|
Irreversible
disability is traditionally associated with cerebral vascular
disease (CVA) and it is under-estimated that there are 2 million
fatalities from vascular disease every year. Although medical
measures help in acute ischemia, they are only palliative in an
established stroke and in prevention of a repeat stroke.
Cerebral
revascularization is the goal. Of late, there is an increasing
acceptance of surgical revascularization even in acute episodes.
Etiology:
Arterial
thrombosis and atherosclerosis with occlusion of the
cerebral arteries is the single most common cause of stroke in more
than 50 percent of patients.
Thirty
to 50 percent of the cases have had previous transient ischemic
attacks.
Other
rarer
causes include trauma to the carotid/vertebral arteries,
collagen diseases, moyamoya disease, fibromuscular dysplasia,
vasospastic conditions (SAH, migraine etc), and the conditions which
alter the rheological properties if the blood such as,
polycythemia, leukemia etc.
There
are risk factors, such as, hypertension, hypercholesterolemia,
atherselerosis, cardiac abnormalities, diabetes mellitus, obesity,
and lack of physical activity..
Clinical
features:
The
earliest sign of the CVA is the transient ischemic attack (TIA).
The other findings may be a history of diplopia, atherosclerosis of
the retinal arteries, speech difficulties, motor or sensory changes,
abnormalities of cerebellar function etc.
Transient
ischemic attacks (TIAs) are
usually described as related to the carotid or vertebral-basilar
arterial systems. It is defined as an
acute cerebral dysfunction resulting from vascular problem, which
recovers within 24 hours.
Carotid
territory:
The
classic history for transient ischemic attack in the carotid system
is one of swift onset of contralateral weakness or numbness of the
arm or leg. Dysphasia occurs if the dominant hemisphere is involved.
Impaired vision of the eye on the side of the diminished carotid
flow takes place. This clinical phenomenon usually indicates a
decrease in regional cerebral perfusion, and produces a neurological
deficit, the onset of which is usually sudden with gradual
progression of the symptomatology.
Carotid
artery occlusion is caused by atherosclerosis, arteriosclerosis and
atheroma, and is compounded by the extension of cholesterol and
calcium deposits into the branches of the common carotid artery,
specifically the internal carotid artery.
There are five
items, which would bring one to suspect involvement of the carotid
arteries:
1. Blindness in one
eye during the TIA attack.
2. Emboli in the
retinal vessels.
3. Bruit over the
carotid artery.
4. Significant
lowering of the retinal arterial pressure on the affected side.
5. Any sign of
retinal artery ischemia.
Vertebral-basilar
territory:
Damage to this
system is also characterized by a very swift onset of symptoms with
neurological phenomenon such as ataxia, monoparesis, hemiparesis,
quadriplegia, numbness (frequently shifting from one side to the
other), vertigo, defects in either visual field, diplopia,
dysarthria, aphasia and occasionally, clouding of consciousness.
Vertigo is perhaps the most common symptom of TIA in this
distribution.
Prolonged
reversible ischemic defect (PRIND) is one where the signs
and symptoms lasts for a week followed by recovery.
Progressing
stroke (PS) is one where the deficit continues to progress
in a stepwise fashion despite adequate medical
therapy.
Stroke is
a sudden, unheralded progressive neurological deficit due to a
vascular pathology; the deficit becomes complete in few hours. It is
usually associated with altered sensorium and hypertension.
Associated carotidynia
(pain over the carotids) suggest a carotid pathology.
Investigations:
TIAs should be
regarded as an emergency. The risk of stroke is greatest in the
weeks following TIA and patients should be referred for further
investigations at the earliest. The initial evaluation of a
patient in whom a transient ischemic attack is suspected should
include laboratory tests, electrocardiography, and imaging studies.
Since imaging of the head may reveal a nonischemic cause, such as a
tumor or subdural hematoma, and may provide information about the
cause of ischemia, it is recommended that CT or MRI of the head be
part of the evaluation of all patients. Doppler ultrasonography or
other noninvasive investigations of the carotids should be performed
rapidly, ideally within 24 hours.
| CT
will demarcate the area of ischemia and exclude
hemorrhage and also the previous infarcts. Small
lacunar infarcts suggest an arteriolar pathology (of the
penetrating branches of major cerebral arteries). Wedge
shaped infarcts suggest thromboembolism. Ill defined border
zone infarcts suggest hemodynamic ischemia. Good recognition
of a perimesencephalic pattern of hemorrhage is
possible on unenhanced CT,
and CT
angiography
accurately excludes and detects
aneurysms and AVMs. DSA can be withheld in
patients with a perimesencephalic pattern of hemorrhage and
negative CT
angiography.
CT angiography of cervical vessels reveals
enough vascular detail to be useful as a
diagnostic screening method in patients with presumed atherosclerosis
of the carotid bifurcation. |
|

