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166
39 Carotid Endarterectomy forSymptomatic Radiation Induced Carotid Stenosis
Invited Commentary fromBenjamin
D.Colvard, MD, andVikram
S.Kashyap, MD
The author describes a carotid endarterectomy
performed on a patient with radiation induced
carotid stenosis, which was causing transient
ischemic attacks. The operation was complicated
by dysphagia and a large cervical hematoma
requiring evacuation. Fortunately, the patient had
a good outcome following appropriate management of the complications. Of note, the patient
underwent uneventful carotid artery stenting on
the contralateral side 2 months later.
CEA is the gold standard for management of
symptomatic carotid stenosis. Select groups have
however been shown to benet from carotid
stenting, including those with radiation induced
carotid stenosis. Specic complications associated with CEA that can be avoided with stenting
include cranial nerve injury, poor wound healing,
and postoperative neck hematoma. The decision
to perform CEA in a patient with an irradiated
neck should be heavily based on the physical
examination, in addition to routine imaging and
clinical evaluation. Stiff and woody neck skin
portends a higher likelihood of difcult dissection and poor wound healing [3]. While nerve
injury is an often cited and feared complication
of CEA in irradiated eld, an important consideration is also the quality of the artery once it is
safely exposed. Just as the tissue planes of the
neck may be obliterated, so too can the planes
between the layers of the artery, which may result
in the need to replace the carotid artery with an
interposition graft rather than proceeding with
an endarterectomy and patch angioplasty.
Subsequently, these patients must be monitored
closely to ensure adequate wound healing.
In our experience, a majority of patients with
irradiated necks have undergone carotid artery
stenting with good results, and this has become
our standard approach to this patient population.
Of note, this can be done via a transfemoral or
transcarotid approach depending on the anatomy
and extent of neck radiation injury.
References
1. Tallarita T, Oderich GS, Lanzino G, Kloft H, Kallems
D, et al. Outcomes of carotid artery stenting verses
historical surgical control for radiation – induced
carotid stenosis. J Vasc Surg. 2011;53:629–36.
2. Magne JL, Pirvu A, Sessa C, Cochet H.Carotid artery
revascularization following neck radiation: immedi-
ate and long-term results. Eur J Vasc Endovasc Surg.
2012;43(1):4–7.
3. Kashyap VS, Moore WS, Quinones-Baldrich
WJ.Carotid artery repair for radiation associated ath-
erosclerosis is a safe and durable procedure. J Vasc
Surg. 1999;29(1):90–6.
4. Leseche G, Castier Y, Chataigner O, Francis F, et al.
Carotid artery revascularization through a radiated
eld. J Vasc Surg. 2003;38(2):244–50.
Nonconvulsive Status Epilepticus Following Carotid Endarterectomy
40
History andProcedures
A 67-year-old left-handed male presented with
severe right ank pain on September 27, 2010,
and underwent emergent open repair of ruptured
abdominal aortic aneurysm (AAA). In the recovery room, the patient developed severe ischemia
of the left lower extremity and was taken back to
the operating room. Thrombosed left popliteal
aneurysm was encountered with no runoff vessel
available to perform a distal bypass. The patient
underwent four compartment fasciotomy. On the
third postoperative day, the patient on the ventilatory support was found to have right hemiplegia.
Computed tomography (CT) scan of the head
showed ischemia in the left frontoparietal area in
the distribution of the left middle cerebral artery.
Carotid duplex showed right internal carotid
artery occlusion and severe stenosis of the left
internal carotid artery (80–90%). The patient
underwent left above-knee amputation on
October 8, 2010, for irreversible ischemia. The
patient started to show signicant improvement
from the hemiplegia and was subsequently discharged to an extended care facility for 6 weeks.
Repeat CT scan of the head showed left frontal
infarct and a small parietal infarct. The patient
was subsequently seen as an outpatient in January
2011 with normal speech and complete motor
recovery of right lower extremity and excellent
motor function in the right upper extremity with
only slight residual weakness in the right hand.
