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and its consequences. Despite ongoing treatment, the five-year
assessed for each patient. Early consultation is desirable to define
mortality rate for high-risk patients can be as high as 30%. In one
the arterial involvement, review aortography, assess the cardio-
series, treatment failed to induce a remission in 25% patients with
vascular status, and control BP.96,97 Patients with mild disease
TA, and half of those who achieved remission later relapsed.88
have little hemodynamic compromise. Electrocardiogram, pulse
Patients with less severe forms of TA do significantly better, with
only one death in another series of 31 patients with mild TA.86 oximetry, and noninvasive BP monitoring is adequate for these
women. When TA affects peripheral arteries, however, noninva-
Morbidity is caused by severe uncontrolled hypertension with
sive BP measurements may be inaccurate or unobtainable. In
end-organ dysfunction (e.g. renal insufficiency) and stenosis of
such cases a peripheral arterial catheter should be inserted,83
major blood vessels affecting regional circulation. Death can
but occasionally a central arterial catheter introduced via the
result from congestive heart failure or CVA.
femoral artery may be required.98 The use of such catheters
carries a risk of arterial occlusion at the site of insertion.99,100,101
Takayasu arteritis and pregnancy
When TA is associated with heart failure, it is necessary to
monitor central venous, right heart, and pulmonary capillary
Pregnancy in patients with early TA is not associated with an
increased risk for obstetric complications.90 One case report wedge pressures. Calculation of CO, systemic, and pulmonary

Chapter 3

the use of spinal anesthesia for C/S in a patient with TA.108
vascular resistance helps to prevent heart failure and maintain
adequate cerebral and renal perfusion.102 For labor and delivery, Preoperative volume expansion with 15“20 ml/kg of a glucose-
epidural analgesia has the advantage of providing effective pain free crystalloid solution, and judicious use of ephedrine or other
relief while preventing acute catecholamine release associated pressors are especially important in maintaining BP and vital
organ perfusion during spinal anesthesia.99 Left uterine displace-
with labor pain. The anesthesiologist should carefully titrate the
dose of local anesthetic in order to produce a level satisfactory for ment is even more critical in these patients when regional
delivery without causing severe hypotension, which could lead to anesthesia is administered.
cerebral ischemia.103 Supplemental oxygen, and laboring in the Patients with TA frequently receive anticoagulants and corti-
lateral position, help ensure adequate oxygen delivery to the fetus. costeroid therapy. Coagulation abnormalities must be corrected
Any contemporary epidural technique would be suitable as before instituting regional anesthesia in order to avoid an epi-
long as dilute solutions of local anesthetic are used (e.g. dural hematoma. Adrenal suppression may be assumed and sup-
0.125% bupivacaine) in conjunction with supplemental epi- plemental perioperative steroids considered.
dural opioids (e.g. fentanyl). Vasoactive drugs should be readily In summary, Takayasu arteritis presents in women of child-
available to treat potential fluctuations in BP. bearing age with a variety of signs and symptoms depending on
For C/S, epidural anesthesia must be induced slowly and incre- the stage of the disease, its progression, and response to treat-
mentally using whatever combination of local anesthetic and ment. The impact of pregnancy on the disease is unclear, but
opioid you would normally use. It is questionable whether epi- worsening ischemic symptoms, cardiac failure, cerebral hemor-
dural epinephrine should be used in parturients with TA. One rhage, and uncontrolled hypertension can occur. Noninvasive
advantage of regional anesthesia for C/S is that the patient technologies, such as MRI, assist in the diagnosis of TA during
pregnancy, avoiding angiography until the postpartum period.109
remains awake. This gives the anesthesiologist a clinical assess-
ment of cerebral perfusion, which central or peripheral arterial In addition, interventional radiologists can help improve out-
pressures may not accurately reflect. Epidural and CSE anes- comes by performing percutaneous transluminal angioplasty
thetics have been described for C/S in women with TA.104,105 and wall stents, when indicated.110
Spinal anesthesia has been successfully used for termination of
pregnancy in a woman with TA, but the usual risks related to
Marfan syndrome
potential hypotension must be considered before using spinal
Incidence and clinical findings
General anesthesia can be given for C/S, although evaluation of
cerebral perfusion becomes more difficult or impossible, even Marfan syndrome (MFS) is a hereditary disorder of connective
with an electroencephalogram (EEG). Patients with severe carotid tissue affecting collagen and elastin. It is a disorder caused by
disease, however, should have EEG monitoring to help prevent mutations in the gene that encodes fibrillin-1 (FBN-1) located on
cerebral ischemia during general anesthesia. One case report chromosome 15. More than 500 mutations have been identified
and almost all are unique to an affected individual or family.111
described the use of general anesthesia with processed EEG mon-
itoring in a woman with TA and bilateral carotid artery steno- Marfan syndrome is transmitted in an autosomal dominant man-
sis.106 She refused regional anesthesia for C/S and the general ner without gender or racial preference. Marfan syndrome occurs
anesthetic was uneventful. in 4“6 of 100 000 births and, although there is often a family
history, 15% of cases are thought to arise as new mutations.112
Pretreatment with beta-adrenergic blockers (e.g. labetalol in
5 mg to 10 mg increments titrated to the desired response), nit- Genotype“phenotype correlations in MFS have been complicated
roglycerin (50 mg to 100 mg) or lidocaine (1“1.5 mg/kg) i.v. can by the large number of unique mutations reported, as well as by
attenuate the rise in systolic BP that accompanies endotracheal clinical heterogeneity among individuals with the same muta-
intubation. Rapid sequence induction with thiopental and succi- tion. Further studies are needed to investigate the role of modu-
nylcholine is performed and the airway secured. During endotra- lating genes and genotype“phenotype correlations. Long-term
cheal intubation, extreme extension of the patient™s neck must be follow-up studies may reveal the prognostic significance of aortic
avoided because stenosis of the carotid arteries predisposes to elasticity and may identify patients at risk of aortic complications.
occlusion and hence the risk of cerebral ischemia. Nitrous oxide When one parent has Marfan syndrome, the fetus has a 50% risk
of inheriting the mutant gene.113
must be avoided if pulmonary vasoconstriction and hypertension
are present. Nitrous oxide has been used without adverse reaction There are a number of clinical manifestations of MFS (see
in a parturient with TA, but pulmonary hypertension was ruled Table 3.4), but the most important is aortic root dilatation,
out before its administration.107 Oxytocin has been given to pro- which can lead to dissection and rupture. The defect in the vessel
vide uterine contraction safely following delivery, but prostaglan- wall is caused by cystic medial necrosis. The ascending aorta is
din F2a and ergot alkaloids should be used cautiously as they can the most frequent site of dissection because it sustains the great-
cause systemic and pulmonary hypertension. For a review of the est stress during systole. Aortic elasticity determined by measure-
anesthetic management issues in women with TA, the reader is ment of local distensibility and flow-wave velocity with MRI is
referred to a case series by Kathirvel et al.108 decreased in nonoperated patients with Marfan syndrome. Aortic
Spinal anesthesia in TA is controversial because of an increased distensibility of the thoracic descending aorta appears to be the
risk of hypotension. There is one published article that described strongest predictor for descending aortic complications. Over the

