With the improvements in maternal care that have occurred over the last several decades, the relative percentage of maternal morbidity and mortality due to nonobstetric causes has risen. Trauma is the leading nonobstetric cause of maternal mortality and central nervous system trauma contributes significantly to the risk of both maternal and fetal death (1). Cerebrovascular events not associated with obstetric disease were responsible for 13.5% of nonobstetric maternal deaths in a recent survey of maternal death in the United States (2). Some diseases of the central nervous system and spinal cord found in the parturient most often predate pregnancy, such as tumors, idiopathic intracranial hypertension, hydrocephalus, and Arnold–Chiari malformation (ACM), while others have an increased incidence during pregnancy such as stroke due to either intracranial hemorrhage, and arterial or venous occlusive disease. Anesthesiologists may also be called upon to provide care for a parturient with brain death. Published data on pregnant women with these disorders is limited, so only case reports and small case series are available to guide neurosurgical, obstetric, and anesthetic management. A multidisciplinary approach to individual case management is most often required and should occur as early in pregnancy as practical. Neuraxial techniques for labor, and both vaginal and cesarean delivery, can be safely used in many cases.

The incidence of new brain tumors during pregnancy is the same as for an age-matched nonpregnant population and occurs in approximately 90 pregnant women in the United States yearly (3). Malignant tumors comprise approximately 50% of brain tumors with a frequency of 3.6/10⁶ to 3.2/10⁵ live births (3). The distribution of primary tumor types also appears similar to that of the nonpregnant population (Table 33-1) (3). Pregnancy may aggravate the natural course of primary intracranial tumors by accelerating tumor growth, increasing peritumor edema due to the generalized fluid retention associated with pregnancy, blood vessel engorgement of the vessels feeding a tumor, and immunologic tolerance (4). In addition, the hormonal changes associated with pregnancy may influence the growth of some tumors as 90% of meningiomas and some gliomas exhibit progesterone receptor activity, and hormonal stimulation may accelerate the growth of preexisting pituitary tumors particularly prolactinomas (5). Choriocarcinoma is associated with a high percentage of brain metastases and is a tumor unique to pregnancy. Metastatic brain tumors would be expected to occur less frequently as systemic cancer is relatively rare in women of childbearing age (3).

Gliomas are the most common intracranial tumor diagnosed during pregnancy and account for 38% of all tumors (Table 33-1) (3). Tumors less often arise from astrocytes or oligodendrocytes and are graded as to potential invasiveness: Low-grade (grade II), anaplastic (grade III), or glioblastoma multiforme/anaplastic astrocytoma (grade IV) (3). Tumor grading is important for gauging prognosis and guiding decisions as to surgical intervention during pregnancy (3). Urgent neurosurgical treatment of low-grade tumors is rarely necessary and resection can be delayed until later in pregnancy or after delivery (6) while high-grade lesions require prompt diagnosis and treatment regardless of gestational age (1).

Meningiomas are histologically benign, are usually slow growing, and arise from the membranous arachnoid layer. They eventually cause symptoms from compression of brain tissue. Pregnancy may accelerate the growth of preexisting meningiomas due to generalized fluid retention during pregnancy and resultant cerebral edema, and estrogen and progesterone effects may stimulate tumor growth, mediated through receptors for both hormones are commonly expressed in meningiomas (3). Surgical treatment, which is typically curative, can most often be delayed until after delivery.

Acoustic neuromas, which occur with greater frequency in patients with neurofibromatosis, arise from the vestibular portion of the vestibulocochlear nerve (8th cranial nerve) and present with progressive hearing loss, tinnitus, and dizziness (3). Like meningiomas, their size may increase dramatically during pregnancy, possibility linked to the high expression of estrogen receptors by these tumors, although these tumors are typically slow growing and surgical resection can be delayed (3,5).

