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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3710_Библиотеки_им_академика_М_И_Перельмана.pdf
Carotid Endarterectomy
withIntraoperative Stroke
DuetoPlaque Embolization
During Shunt Insertion
Physical Examination andHistory
A 71-year-old male was scheduled to undergo left
carotid endarterectomy for progressively worsening carotid stenosis which was in critical range
(80–99%) with carotid duplex study and conrmed
by CT angiography of the carotid arteries. His
medical comorbidities included Type II diabetes
mellitus, hypertension, and dyslipidemia. Past surgical history includes coronary artery bypass graft
and right carotid endarterectomy. CT angiography
of the carotid arteries showed 80% stenosis at the
origin of the left internal carotid artery with mixed
heterogeneous plaque which was both calcied and
non- calcied. In addition, there was evidence of
40–50% stenosis of the left common carotid artery
in the middle of the neck (Fig.37.1).
37
Procedure
Through an oblique incision on the left side of
the neck under cervical block anesthesia, the
common carotid artery was clamped following
systemic heparinization. Carotid stem pressure
was measured (35mm Hg). After about 10 minutes of carotid clamping, the patient was unable
to squeeze his right hand.
A Sundt (Integra LifeSciences, Plainsboro,
NJ) 3 × 4 mm shunt was inserted. The smaller
end into the internal carotid artery was inserted
rst, and a small Javid clamp was applied. As at
© Springer Nature Switzerland AG 2020
S. S. Hans, Challenging Arterial Reconstructions, https://doi.org/10.1007/978-3-030-44135-7_37
Fig. 37.1 Showing high-grade stenosis at the origin of
the left internal carotid artery and moderate stenosis in the
middle common carotid artery
the larger end, 4 mm was inserted through the
common carotid artery, one could see a plaque
embolus in the shunt. The shunt was immediately
removed from the internal carotid artery, and
antegrade ushing of the shunt was performed
before reinserting the shunt. Flow in the shunt
was conrmed by Doppler probe. Following
insertion of the shunt, the patient’s speech
returned, but he could not squeeze with his right
155
37 Carotid Endarterectomy withIntraoperative Stroke DuetoPlaque Embolization During Shunt Insertion
156
Fig. 37.2 Completion carotid arteriogram showing satisfactory endarterectomy site with satisfactory lling of the
anterior and middle cerebral artery
hand. Left carotid endarterectomy was completed
with shunt in place, and the plaque in the common carotid artery was also removed by extending the arteriotomy proximally. A bovine
pericardial patch (LeMaitre Vascular, Inc.
Burlington, MI) was sutured with 7-0 cardiovascular prolene. A completion arteriogram via a
20-gauge catheter was performed (Fig. 37.2).
There was good lling of the anterior cerebral
artery and superior and inferior divisions of the
middle cerebral artery. After the completion of
the operation, the patient was transferred to the
intensive care unit. He continued to show
improvement in his neurological function. He
was then transferred to the rehabilitation unit of
the hospital. His neurological function has
improved, with NIH scale of eight. Non-contrast
CT scan of the head 3 days after the neurological
decit shows small infarct in the peripheral
branches of the left middle cerebral artery and
shows low attenuation density in the left corona
radiata superior and inferior frontal region suggestive of a recent infarct (Fig.37.3). Patient has
shown signicant improvement in his neurologi-
Fig. 37.3 CT of the head showing small infarct in the
distribution of peripheral branches of the middle cerebral
artery
cal status with NIH score of 6 at his last evaluation in January 2020.
References
157
Discussion
Most carotid endarterectomies can be performed without the use of indwelling shunt.
Patients undergoing carotid endarterectomy
under cervical block anesthesia require shunt
placement from 7 to 12% of cases, and, under
general anesthesia with EEG monitoring, the
shunt usage is reported to be 12–18% as EEG is
highly sensitive to cerebral ischemia [1]. There
are three approaches to the use of shunt during
carotid endarterectomy. There have been few
reports that carotid endarterectomy can be performed with satisfactory results without the use
of shunt. On the other hand, there are surgeons
who routinely use shunt in every patient undergoing carotid endarterectomy [1, 2]. The author
uses selective shunting based on ischemic
changes during carotid cross clamping under
cervical block anesthesia and ischemic EEG
changes in somatosensory evoked potentials
under general anesthesia.