1 Cardiovascular and respiratory disorders

among individuals. Life-threatening complications of aortic dis-
Table 3.4 Clinical features of Marfan syndrome ease are more common after the aortic root dilates to > 60 mm.
The normal aortic root diameter is about 22 mm. One study
Eyes ectopia lentis
indicates that patients who have an aortic root diameter
> 30 mm should be considered for prophylactic aortic surgery.117
Skeletal arachnodactyly
The aortic root lies in the cardiac shadow on CXR, and thus
pectus deformity
aortic dilatation can be missed unless echocardiography, CT, or
MRI is performed.114 Patients should have an echocardiogram
high narrow palate
performed annually to look for changes in the aortic root
increased bone length
cervical spine abnormalities
Advances in surgical and medical therapy over the past two to
Pulmonary Propensity to develop:
three decades have decreased the mortality of affected indivi-
 pneumothorax (4.4%) a
duals. However, significant mortality still occurs, peaking in the
 bullous emphysema
third and fourth decades of life. Although surgery usually provides
 restrictive lung disease
successful treatment of aortic dissection, it is uncertain whether
Cardiovascular Cystic medial necrosis of aorta:
surgical repair confers a mortality advantage.118 Some authors
 aortic dilatation
suggest that patients with MFS and thoracic aortic disease should
 aortic dissection and rupture
have elective valve-sparing surgery rather than composite graft,
 mitral valve prolapse
primarily to avoid the complications of anticoagulation.118
 premature coronary artery disease
Emergency surgery and a history of aortic complications in first-
Ref. Hall, J. R., Pyeritz, R. E., Dudgeon, D. L. & Haller, J. A., Jr. degree relatives are associated with a higher mortality. Chronic
Pneumothorax in the Marfan syndrome: prevalence and therapy. beta-blocker therapy may slow the rate of aortic dilatation and
Ann. Thorac. Surg. 1984; 37: 500“504. may be associated with a more favorable prognosis.