Pituitary adenomas are diagnosed infrequently during pregnancy, although autopsy and MRI studies suggest that the incidence may be from 10% to 13% in adult women (3,5). They may present clinically as an endocrinopathy or with neurologic symptoms, often as visual field defects (5). Approximately, 23% of tumors produce no hormones, while 35% produce prolactin, with the rest more commonly producing growth hormone and ACTH, and rarely, TSH and FSH (5). Prolactin adenomas, may more likely than other pituitary tumors, enlarge during pregnancy due to the normal stimulatory effects of pregnancy on pituitary tissue to increase prolactin levels (3). Surgical resection is curative in 90% of microadenomas (5), but observation of pregnant women without significant imaging findings and or visual field defects is appropriate. Bromocriptine administration is effective in lowering prolactin levels and shrinking the size of prolactin secreting adenomas and is generally considered safe during pregnancy (6). Transsphenoidal surgical resection is necessary for large tumors and can be done safely during
pregnancy in most large referral centers (3), while radiotherapy is reserved for recurrent disease and infrequently indicated during pregnancy (5).

Metastatic brain lesions do not occur more frequently in pregnancy than in nonpregnant women, except for choriocarcinoma which occurs in 1 in 50,000 term pregnancies and 1 in 30 molar pregnancies (7). Metastases to the brain occur in 4% to 17% of these women and an acute onset of neurologic symptoms may occur in association with hemorrhage into the tumor, which occurs often (7). Craniotomy is not often needed as radiation therapy and chemotherapy lead to a good overall prognosis (3).

The four most common presenting signs and symptoms of both primary and metastatic intracranial neoplasms during pregnancy are headache, nausea and vomiting (indicators of increased intracranial pressure), new onset of seizure activity, and progressive focal neurologic deficits (5,8,9). Unfortunately, headache occurs frequently during normal pregnancy and makes use of this symptom less helpful in pregnant women, but headache that has a gradual onset, an unremitting course, and is exacerbated by activities that increase intracranial pressure (cough, Valsalva maneuvers, etc.) should prompt investigation (3,8). Likewise, nausea and vomiting occur frequently during pregnancy, but persistence into the second and third trimesters suggests the need for further evaluation (10). The onset of new seizure activity during the first and second trimesters requires prompt neuroradiologic evaluation as the likelihood of eclampsia is low (8). Focal seizures that occur in the third trimester, especially if not accompanied by hypertension and proteinuria, indicate the need for further investigation as eclamptic seizures usually exhibit generalized motor activity (3). The extent and type of focal neurologic deficit depends on the location of the tumor and the extent of its invasion of normal tissue. Brain edema and hemorrhage may also increase intracranial pressure and the significant intravascular volume expansion that accompanies pregnancy may cause rapid deterioration (5).

The diagnosis of brain tumors in pregnancy requires neuroimaging with MRI and CT which can be safely obtained throughout pregnancy (3,5,8,9,10,11). MRI is preferable to CT scanning for tumor diagnosis as it is more sensitive in detecting tumors, detects radiologic features that lead to a shorter differential diagnosis of tumor type and the grade of malignancy, and does not expose the mother or fetus to ionizing radiation (3,9). The increases in tissue temperature with scanners that use a magnetic field strength of 3 T is of little clinical consequence (11). Head CT scanning is very safe for the fetus as tight collimation and abdominal lead shielding reduces radiation exposure to approximately 1 mrem, equivalent to that of 2 weeks of background cosmic radiation, and no study has documented deleterious fetal effects (12). MRI and CT studies should involve the use of IV contrast material and the patient scanned before and after its use as the diagnostic information obtained far outweighs the risks it administer (3). The IV contrast material used for CT scanning is composed of iodinated compounds that are renally excreted with well-documented minimal risks for maternal allergic reaction and nephrotoxicity, and hypothyroidism in the fetus (11,12,13). Gadolinium has a much lower risk for allergic reaction (1:350,000) (12), and despite readily crossing the placenta, has not been associated with fetal adverse outcomes when administered during pregnancy (11,12,13).

