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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 fetal harm. Therefore, the major challenge of neuroanesthesia during pregnancy is to provide an appropriate balance between competing, or even contradictory, clinical goals.
The discussion 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).

I. Maternal physiologic alterations during pregnancy

Neurologic changes
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 nonpregnant patients can lead to severe cardiopulmonary depression during pregnancy.
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.
Respiratory changes
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 preeclamptic patients. A 6 mm endotracheal tube is therefore appropriate for most pregnant patients.
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 face mask before the induction of general anesthesia during pregnancy.
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 carbon dioxide (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.
Cardiovascular changes
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%.
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).
CO 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.
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 decrease significantly. Because both regional and general anesthesthetics 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.
Gastrointestinal changes
Gastric acid production. The placenta produces ectopic gastrin. This leads to increases in both the volume and the acidity of gastric secretions.
Gastric emptying. Contrary to common belief, gastric emptying is not significantly altered during pregnancy. With the onset of painful contractions, however, gastric emptying is slowed. Systemic opioids administered during labor have a similar effect.
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.
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 longer are assumed to have a full stomach. They should therefore receive aspiration prophylaxis with either a nonparticulate antacid or a combination of an 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.
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 either to 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 nonpregnant women. What would be considered a normal or only mildly elevated BUN and creatinine in nonpregnant 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.
Epidural vascular changes
Epidural venous pressure is increased mainly by global elevation of intra-abdominal 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.
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

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.
Factors decreasing uterine arterial pressure
Hypovolemia
Sympathetic blockade
Aortocaval compression
Anesthetic overdose
Vasodilator overdose
Excessive positive pressure ventilation
Factors increasing uterine venous pressure
Vena caval compression
Uterine contractions
Uterine hypertonus
1. Oxytocin overstimulation
2. Alpha-adrenergic stimulation
Factors increasing uterine vascular resistance
Endogenous catecholamines
1. Untreated pain
2. Noxious stimulation (laryngoscopy, skin incision)
Preeclampsia
Chronic hypertension
Exogenous vasoconstrictors
Ephedrine is the drug of choice for treating maternal hypotension. Because of its mixed alpha and beta effects, it increases maternal blood pressure (and therefore UAP) without increasing UVR. It therefore maintains UBF. The use of the pure alpha-agonist phenylephrine during pregnancy is being revisited. In high doses, it increases maternal blood pressure but decreases UBF because it is a potent uterine artery vasoconstrictor. UBF is well maintained when phenylephrine is given in low doses of 50 to 100 mcg intravenously. Recent studies have revealed less neonatal acidosis after spinal anesthesia for cesarean section with the combination of phenylephrine and ephedrine for maternal blood pressure support than when ephedrine is used alone.

