LINEBURG


<< . .

 35
( 87)



. . >>

For C/S in a parturient with raised ICP, preinduction measure-
ment and control of ICP and BP is mandatory. An arterial line and
Neurosurgical management
ventriculostomy with an ICP pressure transducer assist in con-
Low-grade gliomas are slow growing and usually are surgically trolling the response to tracheal intubation, as therapy (antihy-
removed electively after delivery. High-grade gliomas are surgi- pertensive drugs, hyperventilation, and mannitol) can be titrated
cally removed without delay with concomitant radiotherapy and to maintain homeostasis. Anesthesia for neurosurgical interven-
chemotherapy. Since these treatments pose a significant risk to tion during pregnancy is discussed later in the chapter.
the fetus, decisions about treatment must be individualized. In
the case of a slow-growing meningioma, 30% can be completely
Central nervous system infection
resected while the remainder requires subtotal resection or radia-
tion. Pituitary tumors are treated by trans-sphenoidal resection Infection of the brain and spinal cord can become organized into
or, in the case of prolactinomas, bromocriptine therapy. For abscesses, which produce symptoms similar to other mass
lesions.88,89,90,91,92 Anesthetic considerations are the same as
choriocarcinoma, radiation and chemotherapy are used and sur-
gery is reserved for those with a single metastatic lesion to the those for brain tumors and other space-occupying lesions.



173
3 Nervous system disorders


disorders, hypertension, and cocaine abuse.98 Arteriovenous mal-
Table 9.6 Types of strokes during pregnancy or puerperium in formations can occur in most parts of the brain and spinal cord
15 women at Parkland Memorial Hospital from 1984“199024 and are abnormal, thin-walled communications between the
arterial and venous system, which are prone to rupture.99 A
Hemorrhagic strokes (6)
large malformation can produce an arteriovenous shunt suffi-
Saccular aneurysm 1
cient to raise the cardiac output.
Arteriovenous malformation 1
Hypertensive 3
Clinical presentation and diagnosis
Unknown 1
Unruptured aneurysms are usually asymptomatic while large
Ischemic strokes (9)
aneurysms can produce headache and focal neurologic signs
Arterial thrombosis 2
depending on their location. Subarachnoid hemorrhage may pro-
Arterial embolism 3
duce severe headache, photophobia, nausea and vomiting, peri-
Venous thrombosis 2
orbital pain, nuchal rigidity, and a positive Kernig sign.100
Vasculitis 1
Throbbing headache, changing sensorium, and seizures are
Moyamoya disease 1
more characteristic of hemorrhage into the brain parenchyma
from an AVM. Vasospasm is seen more commonly in patients
Stroke with a bleeding aneurysm than a bleeding AVM.6,101 When a
major hemorrhage occurs, the following can happen.
A stroke is defined as a syndrome of acute neurological injury
 Intracranial pressure approaches the mean arterial pressure,
following rupture or occlusion of vessels in the CNS. Cerebral
decreasing cerebral perfusion and resulting in a transient loss
vessels can rupture from trauma or inherent weakness, and can
of consciousness.
be occluded from within by thrombosis or embolus or externally
 A severe headache occurs either before loss of consciousness or
by a mass lesion (see Table 9.6).2,3,4,5,6,7,11,24,93 The incidence of
upon awakening.
