Carotid Complications Robert S. Dieter, MD RVT

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.

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

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 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.

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

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

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

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: 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 Capture 3500 Stroke Events Distribution all patients

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

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 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 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 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