Keywords STA–MCA bypass - progressive stroke - revascularization
Introduction
The safety and efficacy of endovascular mechanical thrombectomy with or without recombinant
tissue-type plasminogen activator infusion have already been established for acute
embolic major intracranial arterial occlusion.[1 ]
[2 ] However, it is not necessarily effective for atherosclerotic occlusion. Therefore,
maximal medical treatments such as dual antiplatelet therapy, fluid replacement, and
even induced hypertension should be administered to overcome hemodynamic ischemia.
When symptoms progressively worsen even with maximum treatment, emergent bypass would
be the last resort.
Although emergent superficial temporal artery-middle cerebral artery (STA–MCA) bypass
for acute-phase progressive stroke due to atherosclerotic internal carotid artery
(ICA)/middle cerebral artery (MCA) occlusion has attending innate risks such as worsening
cerebral edema and/or hemorrhagic infarction, some reports have demonstrated its effectiveness
in reversing or terminating progressive symptoms, even on maximal medical treatment.[3 ] However, only a few reports have been conducted on emergent STA–MCA bypass in acute
atherosclerotic ICA stenosis/occlusion with concomitant chronic contralateral ICA
occlusion/stenosis, apparently one of the worst hemodynamic situations.
In this report, we introduce the outline, clinical features, and surgical strategy
implemented for two cases with progressive stroke due to ipsilateral acute ICA occlusion/stenosis
with concomitant contralateral chronic ICA stenosis/occlusion, which were successfully
managed with an emergent STA–MCA bypass during the acute period to prevent the progression
of infarction.
Case History
Case 1
A 49-year-old man was referred to our institution with complaints of worsening right-hand
clumsiness/gait disturbance due to right hemiparesis with a manual muscle test (MMT)
score of 1/5 and complete motor aphasia.
Magnetic resonance imaging (MRI) revealed an acute ischemic lesion in the left premotor
cortex on diffusion-weighted imaging (DWI) and contralateral right old prefrontal
infarction on fluid-attenuated inversion recovery imaging. Magnetic resonance angiography
(MRA) revealed a very faint left intracranial ICA signal and almost no signal from
the right intracranial ICA ([Fig. 1 ]).
Fig. 1 Diffusion-weighted imaging (DWI), fluid-attenuated inversion recovery (FLAIR) imaging,
and magnetic resonance angiography (MRA) on admission.
Digital subtraction angiography (DSA) revealed a left ICA occlusion immediately after
the ophthalmic artery, possibly due to acute occlusion with engrafted thrombus on
the preexisting atherosclerotic severe stenosis and right chronic cervical ICA occlusion.
The areas surrounding the bilateral anterior cerebral artery (ACA) and MCA were opacified
by crossflow from the left posterior communicating artery and leptomeningeal anastomosis
from the bilateral posterior cerebral artery (PCA) ([Fig. 2 ]).
Fig. 2 Digital subtraction angiography performed after admission.
Maximal medical treatment with argatroban, clopidogrel, and aspirin combination therapy
was initiated, in conjunction with edaravone (30 mg twice daily) and sodium dextran
sulfate (500 mL daily) injection.
However, the patient's symptoms gradually worsened, and a repeat DWI on day 4 of admission
revealed acute ischemic lesions had extended up to the prefrontal cortex and deep
white matter ([Fig. 3 ]). After a thorough discussion, emergent STA–MCA bypass was performed ([Video 1 ]).
Video 1 We provide a video that shows the actual surgery on a patient who underwent urgent
bypass for progressive cerebral infarction with internal carotid artery (ICA) occlusion
associated with contralateral ICA occlusion.
Fig. 3 Diffusion-weighted images on day 4 of admission. Lt.CCAG, left common carotid angiograms;
Rt. VAG, right vertebral angiograms.