III. Uteroplacental drug transfer and teratogenesis

Drug transfer. A detailed consideration of the various mechanisms (active transport, facilitated diffusion, pinocytosis) by which substances are transported across the placenta is not discussed here, and 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.
Determinants of passive diffusion
1. 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.
2. Substances that have a low molecular weight cross the placenta more readily than those that have a higher weight.
3. Drugs that have high lipid solubility readily traverse the placenta.
4. Ionization limits placental transfer.
5. Membrane thickness can be increased in certain pathologic states, including chronic hypertension and diabetes. The effects of these conditions on drug transfer are of less concern than the resultant limitation of the transportation of oxygen and nutrients. This can lead to intrauterine growth restriction or, in severe cases, fetal demise.
Specific drugs
1. The inhalation agents cross the placenta freely, owing to their low molecular weight and high lipid solubility. The longer the period of fetal exposure to the drug (induction to delivery interval), the more likely the newborn is to be depressed.
2. The induction drugs, thiopental, etomidate, and propofol, are highly lipophilic and unionized at physiologic pH. Placental transfer is quite rapid. Because most of the blood returning to the fetus from the umbilical vein passes through the fetal liver, extensive first-pass metabolism occurs and neonatal depression after an induction dose of these drugs is uncommon.
3. Both depolarizing and nondepolarizing muscle relaxants are highly ionized at physiologic pH. Placental transfer is minimal.
4. The opioids freely traverse the placenta because of their high lipid solubility and low molecular weight.
5. The reversal drugs, neostigmine and edrophonium, are highly ionized and demonstrate minimal placental transfer.
6. The anticholinergic drugs, atropine and scopolamine, freely pass the placenta. Glycopyrrolate is highly ionized and therefore crosses the placenta to a minimal degree.
7. The commonly used anticoagulants, heparin and warfarin, have remarkably different placental transfer. Heparin, a highly ionized polysaccharide molecule, does not reach the fetus. Warfarin, which is uncharged and has a molecular weight of only 330, readily passes across the placenta. Because warfarin can cause birth defects, its use is contraindicated during the period of organogenesis.
8. Antihypertensive drugs. The beta-blocking drugs that have been studied all cross the placenta. Labetalol appears to have the least placental transfer of this group of drugs. High-dose infusions of esmolol have been reported to cause persistent fetal bradycardia lasting up to 30 minutes after the termination of the infusion. The effect of a single dose is not known, but numerous cases of its safe use as a bolus during anesthetic induction have been reported. Sodium nitroprusside (SNP) freely passes the placenta and has implications for fetal toxicity.
Anesthesia during pregnancy and the risk of birth defects
Principles of teratology. It is an established principle that any substance, if administered in large enough quantities for a prolonged period of time during critical periods of gestation, can produce fetal injury ranging from growth restriction to major structural anomalies to death. Therefore, it should be a goal of the anesthesiologists caring for pregnant women to minimize the exposure of their fetuses to potentially toxic substances. Nevertheless, fears regarding the potential for injury should be tempered by the following considerations:
1. Most anesthetics are administered for such a brief period of time that the potential for toxicity is minimal.
2. There is no convincing human evidence that any of the commonly used anesthetics is dangerous to the fetus.
3. Maternal hypotension and hypoxemia pose a much greater risk to the fetus than do any of the anesthetic drugs.
4. Maternal well-being must be our paramount concern. If avoiding a potentially teratogenic drug leads to a poor maternal outcome or maternal death, fetal outcome will be equally compromised.
Evaluation of teratogenic potential. Because of the ethical and logistical difficulties inherent in large-scale prospective studies of the teratogenic effects of anesthetics in humans, we must rely on more indirect evidence to evaluate the teratogenic potential of these drugs. The principal investigative tools used are small animal studies, retrospective studies of the offspring of women who underwent anesthesia during pregnancy, and, in the case of inhalation anesthetics, studies of operating room personnel who were exposed to low-level waste anesthetic gases during pregnancy. The discussion of specific drugs that follows refers to the studies supporting or opposing their teratogenic potential.
Specific drugs
1. Animal studies of the potent inhalation anesthetics have demonstrated conflicting results. Reproductive effects appear to be dose related. These effects are more likely to be from the physiologic disturbances (hypothermia, hypoventilation, poor feeding) produced by the anesthetic state rather than the anesthetic drug itself. When animals are exposed to inspired concentrations that do not impair feeding behavior or level of consciousness, reproductive effects are minimal. Neither studies of operating room personnel exposed to trace anesthetics nor of women undergoing surgery during pregnancy support any teratogenic potential for the potent inhaled anesthetics. Fetal loss is increased in women operated upon during pregnancy, but this is primarily because of the underlying condition requiring surgical intervention and the increased incidence of preterm delivery in women undergoing surgery in close proximity to the uterus.
2. Nitrous oxide has clearly been shown to increase the incidence of structural abnormalities and fetal loss in rats. This was initially thought to be the result of inhibition of the enzyme methionine synthetase and subsequent decreases in the levels of methionine and tetrahydrofolate. This mechanism has been called into question, however, because maximal inhibition of methionine synthetase activity occurs at levels of anesthetic exposure that do not produce teratogenic effects. More recent evidence suggests that the fetal effects of nitrous oxide come from alpha-adrenergic stimulation and subsequent decreases in UBF, which can be reversed by simultaneously administering a potent inhalation drug. Studies of operating room personnel exposed to trace levels of nitrous oxide and of women receiving nitrous oxide anesthesia fail to show any teratogenic effect.
3. Muscle relaxants do not have any teratogenic effect at clinically appropriate doses.
4. Opioids have not been shown to be teratogenic in either human or animal studies.
5. Several human studies have suggested that chronic benzodiazepine therapy during pregnancy increases the incidence of cleft lip and cleft palate. These studies have been faulted for failure to control for concomitant exposure to other potentially teratogenic substances. There is little evidence to suggest that a single dose of a benzodiazepine during pregnancy poses any risk to the fetus.
6. There is no human evidence suggesting that local anesthetics are teratogenic. Chronic cocaine abuse has been linked to birth defects.
7. Coumadin therapy during pregnancy has been correlated with ophthalmologic, skeletal, and central nervous system abnormalities, presumably from microhemorrhages during organogenesis. Because heparin does not cross the placenta, it is the drug of choice in women requiring anticoagulation during pregnancy.

