Neurosurgery in the Pregnant Patient

Knowledge of the physiologic changes of pregnancy is essential to the anesthetic management of the pregnant woman undergoing neurosurgery.

The key to maintenance of fetal wellbeing during surgery is appropriate maternal oxygenation and maintenance of uteroplacental perfusion.

While many anesthetic drugs pass the placenta, there is little evidence that any of the commonly used anesthetics is teratogenic.

Whenever possible anesthetic decision making should be based on the best interests of both the mother and her fetus. When these interests conflict, maintenance of maternal wellbeing is paramount.

Neurologic disorders requiring operation during pregnancy are surprisingly common, and most anesthesiologists eventually encounter a pregnant woman who has such a disorder. The anesthetic management of these patients can be complicated by the significant maternal physiologic changes that occur during pregnancy. These changes may require alterations in anesthetic management that are in opposition to the techniques that would be appropriate for a nonpregnant patient who has the same neurosurgical condition.

Additionally, while maternal considerations must remain paramount, it is important to recognize that interventions that benefit the mother might have the potential for causing harm to the fetus. Therefore, the major challenge of neuroanesthesia during pregnancy is to provide an appropriate balance between competing, or even contradictory, clinical goals.

The discussion in this chapter is limited to the anesthetic management of pregnant women undergoing craniotomy for resection of arteriovenous malformations (AVMs) and intracranial neoplasms, aneurysm clipping, and evacuation of spontaneous spinal epidural hematomas (SSEHs). Because the anesthetic management of these procedures is discussed elsewhere in this book, this chapter deals primarily with the ways in which pregnancy alters the anesthetic management.

I. MATERNAL PHYSIOLOGIC ALTERATIONS DURING PREGNANCY

A. Neurologic changes

1. Inhalation anesthetic requirements. The minimum alveolar concentration (MAC) for inhalation anesthetics decreases by approximately 30% to 40% during pregnancy, a change that occurs as early as the first trimester. This has been postulated to be a result of increased circulating endorphins. Alternatively, an increase in the concentration of progesterone, a hormone with known sedative effects, might account for the diminished anesthetic requirement. As a result of the increased sensitivity to inhalation anesthetics, inspired anesthetic concentrations that would be appropriate in non-pregnant patients can lead to significant cardiopulmonary depression during pregnancy.

2. Local anesthetic requirements. Local anesthetic requirements for spinal and epidural anesthesia are decreased by 30% to 40% during pregnancy. This decrease is in part due to the decreased volume of cerebrospinal fluid in the lumbar subarachnoid space secondary to engorgement of the epidural veins. However, the decrease in local anesthetic requirements predates the onset of significant epidural venous engorgement. A progesterone-induced increase in the sensitivity of neurons to the sodium-blocking properties of local anesthetics is thought to be the cause.

B. Respiratory changes

1. Upper airway mucosal edema. The accumulation of extracellular fluid produces soft tissue edema during pregnancy, particularly in the upper airway where marked mucosal friability can develop. Nasotracheal intubation and the insertion of nasogastric tubes should be avoided unless absolutely necessary because of the risk of significant epistaxis. Laryngeal edema can also reduce the size of the glottic aperture, leading to difficult intubation, particularly in pre-eclamptic patients. A 6 to 6.5 mm endotracheal tube is therefore appropriate for most pregnant patients.

2. Functional residual capacity (FRC). FRC decreases by as much as 40% by the end of the third trimester while closing capacity (CC) remains unchanged. The FRC decreases further in the supine position, a situation in which CC commonly exceeds FRC. When CC exceeds FRC, this leads to small airway closure, increased shunt fraction, and an increased potential for arterial desaturation. Additionally, because FRC represents the store of oxygen available during a period of apnea, decreases in FRC can be expected to lead to the more rapid development of hypoxemia when a patient becomes apneic, as occurs during the induction of anesthesia. Because oxygen consumption increases by 20% during pregnancy, significant desaturation can occur even when intubation is performed expeditiously. This mandates at least 4 minutes of preoxygenation and denitrogenation with a tightly fitting facemask before the induction of general anesthesia during pregnancy.