|

|
|
CT
angio-ICA occlusion
|
MRA-
Basilar occlusion
|
|
MRI
is more sensitive, in particular for previous hemorrhage. MRAngiography,
a noninvasive test, permits the visualization of blood flow in
vessels without the need for catheters or contrast agents. The
technology can yield information regarding collateral blood flow and
is nearly as effective as conventional angiography in estimating
disease at the carotid bifurcation. It is suitable for replacing the
invasive conventional angiography
method in most cases. Further technical developments with
regard to spatial resolution are still required for improved visualization
of small vessels and terminal branches of intracranial vessels.
Ultrasonography,
being cost effective, should be used as a screening tool to exclude
patients with no carotid artery disease from further testing.
B-mode
imaging
provides images of various levels, or planes, enabling the creation
of a three-dimensional image of the carotid artery wall and surround
structures. This technique provides information on the type
and extent of arterial damage, but blood clots sometimes do not
appear and the method cannot distinguish a severely narrowed from a
completely occluded artery.
|
Doppler
testing measures the speed of blood flow through an artery. Two
types of Doppler ultrasound are used to obtain information
on the velocity of blood flow in the carotids. In pulsed
Doppler, the probe is placed over one spot on the neck over
the carotid, and timed measurements are taken to determine
the speed of blood flow in the artery. In continuous wave
Doppler, a probe is moved along the neck over the course of
the carotid, and the velocity of blood passing along the
vessel beneath the probe is averaged out.Duplex
ultrasound (DUS) combines B-mode imaging and pulsed
Doppler ultrasound to provide more detail on the condition
of arteries than either test alone can provide. When
performed in settings in which the results have been
consistently well validated by comparison with angiography,
it is an accepted and accurate technique, but there is risk
of calling a high-grade stenosis total occlusion (1% to 14%
false-positive rate).
|

|
However,
its reliability is highly dependent on the technician. The recent
availability of ultrasound contrast agents helps to distinguish
between pseudo- and true occlusions, improves ultrasound images and
should help to reduce operator variability. Color and spectral
Doppler ultrasound are now recognized as the best screening tests
for carotid artery stenosis. The evidence for its use as the sole
diagnostic imaging modality prior to carotid endarterectomy is
examined. Supplementary imaging is especially advisable
when results of DUS are technically limited.
Transcranial
Doppler (TCD)
assesses intracranial arterial flow in the distal ICA, the middle,
anterior, and posterior cerebral artery stems, and ophthalmic
artery. Hemodynamic significance extracranial and intracranial ICA
occlusion and the availability of collateral circulation may be
studied satisfactorily.Transorbital (ophthalmic artery),
submandibular (distal ICA), transtemporal (Anterior cerebral. Middle
cerebral and posterior cerebral), and foramen magnum (posterior
circulation) approaches are employed for a comprehensive assessment.
Serial TCD examination may reveal dynamic changes in cerebral
circulation that may be missed on a single MRA study. Preoperative
TCD can be used to identify patients who do not require a shunt
during carotid endarterectomy. In acute ischemic stroke, TCD can be
used to elucidate stroke mechanisms, plan and monitor treatment, and
determine prognosis. In an era when stroke is increasingly being
recognized as an emergency requiring immediate treatment, TCD may be
capable of providing rapid information about the hemodynamic status
of the cerebral circulation, within the time frame of the rather
small 'therapeutic window'.
Ophthalmodynametry
and oculoplethysmography
offer
an indirect indication of ipsilateral carotid occlusion. Ischemia of
the macular region is necessary to produce transient monocular
blindness and local retinal blood flow has been reduced to the flow
threshold of electrical failure in patient. Ophthalmic artery
flow reversal is not only quite specific for severe ICA disease, and
also provides additional hemodynamic insights (i.e., the inadequacy
of other collateral channels such as the anterior communicating
artery.
| Conventional
four vessel arteriography should include cerebral,
carotid and arch studies and with cross carotid compression.
One may also find post-stenotic lesions of the bifurcation,
patency of the anterior cerebral vessel, absence of the
vertebral artery, occlusion of the vertebral artery and
partial occlusion of the internal carotid vessels. Internal
carotid patency along with cross filling of the anterior,
middle cerebral and the posterior communicating vessels may
be evaluated. However, conventional arteriography fails
to demonstrate some vascular mural changes that may
intervene in the development of clinical
manifestations, such as intraplaque hemorrhage and
thrombus attached to the arterial wall. These mural changes
may be identified with duplex ultrasound and CT arteriography.
With increasing experience with noninvasive imaging,
angiography may be required less often. Clinicians should be
cautious when using contrast enhanced MRA alone for surgical
decision making in CEA candidates because a significant
number of patients may be misclassified. The rate of
misclassification is reduced when the results of contrast
enhanced MRA and duplex Doppler ultrasound are concordant.
Further study is needed to evaluate the benefits and risks
of endarterectomy without angiography. |
|