Though rare, a shunt can result in carotid
dissection and embolization as was present in
this patient due to injury to the intima. In this
patient, the primary reason of plaque embolization was a lesion in the common carotid
artery (50%) mixed plaque. In retrospect, in
this type of lesion, the larger end of the shunt
should be rst inserted through the common
carotid artery, and antegrade ushing is performed before the shunt is inserted into the
internal carotid artery (usually the smaller end
of the shunt is rst inserted into the internal
carotid artery and then into the common carotid
artery).
Using transcranial Doppler, Halsey et al.
reported severe ischemia in 7.2% of cases during
carotid endarterectomy [3]. There was spontaneous clearing of the ischemia in about half the
cases. In those with persistent ischemia, the rate
of severe stroke was very high, while shunting
protected against stroke in such cases. If ischemia did not occur, the stroke rate was higher
with shunting although not so high as in unshunted cases of severe ischemia [2]. The common cause of intraoperative stroke during carotid
endarterectomy is due to plaque embolization.
Other causes include carotid thrombosis due to
distal intimal ap and postoperative cerebral
hemorrhage. Cerebral ischemia due to cross
clamping is a relatively uncommon cause of
intraoperative neurological decit.
References
1. Hans SS, Jareunpoon O. Prospective evaluation of
electrocephalography, carotid artery stump pressure
and neurological changes during 314 consecutive
carotid endarterectomies were performed in awake
patients. J Vasc Surg. 2007;45:511–5.
2. Calligaro KD, Dougherty MJ. Correlation of carotid
artery stump pressure and neurological changes dur-
ing474 carotid endarterectomies performed in awake
patients. J Vasc Surg. 2005;42:684–9.
3. Halsey JH.Risks and benets of shunting in carotid
endarterectomy. Stroke. 1992;23:1583–7.
Intracerebral Hemorrhage Following Carotid Endarterectomy
38
Physical Examination
A 48-year-old male presented to the emergency
room of the hospital with speech difculty, memory loss, and right-hand weakness in October of
2014. Patient had a minor neurological decit
(pronator drift of the right hand with difculty in
nding words). Patient’s NIH stroke scale was 4.
Carotid duplex and CT angiography of the neck
showed focal 90% stenosis at the origin of the left
internal carotid artery with primarily hypoechoic
plaque (Fig.38.1). MRI of the brain showed diffusion defect in the left parietal lobe involved in
the areas of the insula, basal ganglia, and left
frontal lobe (distribution of the middle cerebral
artery (Fig.38.2).
Procedure
On October 9, 2014, the patient underwent left
carotid endarterectomy under cervical block
anesthesia 3 days after the onset of his symptoms. The lesion in the internal carotid artery
was a mixed plaque with platelet thrombus,
narrowing the lumen to 90% transverse diameter. Distal to the high-grade focal stenosis,
the internal carotid artery was small in caliber.
Ten thousand units of heparin were administered; prior to carotid clamping, ACT was
280seconds.
Following endarterectomy, a bovine pericardial patch was applied, and heparin was reversed
with 25 protamine sulfate. The patient was discharged on the second postoperative day; however at midnight on the third postoperative day,
the patient developed severe headache and collapsed. The patient was taken to a nearby emergency room where a CTA of the neck and head
was performed which showed satisfactory endarterectomy site but a large intracerebral hemorrhage in the left frontal and parietal lobe
(Fig.38.3). The patient subsequently died from
intracerebral hemorrhage.
Discussion
Most neurological complications following
carotid endarterectomy/carotid artery stenting
(CEA/CAS) are ischemic in nature due to plaque
embolization during or immediately following
the procedure. In a small number of patients,
rapid correction of high-grade carotid stenosis
can lead to major increase in regional cerebral
blood ow to the areas of the brain with loss of
autoregulation resulting in hyperperfusion and
intracerebral hemorrhage. Within its milder
form, hyperperfusion syndrome manifests as
headache or seizures. Headache and seizures are
the result of cerebral edema. Following carotid
revascularization, intracerebral hemorrhage
© Springer Nature Switzerland AG 2020
S. S. Hans, Challenging Arterial Reconstructions, https://doi.org/10.1007/978-3-030-44135-7_38
159
160
38 Intracerebral Hemorrhage Following Carotid Endarterectomy
Fig. 38.1 CTA neck showing severe stenosis at the origin of the left internal carotid artery
occurs in less than 1% of patients with mortality
approaching 50% and associated signicant disability in most survivors [1–4]. Most studies
have reported a higher risk of postoperative
intracerebral hemorrhage among patients undergoing CAS as compared to patients undergoing
CEA [2]. In addition, there is a difference in the
risk and time course for hyperperfusion syndrome among patients undergoing CEA or CAS.