Repeat carotid duplex study showed right internal carotid artery occlusion and a very high-grade
stenosis of the left internal carotid artery with
peak systolic velocity of the left internal carotid
artery 641 cms/sec and IC/CC ratio of 7.90
(Fig.40.1).
On January 25, 2011, the patient underwent
left carotid endarterectomy under cervical block
anesthesia. The stump (back) pressure was
42mmHg. Since carotid clamping did not result
in any new neurological decits, a shunt was not
used. Clamp time (cerebral ischemia time) was
32minutes. The patient was found to have severe
stenosis and ulceration in the proximal left internal carotid artery. A Hemashield-Finesse patch
graft was sutured to the common and internal
carotid artery. The patient was transferred to the
recovery room with no new neurological decit.
However, 2 hours following carotid endarterectomy, the patient was found to have change in
mental status. He had decreased alertness and
was poorly responsive. The patient was not able
to speak (akinetic mutism). Postoperative CTA of
the neck and head showed satisfactory endarterectomy site (Fig.40.2). A 21-channel electroencephalogram (EEG) showed recurrent episodes
of partial complex ictal events beginning as intermittent sharp waves localized to the left frontal
and central region evolving into more frequent
and higher-amplitude sharp waves, resolving
briey before another event started with periodic
lateralizing epileptiform discharges (Fig. 40.3).
© Springer Nature Switzerland AG 2020
S. S. Hans, Challenging Arterial Reconstructions, https://doi.org/10.1007/978-3-030-44135-7_40
167
168
Fig. 40.1 Carotid
duplex study showing
severe left internal
carotid stenosis
40 Nonconvulsive Status Epilepticus Following Carotid Endarterectomy
During the recording of EEG, the patient developed a focal seizure involving the right arm and
right leg which responded to intravenous Ativan.
Phenytoin was started intravenously. The patient
remained mute and confused for another 1 hour
and before neurological status reverted to its preoperative state.
EEG on the following day did not show epileptiform pattern. The patient was discharged
home on the third postoperative day in satisfactory condition on oral phenytoin. Immediate
postoperative CT scan of the head did not show
any new ndings (no evidence of white matter
edema). CTA of the carotid artery showed a
widely patent left carotid endarterectomy site
with good lling of the circle of Willis from the
left side. At last follow-up in March 2019, the
patient was doing well without any new neurological symptoms or seizures.
Fig. 40.2 CT angiography showing widely patent left
carotid endarterectomy site
Discussion
Seizures following carotid endarterectomy are a
manifestation of hyperperfusion syndrome. They
were rst described by Wilkinson etal. [1] and
Sundt etal. in 1981 [2]. Since then, many reports
of seizures manifesting 17hours to 13 days fol-
Discussion
Fig. 40.3 EEG showing lateralizing epileptiform discharges
169
lowing carotid endarterectomy have been
reported [3–11]. The exact pathophysiologic
mechanism for cerebral hyperperfusion syndrome is unclear [1–12]. By using Xenon-133
labeled radio nuclear studies, Sundt etal. demonstrated increased cerebral blood ow in patients
with cerebral hemorrhage following carotid endarterectomy [2]. Previous studies focused on the
failure of normal cerebral autoregulation secondary to long-standing changes in perfusion pressures [2–5, 7–10]. Protracted maximal
vasodilation of cerebral arterioles results in loss
of cerebral blood ow autoregulation in areas of
chronically under perfused brain tissue resulting
in cerebral edema and/or hemorrhage. It is also
believed that impaired autoregulation is the result
of endothelial dysfunction mediated by oxygen
free radicals [12]. In the past, using carotid
duplex imaging, investigators have demonstrated
increased mean volume ow and peak systolic
velocity in the operated carotid artery in the
patients with HPS [2, 3, 7, 8]. However, in a
recent study by Karapanayiotides et al. using
transcranial Doppler, middle cerebral artery
(MCA) mean ow velocities were not found to be
increased; therefore authors hypothesized that
reperfusion rather than hyperperfusion is a more
apt description of the hemodynamic mechanism
for this syndrome [6]. The main abnormality in
patients with HPS on CT scan and T2-weighted
MR includes white matter edema (vasogenic)
consistent with breakthrough of autoregulatory
mechanism [4]. In this report, the patient was
found to be poorly responsive and mute and did
not follow commands and subsequently developed focal seizure. It is to be noted by EEG and
clinical examination that the patient was experiencing nonconvulsive status epilepticus followed
by one focal motor seizure on the right side and
then reverted to nonconvulsive status epilepticus
for about 1 hour before showing complete recovery. Since there was no evidence of new cerebral
infarct in this patient, the cause of seizure/status
epilepticus was HPS rather than cerebral embolization. PLED activity in the left front and central areas resulted from the excitability of the
focus in the left frontal infarct. Akinetic mutism
and confusion as a part of nonconvulsive status
170
40 Nonconvulsive Status Epilepticus Following Carotid Endarterectomy
epilepticus could be confused with aphasia
caused by post carotid endarterectomy stroke as
patient developed neurological symptoms 2 hours
following carotid endarterectomy– a period when
post carotid endarterectomy stroke is far more
common than seizures. Patients experiencing new
neurological symptoms following carotid endarterectomy should undergo emergency non- contrast
CT scan of the head, carotid duplex study, and
immediate neurology consultation to rule out HPS
before considering re-exploration of the carotid
artery for post carotid endarterectomy thrombosis.
