Acute Spinal Cord Injury 229 sure is essential to prevent refl ux of gastric contents into the trachea. Once again, the importance of spinal immobilization cannot be overemphasized. Relevant p regnancy p hysiology A number of physiologic changes that occur in the pregnant patient can complicate intubation. There is signifi cant capillary engorgement of the mucosa throughout the respiratory tract leading to swelling of the nasal and oral pharynx, larynx, and trachea, all of which can increase the challenge of intubating a patient involved in an acute spinal cord injury [8] . Additionally, pregnant patients have a decreased functional residual capacity, thus decreasing their oxygen reserves. The initiation of tracheal protective procedures such as jaw - thrust, bag - valve - mask ventila- tion, and cricoid pressure, while necessary, can inadvertently cause movement of the cervical spine and subsequent damage if meticulous stabilization is not practiced [5,6] . Circulatory s ystem c onsiderations The evaluation of the circulatory system in a pregnant trauma patient with acute SCI can be very diffi cult. The typical assess- ment parameters may be obscured by the altered hemodynamics of pregnancy, the autonomic derangements of neurogenic shock, and cardiovascular instability from acute hemorrhage. The pres- ence of hypotension, a common component of both hemorrhagic and neurogenic shock, can be confused with the normal reduc- tion in blood pressure associated with pregnancy itself. Supine hypotension can further complicate assessment of trauma patients as aortocaval compression stimulates sympathetic output, increasing both blood pressure and heart rate. Even the normal dilutional anemia of pregnancy can be misinterpreted as a sign of acute blood loss. Spinal n eurogenic s hock v ersus h ypovolemic s hock If the patient has a cervical or high thoracic injury, the presence of neurogenic shock may obfuscate the assessment of circulatory status. The presenting signs and symptoms of spinal neurogenic shock are typically the exact opposite of those expected with hypovolemia. While both disorders present with hypotension, the classic stigmata of hypovolemia result from enhanced sympa- thetic output. Refl ex sympathetic stimulation maximizes cardiac function and increases peripheral vasoconstriction, resulting in tachycardia, delayed capillary refi ll, and cool, clammy extremi- ties. Conversely, spinal neurogenic shock is due to an acute loss of sympathetic input from below the injury. Subsequently, there is no shunting of blood from the periphery back toward the heart and other critical organs. In addition to warm, dry skin and pre- served capillary refi ll, such patients exhibit a “ paradoxical brady- cardia ” [9] when sympathetic input to the heart is lost, and vagal control predominates. Preserved vasodilation in the periphery promotes heat loss, leading to hypothermia and further exacerba- tion of the bradycardia. Table 18.1 Acute spinal cord injury: basics of emergent care. Goals of therapy Stabilize the patient Immobilize the spine in an attempt to prevent further injuries Evaluate and treat other injuries Achieve early recognition, prevention, and management of frequently encountered complications. Management protocol Achieve initial patient stabilization including stabilization of the patient ’ s neck, airway management, circulatory system assessment, and fetal monitoring. Methylprednisolone should be considered within 8 hours of the SCI and given as a bolus dose of 30 mg/kg, followed by infusion at 5.4 mg/kg/h for 23 – 48 hours. Hemodynamic monitoring may be required for optimum fl uid management of neurogenic shock. Adequate fl uid and pressor support may be necessary during the period of neurogenic shock. Delivery may be indicated for obstetric indications, to facilitate maternal resuscitation, or in conjunction with surgery for other injuries. Table 18.2 Acute spinal cord injury: innervation of spinal segments and muscles and grading scale for evaluating motor function. Spinal segment Muscle Action C5 , C6 Deltoid Arm abduction C5, C6 Biceps Elbow fl exion C6 , C7 Extensor carpi radialis Wrist extension C7 , C8 Triceps Elbow extension C8 , T1 Flexor digitorum profundus Hand grasp C8, T1 Hand intrinsics Finger abduction L1, L2 , L3 Iliopsosas Hip fl exion L2, L3, L4 Quadriceps Knee extension L4, L5, S1 , S2 Hamstrings Knee fl exion L4, L5 Tibialis anterior Ankle dorsifl exion L5 , S1 Extensor hallucis longus Great - toe extension S1 , S2 Gastrocnemius Ankle plantar fl exion S2, S3, S4 Bladder, anal sphincter Voluntary rectal tone Grade Muscle strength 5 Normal strength 4 Active power against both resistance and gravity 3 Active power against gravity but not resistance 2 Active movement only with gravity eliminated 1 Flicker or trace of contraction 0 No movement or contraction The predominant segments of innervation are shown in boldface type. (Reproduced by permission from Chiles BW III, Cooper PR. Acute spinal injury. N Engl J Med 1996; 334: 514. pregnant patient in late gestation has the additional risk of aspira- tion due to her reduced gastric sphincter tone compounded by the mechanical effects of increased gastric pressure from her gravid uterus. Consequently, appropriately applied cricoid pres- Chapter 18 230 Maternal h emodynamic s tatus and a ssessment Whether or not concurrent hypovolemia is present, placement of a pulmonary artery catheter and an arterial line may be advanta- geous in guiding fl uid and pressor administration in the pregnant patient with neurogenic shock. Cardiac output and mean arterial pressure must be carefully monitored to prevent cardiopulmo- nary complications that often accompany spinal cord injury [4] . If an initial search for subclinical bleeding (chest and pelvic radio- graphs, pericardial and abdominal ultrasound, peritoneal lavage, or CT) fails to reveal evidence of hemorrhage, neurogenic shock is presumed to be the cause of the patient ’ s hypotension [5] . Attention should then be directed toward countering the cardio- pulmonary dysfunction associated with neurogenic shock, and measures to maximally preserve residual spinal cord function should be instituted. To this end, intravenous fl uid administra- tion is decreased to maintenance rates and therapy with pressor agents (dopamine and dobutamine) is started. The period of neurogenic shock can last weeks. During this time, sympathomi- metics and occasionally atropine sulfate are essential to counter parasympathetic dominance and to facilitate restoration of vas- cular tone and cardiac performance. Maintaining perfusion of injured spinal tissue and oxygen supplementation reduces the threat of secondary ischemic damage to traumatized tissue. Consultation with an expert in blood pressure management under these circumstances is important. Corticosteroids In patients with blunt spinal cord injury, the administration of high - dose methylprednisolone early in treatment has been rec- ommended