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