|
|
4
vessel angiography-ICA occlusion
|
|
Doppler CO2
/ Acetazolamide (diamox) test:
CBF measured early after acetazolamide administration could
be useful to confirm the clinical diagnosis of TIA. No
increase in CBF during hypercapnia or following acetazolamide
suggests that the cerebral arterioles are maximally dilated and the
procedures to improve the blood flow, such as EC-IC bypass will not
help.
|
Single-photon
emission computed tomography (SPECT)
studies combine nuclear medicine with computed tomography. Used
in early hours after infarction, cerebral SPECT is able to
reveal a deficit in local blood flow before changes appear
on CT or MRI. However, SPECT does not reliably
distinguish between hemorrhage and infarction, and it is
unclear whether the method will predict the potential for
clinical recovery. In patients who are marginal
candidates for endarterectomy, the hemodynamic
effect of stenosis on cerebral perfusion may be
assessed with SPECT, and is useful in predicting
neurological outcome in ischemic stroke patients.
Positron
emission tomography (PET)
can be used to measure cerebral blood flow (CBF), cerebral
blood volume (CBV), and metabolism (CMR). Patients with low
CBF and high oxygen extraction (OEF) have compromised
cerebral circulation and are expected to benefit from
revascularization. These studies are helpful in an
established stroke, and to differentiate between flow
related TIAs, and thromboembolic TIAs. None of these
applications is sufficiently widely used in the
clinical practice of neurology to provide a
recommendation.
|
|

