Carotid Endarterectomy

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Introduction   

Atherosclerosis in the carotid artery can lead to stenosis, increasing an individual’s risk for cerebrovascular disease or stroke. Various revascularization techniques treat carotid artery stenosis, a significant risk factor for stroke. Carotid Endarterectomy (CEA), the gold standard, involves removing plaque from the common and internal carotid arteries to improve blood flow and reduce stroke risk [1][8].  

This procedure, first performed in the early 1950s, has evolved in technique and indications, decreasing stroke risk, and improving survival in patients with moderate to severe carotid disease. 

Neurologic dysfunction from microemboli can manifest as sudden or transient symptoms, including unilateral motor and sensory loss, aphasia, or dysarthria, often termed Transient Ischemic Attack (TIA) [1]. The majority of TIAs are brief, and by definition, lasting less than 24 hours [2]. A stroke, also known as a cerebrovascular accident, occurs when there is an acute disruption in cerebral perfusion or vasculature, making it a medical emergency [3]. 

Extracranial carotid disease often presents with symptoms caused by embolization, with arterial emboli accounting for approximately 25% of strokes in Europe and North America [3]. A majority (80%) of these emboli originate from atherosclerotic lesions in the neck at the bifurcation of the carotid artery [3]. Transcranial Doppler studies reveal that emboli are present in about 20% of patients with moderate stenosis (>50%) and are even more common in those with severe stenosis (>70%) [4] [5]. Symptomatic patients exhibited a higher incidence and frequency of emboli [4] [5]. 

Atherosclerotic lesions in the internal carotid artery develop along the carotid bulb wall, opposite the external carotid artery origin [3]. The bulb’s enlargement creates an area of low wall shear stress, promoting atherogenic particle interaction with the vessel walls and localized plaque formation at the bifurcation [3]. This localized atheroma’s accessibility facilitates effective plaque removal, reducing stroke risk. Without treatment, 26% of patients with TIAs and over 70% with severe stenosis will develop permanent neurological impairment within two years. Plaque removal can reduce this risk to 9% [3].  

Carotid endarterectomy (CEA) is a surgical procedure aimed at unblocking a carotid artery to prevent stroke. The risk of stroke during CEA is about 2%, due to emboli or cross-clamp-related ischemia [8]. Monitoring cerebral blood supply during CEA is critical under general anesthesia, where surgeons use EEG or transcranial Doppler. Cerebral near-infrared spectroscopy (NIRS) serves as a dynamic tool for assessing and optimizing cerebral perfusion [7]. Providers use NIRS to monitor cerebral blood flow and make necessary adjustments during procedures. Inducing hypertension or placing an intracarotid shunt can maintain cerebral perfusion, though each method carries its own risks [6]. 

Carotid angioplasty and stenting have emerged as alternatives to CEA for treating carotid artery stenosis [9]. These techniques, similar to those used in cardiovascular disease, are useful in patients with restenosis following CEA. While EEG monitoring is not routine during these procedures, the role of these alternatives in managing symptomatic and asymptomatic carotid artery disease remains under study. 

Anatomy and Physiology of the Carotid Arteries 

The carotid arteries, a pair of vessels, transport oxygen-rich blood from the heart to the brain [10]. Traversing up either side of the neck, these arteries enter the brain, where they play a critical role in supplying most of the brain with blood [10]. The anatomical structure of the carotid arteries allows for significant redundancy; four out of five people can maintain adequate cerebral blood flow with just one carotid artery due to the anastomoses of other arteries [10]. However, the exact nature of these arterial connections can vary between individuals.  

Understanding the anatomy and physiology of the carotid arteries is essential in comprehending the pathophysiology of carotid artery disease and its implications for stroke risk. This knowledge underpins the clinical approach to diagnosing, managing, and treating conditions like carotid stenosis, aiming to reduce the incidence of stroke and improve patient outcomes. 

Structure and Bifurcation 

The carotid arteries consist of the common carotid arteries, which bifurcate into the internal and external carotid arteries at the level of the fourth cervical vertebra (C4), near the superior border of the thyroid cartilage [10]. This bifurcation occurs within the carotid sheath, a structure formed by the deep cervical fascia that also contains the internal jugular veins and vagus nerves [10]. 

The internal carotid artery (ICA) ascends into the skull to form part of the Circle of Willis, supplying blood to the brain and eyes [10]. The external carotid artery (ECA) branches off to supply blood to the neck, thyroid gland, face, and scalp [10]. 

Carotid Stenosis and Atherosclerosis 

Carotid stenosis occurs when one or both carotid arteries narrow due to plaque buildup, a condition known as atherosclerosis [11]. Plaque accumulates at the bifurcation of the common carotid artery into the ICA and ECA [12]. This buildup narrows the lumen—the inside opening where blood flows—altering blood flow dynamics and increasing the risk of blood clot formation [12].  

