the sacral nerves S₃-S₄-S₅ (Fig. 20-7). The transvaginal approach points the needle behind the sacrospinous ligament aiming toward the ischial spine. Up to 5 mg/kg of lidocaine (1% solution without epinephrine) total dose provides relief of perineal pain within 3 to 5 minutes (Figs. 20-8 and 20-9).

Bilateral Paracervical Block

Paracervical block interrupts uterine nociceptive pain pathways T₁₀-L₁, effecting complete relief from pain of the first stage of labor (Fig. 20-10). This does not, however, relieve any perineal pain of the second and third stages of labor. Using up to 5 mg/kg of lidocaine in a 1% solution total dose will give good pain relief for approximately 2 hours. Associated transient fetal bradycardia has been reported with the use of paracervical blockade and therefore should be used with caution. Local anesthetics with epinephrine should not be used because the fetal head is so close to the injection site and the proximate location of the uterine artery and venous plexus that it may increase the risk of epinephrine uptake by mother and/or fetus.

Spinal Anesthesia

The advantages of spinal anesthesia responsible for its current popularity include relative simplicity, rapidity, certainty, duration, low failure rate, and minimal side effects. It also offers the lowest drug exposure as local anesthetic is being exposed directly to nerve fibers with minimal systemic uptake of the drug.

The primary disadvantages of spinal anesthesia are the effects of high T_2-4 blockade with maternal hypotension and postural puncture headaches (Table 20-8). The risk of the high spinal includes sympathectomy with resultant unopposed parasympathetic stimulation. This leads to hypotension, increased gastric motility, increased nausea/vomiting, and instability of uterine perfusion. In parturients with severe asthma or reactive airway disease, this may precipitate bronchospasm. Also, the high motor blockade may inhibit motor fibers of the respiratory muscles impairing normal ventilation.

The postdural puncture headache risks are directly related to the size and type of needle used. With the 24/26 G Sprotte (blunted) needles now in use, the risk is less than 1% in this age group of patients. An important factor in the dispersion of the local anesthetic is the position of the patient. As shown in Fig. 20-11, the lowest point of the spine is T₅. Care, therefore, should be directed toward raising the patient’s head in an effort to reduce the inadvertent cephalad spread of the drug. Complications of subarachnoid block include the following:

• Physiological: Hypotension, bradycardia, or possible cardiac arrest

• Nonphysiological: Respiratory arrest and toxicity reactions

• Neurological: Paraplegia, arachnoiditis, or postdural puncture headache

General Anesthesia for Cesarean Section

General anesthesia is reserved for life-threatening situations, including severe fetal distress, cord prolapse, shoulder dystocia, intrauterine exploration for retained placenta or a twin, and replacement of an inverted uterus. In obstetric anesthesia, the anesthesiologist is responsible for 2 lives: the mother and the baby.

Preanesthetic preparation includes a history and physical examination with emphasis on cardiac and pulmonary disease, evaluation of the airway, height/weight comparison, allergies, current medications, intravenous access, and blood product availability. Every pregnant woman beyond the first trimester is considered to have a full stomach and is at risk for aspiration of gastric contents. This demands prophylaxis with a nonparticulate antacid, an H₂-blocker, and metochlorpropamide (Reglan). The most common cause of maternal death related to general anesthesia is aspiration pneumonia secondary to inability to secure the airway with an endotracheal tube (ETT).

Induction of Anesthesia

The patient should be placed on the operating table with a leftward pelvic tilt to prevent aortocaval compression with monitors applied. She should receive a 500-cc to 1000-cc lactated Ringer bolus while preoxygenation is performed. Cricoid pressure should be applied as the Sellick maneuver is achieved to prevent regurgitation of stomach contents into the lung. The obstetrician who is prepared and ready to make an incision with one hand may place the other hand on the patient’s epigastric area. Intravenous induction (using the patient’s ideal body weight) with thiopental (3-5 mg/kg), propofol (1-2 mg/kg), ketamine (1 mg/kg), or etomidate (0.2-0.3 mg/kg) may be used. Succinylcholine 1 mg/kg IV is given to achieve muscle relaxation to facilitate endotracheal intubation. Once the ETT is placed, the first breath given by the anesthesiologist should not be felt by the obstetrician’s hand over the stomach. If a belch of air is perceived, the ETT may not, in fact, be in the trachea. This team approach ensures maximal security of a protected, intubated airway prior to surgical incision. Maintenance of a balanced general anesthesia with both inhalational agents and intravenous muscle relaxants is performed until delivery of the baby. At this time, narcotics may be given to reduce the concentration of inhalational drugs needed.