References
1. Wilkinson JT, Adams HP, Wright CB. Convulsions
after carotid endarterectomy. JAMA.
1980;224:1827–8.
2. Sundt TM, Sharbrough FW, Piepgras DG, Kearns TP,
Messick JM, O’Fallon WM.Correlation of cerebral
blood ow and electroencephalographic changes during carotid endarterectomy. With results of surgery
and hemodynamics of cerebral ischemia. Mayo Clin
Proc. 1981;56:533–43.
3. Ascher E, Markevich N, Schutzer RW, Kallakuri
S, Jacob T, Hingorani AP. Cerebral hyperperfusion
syndrome after carotid endarterectomy: predictive
factors and hemodynamic changes. J Vasc Surg.
2003;37:769–77.
4. Naylor AR, Evans J, Thompson MM, London NJ,
Abbott RJ, Cherryman G, Bell PR. Seizures after
carotid endarterectomy: hyperperfusion, dysautoregulation or hypertensive encephalopathy? Eur J Vasc
Endovasc Surg. 2003;26:39–44.
5. Kieburtz K, Ricotta JJ, Moxley RT. Seizures following carotid endarterectomy. Arch Neurol.
1990;47:568–70.
6. Karapanayiotides T, Meuli R, Devuyst G, PiechowskiJoswiak B, Dewarrat A, etal. Post-carotid endarterectomy hyperperfusion or reperfusion syndrome.
Stroke. 2005;36:21–6.
7. Wagner WH, Cossman DV, Farber A, Levin PM,
Cohen JL. Hyperperfusion syndrome after carotid
endarterectomy. Ann Vasc Surg. 2005;19:479–86.
8. Reigel MM, Hollier LH, Sundt M, Piepgras DG,
Sharbrough FW, Cherry KJ. Cerebral hyperperfusion syndrome: a cause of neurologic dysfunction after carotid endarterectomy. J Vasc Surg.
1987;5:628–34.
9. Youkey JR, Clagett GP, Jafn JH, Parisi JE, Rich
NM.Focal motor seizures complicating carotid endarterectomy. Arch Surg. 1984;119:1080–4.
10. Nielsen TG, Sillesen H, Schroeder TV. Seizures
following carotid endarterectomy in patients with
severely compromised cerebral circulation. Eur J Vasc
Endovasc Surg. 1995;9:53–7.
11. Coutts SB, Hill MD, Hu WY, Sutherland
GR.Hyperperfusion syndrome: toward a stricter denition. Neurosurgery. 2003;53:1053–60.
12. Van Mook WNKA, Rennenberg RJMW, Schurink
GW, Oostenbrugge RJV, Mess WH, Hofman PAM,
de Leeuw PW. Cerebral hyperperfusion syndrome.
Lancet Neurol. 2005;4:877–88.