IV. Epidemiology of intracranial disease in pregnancy and the effect of pregnancy on intracranial disease

Subarachnoid hemorrhage (SAH): aneurysm and AVM. The causes of SAH during pregnancy are numerous, including hypertensive intracerebral hemorrhage, vasculitis, and bacterial endocarditis, but by far the most common are aneurysmal rupture and bleeding from an AVM. The overall incidence of SAH during pregnancy is approximately 1 in 10,000, which is similar to the incidence in the general population. SAH is responsible for approximately 4% to 5% of maternal deaths and has been reported to be the fourth most common nonobstetric cause of death after trauma, malignancy, and cardiac disease.
In 1990, Dias and Sekhar published a review of 154 published cases of SAH during pregnancy. The ratio of aneurysms to AVMs was approximately 3:1. There was no link between increasing parity and the incidence of hemorrhage. For both AVMs and aneurysms, there was an increasing incidence of hemorrhage with advancing gestational age, which may be from increases in CO or possibly hormonal influences on vascular integrity. Interestingly, few women bled during labor and delivery, which is consistent with the observation that >90% of all hemorrhages in nonpregnant patients occur at rest. Of the patients whose rupture occurred during labor and delivery, 34% had hypertension, proteinuria, or both, suggesting that the differentiation between SAH and preeclampsia may be difficult on clinical grounds alone.
Neoplastic lesions. The incidence of intracranial neoplasms does not appear to be appreciably different in pregnant compared with nonpregnant women. However, as mentioned previously, some tumors appear to grow more rapidly or become symptomatic during pregnancy. This may be because of an increase in either peritumoral edema secondary to increased sodium and water retention or blood volume in vascular tumors such as meningiomas.
Considerable evidence indicates that hormonal influences affect the growth of brain tumors, particularly meningiomas. The incidence of meningioma is higher in women than in men but decreases significantly after menopause. Progesterone receptors have been identified in both meningiomas and gliomas. Accelerated tumor growth during pregnancy is likely, owing in part to the high levels of circulating progesterone that occur with gestation.