|
|
SPECT-Rt.parietal
ischemia
|
|
Surgical
revascularization:
a) Carotid
territory:
The overall risk of
a stroke, following a TIA, is about 12% during the first year,
rising to 30% within 5 years.
The risk is higher,
about 30%, with internal carotid stenosis, whereas those with
complete carotid stenosis are unlikely to develop a stoke in the
same territory.
The stenosis will
progress in more than 50% of cases over the subsequent 1-5 years.
The role of carotid
endarterectomy is now well established.
Various other
procedures are being tried with no satisfactory evidence based
benefit.
1) Carotid
endarterectomy:
Indications:
The
ideal patient for carotid endarterectomy is one who presents with a
history of transient ischemic attack, hemispheric or retinal and
has no neurological deficit on physical examination and who
has a stenotic lesion at the orifice of the internal carotid artery.
TIAs
of embolic origin do well with endarterectomy, whereas, the flow
related ones do not do as well.
Patients
with stroke within previous 6 months with 70%-99% stenosis of
ipsilateral ICA.
Patients
with lesser stenosis but an ulcerative plaque.
Traumatic
occlusion of the carotid and spontaneous dissection of the carotid
may be considered for endarterectomy.
Acute
stroke, when the procedure can be performed within 2-3 hours of the
onset (with no evidence of infarct on CT), is a controversial
indication, becoming less and less controversial of late.
Progressive
stroke despite effective medical measures, and occlusion of an
asymptomatic carotid, while investigating the symptomatic carotid or
vertebro basilar territory are other controversial
indications.
Surgical
technique:
Preoperative
counseling is important as preparation of the patient mentally helps
a great deal in overcoming the fear and anxiety. If the patient is
on antiplatelets already, ASA may be continued through the
procedure. But Clopidogrel is stopped two days pre operatively in
our practice.
In
the operative room patient is sedated with 1mg Medzolam
intravenously after securing venous access and arterial pressure
monitoring catheter. Arterial pressure is monitored continuously as
fluctuation during the procedure can affect the cerebral
circulation.
Positioning
of the patient is extremely important as hyperextension of the neck
may kink the vetebrals which will be the likely source of blood
supply during cross clamping of ICA.
Intraop
monitoring: 1)
EEG:
Electroencephalography is a sensitive detector of cerebral ischemia
and a valuable tool for determination of need for shunting during
carotid endarterectomy. A statistically significant increase in
intraoperative stroke rate is associated with the development of an
abnormal EEG (1.1%), contralateral internal carotid artery occlusion
(1.8%), and the combination of both abnormal EEG and contralateral
internal carotid occlusion (3.3%).
2)
SSEP:
If available, use of SSEP is the ideal monitoring under general
anesthesia. Registration of SEPs is simple to perform and indicates
with a high sensitivity and specificity critical cerebral
hypoperfusion during cross-clamping. Progressive reduction of up to
50% of N20, P25 amplitude is suggestive of ischemia. SSEPs not only
help to identify patients with insufficient collateral blood flow
who benefit from specific cerebral protection, such as shunt, but
also to avoid improper and hazardous application of these measures
in patients with sufficient cerebral perfusion. In addition, correct
shunt function is immediately indicated by recovering potentials.
3)
Stump pressure measurement:
Measurement of ICA stump backpressure helps in deciding on the need
for a shunt. Reports suggest that surgery without a shunt when
the ICA back pressure is low(less than 50 mm/hg), produce
significant deficit.
4)
Transcranial Doppler (TCD):
The perioperative stroke rate can be reduced by appropriate
measures, taken by the surgeons, based on findings of TCD
monitoring.TCD will help detect high blood flow velocities.The
clinical significance of bilateral flow velocity increases soon
after surgery is uncertain, but very high blood flow velocities
might be a signal for cerebrovascular hyperperfusion. In those
patients, increased postoperative surveillance is recommended.
None
of the haemodynamic criteria by stump pressure and TCD are
absolutely reliable in predicting the need for carotid shunt.
The usefulness of monitoring cerebral function during the procedure
is closely related to the experience of the surgical team. No one
method of monitoring in selective shunting has been shown to produce
better outcomes. No prospective randomised or quasi-randomised
trials have been performed and the conclusions therefore remain
unchanged. Recommendations whether to practise cerebral monitoring
or not, and what method should be used for this purpose, cannot be
given presently.
Procedure:
We
prefer regional anesthesia. It obliviates the need for extensive
introperative monitoring for cerebral ischemia. Careful assessment
of cerebral perfusion can be made by direct interaction with the
patient. This is by far the best mode of assessment of cerebral
perfusion when compared to other modalities like TCD and SSEP.
Regional anesthesia is obtained by both superficial and deep
cervical block. Deep cervical block involves infiltration of local
anesthetic agents around C2, 3, and 4 at the exit foramina.
Superficial block involves infiltration around the cervical plexus
at the lateral border of the sternocleidomastoid muscle at the level
of external jugular vein. We use approximately 40cc of 0.375%
Bupivacaine for this as the anesthetic effect lasts as long as
6-8hrs.
Just
before making the incision patient is given Fentanyl 25mg