Carotid Endarterectomy Followed
by Retrieval ofPlaque Embolus
fromM-1 Segment oftheMiddle
Cerebral Artery
41
History andPhysical Examination
A 59-year-old male underwent left carotid endarterectomy for 80% asymptomatic stenosis of the
left internal carotid artery on December 10, 2015,
under general anesthesia, with EEG and median
nerve evoked potential monitoring. Prior to
carotid endarterectomy, patient had undergone
carotid duplex study and CT angiography of the
neck showing 80% stenosis of the left internal
carotid artery with proximal plaque extension
into the distal common carotid artery. Patient
denied any history of focal neurological symptoms, transient loss of vision, or history of stroke.
Medical comorbidities included hypertension
and nicotine abuse (80 pack years).
Procedure
During the operation, plaque was noted to be
quite high, and in order to reach the distal end of
the plaque, sternocleidomastoid branch of the
occipital artery and the occipital artery itself
needed division and ligation. Hypoglossal nerve
was mobilized cephalad, and a silastic vessel
loop was passed to gain distal exposure. Severe
stenosis of the internal carotid artery with ulceration in a very long plaque was observed. Plaque
extended for 3–4cm into distal common carotid
artery and sharp division of the plaque resulted in
its separation from the arterial wall; therefore
plaque was removed up to the tightly applied
proximal common carotid artery clamp.
Indwelling shunt was not used as EEG, and
median nerve evoked potentials remain normal
during carotid cross clamping. Stump (back)
pressure was 41 mm Hg. A bovine pericardial
patch was applied after removal of the plaque,
incision was closed, and patient was extubated.
At the time of extubation, median nerve conduction velocity showed latent interval (abnormal)
though EEG did not show any evidence of ischemia. Patient woke up with right-sided paralysis.
Incision was reopened, and carotid/cerebral arteriogram was performed through superior thyroid
artery; it showed a widely patent common carotid
endarterectomy site. A very small defect at the
site of proximal clamp was noted and absence of
lling of the M-1 middle cerebral artery
(Figs.41.1 and 41.2).
Patient was seen by endovascular neurosurgeon on an urgent basis. Using a right femoral
access, a pigtail catheter was placed in the aortic
arch and was exchanged for a Simmons II glide
catheter. Antegrade catheterization of the left
common carotid artery was performed which
showed patent common carotid endarterectomy
site. Over an exchange wire, a Mercy 8F balloontipped guide catheter attached to heparinized
saline ush to which 1 mg intra-arterial nitroglycerin was infused to prevent and treat the
catheter- induced spasm. A Rebar microcatheter
was advanced over a Synchro 14 wire from
© Springer Nature Switzerland AG 2020
S. S. Hans, Challenging Arterial Reconstructions, https://doi.org/10.1007/978-3-030-44135-7_41
171
41 Carotid Endarterectomy Followed by Retrieval ofPlaque Embolus fromM-1 Segment oftheMiddle…
172
Fig. 41.1 Left carotid artery showing patent endarterectomy site clamp defect in the common carotid artery and spasm
of the internal carotid artery near the base of the skull
extracranial to intracranial circulation and placed
in the superior division of the middle cerebral
artery. A solitaire 4 × 20 embolectomy device
was deployed from the superior division of M-1
segment of the middle cerebral artery. After 6
minutes, balloon temporary occlusion was initiated, and aspiration was started. Embolectomy
was performed. Multiple pieces of plaque were
noted within the embolectomy device (Fig.41.3).
Angiography revealed T1C1 III ow (Fig.41.4).
Angio-Seal device was used to close the femoral
artery. In the ensuing 4–6 hours, he regained
complete neurological function.
Patient underwent neck exploration for a
large left neck hematoma and placement of a
JP drain. Two weeks following endarterec-
Fig. 41.2 M-1 segment occlusion of the left middle cere-
bral artery
tomy, and retrieval of plaque from the middle
cerebral artery, patient was seen in the ofce
Discussion
173
Fig. 41.3 Retrieval of plaque embolus using microwire/catheter and solitaire device
without any motor weakness but with occasional mild expressive speech difculty. He
he has continued to smoke in spite of repeated
counseling.
underwent speech therapy, and subsequently
his speech became completely normal in
February of 2016. Patient was last seen in July
Discussion
2019, and he is undergoing serial duplex imaging of the neck which showed no evidence of
stenosis of the right common and internal
carotid artery and an asymptomatic 60–69%
stenosis of the left internal carotid artery for
which he is undergoing medical treatment. But
Perioperative stroke is the most serious complication of carotid endarterectomy and occurs in
1–5% of patients undergoing the procedure [1].