V. Management of anesthesia for craniotomy during pregnancy

Timing of surgery in relation to delivery
General concerns. When craniotomy during pregnancy is contemplated, the physicians caring for the pregnant woman must decide whether to allow the pregnancy to proceed to term or whether simultaneous operative delivery will occur. The gestational age of the fetus, with 32 weeks commonly used as the cutoff, determines the decision. Before 32 weeks, pregnancy is allowed to continue; after 32 weeks, cesarean delivery is performed and followed by immediate craniotomy. This determination is not only because viability improves at 32 weeks but also the risks of preterm delivery are believed to become less than the risks to the fetus of such maternal therapies as controlled hypotension, osmotic diuresis, and mechanical hyperventilation.
Aneurysm clipping. Dias and Sekhar demonstrated a significant improvement in survival for both mother and fetus when aneurysm clipping was performed after SAH as compared with nonsurgical management. Therefore, in patients who have good grades after SAH, aneurysm clipping should be performed as soon as possible to prevent rebleeding. Clipping unruptured contralateral aneurysms can be delayed until the postpartum period.
AVM resection. Resection of unruptured AVMs can be delayed until after delivery with no apparent increase in maternal mortality. Conversely, resection of symptomatic AVMs is usually performed regardless of gestation. The management of women who have a ruptured AVM but are neurologically stable is controversial. Dias and Sekhar showed improved maternal outcome with early operation, but this difference did not reach statistical significance. Therefore, the question of early operation for ruptured AVM during pregnancy remains unanswered at this time.
Neoplasm resection. Resection of a histologically benign neoplasm such as a meningioma can be delayed until after delivery but only if frequent follow-up and careful monitoring for neurologic deterioration can be ensured. Surgery for presumed malignant tumors and for those masses producing worsening neurologic deficits should be performed regardless of gestational age.
Anesthetic management
Sedative premedication may be appropriate in extremely anxious patients, but the risk of hypoventilation, hypercarbia, and subsequent increases in intracranial pressure (ICP) should be considered and guarded against. It might be more appropriate to defer the administration of sedative medications until the patient arrives in the preoperative holding area where careful observation can be maintained. Because pregnant patients must be considered to be at increased risk for regurgitation and aspiration of gastric contents, medications to decrease the acidity and the volume of the gastric contents should be administered. These include a nonparticulate antacid; metoclopramide, 10 mg; and an H2 blocking drug such as ranitidine, 150 mg.
Anesthetic induction in the pregnant patient who has an intracranial lesion provides the clearest example of the need to reconcile competing clinical goals. A rapid-sequence induction designed to prevent aspiration does little to prevent the hemodynamic response to intubation that can be catastrophic for the patient who has an intracranial aneurysm or increased ICP. At the same time, a slow "neuro induction" with thiopental, a narcotic, a nondepolarizing muscle relaxant, and mask ventilation does little to decrease the risk of aspiration. This technique can also be expected to lead to neonatal depression should a cesarean section be performed as part of a combined procedure.
One acceptable technique for anesthetic induction is described in the Table 15-1; other approaches that accomplish the stated goals are equally acceptable. As described previously, aspiration prophylaxis is mandatory. Cricoid pressure should be maintained from the point at which consciousness is lost until intubation is confirmed by capnography. If cesarean delivery is performed as part of a combined procedure, the physician caring for the newborn should be alerted to the likelihood of neonatal depression and the need to provide ventilatory support.
In addition to the standard maternal monitors, fetal heart rate (FHR) monitoring can be extremely useful during craniotomy, not because an ominous FHR indicates when cesarean delivery should be performed but because it should lead to a rapid search for potentially reversible causes of decreased uteroplacental perfusion, such as hypotension or hypoxemia. FHR monitoring usually becomes technically feasible at approximately 20 weeks of gestation. Note that decreases in short- and long-term variability, as well as a decreased baseline FHR, are commonly seen even in the healthy, uncompromised fetus whose mother is receiving general anesthesia.

Table -1. Anesthetic induction for craniotomy

Thiopental 5-7 mg/kg
Fentanyl 3-5 mcg/kg
Lidocaine 75 mg
Rocuronium 0.9-1.2 mg/kg
Mask ventilation with cricoid pressure, 100% O2

 

Table-2. Anesthetic maintenance for craniotomy

Fentanyl 1-2 mcg/kg/hr
Isoflurane 0.5-1%
Nondepolarizing muscle relaxant Thiopental 5-6 mg/kg/hr for "tight brain"