Obstetric and neurosurgical management depend upon the size and location of the tumor, the potential for tumor growth during pregnancy, and the ability of the patient to accommodate increases in intracranial pressure (3,8). These considerations govern the progression of neurologic findings which guide clinical management (3,5,14). Ng and Kitchen have suggested an algorithm for the neurosurgical management of the pregnant patient with a brain neoplasm (Fig. 33-1) (14). Surgical removal of benign slower growing tumors
can often be delayed until after delivery (5,6,14). Management of malignant tumors that create significant symptoms may require elective surgery during pregnancy as a delay can allow significant maternal deterioration and increase the risk for fetal wastage in association with emergency treatment (4). If surgery can be delayed until the chance of fetal survival is good, then cesarean delivery followed by craniotomy is a reasonable approach (3,5,14). Unfortunately, radiation therapy and maternal chemotherapy pose significant risks to the fetus, particularly if instituted during the first trimester, although the risk for teratogenicity is significantly reduced if these treatments can be delayed into the late second or early third trimester (3,5). Fetal exposure during radiation therapy can be minimized if appropriate shielding is employed (9,11,12). For many tumors, it may be reasonable to delay chemotherapy treatment until after delivery as it may offer only a small increase in maternal survival and delay may not reduce the benefits of its use (3).

The control of intracranial pressure is of great importance during labor and delivery. The classic work by Marx et al. documented a rise in CSF pressure of 53 cm H₂O during painful uterine contractions and rise of 70 cm H₂O during the second stage with maternal bearing down during contractions (15). These changes are well tolerated by women with normal intracranial compliance, but will likely lead to significant neurologic deterioration in women with impaired compliance. Patients with small pituitary tumors or small benign lesions should tolerate vaginal delivery well, but in patients with larger lesions labor analgesia is advised. Consideration may also be given to an instrumental vaginal delivery to minimize pushing during the second stage. Alternatively an elective cesarean delivery may be the best option for some patients, especially when regional anesthesia is contraindicated (3,5,6). A multidisciplinary approach as to the mode of delivery and other management that involves the obstetrician, neurosurgeon, neuroradiologist, anesthesiologist, midwife, and neonatologist is required (3,5,6,14).

Anesthetic management for labor and delivery or cesarean section is based upon the reports of individual case management or small case series (8). Successful epidural analgesia for labor and delivery has been reported (16,17) and would be expected to prevent the increase in intracranial pressure that would accompany painful labor (17) and the increases that would be expected during bearing down during the second stage of labor (4,16). One case report describes successful spinal anesthesia for cesarean section utilizing a 24 g pencil point needle in a patient with symptoms consistent with increased intracranial pressure (18) and another, successful cesarean delivery with spinal anesthesia (17); however, other case reports describe fatal brain stem herniation shortly after delivery in patients with unsuspected neoplasms who received an unintentional dural puncture during an epidural catheter placement (19,20). Other case reports of cerebral herniation in association with lumbar cerebrospinal fluid leak in other settings have been reported as well (21). However, cerebrospinal fluid drainage catheters are often employed during intracranial surgery to improve surgical exposure and reduce intracranial pressure most often without sequelae (22). Examination of these reports does not allow for the identification of those patients who would be at greatest risk for cerebral herniation in the setting of dural puncture during the performance of neuraxial anesthesia. In addition, injection of fluid into the epidural space is associated with increases in intracranial pressure (23). Studies in animal models of baseline elevated intracranial pressure show significant decreases in cerebral blood flow that accompany increases in intracranial pressure (24). The onset of new neurologic symptoms has been reported in one case report of epidural placement in a mother with an unsuspected cerebellopontine angle tumor and obstructive hydrocephalus (25). Such considerations lead many anesthesiologists to select cesarean delivery under general anesthesia in parturients with increased intracranial pressure (6,12) despite the loss of intraoperative monitoring of maternal neurologic status in an awake patient and the need to control rises in intracranial pressure that may accompany anesthetic induction and endotracheal intubation. However, general anesthesia may facilitate maternal blood pressure control and the management of maternal intracranial pressure through hyperventilation and drug administration (12). Several case reports support the safety of general anesthesia when used for emergent and urgent cesarean section due to fetal concerns (12,26).