as a proactive measure to reduce the extent of paraly- sis in the long term [4,9,10,14] . This recommendation is based on fi ndings from two multicenter, double - blind, randomized trials in which patients received placebo, naloxone, or very high - dose methylprednisolone therapy within 8 hours of their injury. The methylprednisolone group experienced signifi cantly greater improvement in sensation and motor function up to 1 year after injury [15,16] . Theorized mechanisms by which methylpredniso- lone improves neurological outcome include blocking PGF - 2 α - induced membrane lipid peroxidation [17] , potentiating the neuroprotective/regenerative effects of taurine in the damaged cord [18] , and suppressing expression of neurotropin receptors involved in secondary cell death [19] . Follow - up multicenter ran- domized trials by the same investigators verifi ed effi cacy and refi ned treatment protocols [20,21] . In the recommended regi- mens, all patients less than 8 hours from the occurrence of blunt spinal trauma receive a 30 mg/kg loading dose of methylpredniso- lone over 15 minutes. If the initial bolus was administered within 3 hours of injury, a continuous drip of 5.4 mg/kg/h methylpred- nisolone is infused for 23 hours. Patients loaded between 3 and 8 hours after injury receive the same postbolus infusion but it is extended over a longer interval (48 hours). There is no proven benefi t to initiating high - dose steroid therapy to any patient beyond 8 hours from their injury. Perils with h ypotension and fl uid r esuscitation The emergency team must be alert to the contradictory infl uences of pregnancy, hypovolemia, and neurogenic autonomic disrup- tion while evaluating and stabilizing the pregnant trauma patient. Because of time constraints in deciphering these various factors, the presence of signifi cant hypotension should be considered and treated as hypovolemia until safely proven otherwise. The primary survey should be accompanied by simultaneous intravenous fl uid resuscitation through two large - bore IV cannulae, serial vital sign measurements, and the placement of a foley catheter [9] . While fl uid resuscitation is imperative in the acute setting, providers must remain cognizant of the increased risk of pulmonary edema during pregnancy secondary to a low colloid oncotic pressure and hypoalbuminemia. Conventional wedging of the patient ’ s back to avoid caval compression can result in exacerbation of spinal trauma. However, these same benefi ts may be achieved by a 15 ° tilt of the backboard if the patient is immobilized, or by simple manual displacement of the gravid uterus to the left. Obvious external bleeding is controlled, and a search is initiated for evi- dence of internal hemorrhage. Use of u ltrasound Ultrasound provides rapid assessment for fl uid in the cul de sac, abdominal cavity, renal gutters, and perisplenic, perihepatic, pericardial, and retroplacental areas and, if negative, may allow avoidance of peritoneal lavage and its associated risks [10,11] . If ultrasound is not immediately available, there is no other expla- nation for the patient ’ s shocked state, or there is obvious severe abdominal/thoracic trauma, peritoneal lavage is required to rule out intra - abdominal hemorrhage. An open entry technique is recommended during the late second and third trimesters to minimize risk to the gravid uterus [10,12] . This is best performed with sharp dissection at or above the umbilicus while elevating the anterior wall away from the uterus. The anterior abdominal peritoneum can then be opened under direct visualization. The procedure is considered diagnostic if either greater than 100 000 RBCs per mL are detected or bowel contents are present in the effl uent. Fetal s tatus r efl ects m aternal s tatus The status of the fetus is not only important in its own right, but also serves as a marker of changes in maternal hemodynamics. A previously normal fetus can tolerate a remarkable diminution in uterine blood fl ow before abnormalities supervene in the fetal heart tracing [13] . The onset of tachycardia, late decelerations, bradycardia, or a sinusoidal pattern can herald a deleterious change in maternal oxygenation, acid – base balance, or hemody- namic status. Likewise, adequate correction of maternal meta- bolic or hemodynamic derangements may be signaled by a return to a reassuring fetal heart rate tracing. Placental abruption occurs in up to 50% of women involved in major trauma, contributing to both fetal compromise and further vascular insult to the preg- nant patient [3] . Acute Spinal Cord Injury 231 response to CPR within 4 minutes, with the intent to complete delivery by 5 minutes [26] . Delivery relieves caval compression and also allows for a large autotransfusion of blood back into the circulation when the uterus is evacuated and contracts. These events, together with maintaining a leftward tilt, increase venous return, the effi cacy of chest compressions, and ultimately sur- vival. Direct access to the maternal aorta via the abdominal inci- sion may also allow its compression above the renal arteries and optimization of blood fl ow to the brain and heart. Cesarean d elivery If the mother is stable, cesarean delivery should also be performed as a rescue procedure for a stressed/distressed but viable fetus. Documentation of the fetal heart rate should ideally be included as part of the primary survey on a pregnant trauma patient ascertained to be in the third trimester of her pregnancy [27] . Continuous electronic fetal heart rate monitoring usually is initi- ated with completion of the primary survey in patients with a viable and potentially salvageable baby. When immediate delivery for fetal indications is necessary and no anesthesia is available, cesarean section without anesthesia has been reported in patients with neurogenic shock and a lesion above T10 [10] . However, anesthesia is generally required and recommended for all SCI patients undergoing cesarean delivery. The clinician should anti- cipate the possibility of uterine atony if dopamine is being used to treat neurogenic shock secondary to its uterine relaxant effect [10] . Potential f etal h azards with d iagnostic r adiography The pregnant women with SCI may require many examinations involving radiation, both acutely and later in her care. Currently, a cumulative radiation exposure of up to 5 rad or less is regarded as unlikely to have signifi cant teratogenic effects [28,29] . With the exception of CT, individual diagnostic procedures typically deliver radiation in the millirad range (Table 18.3 ) which will not Potential c omplications with c orticosteroids Although high - dose steroid therapy is approved by the Food and Drug Administration (FDA) and considered by many to be a best practice, discussion continues about the pros and cons of its use in part because the dosages employed are some of the highest used in any clinical scenario [22 – 24] . Patients receiving