intavenously for additional sedation. Incision is made parallel to
anterior border of sternomastoid from the level of thyroid in
cartilage to just below mastoid process.
|
A
long high incision is made along the anterior border of the
sternomastoid muscle, almost to the mastoid tip. It often
necessitates the division of a branch of the great auricular
nerve as it crosses the anterior margin of the sternomastoid
muscle, resulting in usually temporary ear and/or lower jaw
skin numbness.
The
plane beneath the investing fascia of the neck is followed
under the sternomastoid muscle, and after the sternomastoid
muscle is mobilized, blunt self-retaining retractors are
used to expose the underlying areolar tissue, beneath which
lies the internal jugular vein and carotid sheath.
Sharp
dissection is continued, first skeletonizing the internal
jugular vein and the common facial vein. The common facial
vein and any nearby vein emptying directly into the internal
jugular vein are divided so that the jugular vein can be
retracted posteriorly, exposing the carotid arteries
beneath.
The
carotid sheath is opened to expose the common carotid artery
above the upper margin of the overlying omohyoid muscle, and
dissection proceeds distally to the bifurcation and to the
external and internal carotid arteries.
It is
necessary at all times but particularly at this stage to
handle the tissues gently and disturb the arteries from
their bed as little as possible, especially when
manipulating the internal carotid artery near the plaque. It
is not wise to palpate plaque within the internal carotid
artery, which is usually located at the site where the
artery is most adherent to adjacent tissue, because of the
risk of dislodging an intraluminal thrombus into the
cerebral circulation. Sinus nerve at the bifurcation of
the carotids is blocked with 1% lignocaine during carotid
dissection.
During
distal exposure of the internal carotid artery, care is
taken not to injure or excessively manipulate hypoglossal,
vagus, and accessory nerves, although the latter is high and
posterior in the carotid sheath and infrequently exposed.
The hypoglossal nerve, which is routinely exposed, descends
deep to and beneath the digastric muscle and curves forward
superficially to the external carotid artery; it often can
readily be traced to this location by following a branch,
the descendens hypoglossi, proximally from its course within
the carotid sheath.
Vessel
loops are then passed around the common, external, and
internal carotid and superior thyroidal arteries, and
heparin (75 I.U/kg) is administered. Mean arterial pressure
has to be maintained around 100mmHg before carotids are
clamped. After three minutes, carotids will be cross clamped
sequentially. Care should be taken to palpate the artery at
the precise point where one intends to put the clamp and one
should be certain that it is below a hard, calcified plaque,
which could easily fracture. Internal carotid first
followed by common carotid and external carotid. Superior
thyroid artery which arises from external carotid close to
bifurcation has to be occluded separately.
At
this stage careful neuro monitoring is done by anesthetist
by assessing the level of consciousness and motor activity.
Any deterioration in the assessment at any stage will be an
indication for shunt insertion to protect the cerebral
circulation.
An
arteriotomy is extended proximally from the common carotid
artery, with care being taken to keep it in the middle of
the lateral exposure of the internal carotid artery and away
from the apex of the carotid bifurcation. Internal carotid
clamp is opened to asses the back bleeding which is another
indicator of cross circulation.
The
atheroma is separated, particularly at the distal end of the
internal carotid endarterectomy, followed by complete
removal of all small, loosely adherent circumferential
plaque remnants from the endarterectomy site. Constant
heparinized saline irrigation is recommended.
The
greatest of care should be taken with the upper end of the
endarterectomy, and if the plaque has not come out smoothly,
the surgeon should be prepared and able to open the internal
carotid artery another 5 mm in order to improve the distal
repair. Any significant distal intimal step-off or shelf not
firmly adherent to the arterial wall should be tacked down
with 7-0 monofilament sutures. A partial or circumferential
plaque should never be pulled down and away from above the
level of the arteriotomy within the internal carotid,
because a loose distal intimal attachment, vulnerable to
subintimal dissection and carotid occlusion, can neither be
fully appreciated or properly repaired in this location. The
atheroma extending up the external carotid artery is
mobilized circumferentially, and the plaque is everted from
the arterial lumen. Microsurgical method increases the
precision and safety of every aspect of carotid
endarterectomy, including complete plaque removal,
prevention of intimal flaps, nonstenosing arteriotomy
closure.
After
irrigation of the area the arteriotomy is closed with 6.0
prolene. Before the final arteriotomy suture, the internal
carotid artery temporary clip and the common carotid artery
clamp are removed momentarily in turn, allowing air to be
expelled from the nearly repaired arteriotomy. If the
internal carotid artery is small which is the case in small
built females a Gortex patch can be used as angioplasty.
Patients
with complicated recurrent atherosclerosis can be treated
with endarterectomy and patch grafting, but interposition
vein grafts should be considered in cases in which the
vessels are extensively damaged by the
|
|