A more detailed discussion of the anesthetic management of the parturient undergoing neurosurgery is described in Chapter 50. The management of general anesthesia for a procedure that combines delivery followed by tumor resection or cesarean delivery followed later by a neurosurgical procedure requires an understanding of the physiologic changes associated with pregnancy, and preparations to control maternal intracranial pressure and hemodynamics. The administration of medication to reduce the risk of aspiration, such as an oral or IV H2 receptor antagonist to reduce gastric acid secretion and oral sodium citrate to neutralize stomach acid should be given approximately 1 hour prior to induction (27). Preoperative placement of intra-arterial blood pressure monitoring is recommended to facilitate moment to moment blood pressure monitoring. Blood pressure should be maintained within narrow limits as hypertension can lead to increases in intracranial pressure (27) and hypotension to decreases in cerebral and uterine perfusion pressures (3). A rapid sequence induction should balance the need to protect the mother against the risk of aspiration and to control the intracranial pressure during endotracheal intubation. The administration of both thiopental and propofol reduces the hypertensive response associated with intubation and attenuates the intracranial pressure rises and cerebral metabolism (27), although propofol may be more effective in blunting maternal hypertension (28). Some anesthesiologists avoid the use of succinylcholine for fear that its administration will increase intracranial pressure, but others find this to be of little clinical significance (27). Other approaches to reduce the hypertensive response to tracheal intubation include the administration of a continuous sodium nitroprusside infusion, (29) small IV bolus dosing of nitroglycerin, (30) and moderate dosing of IV opioids (27). The short acting opioid remifentanil in doses of 1 μg/kg over 1 minute prior to intubation has been shown to be particularly effective and safe when used during cesarean delivery (31). IV magnesium sulfate in doses of 30 to 60 mg/kg may be effective as well as intravenous lidocaine in doses of 1 mg/kg (32). Aortocaval compression should be avoided by the use of left uterine displacement. Maternal ventilation during anesthesia should be set to keep maternal PaCO₂ values at 30 to 32 mm Hg, normal for the parturient at term. Although controlled hyperventilation can acutely reduce intracranial pressure, decreases in PaCO₂ of <25 mm Hg can lead to uterine artery vasoconstriction and a left shift of the maternal oxyhemoglobin dissociation curve and reduce fetal oxygen transfer (33). Prolonged severe hyperventilation is associated with poor patient outcomes in other populations of neurosurgical patients (30). Intravenous fluids that
are administered intraoperatively should be isonatremic, isotonic, and glucose free to reduce the risk of cerebral edema associated with hypotonic, hyponatremic fluids and poor neurologic outcome associated with hyperglycemia (27). Diuretic administration may be indicated to control intracranial pressure. Although mannitol accumulates in the fetus and leads to fetal physiologic changes such as reduced urine production, hypernatremia, and dehydration (34), doses of 0.25 to 0.5 mg/kg appear to be safe (26,27). Furosemide causes a fetal diuresis in animal models but offers a safe alternative to osmotic diuretics (27). Patient positioning in a slight head-up posture can also be effective in reducing intracranial pressure as well as the use of low tidal volumes during positive pressure ventilation (27). Oxytocic drug administration has not been well studied in patients who have undergone neurosurgery, but 5 unit bolus dosing of oxytocin following delivery has been reported as safe in case reports (26). Hypotension can accompany its use and should be treated appropriately (35). The use of other oxytocics in this setting appears to not have been reported, but prostaglandin F2α administration may be associated with systemic and pulmonary hypertension (36). Ergometrine may create hypertension through its vasoconstrictor effect and thus increase intracranial pressure (37), while vaginal prostaglandin E1 administration is associated with little maternal hemodynamic effect (38).