steroids have an increased incidence of pneumonia and require more ventilation and intensive care nursing [25] . Those receiving the 48 - hour regimen are also more likely to have more severe sepsis and severe pneumonia than patients who receive the 24 - hour regimen [21] . Thus, if steroids are administered, vigilance for, and prophylaxis of, anticipated steroid - related complications (infections, gastrointestinal bleeding, wound disruption, steroid myopathy, avascular necrosis, and glucose intolerance) are necessary. Radiologic i maging c onsiderations The secondary survey of the pregnant patient with an acute SCI focuses on more precisely defi ning the nature and extent of the lesion and determining the status of the fetus. A thorough neu- rological exam is required and complete documentation is important so that improvement or deterioration of the lesion can be monitored with serial examinations. Once the lesion has been clinically identifi ed, a number of radiological studies may be nec- essary to further defi ne it and help with planning for appropriate treatment. Radiographs of the cervical spine are the standard initial studies used to assess the injury and dictate what further modalities may be needed. CT is best for bony detail and may become necessary to clarify fractures revealed by radiographs especially if: (i) neurologic injury is present; (ii) more extensive injury is clinically apparent than is seen on the radiograph; or (iii) injury detected on the radiograph suggests instability. If a neurologic lesion appears to be progressing, CT myelography may be required to exclude spinal cord compression by an extrin- sic mass such as a hematoma [5] . As will be discussed later, ion- izing radiation can have adverse fetal consequences. The input of the obstetrician may be helpful in minimizing fetal radiation exposure. Acute c are of s pinal c ord i njury: f etal c onsiderations Mother fi rst ( u sually) with e xceptions While it is important to remember that there are at least two individuals to be cared for in every pregnant trauma patient, initial efforts should be focused primarily on the stabilization of the mother. There are two exceptional circumstances where it may be more appropriate to attend to the fetus fi rst: (i) a viable fetus in a dying mother; or (ii) a dying viable fetus in a stabilized mother. In either case, prompt cesarean delivery is indicated. Because 48% of SCI patients die as a result of their injuries [4] , the possibility of perimortem cesarean delivery is very real in these patients. The procedure should be initiated if there is no Table 18.3 Estimated radiation exposure (millirads) associated with commonly used trauma radiography. Cervical spine < 1 mrad Chest (two views) 0.02 – 0.07 mrad Abdomen (one view) 100 mrad Pelvis 200 – 500 mrad Lumbar spine 600 – 1000 mrad Hip (one view) 200 mrad CT head/chest < 1000 mrad CT abdomen/lumbar spine 3500 mrad CT pelvis 3000 – 9000 mrad (Derived from Jagoda A, Kessler SG. Trauma in pregnancy. In: Harwood - Nussa, ed. The Clinical Practice of Emergency Medicine , 3rd edn. Philadelphia, PA: Lippincott, Williams and Wilkins, 2001 and the American College of Obstetricians and Gynecologists Committee Opinion. Guidelines for Diagnostic Imaging during Pregnancy , no. 158, Sept 1995). Chapter 18 232 sures as high as 260 mmHg and diastolic pressures in excess of 200 mmHg have been reported [35] . Left untreated, such hyper- tensive crises can quickly lead to retinal hemorrhage, cerebrovas- cular accidents, intracranial hemorrhage, seizures, encephalopathy, and death [36] . In addition, placental abruption is a signifi cant fetal as well as maternal concern. Paradoxical b radycardia The same spinal cord lesion that blocks the ascent of sensory impulses that trigger sympathetic discharge also prevents the descent of central supraspinal inhibitory impulses. Intense com- pensatory refl ex parasympathetic output is thus channeled outside of the spinal system via the vagus nerve. Consequently, the patient with autonomic hyperrefl exia can present with para- doxical bradycardia and cardiac dysrhythmias in synchrony with the manifestations of unrestrained sympathetic activity. Prevention Recognition and prevention are paramount in avoiding the potentially lethal consequences of AH. It can occur in response to virtually any sensory stimulus below the level of the lesion, during any stage of pregnancy. It has been reported in conjunc- tion with cervical examination, bladder and bowel distention, catheterization, rectal disimpaction, breastfeeding, and episiot- omy [37] . Hence, any potentially noxious stimuli should be con- sciously avoided or minimized by employing topical anesthetic jelly for digital exams, catheterization, and fecal disimpaction [38] . While bladder distention is the most common precipitant of AH [39] , labor is a potent stimulus for the pregnant SCI patient. Confusion with p re - e clampsia In AH - susceptible patients, it should be anticipated and differen- tiated from pre - eclampsia. Maternal death secondary to intracra- nial hemorrhage has been reported when AH was misdiagnosed as pre - eclampsia [36] . The hypertension of pre - eclampsia usually persists into the immediate puerperium, often resolving slowly in the fi rst days postpartum. In contrast, the hypertension of AH crescendos with each contraction and subsides in the interim between contractions, with occasional patients actually becoming hypotensive between contractions. It abates abruptly with removal of the noxious stimulus. Patient familiarity and experi- ence with AH is also helpful for rapid differentiation between these disease entities. Treatment of a utonomic h yperrefl exia Immediate management of AH is orientated towards identifying the inciting stimulus and normalization of blood pressure. The patient should be assessed for bladder distention from lack or obstruction of drainage, uterine contractions, perineal distention, and fecal impaction. Tight clothing, footwear, or external fetal monitoring straps can also cause AH. Blood pressure can be lowered quickly simply by changing the maternal position from supine to erect. Short - acting pharmacologic agents such as nife- subject the fetus to enough ionizing radiation to infl ict harm. However, the cumulative dose of the studies required to defi ne and treat a patient with SCI may approach the critical threshold. The radiation exposure from numerous higher - dose studies, such as abdominal or pelvic CT scans, barium studies, and intravenous pyelography, can quickly add up to more than 5 rad [30] . In a study involving 114 pregnant patients admitted to a trauma center between 1995 and 1999, the mean initial radiation expo- sure was 4.5 rad. Cumulative radiation exposure exceeded 5 rad in 85% of patients [31] . Minimizing fetal exposure is a funda- mental component of patient care. While there should be no hesitation to perform necessary radiological studies in patients