maternal stroke secondary to a bleeding cerebral aneurysm is
 Rarely, acute vascular spasm leads to additional focal neurolo-
1:60003 to 1: 30 00024 pregnancies with a 20% mortality and a
gic signs with stupor and impaired autoregulation.
50% incidence of permanent neurological sequelae.3 The risk of
 The electrocardiogram (EKG) often shows ST and T wave
stroke from cerebral infarction and intracerebral hemorrhage
changes similar to those of myocardial ischemia, along with a
(ICH) is increased in the six weeks after delivery but not during
prolonged QRS complex, increased QT interval, and prominent
pregnancy.8
peaked or inverted T waves. The cause of these EKG changes
has been debated, but there is evidence that structural myo-
cardial lesions may occur, possibly secondary to intense sym-
Central nervous system hemorrhage
pathetic activity.11,95 These lesions are usually not associated
Intracranial hemorrhage has an incidence of 1 to 5 per 10 000 with an elevated creatine kinase. The EKG changes generally
pregnancies and is either subarachnoid (SAH), bleeding into the do not correlate with the extent of cardiac injury. The grade
subarachnoid space from lesions near the surface of the brain, or of SAH may correlate with wall motion abnormalities on
intracerebral, bleeding into the brain parenchyma.11 The patho- echocardiography.
physiologic effects of intracranial hemorrhage result from a com- After a bleed the following complications can occur.
pressive mass effect and irritation from blood and its breakdown  Rebleeding in 10“30% of patients during the first three weeks
products. Intracerebral structures are relatively noncompress- following aneurysmal rupture, with a mortality of 50“60% with
ible, so even a small hemorrhage can result in significant ana- each rebleed.
tomic distortion, a large increase in ICP, and a reduction in  Vasospasm occurs in 35% of patients 4 to 11 days following
cerebral perfusion. SAH, leading to further neurological deterioration.
 Hydrocephalus occurs in 15“20% of patients following SAH,
from blood and cellular exudate blocking efflux of CSF. This is
Subarachnoid hemorrhage
manifested by a gradual decrease in the level of consciousness.
 Cerebral edema or hyponatremia from inappropriate ADH
Subarachnoid hemorrhage occurs in 0.01 to 0.05% of pregnan-
cies2,5,9,10,11,24,94,95,96,97 and is associated with either a saccular (SIADH) secretion can be seen.
(Berry) aneurysm in 77% parturients, or an arteriovenous mal- Subarachnoid hemorrhage is life threatening and surgery can
formations (AVM) in 23% parturients, with an overall mortality of be life saving, therefore a CT scan, MRI, and possibly lumbar
5“12%.24 Intracranial aneurysms result from a weakening of the puncture (presence of blood/xanthocromia) should be carried
internal elastic lamina of large arteries at the base of the brain, out promptly. Angiography is performed to define the lesion for
usually at a bifurcation. Often the vessel wall is thinnest at the surgical intervention.
dome of the aneurysm, and it ruptures into the subarachnoid
Neurosurgical management
space of the basal cisterns, the subdural space, or directly into
the underlying brain parenchyma. Aneurysms can leak sponta- Controversy exists over the optimal time to operate on parturients
suffering from SAH.2,9,10,24,93 Early surgery reduces the incidence
neously. Precipitating factors for rupture include: bleeding