The patient should be completely awake and in control of her airway protective reflexes before extubation occurs. It is important to understand that the risk of aspiration at the end of surgery (extubation) is just as great as at the start (intubation).

Figure 20-12 is a guide to failed intubation events with/without a known difficult airway, with/without the ability to ventilate, and with/without fetal distress.

The GlideScope is a video laryngoscope system that can now be used within the difficult airway algorithm if traditional intubation techniques fail. This can be used prior to awakening a patient for an awake intubation.

Cesarean Under Local Anesthetic Infiltration

American College of Obstetricians and Gynecologists (ACOG) notes that maternal request is sufficient reason to provide pain relief. Infiltration of local anesthesia can be used for cesarean delivery when adequate general or regional anesthesia is available. If the anesthesiologist is not ready to proceed with anesthesia yet the obstetrician declares the need to proceed if the fetus’ life is at risk, the obstetrician has the option to proceed under local infiltration. The anesthesiologist is neither expected nor requested to put a mother’s life in danger by administering an anesthetic if they deem to be unsafe or life-threatening to the mother (see section Local Anesthetic Dosages and Toxicity).

Preeclampsia

Preeclampsia is a multisystem disease. Although its hallmarks are hypertension and proteinuria, patients may develop renal failure, thrombocytopenia, hemolysis, liver dysfunction, and CNS involvement. For labor, epidural or epidural/spinal with narcotic/local anesthetic combinations are optimal to reduce the added stress related to pain. For cesarean section delivery, controversy remains whether epidural or general anesthesia is best. Epidural anesthesia for cesarean section requires a high block-T₄ with the associated risk of maternal hypotension. General anesthesia requires intubation, which with tracheal stimulation may result in dangerous hemodynamic aberrations, including hypertension, increased mean pulmonary artery pressure, and increased pulmonary capillary wedge pressure. With adequate invasive monitors such as an arterial line with careful coloading hydration, use of Neo-Synephrine, and slow onset of the block, epidural blockade can be safely conducted. Transthoracic echocardiography (TTE) is also readily used for investigation of cardiac function, identification of valvular competency, congenital cardiac anomalies, detection of blood clots, masses or tumors and color Doppler flow of blood within the heart and pulmonary blood vessels. Also, the use of β-blocker agents (preinduction) or lidocaine to blunt the tracheal stimulation of intubation can also be safe. Magnesium sulfate interacts with both depolarizing and nondepolarizing neuromuscular blocking drugs, so dosages must be altered accordingly. Close monitoring of the patient and open discussion of the patient’s preoperative status with the obstetrician is helpful in determining the optimum anesthetic plan for mother and baby (see Chap. 5).

Preterm Birth

Patients with preterm labor, for whatever reason, will most likely have been on tocolytic drugs. If β-adrenergic drugs were used to secure uterine relaxation, care must be taken to observe for tachycardia, hypertension, chest pain, myocardial ischemia, arrhythmias, pulmonary edema, anxiety, nausea/vomiting, hyperglycemia, or hypokalemia that may be exaggerated by general anesthetics. In parturients on intravenous magnesium sulfate as a tocolytic agent, potentiation of muscle relaxant drug activity should be anticipated. Because preterm fetuses are often low birth weight, with diminished compensatory reserve, special attention should be directed at maintaining uteroplacental perfusion (see Chap. 22).

HIV-Infected Parturients

Concern has been voiced in published literature that HIV-positive parturients may not be candidates for regional anesthesia. The fear of spreading the infection to the CNS, adverse neurologic sequelae, or attenuation of the immunologic status of the patient has been questioned. To date, the available data support the use of epidural anesthesia in these patients with no substantiated evidence that these concerns are valid (see Chap. 26).