with an acute SCI, one should insure that only those studies that are truly indicated are obtained. Whenever possible, the number of views obtained should be minimized and radiologic techniques employed to diminish the dose absorbed per view [28] . Monitoring devices such as personal radiation monitors or thermoluminescent dosimeters can be used to provide an accu- rate measure of cumulative radiation exposure [32] . Long t erm a ntepartum – i ntrapartum m aternal c oncerns Autonomic h yperrefl exia Long - term care of the pregnant patient with SCI requires cogni- zance of the specifi c, predictable medical complications that may occur in such pregnancies. The acute care of the SCI patient revolves around treatment of neurogenic shock and minimizing secondary injury to the cord. Of primary importance in manag- ing the chronic SCI patient is the prevention, prompt recognition of, and treatment of, autonomic hyperrefl exia (AH) [33] . This potentially life - threatening complication occurs in up to 85% of patients with lesions at or above T5 – 6, although it has been reported with lesions as low as T10 [34] . Refl ex activity generally returns within 6 months of injury, at which time those patients with damage above the region of splanchnic sympathetic outfl ow (T6 to L2) become susceptible to the development of AH [35] . With this complication, noxious stimuli create impulses that enter the cord at different levels and progress upward until they are blocked by the lesion. Unable to ascend further, afferent impulses are channeled instead by interneurons to synapse with sympathetic nerves, resulting in an extensive, multilevel dispersal of sympathetic activity [35] . This explosive autonomic discharge can manifest suddenly and dramatically. The patient typically develops an intense, pounding headache, profuse sweating, facial fl ushing, and nausea. Nasal congestion, piloerection, and a blotchy rash above the level of the lesion are also frequently present. Severe s ystolic h ypertension Impressive signs accompany the physical expressions of sympa- thetic discharge. In a matter of seconds, blood pressure can increase threefold to reach malignant levels. Systolic blood pres- Acute Spinal Cord Injury 233 consumption, can culminate in the need for assisted ventilation in SCI patients. Thus, ventilatory function should be monitored with serial vital capacity measurements [38] and ventilatory support initiated when the VC falls below 15 mL/kg [42] . Summary Care of the acute spinal cord patient requires an awareness of commonly occurring serious or life - threatening complications. Immediate care consists of initial stabilization, treatment of neu- rogenic shock, and the avoidance of secondary cord damage by minimizing physical manipulation and cord hypoxia. Extended antepartum and intrapartum care is focused on prevention, rec- ognition, and expeditious management of AH. Comprehensive management of pregnant SCI patients necessitates attention to the multitude of medical complications that accompany chronic SCI including urinary hygiene, frequent urinary tract infections, pressure sores, thromboembolic surveillance, pulmonary toilet, and the potential for unattended delivery secondary to unper- ceived labor. Additionally, muscle spasms may require specifi c medications for control, as well as altering the mode of delivery, depending on their severity. References 1 Blackwell TL , Krause JS , Winkler T , Stiens S . Spinal Cord Injury: Guidelines for Life. Care Planning and Case Management . Appendix A: Demographic characteristics of spinal cord injury. New York : Demos Medical Publishing, Inc. , 2001 : 133 – 138 . 2 National Spinal Cord Injury Statistic Center . Spinal Cord Injury: Facts and Figures at a Glance . Birmingham, Alabama : National Spinal Cord Injury Statistic Center , 2000 . 3 Atterbury JL , Groome LJ . Pregnancy in women with spinal cord inju- ries . Orthoped Nurs 1998 ; 33 ( 4 ): 603 – 613 . 4 Marotta JT . Spinal injury . In: Rowland LP , ed. Merritt ’ s Neurology , 10th edn. Philadelphia, PA : Lippincott Williams and Wilkins , 2000 : 416 – 423 . 5 Ward KR . Trauma airway management . In: Harwood - Nuss A , ed. The Clinical Practice of Emergency Medicine , 3rd edn. Philadelphia, PA : Lippincott Williams and Wilkins , 2001 : 433 – 441 . 6 Donaldson WF III , Towers JD , Doctor A , Brand A , Donaldson VP . A methodology to evaluate motion of the unstable spine during intuba- tion techniques . Spine 1993 ; 18 ( 14 ): 2020 – 2023 . 7 Donaldson WF III , Heil BV , Donaldson VP , Silvaggio VJ . The effect of airway maneuvers on the unstable C1 - C2 segment. A cadaver study . Spine 1997 ; 22 ( 11 ): 1215 – 1218 . 8 Munnur U , de Boisblanc B , Suresh MS . Airway problems in preg- nancy . Crit Care Med 2005 ; 33 ( 10 ): S259 – S268 . 9 Mahoney BD . Spinal cord injuries . In: Harwood - Nuss A , ed. The Clinical Practice of Emergency Medicine , 3rd edn. Philadelphia, PA : Lippincott Williams and Wilkins , 2001 : 495 – 500 . 10 Gilson GJ , Miller AC , Clevenger FW , Curet LB . Acute spinal cord injury and.neurogenic shock in pregnancy . Obstet Gynecol Surv 1995 ; 50 ( 7 ): 556 – 560 . dipine or hydralazine are also useful for lowering the blood pres- sure until more defi nitive therapy with regional anesthesia is feasible. Short - acting agents are preferable to longer acting drugs since they allow avoidance of prolonged hypotension between contractions once the stimulus is removed or suppressed. Calcium channel blockers must be used judiciously, since common side effects include headache, fl ushing, and palpitations, symptoms that can easily be confused with those of AH. Additionally, it is recommended that an arterial line be placed to provide continu- ous evaluation of the extremely labile pressures associated with AH. Regional a nesthesia Prophylactic and therapeutic administration of regional anesthe- sia is the cornerstone of labor management of the SCI patient at risk for AH. Epidural anesthesia effectively disrupts the propaga- tion of sympathetic afferent impulses through the spine. Although obtaining a good regional block in patients with prior neurologic damage or back surgery can be technically diffi cult, it is nearly universally successful in preventing or aborting an episode of AH [37 – 40] . Failure of regional anesthesia to arrest ongoing AH is one of the few unique indications for cesarean section in a patient with SCI. The depth of general anesthesia typically required to suppress AH often results in neonatal suppression. When feasi- ble, supplemental regional anesthesia should be employed for cesarean section patients with high spinal lesions [37] . Alternatively, if general anesthesia is used, adequate neonatal resuscitation expertise and equipment should be immediately available at the time of delivery. Labor and d elivery c onsiderations Given the potential for serious maternal morbidity and death, the possibility of AH should be anticipated in patients with