Hyperperfusion typically occurs in the rst
24hours following CAS in 2–7days following
CEA. One of the important factors associated
with hyperperfusion syndrome and intracerebral
hemorrhage is systemic hypertension after
carotid revascularization [2].
In this patient, the stroke was minor (NIH
stroke scale 4), and MRI of the brain showed
insular and left frontal lobe infarct. Ay etal. using
Discussion
Fig. 38.2 MRI brain showing infarct in the distribution
of the left middle cerebral artery
161
acute diffusion and perfusion-weighted MRI
within the rst 12 hours of symptoms of onset
and on day 5 or later reported increased conversion of ischemic but potentially viable
neighboring tissues into infarction involving the
insula [1]. Clinically, this patient did not experience any worsening of neurological decit following admission, but it’s possible that insula
infarct may have extended from the time MRI
scan was taken and the patient underwent
CEA. Postoperative blood pressure was well
maintained, and it is unlikely that postoperative
hypertension had a signicant role with the
development of intracerebral hemorrhage in this
patient.
This patient did not receive thrombolysis (tPA)
at the time of admission into the emergency room.
The role of intravenous tPA as a risk factor for
symptomatic intracerebral hemorrhage following
CEA has produced conicting results. Vellimana
reported increased risk of intracerebral hemorrhage following CEA in patients receiving intravenous tPA for acute ischemic stroke [3]. Bazan
et al. reported that urgent carotid intervention
Fig. 38.3 Postoperative CTA showing large left hemi-
sphere hemorrhage and satisfactory endarterectomy site
(CEA and CAS) is safe after thrombolysis for
minor to moderate acute ischemic stroke (NIH
stroke score<10) [4]. They performed 165 urgent
carotid interventions (CEA 135, CAS 30). Of
these, 19% (31 patients, CEA 25, CAS 6) had tPA
for acute stroke. The 30-day stroke, death, and
myocardial infarction rates were 9.7% for the tPA
group compared with 4.5% for the non-tPA group
(p = 0.37). In some patients with intracerebral
hemorrhage localized in the frontal lobe of the
brain, neurosurgery consult for possible craniotomy should be considered. However, in majority
of patients with intracerebral hemorrhage, location of the hemorrhage and severe neurological
decit predict craniotomy.
162
38 Intracerebral Hemorrhage Following Carotid Endarterectomy
References
1. Ay H, Arsava EM, Koroshetz WJ, Sorensen AG.Middle
cerebral artery infarct encompassing the insula are
more prone to growth. Stroke. 2008;39:373–8.
2. McDonald RJ, Cloft HJ, Kallems DF. Intracranial
hemorrhage is much more common after carotid stent-
ing than after endarterectomy: evidence from national
inpatient sample. Stroke. 2011;42:2782–7.
3. Vellimana AK, Yarborough CK, Blackburn S, Strom
RG, etal. Intravenous tPA therapy is an independent
risk factor for systemic intracerebral hemorrhage
following carotid endarterectomy. Neurosurgery.
2014;74:254–61.
4. Bazan HA, Zea N, Jennings B, Smith D, etal. Urgent
carotid intervention is safe after thrombolysis from
minor to moderate acute ischemic stroke. J Vasc Surg.
2015;162(6):1529–38.