|
|
Skin
incision
|
|

|
|
Exposure
of carotids
|
|

|
|
Arteriotomy
|
|

|
|
Removal
of atheromatous plaque
|
|

|
|
Endarterectomy
completed-javed shunt being inserted
|
|

|
|
Arteriotomy
closure with a patch
|
|

|
|
Completed
closure with a patch
|
|

|
|
Atheroma
|
|
recurrent
plaque or with an unexplained thrombus at the site of previous
endarterectomy. Clamps are sequentially released after arteriotomy
closure. External carotid circulation is established first as any
small debris from the operative site may be released into extra
cerebral circulation. Internal carotid clamp is released at the end.
If the haemostasis is satisfactory reversal of the heparin may not
be required.
The wound is
closed after placing a suction drain as the wound is likely to ooze
due to preoperative antiplatelet therapy.
Post
operatively, close neurological observation is necessary by a
dedicated nurse. Post operatively patient can be started on oral
fluids after two hours and all the medication as before including
anti platelets. There is no indication for routine anticoagulant
therapy.
Use
of Shunt:
The only method currently accepted by all surgeons to achieve
cerebral protection, is the use of shunt during carotid
endarterectomy. The relative risk of shunting versus not shunting
during carotid endarterectomy was analyzed by Sundt TM jr et al
retrospectively in 1935 cases undergoing carotid endarterectomy for
carotid ulcerative stenosis. The need for shunting was based on a
correlation between electroencephalographic changes and a fall in
cerebral blood flow below the critical level required for adequate
perfusion during the period of carotid occlusion. Patients were
divided into four risk categories for surgery, based on medical and
neurological risks and angiographic findings. Shunts were required
in 30% of the low risk group and 56% of the high risk group. Based
on the severity of reductions of cerebral blood flow during the
period of carotid occlusion it is concluded that 12% of all patients
would have sustained a major deficit, 15% a minor or transient
deficit, and 20% a transient deficit without shunting. The risk of
shunting 792 cases in this series was 0.5%. Overall minor morbidity,
major morbidity, and mortality each approximated 1% in this series.
It has been
suggested that external shunts, placed between the common carotid
artery and the internal carotid artery (ICA), is safe and
efficacious in cases that do not permit the placement of an internal
shunt.
A new type of temporary extraluminal shunt, connecting the femoral
to the internal carotid artery with the interposition of a roller
pumps to regulate the blood flow has been reported. This method
allows one to perform carotid endarterectomy without interrupting
the blood flow to the brain.
Complications:
The
operative mortality and morbidity is 1-5% in various studies.
The
majority of strokes after carotid endarterectomy are
thromboembolic and many can be traced to technical failures, such as
the creation of an intimal flap, incomplete plaque removal, or the
creation of kinking or stenosis during arterial closure. Severe and
damaging cross-clamp ischemia in patients with poor collateral flow
to the ipsilateral hemisphere underlies fewer postoperative strokes
but may be detectable with intraoperative cerebral monitoring.
Intraoperative
shunts may reduce the risk of stroke in this subgroup of
patients; some surgeons use intraoperative shunts in all patients.
Microsurgical
method increases the precision and safety of every aspect of carotid
endarterectomy, including complete plaque removal, prevention of
intimal flaps, nonstenosing arteriotomy closure, and intraoperative
shunt insertion when necessary.
Restenosis
occurs in about 20%; use of dacron or vein patch during
arteriotomy closure when ICA internal diameter is <5mm is
recommended.
To
improve the prospects for postoperative carotid artery patency, use
of antiplatelet therapy both preoperatively and postoperatively is
advised.
|
Results:
The first
report from the North American Symptomatic Carotid
Endarterectomy Trial (NASCET), which concluded that
carotid endarterectomy is highly beneficial to patients with
recent hemispheric and retinal transient ischemic attacks or
nondisabling strokes and ipsi-lateral high-grade stenosis
(70-99%) of the internal carotid artery, reported a
cumulative 9% risk of any ipsilateral stroke over 2 years in
the surgical group of 328 patients. In the perioperative
period, 18 surgical patients (5.5%) had cerebrovascular
events: 12 minor (3.7%), 5 major (1.5%), and 1 fatal (0.3%).
|
 |
 |
|
pre-op |
post-op |
|
|
angio
- ICA stenosis |
|
|
In that study, three
of the major strokes were due to carotid occlusion in the early
hours after endarterectomy, and 10 of the minor strokes were also
delayed in onset and were presumably embolic.
MRC European Carotid
Surgery Trial (ECST) suggests the patients with a
stenosis <30% need not be operated; benefit of surgery in those
with 30-69% stenosis is not conclusive.
2)
Extracranial to intracranial (EC-IC) bypass:
Superficial
temporal to middle cerebral artery bypass (STA-MCA): Small
vessel disease (about 20% of all ischemic patients), middle cerebral
artery occlusion where endovascular thrombectomy has failed or is
not feasible, and total ICA occlusion may benefit from a EC-IC
bypass procedure.
This procedure
was popular in the 70s. It involves anastomosis of the superficial
temporal artery to one of the cortical branches of the middle
cerebral artery.
The skin in
incised over the proximal STA, just above the zygoma. The STA has at
least two major branches (frontal and parietal) and they should both
be followed distally. The STA is dissected with a small cuff of
tissue to prevent vessel injury. The larger branch is freed.
A small
craniotomy centered over the sylvian fissure is made and a recipient
artery is selected and dissected from the archnoid to follow
anastomosis.
The STA is
ligated and divided and the proximal STA is occluded with a
temporary clip.
The recipient
art is transiently occluded between two temporary clips and an end
to side anastomosis is performed with 10-0 monofilament suture.
Cerebro-protective techniques, including hypothermia and
barbiturates help.
This provides
initial flows of 25-50ml / minute; with time the bypass may mature,
allowing enlargement of STA and delivery of a higher flow. Occipital
artery to the intracranial circulation has also been tried.
Interposition
vein graft is
recommended by some, especially when STA is not satisfactory.
Complications
include aneurysmal dilatation and rupture of the graft and emboli
from the graft site.
Anecdotal
reports and uncontrolled patient series suggested that STA-MCA
bypass may be beneficial. However the National institutes of health
(NIH) study in 1985 concluded that these procedures do not help in
preventing a stroke, despite an overall graft patency rate of 96%
and low surgical morbidity. They may have a place when everything
else fails in the highly selected patients where the metabolic
reserve studies suggest a compromised CBF. In the treatment of
inoperable ICA giant aneurysms where the risk of ischemic
complications due to ICA ligation is high, EC-IC bypass may be used
as a prelude to ICA ligation. Chronic biochemical
abnormalities due to brain ischemia may improve after cerebral
revascularization.
Vertebro-basilar
territory:
The cerebellar
infarctions carry poor prognosis with an acute mortality rate of
20-30%. They are mostly due to poor flow (due to stenosis and poor
collaterals) due to diffuse atherosclerosis of the vessels. Medical
therapy is the first line of therapy. Several procedures have been
tried in those with persisting symptoms.
There
has been no randomized study.
The simplest
procedure, perhaps, is carotid endarterectomy if a significant
stenosis is found while investigating a vertebrobasilar TIA; the
stenosed carotid may be asymptomatic. It is most readily accepted if
the angiogram shows filling of the posterior cerebral artery via the
stenotic ICA, or filling of the posterior circulation from the ICA
because of vertebral occlusion or a persistent hypoglossal or
trigeminal artery.
Good
outcome with vertebral endarterectomy, which is similar to carotid
endarterectomy, has been reported. Posterior circulation bypass (
occipital artery to PICA for occlusion proximal to the PICA and a
superior cerebellar artery or P1 segment of the posterior cerebral
artery anastomosis for lesions at the mid or distal basilar) have
been described.
Extra
cranially, the left subclavian artery, next to the carotids and the
vertebrals, is most commonly involved in atheroscleorosis.
Subclavian syndrome is most commonly treated by carotid-subclavian
bypass. The cervical vertebral artery may occasionally compressed by
cervical osteophytes. Anterior cervical decompression
,reportedly, helps.
b)
Indirect revascularization procedures:
| Intracranial
nonatherosclerotic occlusive diseases form a heterogeneous
group with diverse pathogenesis. Moyamoya is the commonest.
Moyamoya is a progressive occlusive cerebrovascular disorder
characterized by bilateral stenosis and occlusions of
intracranial arteries with extensive neovascularisation at
the base of brain. It was first described in Japan and now
reported from all over the world. Genetic linkage studies
and study of the factors possibly involved in its
pathogenesis have shed new light on this disease. There is
some suggestion that the pathogenesis may vary between
races. In pediatric-onset moyamoya disease, asymmetrical
involvement of bilateral ICAs and PCAs was common, and the
ipsilateral ICA and PCA tended to be predominantly involved. |
|

