1. Carotid Complications
Robert S. Dieter, MD RVT

2. I/we have no real or apparent conflicts of interest to report.
Robert S. Dieter, MD, RVT
I/we have no real or apparent conflicts of interest to report.

3. Complications of Carotid Stenting
Minor complications
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

4. 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)

5. 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 re-stenotic 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.

6. Carotid Sinus Baroreflex
Caudal
Ventrolateral
Medulla
Excitatory fibers
Nucleus Tractus Solitarious
(brainstem)
Excitatory fibers
Inhibitory fibers
CN IX Glossopharyngeal
(Hering)
Nucleus
Ambiguous
(Vagal nuclei)
Rostral
Ventrolateral
Medulla
(regulates SNS)
Carotid Sinus
Stretch sensitive mechanoreceptor
Increased stretch--> increased frequency of discharge
Increased BP --> increased frequency of discharge
Excitatory fibers
Sympathetic preganglionic neurons
Intermediolateral nucleus of the spinal cord

7. Carotid Sinus Baroreflex
Caudal
Ventrolateral
Medulla
Excitatory fibers
Nucleus Tractus Solitarious
(brainstem)
Excitatory fibers
Inhibitory fibers
CN IX Glossopharyngeal
(Hering)
Nucleus
Ambiguous
(Vagal nuclei)
Rostral
Ventrolateral
Medulla
(regulates SNS)
Carotid Sinus
Stretch sensitive mechanoreceptor
Increased stretch--> increased frequency of discharge
Increased BP --> increased frequency of discharge
Vagal stimulation
Excitatory fibers
Sympathetic preganglionic neurons
Intermediolateral nucleus of the spinal cord
Sympathetic withdrawal

8. Carotid Sinus Baroreflex
Caudal
Ventrolateral
Medulla
Excitatory fibers
Nucleus Tractus Solitarious
(brainstem)
Excitatory fibers
Inhibitory fibers
CN IX Glossopharyngeal
(Hering)
Nucleus
Ambiguous
(Vagal nuclei)
Rostral
Ventrolateral
Medulla
(regulates SNS)
Carotid Sinus
Stretch sensitive mechanoreceptor
Increased stretch--> increased frequency of discharge
Increased BP --> increased frequency of discharge
Anti ACh Rx
Pacemakers
Excitatory fibers
IV fluids
Vasopressors
Sympathetic preganglionic neurons
Intermediolateral nucleus of the spinal cord

9. 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?)

10. 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:
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

11. 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

12. Distal embolization (minor: TIAs; MAJOR: STROKES)
Intracranial angiogram
Careful review
Consider other etiologies to neuro status changes:
Hemorrhage
Contrast induced encephalopathy
Hyperperfusion syndrome

13. CAPTURE strokes relative to procedure time
Capture 3500 Stroke Events Distribution all patients

14. Intracranial hemorrhage
0.3%
Usually fatal
Risk factors:
Excessive anticoagulation
Poorly controlled blood presure
Aggressive attempts at neuro rescue
Recent, large ischemic stroke
Reverse anticoagulation
Neurosurgery consultation

15. 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)

16. Hyperperfusion syndrome%
Following revascularization, the increased perfusion pressure overwhelms the ability of the dilated arterioles to constrict, resulting in the development of the clinical syndrome.

17. Patient related factors
Diabetes
Long standing HTN
HTN microangiopathy
CVA / TIA on presentation
Age ≥72 yo
Recent (<3m) contralateral CEA
High-grade carotid stenosis

18. Flow related risk factors
Poor collateral flow
Contralateral carotid occlusion
Incomplete circle of Willis
Periprocedural hypoperfusion
Decreased cerebrovascular reserve

19. Treatment
Strict blood pressure control for up to six months or Doppler guided
Avoid nitrates, nipride and CCB
BB little effect on CBF
labetalol
Clonidine

20. Supportive Anticonvulsant therapy: Cerebral edema: Hyperventilation
Treat fever aggressively
Mannitol or hypertonic saline
Batbiturates
Steroids

21. 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