As the direct obstetrical causes of maternal death have declined, cerebrovascular accidents have become a proportionally more important cause for maternal morbidity and mortality. Stroke during pregnancy is relatively rare, occurring at an estimated rate between 11 and 26 deliveries per 100,000, but is a cause of 12% of all maternal deaths (39). The death rates cited in older studies are widely variable, with rates as high as 210/100,000, but methodologic weaknesses and inclusion of data from underdeveloped countries may overestimate the rate in developed countries (40) which suggests a rate at the lower end of the range cited above (9 to 11 per 10,000 deliveries). However, one recent well-conducted review of data from approximately 1,000 United States hospitals identified a higher rate of 34.2/100,000 deliveries (40), which contrasts with a rate of 10.7/100,000 women-years reported among nonpregnant women of childbearing age (39). The stroke rate would be expected to be higher during pregnancy as the increases in hypercoagulability and venous stasis that accompany pregnancy, and the increased risk for endothelial trauma during delivery, would increase the risk for thrombotic stroke (8). The risk for stroke due to cerebral hemorrhage would also be increased due to the pregnancy-associated hypertensive disorders that affect up to 10% of all pregnancies (8).

Stroke can be broadly categorized into ischemic and hemorrhagic causes (8). Feske in a recent review of single and multiple hospital experiences with pregnancy-related stroke, noted that the causes were nearly evenly divided between both (41). Age greater than 35 years and black ethnicity convey increased risk (40). Significant risk factors associated with pregnancy and delivery are postpartum infection, pregnancy-related transfusion, increased parity, multiple gestation, and cesarean delivery (Table 33-2) (40). Cesarean delivery is more likely among women who have had a stroke prior to delivery and other pregnancy-related disorders associated with stroke such as preeclampsia (39). Maternal medical conditions that are most associated with pregnancy-related stroke include hypertension, heart disease, history of migraine headaches, lupus, sickle cell disease, smoking, alcohol and substance abuse, thrombophilias, and postpartum infection (Table 33-3) (40). Pregnancy-induced hypertension appears to convey the greatest risk as one large retrospective review found that 24% of cerebral infractions and 14% of intracerebral hemorrhages (ICHs) occurred in association with hypertensive disorders (42). Although one retrospective study found a risk for arterial strokes that increased during the third trimester and postpartum, that same study found that most strokes due to venous occlusion occurred in the puerperium (43). Virtually all studies note an increased risk of stroke regardless of cause during the third trimester and postpartum with the exception of those associated with hemorrhage due to intracranial arteriovenous malformations (AVMs) that occur throughout pregnancy (Fig. 33-2).

Intracranial hemorrhage occurs in 5 to 31 per 100,000 pregnancies (41) and is due to subarachnoid hemorrhage (SAH) and ICH. The reported percentage of pregnancy-related SAH due to cerebrovascular malformations ranges from 20% to 67% (45) with ruptured intracranial aneurysms affecting 77% of patients and arteriovenous malformation occurring in 23%, and other causes very rarely (46). ICH occurs during pregnancy at a rate of 7.1/100,000 at risk person years, which is higher than the rate of 5/10,000 at risk patient year for nonpregnant women (45). Both SAH and ICH convey substantial risk for maternal and fetal death. SAH accounts for 5% of all maternal deaths and is the third leading cause of nonobstetric maternal death (14). The in-hospital maternal
mortality associated with maternal ICH was 20.3% in a recent survey of 10 years of data from 20% of United States non-Federal hospitals (45). Fetal mortality from maternal SAH was 25% in one survey (46).