Coagulopathies

The preoperative laboratory tests recommended in a parturient with a suspected coagulopathy include hemoglobin, hematocrit, platelet count, prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen, and fibrin degradation products. There is no one source (authority) that specifies the best test or laboratory value in determining risk for epidural hematoma. The following are examples when epidural anesthesia is not recommended:

• Parturient on heparin therapy with elevated PTT or heparin level greater than 0.24 μ/mL

• Parturient with known factor deficiency, for example, von Willebrand with low factor 8 levels

• Parturient with severe HELLP (hemolysis, elevated liver transaminases, low platelets) syndrome

• Parturient with disseminated intravascular coagulopathy

• Parturient actively bleeding and hemodynamically unstable

• Many examples of stable, but abnormal laboratory values may be amenable to an epidural technique. However, discussion with the obstetrician about whether active bleeding is occurring and about overall risks versus benefits of general anesthesia as compared to conduction anesthesia, in a given high-risk circumstance, may help determine the parturient’s best overall anesthetic management.

The degree of shunting of blood in women with intracardiac defects is primarily determined by the balance of resistances in the systemic (systemic vascular resistance) and pulmonary vascular beds (pulmonary vascular resistance). During pregnancy, these resistances decline proportionally during the various stages of pregnancy. With atrial septal defect (ASD), ventricular septal defect (VSD), or patent ductus arteriosus (PDA) with a left-to-right shunt, these parturients usually tolerate pregnancy, anesthesia, and delivery well. Reminders are to be aware of arrhythmias, systemic embolism, right ventricular hypertrophy and failure, and pulmonary hypertension. These concerns are especially problematic in the postpartum period when placental shunting is gone (increased blood volume), resulting in an increased preload that places a strain on the shunt balance. Parturients with right-to-left shunts such as uncorrected tetralogy of Fallot or Eisenmenger syndrome can be exacerbated by hypoxemia, hypercarbia, and decrease in systemic vascular resistance.

In right or left ventricular outflow obstruction such as valvular stenosis or coarctation of the aorta, volume depletion, or decrease in systemic vascular resistance can significantly exacerbate symptoms. With careful monitoring and attention to the specifics of the cardiac lesion and resultant cardiopulmonary pathophysiology, anesthesia and analgesia can be safely conducted in the high-risk parturient (see Chap. 8).

Pulmonary edema, when it occurs during pregnancy, invariably has a predisposing etiology (Table 20-9). Basic management of this condition includes establishing the cause and reversing the effects of hypoxemia. The use of transesophageal echocardiography (TEE) or TTE monitoring and arterial line can be extremely useful in elucidating the etiology and most appropriate treatment for pulmonary edema (see Chap. 12).

Anesthetic management for delivery of the baby, in most circumstances, may be in the form of a conduction anesthetic. However, the parturient with severe respiratory failure may require general anesthesia with endotracheal intubation to obtain stability.

In September 2010, ACOG changed the standard of care to giving antibiotics before skin incision for cesarean deliveries, rather than after umbilical cord clamping. Giving antibiotics to within 60 minutes prior to skin incision reduced wound infection from 1.4% to 0.6%.

Prevention of Neuraxial Infections

Neuraxial infections due to regional anesthesia are rare. In 2010, the ASA Practice Advisory of Prevention of Infection made recommendations based on both scientific evidence and opinion-based evidence to support their recommendations.

The use of alcohol with chlorhexidine is the preferred prep solution for the best antibacterial effect for the longest period. Although the Food and Drug Administration (FDA) has not approved this owing to animal studies producing neurotoxicity due to intrathecal chlorhexidine, retrospective studies in humans showed no difference in neurologic complications using chlorhexidine prep compared to others in the literature, with symptoms resolving in 30 days (0.0%).

In conclusion, once an understanding of the nature of the parturient’s pain is recognized, with techniques available to the anesthesiologist and obstetrician, an optimal care plan can be attained, even for high-risk parturients.