Since severe hemodynamic impairment had been expected, edaravone (30 mg) was administered
immediately before cross-clumping the recipient artery,[4 ] and minocycline (200 mg/day for 5 days) was given for neuroprotection perioperatively.[5 ] The intraoperative mean blood pressure was maintained at 80 to 100% of preoperative
blood pressure. Shortening the anastomosing and operation times is also extremely
essential during the emergent STA–MCA bypass for patients with contralateral ICA stenosis/occlusion
because their ischemic resistance is extremely low. For that purpose, reliable and
efficient hand movement during anastomosis is essential. These steps can be viewed
on the operative video provided ([Video 1 ]).
Arterial spin labeling (ASL) MRI on postoperative day (POD) 1 showed increased blood
flow on the operated side; however, clinical signs of cerebral hyperperfusion (CH)
did not become symptomatic by strictly controlling the systolic blood pressure at
less than 130 mm Hg until the ASL findings stabilized on POD 5. Postoperatively, no
additional ischemic lesions were observed on repeat DWI, the exacerbation of clinical
symptoms ceased, and the patient's condition gradually stabilized.
Approximately 1 month after admission, STA–MCA bypass surgery was also performed for
contralateral ICA occlusion. Finally, after rehabilitation, the patient's right hemiparesis
recovered from MMT 1/5 to MMT 3/5 with independent/voluntary movement of his right-hand
fingers. Additionally, simple spontaneous utterances such as “yes” and “no” were observed,
and the patient was transferred to a rehabilitation hospital for further improvement
with a modified Rankin Scale (mRS) score of 4. [Fig. 4 ] shows MRI findings performed immediately before discharge.
Fig. 4 Magnetic resonance imaging immediately before discharge. DWI, diffusion-weighted
imaging; FLAIR, fluid-attenuated inversion recovery; MRA, magnetic resonance angiography.
Case 2
A 62-year-old man with a history of the occipital artery (OA)–MCA bypass surgery for
right ICA occlusion 8 years prior was admitted to our institution with disturbed consciousness,
severe dysarthria, and right hemiparesis with an MMT score of 4/5.
Upon presentation (day 0), DWI showed only a faint acute ischemic lesion along the
left watershed area and the right old prefrontal infarction, whereas MRA demonstrated
an old right ICA occlusion, a severe left C2 stenosis, and a visible distal left MCA
signal ([Fig. 5 ]). On day 1, DSA showed a chronic right ICA occlusion and moderately developed right
OA–MCA bypass. However, the right ACA area was poorly opacified in the right common
carotid artery angiography and supplied by collateral flow from the right posterior
pericallosal artery, indicating the low ischemic resistance of the right cerebellar
hemisphere. The left supraclinoid ICA showed severe stenosis with a slightly delayed
distal left MCA opacification. Bilateral ACA areas were poorly visualized. On right
vertebral angiography, leptomeningeal anastomosis from bilateral PCA perfused the
bilateral MCA area only moderately ([Fig. 6 ]). On day 2, MRA demonstrated progressive worsening of the left ICA stenosis with
an extremely poor signal of the distal left MCA ([Fig. 7 ]), whereas DWI showed only small ischemic lesions scattered along the left watershed.
Fig. 5 Diffusion-weighted and fluid-attenuated inversion recovery images on admission. DWI,
diffusion-weighted imaging; MRA, magnetic resonance angiography.
Fig. 6 Comparison of post-discharge digital subtraction angiography (DSA) with 2008 DSA.
Rt.CCAG, right common carotid angiograms; Lt.ICAG, left internal carotid angiograms;
Rt.VAG AP, right vertebral angiograms A-P view; Rt.VAG LAT, right vertebral angiograms
lateral view.
Fig. 7 Magnetic resonance angiography findings on days 2. MRA, magnetic resonance angiography.
Besides the usual aspirin and cilostazol therapy, daily injections of argatroban,
edaravone (30 mg twice daily), and sodium dextran sulfate (500 mL) were administered.