Most cases of SAH during pregnancy are caused by intracranial aneurysm bleeding, which occurs with an incidence of 3 to 20 per 100,000 deliveries, (42,47) with bleeding from AVMs less frequently a cause (14). The incidence of SAH due to aneurysmal bleeding is thought to increase with increasing gestational age due to the increases in maternal blood volume and changes in arterial wall strength that accompany pregnancy with an increased risk compared to nonpregnant women until 6 weeks postpartum (47). Most aneurysms are due to congenital or acquired defects in the muscularis or media of the arterial wall and 85% occur in the anterior cerebral circulation at the base of the brain at the bifurcations of arterial vessels (48). Maternal coagulopathy and uncontrolled hypertension are the risk factors for bleeding from both aneurysms and AVMs (49).

Aneurysms and AVMs that have not bled usually do not cause symptoms unless they are large enough to cause persistent headache or focal neurologic signs (49). The clinical presentation of SAH in pregnancy is the same as in nonpregnant women (14). A sudden onset of severe headache, usually with vomiting and photophobia, occurs in up to 97% of cases with periorbital pain, neck pain, nuchal rigidity, and frequently a positive Kernig’s sign (14,50). Up to 60% of patients will report sentinel headaches that precede the SAH by several weeks (6,14). Loss of consciousness due to rapid increases in intracranial pressure that reduce cerebral perfusion can occur (51). Focal neurologic signs can occur due to acute vasospasm (51) and the electrocardiogram can show changes similar to those associated with myocardial ischemia as well as prolonged QRS complexes and tall and inverted T waves (8,14). The patient’s presenting clinical condition is an important guide to prognosis and worsening grade on the World Federation of Neurological Surgeons scale (Table 33-4), a score that combines the Glasgow Coma Score (GCS) (Table 33-5) and assessment of best motor function, correlates with poorer outcome
(50). All patients with suspected SAH due to either aneurysm or AVM bleeding should undergo urgent neuroradiologic examinations with computed tomographic scanning and MRI studies, both with contrast, (6,11,14,39,47,48,49,50,51) and lumbar puncture looking for persistent blood staining and xanthochromia (14). Neurosurgical referral is mandatory to monitor for re-bleeding, and the management of vasospasm. Re-bleeds occur in 10% to 30% of patients within the next month following an aneurysmal rupture (14,52) and the chance of re-bleeding during pregnancy from an initial AVM bleed is 25% (52). Vasospasm occurs in 35% of patients with an aneurysmal rupture within 4 to 11 days, but less often following AVM bleeding (52) with significant morbidity and mortality in up to 75% of patients (51). Hydrocephalus occurs in 10% to 25% of patients with SAH, and a syndrome of inappropriate ADH secretion occurs infrequently (51).

Neurosurgical and medical management of the pregnant patient with SAH should be the same as in the nonpregnant patient (6,14,39,47,48,49,50,51,52) and a multidisciplinary approach involving the obstetrician, neurosurgeon, neuroradiologist, neonatologist, and anesthesiologist is required. In the patient with a ruptured aneurysm, the optimal time for surgical intervention is controversial (45,47,48,49,50,51,52); however, early operative intervention, either through endovascular embolization or through intracranial surgery to clip the aneurysm, is usually considered as early interventions reduce the incidence of vasospasm and re-bleeding (6,14,24,53). Ng and Kitchen have suggested an algorithm for the management of a ruptured aneurysm and the timing of a concurrent cesarean delivery based on patient stability and gestational age (Fig. 33-3) (14). Although case series of intracranial surgery for the clipping of aneurysms have uniformly reported good maternal and fetal outcomes (6,14,52), endovascular embolization has become the primary treatment modality for nonpregnant patients with SAH due to aneurysmal bleeding (54). These results may not be totally applicable to the pregnant patient as the International Subarachnoid Aneurysm Trial which reported on outcomes of surgical clipping versus endovascular coiling did not include any pregnant patients (54), although there have been several small case series reports of good outcomes (55). Practical problems include the need for systemic anticoagulation for up to 48 hours following endovascular coiling and the need to deliver general anesthesia in an area outside the conventional operating room environment (6,14). Preparations for possible delivery in the radiologic suite may be considerations in weighing the choice between clipping and coiling (6,14). Cerebral vasospasm may warrant the use of “Triple H” therapy: Hypervolemia, hemodilution, and systemic hypertension in nonpregnant women; however, since pregnancy creates a state of hypervolemia and relative hemodilution, its use in pregnant women may not be indicated (14,27). Nimodipine is commonly administered to reduce vasospasm in nonpregnant patients and has been used in the treatment of preeclampsia without significant maternal and fetal effects, but the use of Triple H therapy or nimodipine administration for the treatment of vasospasm has not been reported in pregnant women (27). The International Study on Unruptured Intracranial Aneurysms (ISUIA) noted that the annual risk of rupture with aneurysms of <10 mm and <7 mm was 0.05% and 0% respectively (56), and that the risks of treatment outweighed the risk of nontreatment in patients with small aneurysms. However, the study did not report on any pregnant women and extrapolating the results may not be justified.