3. Ventilation. Significant increases in minute ventilation occur as early as the end of the first trimester. At term, minute ventilation increases by 50% owing to increases in both tidal volume (40%) and respiratory rate (15%). It has been postulated that these increases occur because of a progesterone-induced increase in the ventilatory response to CO₂. Because the increase in ventilation exceeds the increase in CO₂ production, the normal arterial partial pressure of CO₂ (PaCO₂) decreases to approximately 32 mm Hg. The increased excretion of renal bicarbonate partially compensates for the hypocarbia so that pH increases only slightly to approximately 7.42 to 7.44.

C. Cardiovascular changes

1. Blood volume. Blood volume increases by 35% during pregnancy. Because plasma volume increases to a greater extent than red cell mass (50% vs. 20%), a dilutional anemia occurs. Normal hematocrit at term ranges from 30% to 35%.

2. Cardiac output (CO). Significant increases in CO occur as early as the first trimester. Capeless and Clapp demonstrated a 22% increase in CO by 8 weeks’ gestation which represents 57% of the total change seen at 24 weeks. CO rises steadily throughout the second trimester. After 24 weeks, it remains stable or increases slightly. Earlier studies demonstrating a decrease in CO in the third trimester reflect measurements made in the supine position with consequent aortocaval compression (see subsequent text).

Cardiac output can increase by an additional 60% during labor. Part of this increase is caused by the pain and apprehension associated with contractions, an increase that can be blunted with the provision of adequate analgesia. There is a further increase in CO, unaffected by analgesia, from the autotransfusion of 300 to 500 mL of blood from the uterus into the central circulation with each contraction. Finally, CO increases further in the immediate postpartum period by as much as 80% above prelabor values because of the autotransfusion from the rapidly involuting uterus as well as the augmentation of preload secondary to alleviation of the aortocaval compression.

3. Aortocaval compression. When pregnant women beyond 20 weeks’ gestation assume the supine position, the enlarged uterus can compress the inferior vena cava against the vertebral column. When this occurs, venous return to the heart decreases, sometimes to a marked extent, leading to decreases in CO and blood pressure. This has the potential for decreasing uterine blood flow (UBF) to a level that can impair uteroplacental oxygen delivery. Supine positioning may also produce aortic compression. If this occurs, upper extremity blood pressure might be normal, but distal aortic pressure and therefore uterine artery perfusion pressure both decrease significantly. Because both regional and general anesthetics reduce venous return, the effects of aortocaval compression are magnified in the anesthetized patient. Therefore, the supine position must be avoided in pregnant patients undergoing anesthesia. Tilting the operating table 30° to the left prevents significant aortocaval compression. Placing a roll under the patient’s right hip can also achieve this goal.

D. Gastrointestinal changes

1. Gastric acid production. The placenta produces ectopic gastrin. This leads to increases in both the volume and the acidity of gastric secretions.

2. Gastric emptying. Contrary to common belief, gastric emptying in pregnancy is not significantly altered prior to the onset of labor. With the onset of painful contractions, however, gastric emptying is slowed. Systemic opioids administered during labor have a similar effect.

3. Gastroesophageal sphincter. The enlarging uterus causes elevation and rotation of the stomach, which interferes with the pinch-cock mechanism of the gastroesophageal sphincter. This increases the likelihood of gastroesophageal reflux.

4. Pregnancy and aspiration pneumonia. The changes described make it more likely that a pregnant patient will regurgitate and aspirate and, if this occurs, the pulmonary injury will be greater because of the increased volume and acidity of the gastric contents. These changes occur by the end of the first trimester if not earlier. Therefore, pregnant patients who have an estimated gestational age of approximately 14 weeks or more are assumed to have a full stomach. They should therefore receive aspiration prophylaxis with either a non-particulate antacid and/or a combination of a hydrogen (H₂) blocking drug and metoclopramide. The presence of a full stomach influences anesthetic induction but, as described in the subsequent text, techniques designed to minimize the risk of aspiration might not be ideal for the patient who has an intracranial lesion.

E. Renal and hepatic changes. Aldosterone levels increase during pregnancy with a concomitant increase in total body sodium and water. This increase in total body sodium and water can increase edema in an intracranial neoplasm and lead to either worsening signs and symptoms or the onset of symptoms from a previously unrecognized mass lesion. Renal blood flow and glomerular filtration rate increase by approximately 60% at term, paralleling the increase in CO. Therefore, blood urea nitrogen (BUN) and creatinine are usually one-half to two-thirds the values seen in non-pregnant women. What would be considered a normal or only mildly elevated BUN and creatinine in non-pregnant women should be a cause for concern during pregnancy.