Pregnancy and Marfan syndrome
past 30 years, improvement of diagnostic modalities and aggres-
sive medical and surgical therapy have resulted in considerable Effect of Marfan syndrome on pregnancy outcomes
improvement of life expectancy of patients with MFS.111 Selected
In a retrospective study of 63 of the 122 enrolled women with
manifestations of MFS reflect excessive signaling by the trans-
MFS,119 142 pregnancies were reported, including 111 that
forming growth factor-beta (TGF-beta) family of cytokines. Aortic
reached > 20 weeks™ gestation, 28 (20%) that miscarried, and
aneurysm in a mouse model of MFS is associated with increased
three elective abortions. An obstetric and/or neonatal complica-
TGF-beta signaling and can be prevented by TGF-beta antago-
tion occurred in 40% of all completed pregnancies. The most
nists such as TGF-beta-neutralizing antibody or the angiotensin
important complication was an increased number of premature
II type 1 receptor (AT1) blocker, losartan. AT1 antagonism also
deliveries (n ¼ 17, 15%) mostly due to preterm premature rupture
partially reversed noncardiovascular manifestations of MFS,
of membranes and cervical incompetence. This contributed to a
including impaired alveolar septation. These data suggest that
markedly increased combined fetal and neonatal mortality of 7%.
losartan, a drug already in clinical use for hypertension, merits
These findings were the same whether the diagnosis of MFS was
investigation as a therapeutic strategy for patients with MFS and
made prior to conception or after the woman was pregnant.119
has the potential to prevent the major life-threatening manifesta-
tion of this disorder.114
Mitral valve prolapse (most frequently of the posterior leaflet),
Effect of pregnancy on Marfan syndrome
and myxomatous degeneration of the mitral valve occur fre-
During pregnancy, a 30“40% increase in CO by the second trime-
quently in MFS. Mitral valve pathology is detectable by echocar-
diography in at least 68% of these patients.115 Mitral valve ster results from an equal increase in heart rate and stroke
volume.120,121 During labor this increase is more profound (100%
prolapse is suggested by the presence of a systolic click, best
greater than prepregnancy levels), and immediately following
heard just medial to the cardiac apex.
delivery the stroke volume may increase a further 40“50% above
Relatively unknown cardiovascular manifestations of Marfan
prepregnancy levels.122 The high serum estrogen concentration
syndrome include dilatation of the main pulmonary artery and
of pregnancy causes connective tissue changes at the subcellular
early onset coronary artery disease. In a series of 50 patients
level, which produce collagen ˜˜softening™™. The increased stress
with Marfan syndrome, MRI showed 74% had an enlarged
pulmonary artery root above the upper limit of normal.111 placed on the aortic root by increased CO, preexisting cystic
medial necrosis, and estrogen effects all contribute to an increased
Early onset of coronary artery disease may occur in patients
risk for aortic dissection during pregnancy. Half of all aortic dis-
with MFS, producing a high rate of dysrhythmias and conduc-
sections in women of childbearing age occur during pregnancy.122
tion disturbances.116
Women with known MFS who are pregnant or wish to become
For patients with MFS, aortic dilatation begins early in child-
pregnant should first be counseled that half of their children will
hood. Progressive dilatation occurs slowly but at varying rates