In contrast with SAH due to aneurysm bleeding, surgical management of AVMs has not been shown to significantly lower maternal or fetal mortality and endovascular embolization is usually inadequate to completely treat many lesions (14). The management of known vascular malformations which have not bled in pregnant women has to be individualized
recognizing that the risk of hemorrhage from an AVM during vaginal or cesarean delivery is low (14,45,56). If a neurovascular lesion has been successfully repaired, then no special care is required for labor and delivery (6,14,27,46,47,48,49,50,51,52). In a patient with an untreated aneurysm or AVM, maternal hemodynamic fluctuations should be minimized during delivery and current data does not suggest an advantage of cesarean over vaginal delivery (45,47,52,57). Most authors suggest an instrumental delivery under epidural analgesia to avoid bearing down during labor if labor and vaginal delivery are selected. There are fewer reports of anesthetic management for labor and delivery than for cesarean delivery in pregnant women who have untreated aneurysms, but most reports report successful outcomes when epidural analgesia is used for patients with both unrepaired aneurysms and AVMs who undergo either vaginal or cesarean delivery (8,58,59,60,61,62). Considerations for general anesthesia for cesarean delivery are the same as for other pregnant patients with neurosurgical disease and one case report attests to its safety (63). There are many case reports of anesthetic management of pregnant patients undergoing neurosurgical repair of intracranial vascular lesion, many in a combined procedure with cesarean delivery (64,65,66,67). In addition to the considerations outlined above and in Chapter 50, care must be taken to minimize the transmural pressure across the aneurysm wall, especially measures to minimize rises in mean arterial pressure during induction and intubation and drops in intracranial pressure until after the surgeon has opened the dura mater (64,65,66,67). The induction of controlled hypotension may be required and sodium nitroprusside use is safe when used for this purpose (64). Monitoring of the fetal heart rate response after 20 weeks of gestation is indicated to detect potential fetal compromise during the use of deliberate hypotension.

ICH occurs at a rate of 3.8 to 18.1 per 100,000 deliveries (40,42,43). A recent survey by Bateman et al. of discharge data from 20% of non-Federal United States hospital found a rate of 6.1/10,000 deliveries (45). Although older studies suggested that 20% to 67% of intracerebral bleeding was due to cerebrovascular malformations, (39,41,42,43,68) the more recent report by Bateman et al. reported a much lower associated incidence of 7.1% (45,69). The hypertensive disorders of pregnancy are a significant cause, as eclampsia or preeclampsia have been reported in 14% to 50% of patients with ICH (39,41,42,43,45) and it is the most common cause of death in eclamptic patients (8,40,41,42,44). Significant related risk factors in order of increasing strength of association are African-American race, advanced maternal age, alcohol and tobacco use, cocaine abuse, chronic hypertension with and without superimposed preeclampsia/eclampsia, and coagulopathy (40,45). Despite its rarity, ICH accounts for 7.1% of all maternal deaths (45). Most studies show the incidence to be higher postpartum with approximately 60% of ICH occurring after delivery (41,42,45).