The incidence is lowest in patients undergoing
carotid endarterectomy for asymptomatic
41 Carotid Endarterectomy Followed by Retrieval ofPlaque Embolus fromM-1 Segment oftheMiddle…
174
Fig. 41.4 Showing reestablishment of ow in the middle cerebral artery and lling of the middle cerebral artery and
anterior cerebral artery branches
stenosis and highest in patients undergoing carotid
endarterectomy for recent stroke. Most perioperative strokes are ischemic and manifest as a contralateral motor weakness of the upper and lower
extremities with speech involvement in a patient
undergoing left carotid endarterectomy (in righthanded patients). The commonest cause is plaque
embolization either during the operation or in the
early postoperative period. Patient may develop
thrombosis at the endarterectomy site as a result
of intimal ap at the distal end manifesting as a
neurological decit following normal neurological function after completion of carotid endarterectomy. Cerebral ischemia due to nonuse of shunt
or malfunction of the shunt in patients with inadequate cerebral blood ow is usually responsible
for stroke in a smaller number of patients (<10%)
undergoing carotid endarterectomy [2, 3].
If a patient wakes up with a neurological decit in the operating room, the carotid endarterectomy site should be re-explored, and completion
arteriogram performed. If the patient develops
neurological decit in the recovery room or later
(typically 30 mins–12hours following endarterectomy), emergency CT scan of the head should
be performed. It is almost always negative as
intracerebral hemorrhage typically occurs after
24hours of carotid endarterectomy and ischemic
infarct does not become distinctly visible on the
CT scan for a few hours. The earliest CT scan
nding of an intraoperative stroke is hyperdense
segment of a vessel (hyperdense middle cerebral
artery sign). Other early signs include loss of
grey-white matter differentiation and cortical
hypodensity with parenchymal swelling with
resultant gyral effacement. If the intracerebral
hemorrhage is ruled out, patient should undergo
CTA of the neck and head, while the patient is
still in the CT department. If patient has occlusion of the middle cerebral artery (M-1 or M-2
segment), patient should undergo neurovascular
intervention and should be referred for retrieval
provided the stroke is within the 6–8-hour window following the event for successful outcome
[4]. In patients with occlusion of peripheral
branches of the middle cerebral artery (multiple
small emboli), endovascular retrieval is not helpful, and patient should undergo PT/OT and
speech therapy.
Re-exploration of endarterectomy site for suspected thrombosis results in improvement in neurological function in about half of the patients
depending upon the elapsed time period between
the onset of thrombosis and time of re- exploration.
If there is associated occlusion of the middle
cerebral artery, the operative exploration of the
neck will not be helpful. In some patients, early
re-exploration by the endarterectomy site with
removal of fresh thrombus may allow spontaneous extrusion of the remaining thrombus from the
intracranial segment resulting in improved neurological outcome.
References
175
References
1. Goodney PP, Likosky DS, Cronenwett JL. Factors
associated with stroke or death after carotid endarterectomy in Northern New England. J Vasc Surg.
2008;48:1139–45.
2. Calligaro KD, Dougherty MJ. Correlation of carotid
artery stump pressure and neurological changes during 474 carotid endarterectomies performed in awake
patients. J Vasc Surg. 2005;42:684–9.
3. Hans SS, Jareunpoon O. Prospective evaluation of
EEG, carotid artery stump pressure, and neurological changes during 314 consecutive carotid endarterectomies performed in awake patients. J Vasc Surg.
2007;45:511–5.
4. Roth C, Papanagitou P, Behnke S, Walter S, et al.
Stent-assisted mechanical recanalization for treatment
of acute intracerebral artery occlusion. Stroke.
2014;41:2559–67.