Critical Care Obstetrics part 25 pptx

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 circulator

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 sympasympa-thetic 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

C6 , C7 Extensor carpi radialis Wrist 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

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

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]

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 compresinci-sion 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

(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)

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 examinaconjunc-tion, bladder and bowel distenconjunc-tion, 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 expoexpo-sure 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-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

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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

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Regional a nesthesia

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Meticulous and frequent blood pressure monitoring is essential

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Patients with cervical or high thoracic lesions can have

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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

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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

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from a clinical perspective Spinal Cord 2000 ; 38 ( 5 ): 273 – 286

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

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

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

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

[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 (pregpreg-nancy - 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 intracerecere-bral) 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

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, comcom-petitive 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