Carotid Endarterectomy
forSymptomatic Radiation
Induced Carotid Stenosis
39
History andPhysical Examination
A 78-year-old male was admitted with symptoms
of right upper extremity weakness which lasted
30minutes in May of 2019. There was no associated involvement of speech or right lower extremity weakness. Medical comorbidities included
hypertension, hyperlipidemia, and former nicotine abuse. The patient underwent radiation therapy and chemotherapy for carcinoma of the
throat 10 years prior to this admission. Following
radiation therapy, the patient developed dyspha-
gia secondary to radiation induced upper esophageal stenosis, and the patient underwent
esophageal dilatation twice yearly with a pediatric esophagogastroscopy by a gastroenterologist
as an outpatient. Carotid duplex and CT angiography showed bilateral severe carotid artery stenosis (Fig.39.1). The left internal carotid artery
stenosis extended up to the level of C2 vertebral
body. On the right side, the cephalad end of the
plaque ended at the junction of C1 and C2. A
non-contrast CT scan of the head and MRI of the
brain did not show any evidence of acute infarct.
Fig. 39.1 Showing severe bilateral carotid stenosis with high plaque
© Springer Nature Switzerland AG 2020
S. S. Hans, Challenging Arterial Reconstructions, https://doi.org/10.1007/978-3-030-44135-7_39
163
164
39 Carotid Endarterectomy forSymptomatic Radiation Induced Carotid Stenosis
Neurology consultation conrmed transient ischemic attack in the distribution of the left middle
cerebral artery.
Procedure
The patient underwent left carotid endarterectomy under cervical block anesthesia on May
15. Dissection was difcult because of the
extensive scarring from radiation. Left carotid
endarterectomy with bovine pericardial patch
was performed (Fig.39.2). The patient developed increasing dysphagia on the third day following carotid endarterectomy. CTA of the
neck showed satisfactory carotid endarterec-
tomy site but a large hematoma in the neck
with deviation of the trachea toward the right
(Fig.39.3). On May 19, 2019, hematoma was
evacuated, and there was no evidence of any
active bleeding (Fig.39.4). Because of the difculty in swallowing, the patient was started
on total parenteral nutrition (TPN). Symptoms
of dysphagia improved in the ensuing 3 weeks,
and TPN was discontinued. The patient underwent right carotid stenting for symptomatic
right carotid stenosis 2 months later and has
been followed for the past 4 months with follow-up carotid duplex study showing no evidence of recurrent carotid stenosis. The patient
has not experienced any neurological
symptoms.
Fig. 39.2 Intraoperative pictures of carotid endarterectomy
Fig. 39.3 Post-operative CTA of the neck showing patent endarterectomy site with hematoma and neck with medial
deviation of the trachea
Discussion
165
Fig. 39.4 Pictures of the left neck with hematoma
Discussion
External radiation for head and neck cancer may
result in extracranial carotid stenosis; thus radiation represents a risk factor for the development
of stroke [1–4]. The exact mechanism underlying
radiation induced carotid stenosis is not well
understood. The process is inammatory in type,
and plaque characteristics are similar to those
present in atherosclerotic disease. However, the
natural history of radiation induced stenosis is
distinct [1]. Clinically, radiation induced carotid
stenosis is often bilateral, and the plaque extends
for a considerable distance cephalad in the internal carotid artery [1–4]. Carotid endarterectomy
in patients with history of neck radiation is associated with slightly increased incidence of cranial
nerve injury, cervical hematoma, and wound
complications. Carotid artery stenting is preferable in patients with history of head and neck cancer treated with prior radiation with associated
radical neck dissection and tracheostomy. On the
other hand, many investigators have reported satisfactory outcome of carotid endarterectomy in
patients following neck radiation though higher
incidence of recurrent stenosis/occlusion following carotid endarterectomy has been reported as
compared to de novo lesions [1–4].
Hematoma in the neck is a common complica-
tion of carotid endarterectomy and is usually due
to venous bleeding. In this patient, predisposing
factors for the hematoma were history of radiation and patient on Plavix (clopidogrel).
Postoperatively, hematoma in the neck should be
carefully evaluated and drained if there is any
evidence of respiratory compromise or difculty
in swallowing. A small amount of blood in a
closed tracheoesophageal compartment can
prove serious. Sometimes the rst sign of
compressive hematoma in the neck is an inspiratory stridor. If patient has a hematoma in the neck
with associated symptoms with compression of
trachea/esophagus and severe pain associated
with rmness and tenseness of the neck, the
patient should be taken back to the operating
room for re-exploration of the neck as an emergency. Neck sutures should be removed under
local anesthesia to prevent respiratory arrest.
Small hematomas in the neck may resolve on
their own.