Chapter 3

be affected by the disease. If pregnancy is desired, the parturient and acute Type A aortic dissection are often managed by cesarean
delivery and concomitant aortic repair.129
should have a thorough cardiovascular assessment including an
echocardiogram. At least one study has indicated that women In summary, women with MFS are at significant risk of aortic
with MFS whose aortic roots are < 40 mm in diameter seldom dissection during pregnancy even if there is no cardiovascular
have serious cardiovascular complications during pregnancy, abnormality prepregnancy. Aortic root dilatation may be a pre-
and so tolerate pregnancy well.123 Another report has indicated dictor of risk, but dissection can occur without significant dilata-
that pregnancy may be safe with aortic root diameters < 45 mm.124 tion.130 In addition, serial echocardiograms may fail to predict
aortic dissection during pregnancy in women with MFS.131
Those patients whose aortic root diameters > 40 mm should be
counseled against becoming pregnant, irrespective of their New
York Heart Association (NYHA) functional class.124 All pregnant
Anesthetic management of women with
women with MFS are considered high risk, and require on-going
Marfan syndrome
evaluation, including echocardiograms every six weeks during
their pregnancies.125 If the parturient with MFS does not have signs or symptoms of
cardiac failure, and the aortic root diameter is < 40 mm, she does
not require special care for labor and delivery.132 However, anti-
Aortic dissection
biotic prophylaxis against bacterial endocarditis should be pro-
Along with hypertension (most common), connective tissue dis- vided because of the occult collagen changes present in this
orders, and Turner syndrome, MFS is a predisposing condition disorder. Vaginal delivery is permissible for the asymptomatic
for the development of aortic dissection (see Figures 3.7A and patient. Anesthetic management focuses on minimizing aortic
3.7B). Acute aortic dissection has a fatality rate of 36“72% within root shear forces and wall stress through invasive monitoring,
pharmacologic intervention, and pain treatment.120 Epidural
48 hours. Without intervention, 62“91% of patients will die within
one week.126 An aortic dissection is a tear in the intima secondary analgesia for labor should be initiated early in order to prevent
to blood dissecting along the intima (see Figure 3.2). Dissection pain-induced catecholamine release, elevated BP, and increased
causes an intimal flap, which can cause obstruction of the aorta or CO. An infusion of i.v. crystalloid solution can be titrated in 250 ml
its branches or serve as a nidus of thrombus generation. Spiral CT, aliquots slowly up to 750 ml, as required. Slow titration of the
MRI, and transesophageal echocardiography (TEE) are all equally epidural level to a T10 sensory level will help to prevent a sudden
accurate in the diagnosis of aortic dissection.127 The maximal risk fall in SVR and BP. Avoiding epinephrine-containing solutions
of aortic dissection is in the third trimester of pregnancy. More risks poorer quality anesthesia and is of uncertain value in these
than 50% of 40-year-old women in whom an arterial aneurysm patients. Significant hypotension should be treated with phenyl-
ruptures sustain the rupture during pregnancy.128 Stanford Type ephrine to avoid the beta-agonist effect of ephedrine. One
A dissection involves the aorta proximal to the origin of the left case report described labor epidural analgesia in a woman
with MFS.133 The authors used direct arterial BP monitoring and
subclavian artery, regardless of distal extent. Stanford Type B is a
dissection confined to the descending aorta. Most patients with a double-catheter epidural technique with continuous epidural
Type A dissection are treated surgically whereas those with Type infusion of a 0.125% bupivacaine and 0.0002% fentanyl solution.
B dissections are usually managed medically. Women with MFS The baby was delivered vaginally after almost eight hours using

Figure 3.7 (A&B) Aortic dissection in a patient with Marfan syndrome. From: Ioscovich, A. Images in anesthesia: transesophageal echocardiography during Cesarean
section in a Marfan syndrome patient with aortic dissection. Can. J. Anesth. 2005; 52: 737“8. (Used with permission of the author and the journal editor.) Figure 3.7A
shows the aortic dissection at the level of one section of the descending aorta. Figure 3.7B shows the aortic dissection at the level of the aortic arch. They were
both taken at the same time three days prior to the cesarean delivery.