Anesthetic maintenance is not appreciably different between the pregnant and nonpregnant patient undergoing craniotomy (Table 15-2). As is the case during induction of anesthesia, every effort should be made to maintain hemodynamic stability as well as to avoid increases in cerebral blood volume that could interfere with surgical exposure. As stated previously, potentially teratogenic drugs should be avoided, but the commonly used anesthetics do not appear to fall into this category.
Adjuvants to surgery
1. Osmotic diuresis with mannitol is commonly used to decrease brain bulk and facilitate exposure during craniotomy. Because mannitol has been demonstrated in both animal and human studies to produce fetal dehydration, some have advised against its use during pregnancy. However, the doses given in these early studies were considerably higher than those currently in clinical use. There is no evidence that mannitol, 0.5 to 1 g/kg, has any significant adverse effect on fetal fluid balance.
2. Maternal hyperventilation can facilitate surgical exposure by decreasing cerebral blood volume. Severe hypocarbia may impair fetal oxygen delivery, however, by shifting the maternal oxygen-hemoglobin dissociation curve to the left. Hyperventilation can also decrease maternal CO by increasing intrathoracic pressure. Modest hyperventilation to a Paco2 of 28 to 30 mm Hg should provide adequate surgical conditions without compromising the fetus.
3. Controlled hypotension is becoming less common during aneurysm surgery because of the growing use of temporary clip occlusion of proximal vessels. Some situations, however, make this technique necessary. Because UBF varies directly with perfusion pressure, severe hypotension can lead to fetal asphyxia. Blood pressure should therefore be lowered only to that level deemed necessary for maternal well-being and for as brief a period as possible. FHR monitoring might alert the anesthesiologist to the development of fetal hypoxia and lead to the restoration of blood pressure if the need for hypotension is not critical at that time.
There is an additional concern when SNP is used as the hypotensive agent. Because of the limited ability of the fetal liver to metabolize cyanide, it is possible for fetal intoxication to occur in the absence of any signs of maternal toxicity. Although there are several case reports of the safe use of SNP during pregnancy, the duration of administration should be limited to that period deemed essential to maternal well-being. The total dose of SNP can also be limited through the administration of adjuvants such as beta-blocking drugs and inhalation anesthetics.
4. It has been suggested that mild hypothermia (33C to 35C) has cerebral protective effects. This level of hypothermia has no significant fetal effects. More profound hypothermia, however, can cause fetal arrhythmias and should be avoided.
Emergence. Before the removal of the endotracheal tube, the pregnant patient should be fully awake and airway reflexes intact to minimize the risk of aspiration. An alert patient also facilitates early neurologic evaluation and eliminates the need for emergent radiologic evaluation of the persistently obtunded patient. At the same time, however, every effort should be made to prevent coughing and straining on the endotracheal tube because this may cause a catastrophic intracranial hemorrhage. Prevention of coughing and straining on the endotracheal tube may be accomplished through the administration of lidocaine, 75 to 100 mg, and fentanyl, 25 to 50 mcg, at the end of the operation. Because the placement of the head dressing is associated with movement that produces airway stimulation, maintaining neuromuscular blockade until the dressing has been secured is appropriate. These guidelines do not apply to the patient who was obtunded preoperatively or who had a significantly complicated intraoperative course with bleeding, brain swelling, or ischemia. The trachea of such patients should remain intubated until their neurologic status can be evaluated.

VI. Epidemiology of SSEH during pregnancy

SSEH. SSEH is a rare cause of spinal cord compression. Only a handful of case reports having a clear etiology for the pregnant and nonpregnant population have been published since 1869. Bidzinski described the earliest case of SSEH in pregnancy in 1966. Spontaneous, or atraumatic, spinal epidural hematomas are usually associated with congenital or acquired bleeding disorders, hemorrhagic tumors, spinal AVMs, or instances of increased intrathoracic pressure. Considering the physiologic changes of pregnancy and the inherent hypercoagulable state, very few cases have been reported. To date, the English-language literature has reported only six cases. Jea reviewed the cases that involved healthy women in their twenties who were in their second trimester or later. All of the women had profound neurologic deficits, were managed operatively, and exhibited significant neurologic improvement after surgery. Pregnancy was carried to term in three cases, and an emergency cesarean section was performed before evacuation of the spinal epidural hematoma in three cases.