SCI, and a plan for care should be established well in advance of labor [41] . Early antepartum anesthesia consultation is mandatory, not only for those parturients at risk for AH, but for all SCI patients. This allows for the risks and benefi ts of regional anesthesia to be dis- cussed in a controlled setting, and alerts the patient to the pos- sibility, and consequences, of AH in labor. It is recommended that an epidural be placed as soon as the patient presents in labor, as well as before induction or augmentation of labor [39] . Meticulous and frequent blood pressure monitoring is essential. Placement of an arterial line and continuous cardiac monitoring for dysrhythmia are recommended [38] . Continuous bladder drainage is also advisable. An early anesthesia consultation also provides an opportunity for pulmonary function assessment. Patients with cervical or high thoracic lesions can have compro- mised pulmonary capacity secondary to debilitated intercostal muscle function as well as an attenuated cough refl ex. Patients with SCI often have baseline vital capacities measuring less than 2 L, predisposing them to atelectesis and pneumonia, and dimin- ishing their capacity to satisfy oxygen requirements [37] . The burden of pregnancy - related decrements in functional reserve capacity and expired reserve volume, as well as increased oxygen Chapter 18 234 25 Gerndt SJ , Rodriguez JL , Pawlik JW et al. Consequences of high - dose steroid therapy for acute spinal cord injury . J Trauma 1997 ; 42 ( 2 ): 279 – 284 . 26 Katz VL , Dotters DJ , Droegemueller W . Perimortem cesarean deliv- ery . Obstet Gynecol 1986 ; 68 ( 4 ): 571 – 576 . 27 Morris J A Jr , Rosenbower TJ , Jurkovich GJ et al. Infant survival after cesarean section for trauma . Ann Surg 1996 ; 223 ( 5 ): 481 – 491 . 28 International Commission on Radiological Protection . Protection of the Patient in Diagnostic Radiology . ICRP Publication 34. Oxford, England : Pergamon, 1983 . 29 Brent RL . The effect of embryonic and fetal exposure to X - ray, micro- waves, and ultrasound: counseling the pregnant and nonpregnant patient about these risks . Semin Oncol 1989 ; 16 ( 5 ): 347 – 368 . 30 Damilakis J , Perisinakis K , Voloudaki A , Gourtsoyiannis N . Estimation of fetal radiation dose from computed tomography scanning in late pregnancy: depth – dose data from routine examinations . Invest Radiol 2000 ; 35 ( 9 ): 527 – 533 . 31 Bochicchio GV , Napolitano LM , Haan J , Champion H , Scalea T . Incidental pregnancy in trauma patients . J Am Coll Surg 2001 ; 192 ( 5 ): 566 – 569 . 32 Goldman SM , Wagner LK . Radiologic ABCs of maternal and fetal survival after trauma: when minutes may count . Radiographics 1999 ; 19 ( 5 ): 1349 – 1357 . 33 McGregor JA , Meeuwsen J . Autonomic hyperrefl exi: a mortal danger for spinal cord - damaged women in labor . Am J Obstet Gynecol 1985 ; 151 ( 3 ): 330 – 333 . 34 Gimovsky ML , Ojeda A , Ozaki R , Zerne S . Management of autonomic hyperrefl exia associated with a low thoracic spinal cord lesion . Am J Obstet Gynecol 1985 ; 153 ( 2 ); 223 – 224 . 35 Colachis SC III . Autonomic hyperrefl exia with spinal cord injury . J Am Paraplegia Soc 1992 ; 15 ( 3 ): 171 – 186 . 36 Abouleish E . Hypertension in a paraplegic parturient . Anesthesiology 1980 ; 53 ( 4 ): 348 . 37 Baker ER , Cardenas DD . Pregnancy in spinal cord injured women . Arch Phys Med Rehabil 1996 ; 77 ( 5 ): 501 – 507 . 38 Greenspoon JS , Paul RH . Paraplegia and quadriplegia: special consid- erations during pregnancy and labor and delivery . Am J Obstet Gynecol 1986 ; 155 ( 4 ): 738 – 741 . 39 Lindan R , Joiner B , Freehafer AA , Hazel C . Incidence and clinical features of autonomic dysrefl exia in patients with spinal cord injury . Paraplegia 1980 ; 18 ( 5 ): 285 – 292 . 40 Crosby E, St - Jean B , Reid D , Elliot RD . Obstetrical anesthesia and analgesia in chronic spinal cord - injured women . Can J Anaesth 1992 ; 39 ( 5 Pt 1 ): 487 – 494 . 41 Cross LL , Meythaler JM , Tuel SM , Cross AL . Pregnancy, labor and delivery post spinal cord injury . Paraplegia 1992 ; 30 ( 12 ): 890 – 902 . 42 Macklem PT . Muscular weakness and respiratory function . N Engl J Med 1986 ; 314 ( 12 ): 775 – 776 . 11 Goodwin H , Holmes JF , Wisner DH . Abdominal ultrasound exami- nation in pregnant blunt trauma patients . J Trauma 2001 ; 50 ( 4 ); 689 – 693 . 12 American College of Obstetrics and Gynecology . Obstetric Aspects of Trauma Management . Educational Bulletin Number 251, September 1998 . 13 Lucas W , Kirschbaum T , Assali NS . Spinal shock and fetal oxygen- ation . Am J Obstet Gynecol 1965 ; 93 ( 4 ): 583 – 587 . 14 Coleman WP , Benzel D , Cahill DW et al. A critical appraisal of the reporting of the National Acute Spinal Cord Injury Studies of methylprednisolone in acute spinal cord injury . J Spinal Discord 2000 ; 13 ( 3 ): 185 – 199 . 15 Bracken MB , Shepard MJ , Collins WF et al. A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal cord injury. Results of the Second National Acute Spinal Cord Injury Study . N Engl J Med 1990 ; 322 ( 20 ): 1405 – 1411 . 16 Bracken MB , Shepard MJ , Collins WF Jr et al. Methylprednisolone or naloxone treatment after acute spinal cord injury: 1 - year follow - up data. Results of the second National Acute Spinal Cord Injury Study . J Neurosurg 1992 ; 76 ( 1 ): 23 – 31 . 17 Liu D , Li L , Augustus L . Prostaglandin release by spinal cord injury mediates production of hydroxyl radical, malondialdehyde and cell death: a site of the neuroprotective action of methylprednisolone . J Neurochem 2001 ; 77 ( 4 ): 1036 – 1047 . 18 Benton RL , Ross CD , Miller KE . Spinal taurine levels are increased 7 and 30 days following methylprednisolone treatment of spinal cord injury in rats . Brain Res 2001 ; 893 ( 1 – 2 ): 292 – 300 . 19 Brandoli C , Shi B , Pfl ug B , Andrews P , Wrathall JR , Mocchetti I . Dexamethasone reduces the expression of p75 neurotrophin receptor and apoptosis in contused spinal cord . Brain Res Mol Brain Res 2001 ; 87 ( 1 ): 61 – 70 . 20 Bracken MD , Shepard MJ , Holford TR et al. Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the third National Acute Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study . JAMA 1997 ; 277 ( 20 ): 1597 – 1604 . 21 Bracken MB , Shepard MJ , Holford TR et al. Methylprednisolone or tirilazadmesylate administration after acute spinal cord injury: 1 year follow - up. Results of the third National Acute Spinal Cord Injury randomized controlled trial . J Neurosurg 1998 ; 89 ( 5 ): 699 – 706 . 22 Nesathurai S . Steroids and spinal cord injury: revisiting the NASCIS 2 and NASCIS.3 trials . J Trauma 1998 ; 45 ( 6 ): 1088 – 1093 . 23 Hurlbert RJ . Methylprednisolone for acute spinal cord injury: an inappropriate standard of care . J Neurosurg 2000 ; 93 ( Suppl 1 ): 1 – 7 . 24 Short DJ , El Masry WS , Jones PW . High dose methylprednisolone in the management of acute spinal cord injury – a systematic review from a clinical perspective . Spinal Cord 2000 ; 38 ( 5 ): 273 – 286 . 