174
Chapter 9


of vasospasm and rebleeding and seems to be associated with
Table 9.7 Anesthetic goals for clipping a cerebral aneurysm in
lower maternal and fetal mortality.24 However, the patient may be
the parturient
unstable (worsening neurological status, poorly controlled hyper-
tension) and surgery itself may induce vasospasm. Surgery may  Minimize transmural pressure (mean arterial pressure“intracranial
or may not be of benefit after an AVM bleed.24,102 The decision to pressure) a
operate is based primarily on neurosurgical considerations, Prevent hypertension and maintain normal mean arterial and
although advances in the maintenance of normotension, normo- intracranial pressure
volemia, hemodilution, and improved treatment of vasospasm Maintain normal oxygen saturation and normocarbia b

favor early clipping of aneurysms to prevent rebleeding.95,96,97,103  Maintain appropriate analgesia, muscle relaxation, and amnesia
 Close monitoring of volume status
Effect of pregnancy and obstetric management  Mild hypothermia (36“358C) may be considered to reduce cerebral
In the past it was thought that aneurysms, but not AVM, were at metabolic rate “ brain protection (prevent shivering with muscle
increased risk of bleeding with advancing gestational age.100 The relaxation)
current opinion is that both aneurysms and AVM tend to bleed  Vasospasm may require nimodipine treatment and triple ˜˜H™™
more as pregnancy advances, possibly due to the hemodynamic therapy, i.e. hypervolemia, hypertension, and hemodilution
and hormonal changes of pregnancy.24 This explanation does not  Head elevation
account for the rarity of intracranial hemorrhage during labor and  Left uterine displacement to minimize aortocaval compression
delivery when hemodynamic changes are maximal. Hemorrhage  Early awakening
resulting from AVM does not cluster during any particular trime-
a
It is imperative that intracranial pressure not be lowered until the
ster, and the incidence in subsequent pregnancies is increased.99
dura mater is opened to minimize changes in the transcranial pressure
The incidence and mortality from intracranial hemorrhage in par-
gradient on the aneurysm wall and associated bleeding.
turients are similar to that of the general population.24,99
b
Hypocarbia potentially reduces placental perfusion.
If an aneurysm has been clipped, there is no increased risk for
vaginal delivery.104 If the aneurysm is untreated, the risk of intra-
partum rebleeding is greatest if the initial bleed occurred during
hypertension, and all three patients had residual neurological defi-
the third trimester. An uncorrected AVM is more likely to bleed
cits.3 The incidence due to less common etiologies is unknown.
during labor and delivery than an aneurysm. Some authors
recommend elective C/S at 38 weeks™ gestation,102,104,105 but Severe preeclampsia causes arterial vasospasm, multifocal
petechial hemorrhages, and may be accompanied by SAH.123
others have found no advantage over vaginal delivery.24
Hypertensive ICH typically occurs in the basal ganglia, thalamus,
Currently, most would recommend operative delivery with an
cerebellum, or pons. Intracerebral hemorrhage can also accom-
unclipped and previously ruptured aneurysm.
pany SAH caused by aneurysms or AVM. The risk of ICH in
A combined C/S and neurosurgical procedure can be under-
taken when indicated.2,10,93,106,107,108,109 If urgent, the neurosur- pregnancy is increased with metastatic choriocarcinoma,
gical procedure is carried out prior to delivery.110,111 In patients Moyamoya disease, Kaposi sarcoma, occult carotid-cavernous
fistula, bleeding diatheses, and cocaine abuse.5
with obstetrical reasons for expeditious delivery, the neurosurgi-
cal procedure may be performed remote from delivery.
Clinical presentation and diagnosis
95,110,111,112,113
Anesthetic management (see Table 9.7) Pregnant patients with ICH present with an abrupt onset of a
95,112
neurologic deficit referable to the site of the hemorrhage, com-
Aneurysm clipping may be delayed in unstable patients. It is
monly accompanied by headache, nausea, and vomiting. A non-
important to minimize transmural pressure (mean arterial pres-
contrast CT scan is the most sensitive test to diagnose acute ICH,
sure“intracranial pressure) across the aneurysm wall to minimize
but contrast CT scan, MRI scan, or angiography may be needed to
the risk of rebleeding.
exclude a structural etiology. A bleeding disorder should be ruled
General anesthetic considerations for C/S are the same as those
out. It is important to differentiate ICH from SAH, because treat-
for other neurosurgical procedures. Epidural anesthesia has been
used for C/S114,115 and for vaginal delivery116,117,118 in patients ment differs greatly.
with a medically managed intracranial aneurysm. One report has
Neurosurgical management
described the successful use of either epidural or GA for C/S in
three women with AV malformations.119 Intracerebral hemorrhage is often not amenable to surgical cor-
rection and has a poor prognosis.124 Treatment is supportive,
with control of BP and ICP. Surgery is reserved for life-threatening
Intracerebral hemorrhage
elevations of ICP, brain-stem herniation, and evacuation of an
expanding hematoma that is well defined.
Hemorrhage into the brain parenchyma of pregnant patients is rare,
is often secondary to hypertensive disorders,5,10,120 and remains the
most common cause of death in an eclamptic patient.121,122 One Effect of pregnancy and obstetric management
Obstetric considerations should determine the mode and timing
report noted three strokes of hypertensive etiology in 90 000 parturi-
ents studied.3 Two of these parturients had underlying chronic of delivery. Cardiovascular effects of pain and pushing during



175
3 Nervous system disorders


labor and delivery may elevate the ICP and BP during preeclamp- A spinal hematoma is a medical emergency as nerve compres-
sia, worsening the ICH. Cesarean section offers no advantage in sion and ischemia will result in permanent damage “ often in less
limiting hemodynamic stress over painless vaginal delivery modi- than six hours after the onset of symptoms. An MRI is diagnostic.
fied with limited pushing during the second stage, but a perimor- The only effective treatment is emergency decompression if a
hematoma mass-lesion is found.129 Spontaneous partial recovery
tem C/S may be required. If a hematoma is present, surgical
occurs rarely.137,138
evacuation may be required, with delivery at a later date.