|

|
|
Moyamoya-angio(lat)
|
Moyamoya-angio(AP)
|
|
Patients
present with stroke or intracranial hemorrhage due to bleeding from
the friable vessels with major morbidity and mortality. Children
usually present with cerebral ischemia. Intracranial hemorrhage is
common in adults. Without treatment, there is progressive
deterioration of neurologic function and re-hemorrhage.
Treatment
of all these patients with nonatherosclerotic occlusive diseases is
similar to that of moyamoya patients. Medical therapy with
vasodilators, steroids, and antibiotics is only minimally effective.
Various surgical procedures have been tried with mixed results.
STA-MCA
bypass in adults, encephloduroarteriosynangiosis,
encephalomyosynangiosis, and encephaloomental-synangiosis in
children are the available procedures. Direct superficial temporal
artery to middle cerebral artery bypass is considered the treatment
of choice, although its efficacy, particularly for hemorrhagic
disease, remains uncertain.
Encephalomyosynangiosis
involves
direct placement of temporalis muscle on the cerebral cortex. This
may induce seizures.
Encephloduroarteriosynangiosis
developed by Matsushima is popular. STA is mobilized
and placed directly on the cortex. The free artery with a cuff of
surrounding soft tissue is simply sutured to the dura.
Encephaloomental-synangiosis
(omental-cerebral transposition) may provide an alternative. The
omentum is mobilized from the abdomen in a subcutaneous tunnel and
placed over cerebral cortex as a pedicle graft or, as a free graft
with microsurgical anastomosis of the gastroepiploic artery and vein
to the STA and the superficial temporal vein. Omentum contains
biologically active substances taking part in neural transmission
and has angiogenic and neurotrophic action.
Combined
procedures give the best results. Spontaneously developed
leptomeningeal anastomosis might be the key factor for the efficacy
of indirect bypass in elderly patients with moyamoya /stenotic
cerebrovascular disease.
There
is no controlled study available. Satisfactory results are reported.
Surgery
for Acute Stroke:
To
appreciate the role of surgery in acute stroke, it is imperative to
understand the pathophysiology
of stroke.
Recently,
the effectiveness of many medical therapies for brain
edema and the subsequent increased ICP has been challenged. Recent
studies have shown a very high mortality rate despite aggressive
medical treatment strategies to lower ICP, which have included
osmotherapy, hyperventilation, barbiturate administration,
hypothermia, and anticoagulation therapy guided by ICP monitoring.
Compared with these, decompressive craniectomy seems to result
in a much better outcome; surgical decompression should be performed
before inducing deep barbiturate coma in these patients; a surgical
decompression performed after failure of ultrahigh barbiturates is
too late.
1)
Craniectomy and decompression:
A
decompressive procedure in selected stroke patients is the most
practiced surgical intervention in acute strokes. Any surgery should
be effective, rational, and safe. An ipsilateral decompressive
surgery fulfils all three criteria. The procedure is, certainly,
simple and safe.
The
intracranial mass effect can be compensated without an increase in
ICP by resorption of cerebrospinal fluid (CSF) and by shifting CSF
into the spinal canal. When the reserve spaces become completely
exhausted, mass effect leads to an exponential increase in ICP. The
equation is expressed by the pressure-volume curve. The studies
provide evidence that decompression leads to a shift to the right of
the pressure-volume curve and, therefore, to a massive increase in
compliance and a reduction of ICP. The rationale for decompressive
surgery is supported by these studies.
The available
results suggest the effectiveness of decompressive surgery as a
salvage procedure.
Associated
illnesses and the attitude of the family members to accept a severe
neurological deficit, especially in developing countries where there
is no adequate rehabilitation centers, must also be considered. As
in any surgery, patient selection, and meticulous postoperative
management play a major role in the outcome. Associated illnesses
must be attended to.
| Cerebral
infarcts: A
subgroup of patients with a large cerebral infarct qualifies
for a decompressive procedure to prevent uncal herniation
and death. This generally follows a massive multilobar
infarction. They develop space-occupying cerebral edema with
subsequent herniation and death. It is well
recognized that cerebral edema after large MCA
infarcts occurs in up to 10% of all patients.
Even under full supportive therapy, the mortality
rate for this distinct syndrome of malignant MCA
infarction is roughly 80%. If there is no satisfactory
recovery with aggressive medical therapy within few hours,
surgical hemicraniectomy and decompression should be
considered in patients with malignant cerebral edema. |
|