235 Critical Care Obstetrics, 5th edition. Edited by M. Belfort, G. Saade, M. Foley, J. Phelan and G. Dildy. © 2010 Blackwell Publishing Ltd. 19 Pregnancy - Related Stroke Edward W. Veillon , Jr 1 & James N. Martin , Jr 2 1 Maternal - Fetal Medicine, University of Mississippi Medical Center, Jackson, MA, USA 2 Department of Obstetrics and Gynecology, Division of Maternal - Fetal Medicine, University of Mississippi, Medical Center, Jackson, MA, USA Introduction Cerebrovascular accidents (CVAs), also termed “ strokes ” , in the pregnant patient are infrequent but often catastrophic events which account for 12 – 14% of all maternal deaths [1 – 3] . CVA is usually classifi ed as either hemorrhagic or ischemic. Most hemor- rhagic strokes occur secondary to a ruptured aneurysm or arte- riovenous malformation (AVM) or a ruptured blood vessel(s) in association with sustained, severe hypertension. On the other hand, most ischemic strokes occur in relation to thromboembolic phenomena or vasculopathies. Ischemic and hemorrhagic CVAs are further classifi ed according to location within the central nervous system. CVA in the pregnant patient refl ects overall the spectrum of stroke etiologies encountered in young adults [4 – 6] , or they occur secondary to pregnancy - associated or induced disorders such as central venous thrombosis (CVT) and pre - eclampsia/eclampsia [5,7] . When a CVA affects a pregnant patient, the obstetrician - gynecologist and maternal - fetal medi- cine subspecialist physician managing the patient are challenged to collaborate with other specialties including anesthesia, neurol- ogy/neurosurgery and critical care while maintaining an aware- ness of pregnancy physiology, pathophysiology and practice critical to the patient ’ s special disease circumstances and recom- mended obstetric treatment. The concurrence of pregnancy and CVA must not in general alter diagnosis and management of the CVA. A thorough search for less serious medical disorders which can mimic stroke – metabolic, migraine, seizure, toxicology or psychogenic – must be considered and ruled out by appropriate history taking, laboratory tests and imaging studies. Causation and t ime of o ccurrence When CVA occurs during the pregnancy (11%), the peripartum period immediately around labor and delivery (41%) or up to 6 weeks postpartum (48%), it is described as a pregnancy - related stroke or PRS [3] . A tabular presentation of PRS is listed in Table 19.1 and divided between types of stroke incited or induced by pregnancy and types incidental to pregnancy. These have been summarized and described recently in a number of excellent reviews that were used to create Table 19.1 [1 – 27] . Based on published collective reviews through 2006, the worldwide incidence of PRS ranges from 8.9 to 67.1 per 100 000 deliveries or an average of 21.3 per 100 000 [28] . Differences among study fi ndings refl ect the variations in study populations, study inter- vals, study design and methodologies, case defi nitions, case ascer- tainment, neuroimaging techniques and likely other factors. Using data collected from 8 million American women in the 2001 – 2002 Nationwide Inpatient Sample which includes all - payer inpatient care from more than 1000 general and university hospitals in the United States, a national PRS incidence of 34.2 events/100 000 women was derived [3] . Death occurred in 117 of the 2,850 women with PRS, a rate of 1.4 stroke deaths per 100 000 deliveries [3] . Worldwide except for Taiwan the incidence of PRS due to ischemia/infarction is slightly higher than that of hemorrhage [15,16,22,28 – 33] . Pre - eclampsia/eclampsia accounted for 47% of ischemic PRS in the French Study Group and 24% in the Baltimore - Washington Study Group [4,15] . Risk for ischemic PRS remains low throughout gestation until the 2 - day period before delivery and the fi rst day postpartum [11] . During the remainder of the puerperium (6 weeks postpartum), the risk of ischemic and hemorrhagic PRS remains elevated but less so than the peripartum period [11] and during gestation itself [8,15] . A number of factors in any given patient impact her risk of PRS including developments within the pregnancy itself (obstetric) as listed in Table 19.2 . Pregnancy p hysiology and p athophysiology Compared with the non - pregnant state, pregnancy increases by as much as 12 – 13 - fold the risk of CVA [34,35] . One reason for such an increase in stroke potential for the pregnant patient is Chapter 19 236 Table 19.1 Types of pregnancy - related stroke ( PRS ). Pregnancy - induced stroke Pregnancy - incidental stroke Pre - eclampsia - Eclampsia Subarachnoid Hemorrhage Severe Gestational Hypertension Aneurysm HELLP Syndrome Arteriovenous Malformation Cerebral Vein Thrombosis Takayasu ’ s Disease Cerebral Sinus Thrombosis Ischemic Arterial Infarction Dural Sinus Thrombosis Hematologic Sagittal Venous Thrombosis TTP Postpartum Cerebral Angiopathy/Vasculopathy DIC Polycythemia Thrombocythemia Sickle Cell Diseases Paroxysmal Nocturnal Hemoglobinuria Thrombophilias/Prothrombotic States Antithrombin III Defi ciency Prothrombin Mutation Antiphospholipid Antibodies Protein S or C Defi ciency Factor V Leiden Homocysteinemia Nephrotic Syndrome Infl ammatory Disease Postpartum Reversible Encephalopathy Syndrome Metastatic Choriocarcinoma Embolism Amniotic Fluid Air Fat Paradoxical Peripartum Cardiomyopathy Vascular Arterial Dissection Moyamoya Systemic Lupus Erythematosus Sarcoidosis Wegener ’ s Granulomatosis Behcet ’ s Syndrome Others Bacterial Endocarditis Cardiac Arrhythmia Cerebral Ischemia Cocaine/Vasoactive Drugs Head Injury Severe Dehydration Meningitis/Sinusitis/Mastoiditis Systemic Infectious Disease Fibromuscular Dysplasia Marfan ’ s Syndrome Ehlers - Danlos Type IV Neurofi bromatosis Tuberous Sclerosis Osler - Weber - Rendu Syndrome Autosomal - Dominant Inherited Polycystic Kidney Table 19.2 Contributing risk factors for stroke during pregnancy. 