Anesthetic management
Central nervous system ischemia
Blood pressure must be controlled prior to surgery, but may be
Cerebral ischemia
difficult to manage in the hypertensive or preeclamptic parturi-
ent. These patients often have a low intravascular volume, which
Ischemic stroke is uncommon in women of childbearing age and
increases the risk of severe hypotension and decreased placental
results from occlusion of the cerebral circulation (venous or
perfusion following anesthetic induction.10 In these cases, opti-
arterial) due to a variety of causes. In one report, ischemic strokes
mal fluid replacement is guided by the use of a central venous
were observed in 9 of 90 000 pregnancies.3 In another report,
pressure or Swan-Ganz catheter. Diuretics such as mannitol and
cerebral thrombosis was present in 1 of 29 000 pregnancies.139
furosemide may be used intraoperatively to reduce brain bulk
Kittner et al.8 showed that the relative risk for cerebral infarction
and facilitate surface exposure. Mannitol increases the fetal
during pregnancy was 0.7 (adjusted for age and race) compared
osmolality significantly and should be used with caution.125
with a relative risk of 8.7 in the first six weeks after delivery.
Intracranial pressure should also be controlled preoperatively.
Cerebral venous thrombosis (CVT) occurs during the early
Regional anesthesia is generally preferred for hypertensive
postpartum period in most cases. Underlying precipitating fac-
patients, if coagulation status is normal, as it avoids the hyper-
tors for cerebral venous thrombosis are shown in Table 9.8.
tensive response to intubation and reduces the risk of regurgita-
Thrombosis of the sagittal sinus with extension to the cortical
tion and pulmonary aspiration. If GA is used, BP is controlled with
veins is not uncommon. Sagittal sinus thrombosis blocks reup-
labetalol or sodium nitroprusside, using an arterial line to assess
take of CSF and produces intracranial hypertension. Cortical vein
the response to therapy on a beat-to-beat basis. Preeclamptic
thrombosis produces focal cerebral ischemia and edema, and,
patients are observed for postpartum convulsions and managed
when extensive, bland or hemorrhagic infarction. For arterial
with magnesium sulfate and/or benzodiazepines.
occlusion, specific etiologies in parturients are similar to those
in other young adults (see Table 9.9).5
Spinal hematoma
Clinical presentation and diagnosis
Bleeding into the spinal area can occur spontaneously or, rarely, Cerebral venous thrombosis presents with a gradual onset of focal
following regional anesthesia.126,127,128,129,130 Patients who are deficits, while arterial emboli produce a more sudden onset of symp-
treated with anticoagulants may, rarely, develop a spontaneous toms. Cerebral venous thrombosis usually presents with a progressive
bleed.131 The incidence of neurologic dysfunction resulting from headache, nausea and vomiting, blurred or double vision, and altered
hemorrhagic complications associated with central neural block- sensorium secondary to increased ICP. Cerebral venous thrombosis
ade is estimated to be less than 1 in 150 000 epidural and less than 1 may be mistaken for eclampsia (or be associated with it) or aneurysm
in 220 000 spinal anesthetics.132 Risk factors include traumatic nee- rupture. Cortical vein occlusion produces focal or generalized sei-
dle/catheter placement, sustained anticoagulation with an indwel- zures and lateralizing signs that affect the proximal extremities.
ling neuraxial catheter, and catheter removal during therapeutic
levels of anticoagulation.133 Thrombocytopenia accompanying
Table 9.8 Precipitating factors for cerebral venous thrombosis
preeclampsia is also thought to be a risk factor.134,135 Considering
the vascularity of the epidural space, it is surprising that clinically Excessive blood loss during delivery
detectable hematomas are not seen more often following regional Infection
anesthesia. A spinal hematoma can develop rapidly or insidiously Hyperviscosity syndromes
and is usually related to arterial bleeding. The patient may com- Sickle cell disease
plain of severe burning back pain that progresses to motor dysfunc- Malignancy
tion (usually bilateral) and the loss of bowel and bladder function. It Polycythemia rubra vera
is important to follow the American Society of Regional Anesthesia Paroxysmal nocturnal hemoglobinuria
(ASRA) guidelines before and after regional anesthesia, if a parturi- Dehydration
ent takes anticoagulants.134 Procoagulation syndromes
Pain from an epidural hematoma must be differentiated from Antiphospholipid antibody syndrome
the pain and motor dysfunction associated with a prolapsed Deficiency of protein C and S
intervertebral disc and other neurological complications of preg- Arteriovenous malformation
nancy, such as meralgia paresthetica.136 Neurological examina- Endothelial injury
tion usually will differentiate these lesions based on their single Venous statsis
nerve or nerve root distribution.



176
Chapter 9


clopidogrel after the delivery.145 Surgery may be needed if there
Table 9.9 Etiology of arterial occlusion is hemorrhagic transformation of the infarct with mass effect and
increased ICP, or for ventriculoperitoneal shunting and place-
Type Association (risk factors)
ment of ICP monitors.
Arteriopathies Premature atherosclerosis (smoking,
* *