Despite the maximal medical treatment, the patient's clinical symptoms, especially
the progressively worsening disturbed consciousness, suggested that the left C2 near
the occlusion is in a critical state because of the extremely poor crossflow caused
by contralateral chronic ICA occlusion. Therefore, emergent revascularization STA–MCA
bypass was conducted on day 3, and perioperative management was administrated similarly
as in Case 1.
Postoperatively, the patient's consciousness, hemiparesis, and dysarthria gradually
improved. ASL demonstrated focal hyperperfusion around the recipient area of the STA–MCA
bypass, although vigorous blood pressure control prevented it to become symptomatic.
The patient was discharged after rehabilitation with an mRS 1 and was still due to
return for a follow-up visit at the time of this writing. [Fig. 8 ] shows MRI findings at discharge.
Fig. 8 Magnetic resonance images immediately before discharge. DWI, diffusion-weighted imaging;
FLAIR, fluid-attenuated inversion recovery; MRA, magnetic resonance angiography.
Discussion
The effect of STA–MCA bypass on the management of chronic hemodynamic ischemia has
not yet been proven. The Carotid Occlusion Surgery Study (COSS) reported that the
STA–MCA bypass is not superior to the best medical treatment because of its high incidences
of perioperative complications.[6 ]
[7 ]
[8 ] However, in Japan, STA–MCA bypass for ICA occlusion, MCA occlusion, or severe stenosis
has been proven effective as protection from possible ischemic stroke for some patients
who meet the requirements, including decreased vascular reactivity in the acetazolamide
test; increased oxygen uptake rate in positron emission tomography (PET), elapsing
over 3 months since the last attack; and absence of extensive infarction.[9 ] The method is still used as a means of preventing ischemic stroke in patients with
severe hemodynamic insufficiency.
Apart from the STA–MCA bypass for chronic occlusion, one of the possible indications
for emergent STA–MCA bypass might be acute atherosclerotic ICA/MCA occlusion with
progressive stroke despite maximal medical treatment and severe hemodynamic insufficiency.[10 ]
However, urgent bypass surgery for extremely hemodynamically unstable acute cerebral
infarction is expected to have a much higher risk of perioperative complications compared
with that of chronic preventive bypass surgery such as a COSS candidate. Thus, more
cases should be evaluated to elucidate the emergency bypass candidate with a severely
impaired hemodynamic situation and in whom the risk of sticking to the best medical
treatment outweighs the risk of emergent bypass.[11 ]
[12 ]
To date, several retrospective case series have described promising results of emergent
STA–MCA bypass surgery in patients with progressive symptoms.[13 ]
[14 ] Kimura et al reported favorable outcomes in a cohort with mild symptoms as indicated
by lower preoperative National Institutes of Health Stroke Scale (NIHSS) scores.
Among patients with medically intractable progressive stroke, acute ipsilateral ICA
occlusion associated with contralateral chronic ICA occlusion might be the most difficult
situation for an emergent STA–MCA bypass.[15 ] The majority of these patients have more severe cerebral circulatory failure or
low cerebrovascular reserve because of the lack of cross-collateral flow; hence, the
risk of developing cerebral infarction is higher because of general anesthetic management,
temporary clumping of the recipient, and blood pressure control immediately after
surgery, among others. Most patients also presented with relatively severe symptoms
such as preoperative neurological findings; thus, they tended to have poor clinical
outcomes even after an emergent surgery.[3 ]
To overcome bypass surgery in progressive stroke under a significant hemodynamic insufficiency,
some pharmacological affirmative majors that have been reported were followed. Free-radical
scavenger (edaravone) was administered immediately before cross-clumping of the recipient
artery to prevent CH after carotid endarterectomy, especially with preexisting severe
hemodynamic insufficiency.[4 ] We continued free-radical scavenger infusion for several days postoperatively. Moreover,
minocycline (200 mg/day for 5 days), which is reported to alleviate the focal hyperperfusion
and clinical symptom after the bypass surgery for moyamoya disease,[5 ] was administered for neuroprotection perioperatively. Both of our cases showed hyperperfusion
in postoperative and preoperative ASL. Hence, although the clinical symptoms remained
similar or somewhat worse immediately after surgery, we confirmed that this is due
to hyperperfusion and thereby reperfusion itself would be sufficient. Thus, besides
the above two antihyperperfusion majors, postoperative blood pressure was maintained
as low as less than sBP130. Additionally, a single-agent administration of clopidogrel
75 mL was continued as a perioperative antiplatelet agent.