VII. Management of anesthesia for evacuation of spinal epidural hematoma

Timing of surgery in relation to neurologic symptoms
Surgical management. When the hematoma occurs in the thoracic or lumbar region, initial neurologic symptoms and signs consist of lower extremity radicular pain as well as bladder and bowel dysfunction. Motor and sensory deficits are usually progressive within hours of presentation. The definitive diagnosis is made radiologically, and magnetic resonance imaging appears to be the safest imaging modality during pregnancy. For patients who have profound and progressive neurologic deficits, the treatment of choice is surgical evacuation of the hematoma within 4 to 32 hours of the onset of symptoms as recommended in the literature reviewing the cases of pregnant patients. Lawton concluded that neurologic outcome appeared to depend on the length of time that elapsed between the onset of the neurologic deficits and the surgical intervention.
Conservative management. There are no case reports of the conservative management of pregnant patients with SSEH. However, Duffill reported the successful nonoperative management of SSEH in nonpregnant patients. There is some consensus that patients who demonstrate rapid improvement of neurologic symptoms after SSEH may be managed without surgery although these patients must be closely monitored for any renewed deterioration of neurologic status. The decision to manage SSEH conservatively may be influenced by the gestational age of the fetus: being near term may alter the risk considerably. Labor, vaginal delivery, and the related hemodynamic changes can precipitate the expansion of the hematoma and potentially worsen the patient's neurologic status when neurosurgical intervention may be rendered difficult or impossible. Also, cesarean section may be inappropriate during conservative management because there is no way to assess the patient's potentially unstable neurologic status during delivery secondary to the general or regional anesthetic needed for the procedure. If the neurologic status improves dramatically in the pregnant patient who has SSEH and an immature, nonviable fetus (<24 weeks' gestation), conservative management may be appropriate with close neurologic monitoring for potential deterioration. To date, no case of successful conservative management of SSEH in a pregnant patient has been reported. Therefore, caution is indicated in applying the experiences observed in the nonpregnant population to the pregnant patient.
Timing of delivery in relation to surgery depends on gestational age. If the fetus is deemed viable (>25 weeks' gestation) when SSEH is diagnosed, the cesarean section may be performed before neurosurgical evacuation of the hematoma to facilitate optimal neurologic outcome for the patient. If the fetus is determined to be nonviable (at or below 24 weeks' gestation), neurosurgical intervention should be undertaken as soon as possible to improve neurologic outcome with implementation of specific considerations for surgery in the pregnant patient.
Anesthetic management of evacuation of SSEH. The concerns and techniques outlined for anesthetic management of intracranial lesions should be followed for cesarean section and evacuation of hematoma with or without cesarean section, including the recommendations for sedative premedication, anesthetic induction, FHR monitoring, and emergence.
Anesthetic maintenance is not appreciably different from for that in patients undergoing operation for intracranial lesions except for the need to maintain the mean arterial blood pressure in the high normal range (70 to 85 mm Hg in normotensive patients) to ensure optimal UBF until decompression is completed. To avoid uterine atony, the end-tidal concentration of the volatile anesthetic is maintained at a low concentration (0.3%), relying on an opioid-based technique and a nondepolarizing muscle relaxant for maintenance.
Positioning considerations are extremely important in the pregnant patient before thoracic or lumbar laminectomy for hematoma evacuation. Aortocaval compression must be avoided to prevent significant reductions in maternal CO, systemic blood pressure, and UBF in patients for whom prior cesarean section is not performed. Physiologic studies reveal improved relief of uterine compression of the large maternal vessels in the prone position as compared to the sitting or lateral position. The lateral position actually demonstrates an increased incidence of aortocaval compression.
Jea described the use of the four-post Wilson frame with two posts placed just below the clavicles on the chest and the other posts centered on the anterosuperior iliac spines to support the pelvis. With this configuration, the protuberant abdomen hung free of compression between the four posts, encouraging the gravid uterus to migrate off the large vessels. Positioning the patient on the Jackson table would similarly reduce aortocaval compression.
Emergence is managed as for pregnant patients undergoing surgery for intracranial lesions. Additional precautions must be taken to assess the patient's readiness for extubation after remaining in the prone positioning for surgery because of possible edema of the airway. A leak test should be performed when the patient is fully awake before removing the endotracheal tube.

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