1. AGE : PRS risk increases with maternal age [3] 35 – 39 years old = 90% increase in risk 40+ years old = 3.3 fold increase versus < 20 years old 2. RACE : PRS risk varies by race [3] 26.1 : 100 000 deliveries = Hispanics 31.7 : 100 000 deliveries = Caucasians 52.5 : 100 000 deliveries = African Americans 3. HYPERTENSION : PRS Risk varies by type of hypertension: Pre - existing Hypertension (OR 2.61) Gestational Hypertension (OR 2.41) Pre - eclampsia/Eclampsia (OR 10.39) Superimposed Pre - eclampsia/Eclampsia (OR 9.23) 1993 – 2002 Nationwide Inpatient Database [25] 4. HEART DISEASE : Valvular - Arrhythmia - Infection - Infarction OR 13.2 [3] 5. ILLICIT DRUG USE : Cocaine - Amphetamine OR 2.3 [3] 6. TOBACCO USE/ABUSE : OR 1.95 [25] 7. MIGRAINE HEADACHES : OR 16.9 [3] 8. DIABETES : OR 2.5 [3] 9. THROMBOPHILIA : OR 16.0 [3] 10. LUPUS/SLE : OR 15.2 [3] 11. SICKLE CELL DISEASE : OR 9.1 [3] 12. THROMBOCYTOPENIA : OR 6.0 [3] 13. ANEMIA : OR 1.9 [3] 14. OBSTETRIC : POSTPARTUM HEMORRHAGE = OR 1.8 FLUID & ELECTROLYTE IMBALANCE = OR 7.2 TRANSFUSION = OR 10.3 INFECTION = OR 25.0 [3] that she is considered to be in a hypercoagulable state despite an expected decrease in hematocrit, blood viscosity and vascular resistance. Platelet hyperaggregability, decreased fi brinolysis, increases in some clotting proteins (fi brinogen and factors V, VII, VIII, IX, X and XII), decreases in naturally occurring anticoagu- lant proteins (C, S, antithrombin III) in late gestation, acquired increased resistance to protein C and decreased protein C inhibi- tor activity all contribute to a hypercoagulable state that extends several weeks into the puerperium. Blood coagulability may also be enhanced by pregnancy hormones estrogen and progesterone. Finally, hemodynamic changes inclusive of increases in blood volume, cardiac output and venous blood pressure are important factors especially around delivery and if anesthesia and cesarean surgery are employed. General d iagnostic c onsiderations Neuroimaging a pregnant patient raises questions of safety for the fetus. Because head computed tomography (CT) of the mother Pregnancy-Related Stroke 237 [50,51] . It is variably characterized by headache, seizure, altered mental status, visual disturbance and/or focal neurologic distur- bances in a hypertensive patient with preferential localization of focal cerebral edema formation in the posterior cerebral circulation. Categories of p regnancy - r elated s troke As depicted in Table 19.1 , PRS can be divided into CVAs which occur as a consequence of disorders or diseases unique to preg- nancy (pregnancy - induced) or CVAs which occur during gestation that are not primarily due to pregnancy - associated (pregnancy - incidental) pathology. Examples of the former are pre - eclampsia/eclampsia, cerebral venous thrombosis, and post- partum cerebral vasculopathy. Because the spectrum of disease encountered in the stroke patient with gestational hypertension/ pre - eclampsia/eclampsia/HELLP syndrome is broad, the clini- cian can be challenged in some patients to distinguish between a stroke caused primarily by a pregnancy - induced hypertensive disorder versus some other non - pregnancy specifi c cause of cere- bral infarction or intracranial (subarachnoid or intracerebral) hemorrhage. The history and physical examination may provide important clues to type and etiology of stroke. Pregnancy - i nduced s troke Pre - e clampsia - e clampsia - HELLP s yndrome and s evere g estational h ypertension General That patients with hypertensive complications of pregnancy such as gestational hypertension and pre - eclampsia are 2 to 4 times more likely than controls to later suffer a postpregnancy cardio- vascular, thromboembolic or stroke event suggests that there are underlying factors which contribute to a proclivity toward CVA in these women [52 – 54] . Indeed, a strong family history for heart disease or stroke imparts a 3.2 - fold elevation in the risk for pre - eclampsia [55] . CVA is the most common cause of death in patients with eclampsia [56,57] as well as patients with atypical severe pre - eclampsia expressed as HELLP syndrome (hemolysis, elevated liver enzymes, thrombocytopenia) who receive tradi- tional non - steroid obstetric and medical management [58 – 60] . It is less appreciated by clinicians that stroke can occur in the patient with severe pre - eclampsia without HELLP syndrome and in the patient with severe gestational hypertension who at the time of stroke does not have measurable proteinuria to merit a diagnosis of pre - eclampsia. Severe s ystolic h ypertension The importance of preventing severe systolic hypertension ( < 160 mmHg) in the pathogenesis of stroke in patients with a pre - eclampsia disorder has led to a call for a paradigm change in obstetric practice away from an emphasis on high diastolic with the abdomen shielded exposes the fetus to less than 1 mil- lirad, it is considered safe in pregnancy [36,37] . Because magnetic resonance imaging (MRI) involves no radiation exposure and most animal studies have shown no adverse effects on fetal devel- opment, the present consensus is that MRI (magnetic resonance arteriography (MRA) and magnetic resonance venography (MRV)) is probably safe in pregnancy [37] . Triiodinated com- pounds used as intravenous contrast agents for CT and fl uoros- copy are class B pharmaceuticals probably safe for use during pregnancy because they are undetectable in the fetus and amni- otic fl uid, but gadolinium contrast is avoided because it crosses the placenta and has unknown effects on fetal development [38] Conventional head angiography also exposes the fetus to minimal radiation ( < 1 mrad) if fl uoroscopy is short in duration. Cerebrospinal fl uid studies are infrequently undertaken unless vasculitis, infection or subarachnoid hemorrhage is suspected. Echocardiogram is used to detect a patient foramen ovale or right to left shunt in the young pregnant patient since hemodynamic changes and a predisposition to venous thrombosis increase the likelihood of a paradoxical embolus [39] . Until recently, the use of tissue plasminogen activator (tPA) thrombolysis in pregnancy has been regarded as relatively contraindicated, but recent case reports and series have shown some limited use for late pregnancy stroke or life - threatening and potentially debilitating thrombo- embolic disease [40 – 42] . Cerebral b lood fl ow The autoregulatory system of the human brain ensures constant cerebral blood fl ow and tissue perfusion over a wide range of systemic pressures. During normal pregnancy, cerebral hemody- namics change over the course of gestation as measured by Doppler [43] and velocity - encoded phase contrast magnetic reso- nance imaging [44] . The systolic velocity and resistance index in the middle cerebral artery both decrease approximately 20% over gestation, whereas the cerebral perfusion pressure (CPP) is esti- mated to increase by 50% from early pregnancy to term [45,46] although the methodology used has been criticized [47,48] . A similar decrease in fl ow is seen by magnetic resonance imaging studies of the posterior cerebral artery with no change in the middle and posterior cerebral artery diameters during late normal pregnancy [43,44] . The cerebral blood fl ow index (CFI) refl ecting overall cerebral perfusion also increases approximately 10% during pregnancy. Despite this increase, cerebral autoregulation in the normal pregnancy patient remains very effi cient. A small decrease in cerebral resistance occurs as blood pressure increases within the normal range late in pregnancy; if blood pressure increases outside the normal range, a physiological increase in cerebral resistance occurs to limit perfusion [46] . If the upper limit of autoregulation is exceeded by elevated blood pressure and impairments to normal cerebrovascular health such as endothe- lial dysfunction and water homeostasis [48,49] , the subacute neu- rologic syndrome of hypertensive encephalopathy