Slight increases in alanine aminotransferase, aspartic transaminase, and lactate dehydrogenase are not uncommon during normal pregnancy. Plasma cholinesterase levels decrease, but prolonged neuromuscular blockade does not occur in normal parturients receiving succinylcholine.

F. Epidural vascular changes

1. Epidural venous pressure is increased mainly by global elevation of intraabdominal pressure secondary to the pregnant uterus and direct compression of the vena cava. These two factors lead to the diversion of a portion of the venous return from the legs and pelvis into the vertebral venous system with resultant engorgement of the epidural venous plexus. It has been postulated that elevated venous pressure in the epidural space in association with the hemodynamic changes of pregnancy may predispose the pregnant patient to the rupture of a preexisting pathologic venous wall. Epidural veins are a primitive venous system containing no valves. Therefore, abrupt pressure changes, such as straining and coughing, could be transmitted directly from the abdominal cavity to the epidural veins, causing rupture although this is certainly a rare occurrence.

2. Epidural arterial vessels may undergo degenerative structural changes during pregnancy owing to the excess of estrogen and progesterone. The arterial vessels of pregnant women have been shown to demonstrate fragmentation of the reticulin fibers, diminished acid mucopolysaccharides, loss of normal corrugation of elastic fibers, and hypertrophy and hyperplasia of smooth muscle cells. The combination of these structural changes with hemodynamic alterations during pregnancy, particularly in the third trimester, may predispose susceptible patients to the rupture of the epidural arteries.

II. EFFECTS OF ANESTHETIC INTERVENTIONS ON UBF

A. Determinants of UBF. At term, normal UBF is approximately 700 mL/minute which is approximately 10% of total maternal blood flow. The magnitude of UBF is determined by this equation:

UBF = (UAP − UVP)/UVR

where UAP is the uterine arterial pressure, UVP the uterine venous pressure, and UVR the uterine vascular resistance. Alterations in any of these influences UBF and, therefore, the delivery of oxygen and nutrients to the fetus.

B. Factors decreasing uterine arterial pressure

1. Hypovolemia

2. Sympathetic blockade

3. Aortocaval compression

4. Anesthetic overdose

5. Vasodilator overdose

6. Excessive positive pressure ventilation

C. Factors increasing uterine venous pressure

1. Vena caval compression

2. Uterine contractions

3. Uterine hypertonus

a. Oxytocin overstimulation

b. Alpha-adrenergic stimulation

D. Factors increasing uterine vascular resistance

1. Endogenous catecholamines

a. Untreated pain

b. Noxious stimulation (laryngoscopy, skin incision)

2. Pre-eclampsia

3. Chronic hypertension

4. Exogenous vasoconstrictors

Phenylephrine is now commonly used as the first-line pharmacologic treatment for maternal hypotension. Although high doses of phenylephrine decrease UBF owing to its vasoconstrictor effects, UBF is well maintained when phenylephrine is given in low doses of 50 to 100 mcg intravenously. In fact, there is growing evidence that phenylephrine maintains fetal acid–base balance better than ephedrine; it has been postulated that transplacental passage of the ephedrine increases fetal metabolism, leading to relative acidemia.

III. UTEROPLACENTAL DRUG TRANSFER AND TERATOGENESIS

A. Drug transfer. A detailed consideration of the various mechanisms (active transport, facilitated diffusion, pinocytosis) by which substances are transported across the placenta is beyond the scope of this chapter. The discussion here concentrates on passive diffusion, the mechanism by which most anesthetic drugs administered to the mother reach the fetus. This process does not require the expenditure of energy. Transfer can occur either directly through the lipid membrane or through protein channels that traverse the lipid bilayer.

1. Determinants of passive diffusion

a. Concentration gradient is the primary determinant of the rate of transfer of drugs across the placenta. As an example, the initial rate of transfer of an inhalation anesthetic is quite rapid. As the partial pressure of the drug increases in the fetus, the rate of transfer decreases.

b. Substances that have a low molecular weight

Only gold members can continue reading. Log In or Register to continue