|

|
|
Multiteritory
infarct-CT
|
Malignant
MCA infarct-CT |
|
The aim is
patient salvage during the acute period of brain swelling. None of
the available medical therapies provide substantial relief from the
oedema and raised ICP, or at best, they are temporizing in most
cases.
The
technique
is simple. Judicious timing is the key for success. Craniectomy
should be performed early, before severe impairment of brain
perfusion occurs. Computerized tomography might be able to predict
the dynamics of the ensuing clinical course to assist in indicating
early intervention in some patients. There are no systematic reports
about quantitative analysis of the size of craniectomy required to
be effective. Traditionaly, craniectomy is planned according to the
area of infarct. A wide craniectomy with a duraplasty is, routinely,
recommended.
Ideally, as
described by Cushing,, the craniectomy should extend to the
base and include drilling of the sphenoid ridge for adequate
decompression. Achieving a decompression down to the floor of the
middle fossa (subtemporal decompression) seems to be important in
this surgical technique, because this procedure relieves pressure
from the basal temporal lobe. Good results with this technique were
reported even though this form faces the risk of temporal lobe
herniation and necrosis. As the dura is opened, pale infracted brain
herniates out. The herniation may subside with hyperventilation and
osmotherapy. The author recommends excision of persistent herniated
brain to prevent strangulation and necrosis. Duraplasty is performed
with either silastic lyodura or pericranial grafts.The graft is
secured with sutures in a way that allowed the initial incision to
spread not more than 2 to 3 cm.This achieves smooth bulging rather
than fungus like herniation of brain into the craniectomy, avoiding
shearing injuries, impairment of venous drainage, and enhancement of
cerebral edema. It is also recommended that in bifrontal craniectomy,
the sphenoidal ridges and the anterior walls of the middle cranial
fossa be preserved to prevent temporal lobe forward migration. Some
groups have suggested resection of infarcted and even noninfarcted
brain tissue. Some others recommend resection of the infarcted
cerebral tissue and a temporal lobectomy. Japanese surgeons
recommend additional excision of the hippocampal gyrus also to
relieve peduncle compression, and blockage of cerebrospinal fluid
circulation. Another small group of surgeons include a slit in the
tentorium to relieve further compression. The author recommends a
subdural positive pressure drainage at the end of the procedure
helps to facilitate CSF drainage if required post operatively and
may be incorporated with an ICP monitor.
The author
recommends that conservative measures, such as hyperventilation and
osmotherapy, must be tried before surgery is considered and that the
decompressive procedure is performed prior to frank clinical
deterioration. Ideally, the patient should be young with a GCS of
>5, and no serious systemic illness, and must have a supporting
family. There may be occasions when the patient selection needs to
be individualized. The procedure is mainly to give the maximum
chance to preserve life. There is a group of reluctant surgeons who
feel, a decompressive procedure do not alter the final outcome.
Discouraging outcomes in patients do not invalidate the method; good
results confirm its usefulness. The increase in brain edema after
decompressive craniectomy led to a discussion in the neurosurgical
literature and to questioning the usefulness of the procedure when
treating severely brain-injured patients. Brain edema only increases
if the brain is already irreversibly severely damaged. Such patients
have a poor prognosis, which is no argument against decompressive
craniectomy. At present decompressive surgery might be the most
promising therapeutic option. For decisive answers, randomized,
controlled clinical trials are needed.
Cerebellar
infarcts:
Older hypertensive men with diffuse atherosclerosis are commonly
affected. Previous myocardial infarction or cerebral infarcts are
often noted together.Cardiogenic embolus is thought to be the
etiological factor in about 50% of the cases. Trauma is an
occasional cause. Pediatric group is being recognized increasingly.
The infarct is
usually unilateral, and the PICA territory (posteroinferior aspect
of the cerebellum) is the site involved.
The superior cerebellar artery is an uncommon site of occlusion.
Extensive infarction may involve 1/3 or1/2 of the hemisphere and
brainstem compression. 25% of them are hemorrhagic.
| A
history of posterior circulation TIA may alert the
physician. In massive infarction, the patient becomes
progressively obtunded. When the aggressive medical therapy
fails in a reasonable time, surgical decompression should be
considered.Today the only indication that seems to be widely
accepted for performing decompressive surgery is in
cerebellar infarction with continuous clinical
deterioration, as shown in several large trials.
Our
practice is to perform a simple suboccipital craniectomy in
prone position with resection of infarcted tissue. The
posterior arch of the atlas is removed for wider
decompression. Ventricular drainage is established for
concomitant hydrocephalus and converted to a shunt if
necessary at a later stage. It must be understood that
patients with brainstem infarction have poor outcome; but,
brainstem compression is potentially reversible.
|
|

|
|
Cerebellar
infarct-CT
|
|
2)
Revascularization procedures:
The
role of revascularization procedures in acute stroke is still in the
experimental stage. Emergency carotid endarterectomy is a
controversial indication, becoming less and less controversial of
late. Patients must have angiographically demonstrated lesion and no
infarction in a CT. There is no randomized trial. Tissue plasminogen
and interventional endovascular procedures are more often preferred.
Recent
reports suggest moderate success of emergency carotid endarterectomy
in patients a) with cresendo TIAs, b) with severe stenosis in
angiography, and c) with disappearance of a previously auscultated
bruit, presumably indicating acute occlusion. The presence of good
collateral flow is a favorable prognostic sign. The technique is the
same as in elective endarterectomy. Clinical results are best in
patients with mild to moderate deficit and a rapid course from onset
of deficit to surgery.
Despite
excellent postoperative results, the outcomes in patients after
STA-MCA anastomoses are not better than the results from
medically treated patients. Other procedures such as
posterior circulation bypass, vertebral endarterctomy, arterial
anastomses, and corrction of subclavian steal have not been
tested sufficiently.
Hemorrhagic
transformation
is frequently seen on CT scans obtained in the subacute phase of
ischemic stroke. Its prognostic value is controversial. Hemorrhagic
transformation of an ischemic infarct is managed the same way as an
ischemic infarct is.
Hemorrhagic
stroke: (discussed
elsewhere)
|