Download Carotid Sinus

Carotid Complications
Robert S. Dieter, MD RVT
Robert S. Dieter, MD, RVT
I/we have no real or apparent conflicts of interest to report.
Complications of Carotid Stenting
Minor complications
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Carotid artery spasm
hypotension / bradycardia
Carotid artery dissection
Contrast encephalopathy (very rare)
Minor embolic neurological events (TIAs)
Major complications
• Major embolic stroke
• Intracranial hemorrhage
• Hyperperfusion syndrome
• Carotid perforation (very rare)
• Acute stent thrombosis (very rare)
• Complications at the site of the vascular access
Carotid Spasm
• Spasm of the distal internal carotid artery (ICA) following distal
deployment of a filter is a complication that usually resolves
spontaneously after the filter-wire has been removed from the
vessel.
• Gentle approach minimizes the occurrence of distal carotid artery
spasm.
• A flow-limiting spasm could be a potential hazard in the presence of
occlusion of the contralateral ICA or in cases of incomplete circle of
Willis.
• Intra-arterial administration of 100 to 400 micrograms of
nitroglycerin through the guiding sheath generally leads to a rapid
resolution of the spasm.
• When all else fails or BP won’t allow vasodilators…TIME. Spasm will
generally resolve within 5-10 minutes
• (unresolving spasm: important to rule out dissection or thrombus)
Transient bradycardia and hypotension
• 13-38% of cases
• Transient sinus bradycardia or asystole are relatively common
particularly during post-dilatation after stenting
• This phenomenon is less commonly observed with treatment of restenotic lesions following carotid endarterectomy (CEA) because
the receptors may have been denervated by the surgical dissection.
• Effectively avoided by pretreatment with 0.5 to 1 mg of intravenous
atropine
• Exclude other etiologies of hypotension
– Volume depletion
– Cardiac pathologies (primarily preload dependent states: severe
pulmonary HTN, AS, severe diastolic dysfunction)
– Bleeding from the site of vascular access.
Carotid Sinus Baroreflex
Excitatory fibers
Excitatory fibers
Nucleus Tractus Solitarious
(brainstem)
Caudal
Ventrolateral
Medulla
Inhibitory fibers
Nucleus
Ambiguous
(Vagal nuclei)
CN IX Glossopharyngeal
(Hering)
Carotid Sinus
Stretch sensitive mechanoreceptor
Increased stretch--> increased frequency of discharge
Increased BP --> increased frequency of discharge
Rostral
Ventrolateral
Medulla
(regulates SNS)
Excitatory fibers
Sympathetic preganglionic neurons
Intermediolateral nucleus of the spinal cord
Carotid Sinus Baroreflex
Excitatory fibers
Excitatory fibers
Nucleus Tractus Solitarious
(brainstem)
Caudal
Ventrolateral
Medulla
Inhibitory fibers
CN IX Glossopharyngeal
(Hering)
Nucleus
Ambiguous
(Vagal nuclei)
Carotid Sinus
Vagal stimulation
Stretch sensitive mechanoreceptor
Increased stretch--> increased frequency of discharge
Increased BP --> increased frequency of discharge
Rostral
Ventrolateral
Medulla
(regulates SNS)
Excitatory fibers
Sympathetic preganglionic neurons
Intermediolateral nucleus of the spinal cord
Sympathetic withdrawal
Carotid Sinus Baroreflex
Excitatory fibers
Excitatory fibers
Nucleus Tractus Solitarious
(brainstem)
Caudal
Ventrolateral
Medulla
Inhibitory fibers
Nucleus
Ambiguous
(Vagal nuclei)
Anti ACh Rx
Pacemakers
CN IX Glossopharyngeal
(Hering)
Carotid Sinus
Stretch sensitive mechanoreceptor
Increased stretch--> increased frequency of discharge
Increased BP --> increased frequency of discharge
Rostral
Ventrolateral
Medulla
(regulates SNS)
Excitatory fibers
IV fluids
Vasopressors
Sympathetic preganglionic neurons
Intermediolateral nucleus of the spinal cord
Severe, sustained hypotension
• 4-11%
• Associated with:
– Advancing age
– Transient hypotension during balloon dilation
– Severe calcification
• Usually responds to IVF’s
• Occasionally vasopressors required
• (hold anti-HTN Rx morning of procedure?)
Distal embolization (minor: TIAs; MAJOR: STROKES)
• Risk factors for periprocedural distal embolization
– Carotid lesion:
• Soft plaque, fresh thrombus.
– Inadequate medical (pre)treatment:
• Poor pretreatment with double antiplatelet agents
• Insufficient heparin during procedure (check active coagulation time!).
– Stenting technique:
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Unprotected procedure
Aggressive manipulation of the guide wire
Aggressive balloon dilatation prior to or after stent deployment
Forceful introduction of a high-profile stent across a heavily calcified
tight lesion
• Prolonged, aggressive attempts to acess a highly atherosclerotic,
tortuous common carotid artery
Distal embolization (minor: TIAs; MAJOR: STROKES)
• Frequent neuro checks at each step
• If a change:
– Maintain BP (?therapeutic hypertension)
– Maintain heart rate
– Intravenous volume expansion (IVFs)
– Maintain airway
– If agitated or compromised airway- early
assistance of anesthesiologist
Distal embolization (minor: TIAs; MAJOR: STROKES)
• Intracranial angiogram
• Careful review
• Consider other etiologies to neuro status
changes:
– Hemorrhage
– Contrast induced encephalopathy
– Hyperperfusion syndrome
CAPTURE strokes relative to procedure time
100%
% of all patients
90%
80%
70%
58%
60%
50%
40%
30%
23%
20%
20%
10%
0%
Proce dure
Pos t-Procedure
Post-Discharge
Intracranial hemorrhage
• 0.3%
• Usually fatal
• Risk factors:
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Excessive anticoagulation
Poorly controlled blood presure
Aggressive attempts at neuro rescue
Recent, large ischemic stroke
• Reverse anticoagulation
• Neurosurgery consultation
Cerebral Hyperperfusion Syndrome: Mechanism
• Baroreceptor-reflex disruption (denervation after CEA ->
HTN)
• Axon-like trigeminovascular reflex effect (neuropetide
mediated increased in tone; Trigeminal nerve ganglion
stimulation produces frequency related increases in
carotid blood flow)
• Impaired auto-regulation:
– Decreased cerebrovascular reactivity
– Endothelial dysregulation (nitric oxide, free radicals, pH, CO2)
Hyperperfusion syndrome
• 0.3-2.7%
Following revascularization, the increased perfusion pressure overwhelms the ability of the
dilated arterioles to constrict, resulting in the development of the clinical syndrome.
Patient related factors
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Diabetes
Long standing HTN
HTN microangiopathy
CVA / TIA on presentation
Age ≥72 yo
Recent (<3m) contralateral CEA
High-grade carotid stenosis
Flow related risk factors
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Poor collateral flow
Contralateral carotid occlusion
Incomplete circle of Willis
Periprocedural hypoperfusion
Decreased cerebrovascular reserve
Treatment
• Strict blood pressure control for up to six months
or Doppler guided
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Avoid nitrates, nipride and CCB
BB little effect on CBF
labetalol
Clonidine
• Supportive
– Anticonvulsant therapy:
– Cerebral edema:
• Hyperventilation
• Treat fever aggressively
• Mannitol or hypertonic saline
• Batbiturates
• Steroids
Conclusion
• Complications of carotid stenting should be
low
• Solid understanding of risk factors for
complications as well as how to identify and
treat complications is necessary prior to
stenting