can develop Chapter 19 238 of the brain as well as the occipital area [61] . This is consistent with recent data showing magnetic resonance imaging abnor- malities in the occipital and parietal lobes of patients with pre - eclampsia [92] . Hemorrhage can be either intracerebral or subarachnoid [93 – 95] , rarely involving the brainstem [96] . When Doppler and CNS imaging abnormalities are observed in post- partum patients with headache, altered consciousness, vomiting, seizures and focal neurologic signs that is similar to the spectrum of eclampsia, the term “ postpartum cerebral angiopathy ” has been utilized and managed with supportive and antiseizure medi- cations given while awaiting spontaneous resolution [81,86] . The rare complication of cortical blindness is usually reversible since it is due to vasogenic edema in the posterior cerebral circulation of the occipital lobes, but permanent blindness or complete amaurosis rarely follows infarcts of the lateral geniculate bodies [97 – 100] . Pharmacotherapy Magnesium sulfate has been shown to signifi cant reduce eclamp- tic seizures in the MAGPIE trial, although a small percentage of patients develop eclampsia nevertheless and its use does not prevent stroke. Magnesium sulfate ’ s mechanism of action to prevent seizure is still undefi ned, but it has been shown to reduce cerebral perfusion pressure via vasodilatation of constricted cere- bral vessels [46,101] in contrast to nimodipine, a dihydropyridine calcium channel blocker [102] which increases CPP. Recent data suggest that magnesium sulfate acts to maintain cerebral fl ow index while reducing cerebral perfusion pressure in women with elevated CPP, and that its effect is linearly related to the baseline CPP. In other words, patients with a higher starting CPP will demonstrate a greater reduction in CPP following MgSO 4 than women with lesser elevation of their CPP. In addition, women with lower CPP will tend to “ normalize ” their CPP within the 5 – 95% after MgSO 4 infusion. Labetalol has both selective, com- petitive alpha - 1 and non - selective, competitive β - adrenergic blocking actions that produce rapid dose - dependent decreases in blood pressure without refl ex tachycardia or signifi cant reduction in heart rate [103] . In addition, it has been shown to be a membrane stabilizer [104] and it may reduce cerebral perfusion pressure more effectively than magnesium sulfate without affect- ing cerebral perfusion. Hence it is a candidate agent to replace magnesium sulfate as fi rst - line therapy to control blood pressure and prevent cerebral sequelae [46] . Guidelines for the use of labetolol and hydralazine have been published [105,63] ; great individual variation in dosage amount and frequency exist in practices around the United States, suggesting the need for further studies to validate effectiveness of therapy for achieving and maintaining therapeutic goals (ie, a systolic blood pressure < 160 mmHg) by traditional oral and systemic routes or via intra- venous infusions (i.e. labetolol, nicardipine). Immediate postpar- tum or poststroke diuretic therapy as furosemide is recommended for patients with hypertensive encephalopathy and to improve blood pressure control in the severely hypertensive parturient [106 – 108] . ( > 110 mmHg) or mean arterial blood pressures ( > 125 – 140 mmHg) as thresholds to guide antihypertensive therapy [61] . The impor- tance of aggressively treating severe systolic hypertension to < 160 mmHg has been emphasized also by Cunningham [62] and is consistent with recommendations published by the 2000 National Institutes of Health Working Group on High Blood Pressure in Pregnancy [63] . The development of a pulse pressure of more than 60 mmHg difference between systolic and diastolic readings, in association with a systolic blood pressure increase over baseline also of more than 60 mmHg could be as important in the pregnant patient with pre - eclampsia to place her at risk of cerebrovascular accident as exceeding a systolic blood pressure threshold of 160 mmHg [61] . Abnormal c erebral h emodynamics Changes in the cerebral hemodynamics of the pregnant patient with severe pre - eclampsia explain in part the susceptibility of these patients to cerebrovascular accident [46] . Compared to normal pregnant patients or those with mild pre - eclampsia, the majority of patients with severe pre - eclampsia have high cerebral perfusion pressures and cerebral vascular resistance which may cause vascular (endothelial, muscularis, arterial wall stiffness) damage centrally [64 – 66] over time and headache [67] . Women destined to develop pre - eclampsia or superimposed pre - eclamp- sia have cerebral hemodynamic changes that predate by 7 – 10 weeks the development of overt pre - eclampsia [68 – 71] . Cerebral blood fl ow velocity increases signifi cantly in the fi rst 24 – 48 hours postpartum, possibly related to the higher frequency of stroke seen postpartum in women with pre - eclampsia than antepartum in some series [61,72] . These and other central hemodynamic changes can persist for 7 days to 12 weeks postpartum [73 – 74] . Defective c erebral a utoregulation and s equelae A number of investigators have advanced the hypothesis that a protracted period of increased cerebral perfusion pressure in patients with pre - eclampsia/eclampsia may cause barotrauma and vascular damage that causes cerebral autoregulation to fail with overperfusion injury, vasogenic edema [46,75 – 77] and the clinical syndrome of hypertensive encephalopathy. Support for this concept has also been found in small animal studies [48,78,79] . Oehm and colleagues in Germany have reported that a substantial disturbance of dynamic cerebral autoregulation occurs in patients who develop eclampsia [80] . Some patients with severe gestational hypertension/severe pre - eclampsia/ HELLP syndrome develop only symptoms of advanced cerebral pathology and hypertensive encephalopathy [81 – 83] , some man- ifest this as eclampsia with seizure [84 – 87] , while still others instead progress to cerebral hemorrhage or thrombosis [88 – 91,61] during pregnancy or the puerperium. Spectrum and c haracteristics of s troke In the recent series of strokes in 28 severely pre - eclamptic patients reported by Martin, most were hemorrhagic in type, frequently in multiple sites (37%), and present in frontal and parietal lobes . cumulative radiation exposure [32] . Long t erm a ntepartum – i ntrapartum m aternal c oncerns Autonomic h yperrefl exia Long - term care of the pregnant patient with SCI requires cogni- zance. secondary cord damage by minimizing physical manipulation and cord hypoxia. Extended antepartum and intrapartum care is focused on prevention, rec- ognition, and expeditious management of AH. Comprehensive. patients with SCI, and a plan for care should be established well in advance of labor [41] . Early antepartum anesthesia consultation is mandatory, not only for those parturients at risk for AH,