hypertension, diabetes,
Anesthetic management
hypercholesterolemia, homocystinuria,
During labor, hypertension and elevated ICP are avoided by
radiation to the neck, and a family history
careful induction of epidural analgesia/anesthesia and avoid-
of arteriosclerosis)
ance of pushing in the second stage with assisted vaginal deliv-
Arterial dissection (inflamed cerebral
*
ery. Systemic hypotension may reduce cerebral perfusion and
arteries)
blood flow to an already compromised, injured area. In patients
Hematological Sickle cell crises (ischemic injury to the
* *
receiving anticoagulants, precautions outlined in the ASRA
vessel wall)
guidelines should be followed.134 Reversal of therapeutic anti-
Systemic lupus erythematosus (SLE)
*
coagulation may be required if a regional anesthetic technique is
Thrombotic thrombocytopenic purpura
*
considered safe. For C/S, the risk of a dural puncture from an
(TTP)
epidural needle must be weighed against the risks of exacerbat-
Embolism Embolism from artificial valves, mitral
* *
ing hypertension with tracheal intubation in women with ele-
valve prolapse, atrial fibrillation, and
vated ICP. Avoid hyperventilation during GA as it may
subacute bacterial endocarditis
compromise cerebral and uterine blood flow. Postoperatively,
Others: air, fat, and amniotic fluid
*
the patient must be observed for recurrence or extension of
embolism, as well as paradoxical emboli
local thrombus or increased ICP.
from veins in the presence of a patent
foramen ovale
Idiopathic No cause found in 25%
* *
Spinal-cord ischemia
Miscellaneous Migraine related
* *

Anterior spinal artery syndrome has been reported rarely in par-
Drug induced (cocaine, heroin, and
*

turients suffering severe and/or prolonged hypotension and
amphetamines)
presents with painless paraplegia secondary to spinal-cord ische-
mia.146 Spinal-cord ischemia is rarely reversible. See Chapter 10.
Ischemic strokes must be differentiated from hemorrhagic or
structural lesions, which may be surgically treatable. Recurrence
Benign intracranial hypertension
of stroke is common so it is important to diagnose and treat any
underlying medical condition. The diagnosis is based on clinical Benign intracranial hypertension or ˜˜pseudotumor cerebri™™147 is
information, laboratory investigations (including coagulation defined as an increase in ICP without a demonstrable etiology
studies), CT, MRI, and angiography where indicated. Treatment and is a diagnosis of exclusion. Benign intracranial hypertension
of patients with CVT is supportive with administration of anti- is thought to occur in 1:1000 pregnancies, with a 30% recurrence
seizure medication. These patients usually recover rapidly and rate in subsequent pregnancies.148,149 It has been reported to be
spontaneously without neurological sequelae.140,141,142 more common in obese women of childbearing age, suggesting a
hormonal etiology,147 but some evidence suggests that it may not
Effect of pregnancy and obstetrical management be more common in pregnancy.93 It may occur after chronic use
The incidence of cerebral infarction is increased 13-fold during of specific medications such as tetracycline. Over production
pregnancy139 due to the hypercoagulable state of pregnancy and and/or under absorption of CSF are proposed mechanisms. The
hormonal changes.143 Obstetric considerations should determine disease is usually benign, but increased ICP can lead to optic
the mode of delivery. nerve atrophy and blindness.150

Treatment
Clinical presentation and diagnosis
Treatment is based on underlying etiology. During an acute
Headache, stiff neck, papilledema and visual disturbances occur
thrombotic episode the parturient might be treated with anti-
from increased ICP, but consciousness is not affected.
coagulants. Urokinase, intravenous tissue plasminogen activator
Cerebrospinal fluid pressure is elevated to above 200 mmH2O,
(TPA), and heparin (either low molecular weight [LMWH] or
CSF composition is normal, and imaging studies are normal.
unfractionated) have all been used successfully in parturi-
ents.111,144 Low molecular weight heparin is used increasingly as
Neurosurgical management
it has a predictable anticoagulant effect, less frequent dosing, and
requires minimal monitoring. These medications may be chan- Treatment consists of serial lumbar punctures to drain CSF.
ged, after an acute episode, to subcutaneous heparin and aspirin Brain-stem herniation usually does not occur, because the
to minimize recurrence and converted to warfarin, aspirin, or increase in ICP is uniformly distributed throughout the CNS.



177
3 Nervous system disorders


However, two cases of cerebellar tonsillar herniation have been
Table 9.10 Causes of hydrocephalus and increased
reported after diagnostic lumbar puncture in nonpregnant
intracranial pressure
patients with this syndrome.151 These patients presented with
severe headache, neck pain, and focal neurologic signs. If the Hydrocephalus Increased intracranial pressure
patient experiences progressive loss of vision then optic nerve
 Congential aqueductal  Traumatic brain injury

<< . .

 35
( 87)



. . >>

Copyright Design by: Sunlight webdesign