1 Cardiovascular and respiratory disorders

an elective forceps delivery. There were no cardiovascular pain, headache, proximal leg pain, weakness and numbness
complications and the patient was discharged from hospital after above and below the knee, and genital/rectal pain. These symp-
six days.133 toms are moderate to severe, typically occur daily or several times
In low-risk women with MFS, C/S is indicated only for obstet- a week, and are commonly exacerbated by the upright posture but
not always relieved by recumbency.141 Two cases of failed subar-
ric reasons. Either regional or general anesthesia can be used for
C/S, although regional anesthesia is preferred. The same caveats achnoid block for cesarean delivery have been described in
women with MFS who had dural ectasia confirmed by CT.142
should be applied to epidural anesthesia for C/S as for labor and
vaginal delivery. For general anesthesia, the combined use of
beta-blockade and vasodilator therapy will prevent a sudden Moyamoya disease
rise in BP and CO during endotracheal intubation. Volatile agents
Moyamoya disease (MMD) is a condition of unknown etiology
for these parturients are useful because they decrease cardiac
characterized by progressive narrowing and occlusion of basal
contractility.116 Positive pressure ventilation must be used care-
cranial vessels with secondary neoangiogenesis.143 It commonly
fully to avoid inducing pneumothorax (see Table 3.4).
affects the terminal portions of the intracranial carotid arteries.
In women with MFS who are high risk on the basis of cardiac
Moyamoya disease is uncommon outside of East Asia; however,
symptoms, an aortic root size > 40 mm, significant aortic valve
in Japan the incidence of MMD is 5 per 100 000 population with a
disease, or the presence of aortic dissection, it is even more impor-
female to male ratio of 1.8:1.
tant to use invasive monitors and vasoactive infusions to minimize
abrupt swings in BP. Perioperative use of beta-blockers is import-
Clinical characteristics, diagnosis, and management
ant and the use of atenolol, metoprolol, and labetalol has been
described.134 A new selective beta1-adrenergic blocker, landiolol,
Moyamoya disease (see Table 3.5) usually presents in the first dec-
has been used to prevent further dilatation of the aortic root in a
ade of life with transient ischemic attacks and then peaks again in
woman with MFS undergoing cesarean delivery under spinal
anesthesia.135 Landiolol can be continuously infused at a rate of
Table 3.5 Moyamoya disease
0.04 mg/kg/min in order to maintain heart rate at 80“90 bpm (beats
per minute). Calcium channel blockers also are useful for control- Etiology unknown
ling BP in these patients.136 The use of beta-agonists, vagolytics, Most common in Japanese
and ergot derivatives should be avoided because they may cause a Female:male ratio ¼ 1.8:1
rapid rise in CO and increase the risk of dissection. Atropine should Two onset peaks
be used carefully to treat bradycardia-induced hypotension.  first decade (juvenile) “ often presents with TIA
Vasodilators, such as nitroglycerin and nitroprusside, when used  third and fourth decade (adult) “ often presents with cerebral
as a sole agent, cause an increase in left ventricular ejection velocity hemorrhage
by reducing SVR and afterload, which in turn leads to stress on Pathology
the aortic root. If hypertension occurs, therefore, it is best managed  occlusion and narrowing of internal carotid arteries and distal
by the concurrent use of labetalol and nitrate infusions.116 branches
Some reports describe the anesthetic management of  cerebral artery aneurysms
C/S in women with MFS complicated by aortic dissec-  secondary enlargement of perforator arteries around basal ganglia
tion.133,134,137,138,139 Concomitant surgical treatment of the dis- (puff of smoke appearance on angiography)
section usually follows immediately after delivery of the neonate. Clinical risks
General anesthesia is used in such cases, with central venous  cerebral infarction
lines, arterial cannulae, and TEE in place to provide adequate  cerebral hemorrhage
monitoring of cardiovascular function. Other reports describe the  seizures
use of epidural, spinal, and general anesthetics in women with MFS Treatment
undergoing C/S alone. These women either have aortic root dilata-  anticoagulants
tion, or have had prior aortic valve replacement, repair of a prior  platelet inhibitors
dissection, or an existing Type B dissection.134,135,136,137,138,139,140  cerebral vasodilators
The principles for successful anesthetic management involve  anticonvulsants
control of BP, avoidance of shear stress across the aortic root, and  surgical revascularization techniques
vigilance for at least 72 hours postpartum. Goals of anesthetic management
Other anesthetic considerations in women with MFS include  pain-free vaginal or cesarean delivery
potential airway management problems secondary to high arched  maintain normocarbia
palate and the potential for cervical spine instability. Despite the  avoid hypotension and severe hypertension
high incidence of bony and ligamentous abnormalities in patients  epidural anesthesia has been successfully used
with MFS, a routine cervical radiograph prior to general anesthe-  best to avoid spinal anesthesia in order to avoid large fluctuations
sia is not recommended.140 Another concern is the potential for in BP
dural ectasia in patients with MFS. Dural ectasia is the expansion
TIA ¼ transient ischemic attack
of the dural sac surrounding the spinal cord causing low back