Moreover, Kobayashi et al[16 ] reported the outcome of acute STA–MCA bypass for high-grade stenosis in a contralateral
ICA or symptomatic ICA occlusion complicated by an occlusive lesion in four patients.
All of them underwent emergent STA–MCA bypass because of perfusion that was larger
than the infarct area on PET cerebral blood flow and higher brain dysfunctions observed
after the onset of minor stroke. According to this report, of the four patients, three
(75%) developed perioperative cerebral infarction and two developed postoperative
hyperperfusion. Therefore, the incidence of perioperative complications was high.
However, each patient had a perioperative cerebral infarction in an area away from
the anastomotic site, especially in the ACA area, indicating that the watershed shift
might have been generated via a bypass flow competing with a faint antegrade flow
that originally existed. Symptoms due to similar ischemic lesions were also identified
to be transient and improved in the chronic phase. Thus, although the risk of a minor
infarction resulting from hemodynamic changes due to blood flow load exists, the risk
of a major hemodynamic infarction caused by surgery under general anesthesia is likely
to be low. Hypoperfusion symptoms were also transient, and all of them were improved
via strict blood pressure control.
In our two patients, no new developments were observed in the perioperative cerebral
infarction, and no postoperative symptomatic hyperperfusion syndromes were observed.
Hence, the risk of perioperative complications in acute bypass surgery remains high;
however, studies on some cohorts have demonstrated that urgent bypass is superior
to medical treatment. No article has reported the outcomes of medical monotherapy
for progressive cerebral infarction associated with bilateral ICA occlusion and compared
treatment outcomes between medical monotherapy and surgical therapy.[17 ]
[18 ] Although the kind of cohort suitable for urgent bypass remains unclear, at least
in our two patients, cerebral infarction progression was prevented, indicating that
the efficacy of an urgent bypass may be superior to conservative treatment by significantly
improving the surgical technique and perioperative management.
The unified surgical technique is adopted, not limited to urgent bypass, in our facility,
which allows for a stable performance within 5 hours of anesthetic time and 20 minutes
of clamping time during inoculation. Regarding the recipient artery, a larger diameter
is selected at the frontal lobe in the perisylvian area and the M4 segment on the
temporal lobe. Especially for the frontal lobe, the M4 segment toward the frontoparietal
lesion is targeted. For the actual surgical technique, refer to the page and video
of the surgical procedure. Considering the abovementioned measures, a safer emergent
STA–MCA bypass surgery can be performed.
Indications for emergent STA-MCA bypass surgery should be considered when symptoms
progress despite maximum medical treatment.
In particular, emergent STA-MCA bypass surgery is not considered dangerous just because
of contralateral ICA stenosis/occlusion.
Rather, even with severe hemodynamics, the benefits of emergent STA-MCA bypass surgery
may outweigh those of maximum medical treatment.
However, the hemodynamics, indications for each case need to be considered.
Conclusion
An emergent STA–MCA bypass can be considered as a last resort for preventing progressive
neurological deterioration in patients with progressive infarction due to ICA stenosis/occlusion
concomitant with contralateral ICA stenosis/occlusion.
Given that only two cases had been examined herein, our results cannot be generalized
to other patients, suggesting the need for further accumulation of cases.