Chapter 3

the third and fourth decades presenting with symptoms of cerebral trigger leads to massive activation of the immune system, result-
hemorrhage. It may be associated with intracranial aneurysms in ing in a prolonged self-directed immune response at the coronary
about 15% of cases.144 Symptoms may be precipitated by hypocar- arteries.149 The most important clinical features of this disease
bia due to hyperventilation, or by hyperthermia causing an increase are coronary arteritis with aneurysms and thrombotic occlusions.
in the cerebral metabolic rate for oxygen (CMRO2). As with other These may lead to ischemic heart disease and sudden death.
vascular anomalies, the increase in CO that occurs during preg- There are reports of adult survivors of KD some of whom become
nancy and parturition may precipitate intracranial hemorrhage. pregnant. A large survey in Japan identified 46 deliveries in
30 patients with KD.150 One report described a woman with KD
Confirmatory diagnosis is based on the angiographic findings,
which characteristically show narrowing of the carotid arteries who had a successful pregnancy and normal vaginal delivery nine
and/or their distal branches, particularly at the origin of the years after a coronary artery bypass graft for a giant coronary artery
aneurysm.151 The large Japanese survey reported mostly vaginal
anterior and middle cerebral arteries. Compensatory enlarge-
ment of the perforator arteries around the basal ganglia accom- deliveries and the use of epidural analgesia for assisted vaginal
births.150 Mode of delivery was determined primarily on obstetric
panies the changes in the carotid vessels. In Japanese,
˜˜moyamoya™™ means ˜˜something hazy™™ (like a puff of smoke), considerations. Importantly, many women with KD will present
in labor on anticoagulants152 and aspirin therapy. This will need to
and this is the characteristic appearance of the vasculature
around the basal ganglia seen on angiography. Periventricular be taken into consideration when planning neuraxial techniques.
pseudoaneurysms and saccular aneurysms of the circle of Willis The principles for anesthetic management of women with KD
can also be seen angiographically in some patients. will depend on physical status, the nature and location of the
coronary lesion, previous surgery, and current medications.153,154
Typically these patients receive anticoagulants, aspirin for pla-
telet inactivation, and verapamil for cerebral vasodilatation to (See Chapter 1 for details of the management of coronary artery
help prevent cerebral ischemia. Patients with seizure disorders disease in pregnancy.) These patients are at risk for developing
are maintained on anticonvulsant therapy.143 myocardial infarction, ventricular failure, and ventricular dys-
Revascularization surgery is an established treatment of rhythmias, so a defibrillator should be readily available. The
ischemic attacks and includes superficial temporal artery to mid- practical management of a parturient with heart disease has
been reviewed recently by Dob and Yentis.155 Low-dose epidural
dle cerebral artery (extracranial/intracranial) bypass and ence-
phaloduroarteriosynangiosis. However, it is uncertain whether infusions for labor analgesia will be suitable for most women with
these procedures reduce further hemorrhagic events.143 a history of KD assuming that they are not anticoagulated. This
will reduce the stress on the mother and her heart.

Anesthetic management in women with
Klippel-Trenaunay-Weber syndrome
Moyamoya disease
The goal of anesthetic management is to provide a pain-free Klippel-Trenaunay-Weber syndrome (KTWS) is a rare congenital
vaginal delivery or C/S while maintaining cerebral blood flow soft-tissue anomaly characterized by multiple hemangiomas,
varicose veins, AV fistulas, and unilateral limb hypertrophy.156
(see Table 3.5). Hypotension and hyperventilation are avoided as
both can decrease cerebral perfusion. Hypertension associated Klipped-Trenaunay-Weber syndrome is thought to occur sporadi-
with endotracheal intubation should be anticipated and managed cally, but there is evidence of an autosomal dominant inheritance
with familial occurrence.157,158 Vascular morphogenesis is a vital
with i.v. lidocaine and antihypertensive drugs, such as labetalol.
This will minimize the risk of cerebral hemorrhage, particularly in process for embryonic development, normal physiologic processes
those who have intracranial aneurysms. Ideally, operative vaginal (e.g. wound healing), and pathologic processes (e.g. atherosclero-
or abdominal delivery should be performed in order to prevent the sis and cancer). Genetic studies of vascular anomalies have identi-
fied critical genes involved in vascular morphogenesis.159 A
hemodynamic consequences of maternal effort.
Regional anesthesia is preferred for labor and C/S as it allows susceptible gene, VG5Q, has been cloned for KTWS, which encodes
easier neurological assessment of the patient. Epidural and CSE a potent angiogenic factor. Increased angiogenesis is one possible
anesthesia have been described in women with MMD.145,146 molecular mechanism for the pathogenesis of KTWS. There are
many other vascular anomaly genes.159
Spinal anesthesia is best avoided in order to avoid large fluctuations
in BP.143 One case report described the use of transcranial Doppler The vascular abnormalities seen in this condition include

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