A blood clot that breaks away and travels to the brain can obstruct blood flow, leading to a stroke. While a stroke can also occur from insufficient blood flow through a narrowed carotid artery, this is rare due to the collateral circulation provided by the arterial anastomoses. 

Risk Factors and Stroke 

The degree of carotid artery narrowing, often reported as a percentage, is a critical factor in estimating stroke risk. Research has shown that both the severity of stenosis and the presence of symptoms influence stroke risk. A higher percentage of stenosis correlates with a greater risk of stroke if the condition is symptomatic [13]. 

Carotid artery stenosis is a manifestation of systemic atherosclerotic disease. Any risk factor that predisposes a patient to progressive atherosclerosis can lead to carotid artery stenosis, resulting in ischemic stroke or transient ischemic attack (TIA) symptoms [13]. Common risk factors include smoking, hyperlipidemia, male gender, and increased age [13]. 

In a minority of cases, in young females, fibromuscular dysplasia (FMD) plays a more significant role in carotid artery stenosis. FMD is a noninflammatory, nonatherosclerotic condition that affects medium-sized arteries, notably the carotid and renal arteries [3].  

Indications  

Carotid stenosis is a chronic condition that develops as people age due to the accumulation of excess cholesterol in the blood [11]. Low-density lipoprotein (LDL) cholesterol plays a significant role in this process. Over time, LDL cholesterol traps inside the blood vessel walls and adheres to the outside, leading to plaque formation [11]. This process, known as atherosclerosis, narrows the carotid arteries.  

Numerous patients with carotid stenosis do not exhibit symptoms, and healthcare providers often discover the condition as a secondary finding. However, when the narrowing becomes symptomatic, it can cause a transient ischemic attack (TIA) or stroke. A TIA, which does not cause permanent brain damage and is undetectable on MRI or CT scans, shares similar signs with a stroke, including facial droop, speaking difficulties, comprehension, unilateral weakness or numbness, and sudden vision loss in one eye [2]. The side of the body affected by these symptoms is notable; for instance, stenosis in the left carotid artery affects the left eye and the right side of the body, and vice versa for the right carotid artery.  

Amaurosis fugax (AF) is a classic symptom of carotid artery disease, presenting as transient vision loss (TVL) [38]. AF can manifest as either monocular (TMVL) or binocular (TBVL) vision loss [38]. The workup for patients with AF must be evaluated for sources of emboli and ischemia. This involves imaging studies such as bilateral carotid Doppler ultrasonography, magnetic resonance angiography (MRA), or computed tomography (CT) angiography of the neck and head [38]. These diagnostic tools help identify the underlying causes and guide appropriate treatment standards.  

History & Physical  

During a routine medical examination, a primary care provider might listen to the carotid arteries using a stethoscope to check for a bruit, a “whooshing” sound indicative of significant narrowing. If a healthcare provider detects a bruit, they will often schedule a carotid ultrasound for the patient. Carotid stenosis may cause non-specific symptoms such as dizziness, vertigo, lightheadedness, fainting, visual problems, headaches, or weakness [14].  

Several factors contribute to the development of atherosclerotic plaque in the carotid arteries, including genetics, high cholesterol, smoking, a fatty diet, and physical inactivity [14]. Patients who have undergone radiation therapy for head and neck cancers may develop carotid artery stenosis as a result of radiation effects rather than plaque buildup [15]. Some inflammatory conditions can also cause irregularities in the carotid arteries [16].  

Comprehensive Management and Treatment Strategies for Carotid Artery Disease 

Vascular surgeons can perform carotid endarterectomy (CEA) under regional anesthesia in patients with severe chronic obstructive pulmonary disease, coronary artery disease (CAD), and other comorbidities. Carotid stenting is an option for patients with a history of neck irradiation, modified radical neck dissection, or re-operative CEA [3]. Consider combined CEA and coronary artery bypass grafting for patients with concurrent symptomatic carotid stenosis and coronary artery disease (CAD) [3].  

Patients undergoing CEA should take antiplatelet therapy unless contraindicated [17]. A vascular surgeon or neurosurgeon can perform the procedure under general or local anesthesia, with local anesthesia allowing the patient to remain awake but sedated, feeling numb at the surgery site.  

The development of significant restenosis after CEA or carotid angioplasty with stenting poses a risk of ischemic stroke [18]. Treatment strategies play a crucial role in preventing this complication. Surgeons often manage restenosis after carotid angioplasty with stenting by performing CEA and removing the stent, while managing restenosis after CEA involves performing carotid angioplasty with stenting [18] [19]. In cases where stenting is contraindicated, repeated CEA may be necessary, though it carries risks of bleeding and cranial nerve trauma. 

The North American Symptomatic Carotid Endarterectomy Trial (NASCET) and the European Carotid Surgery Trial (ECST) have demonstrated the benefits of CEA over medical management alone for symptomatic patients with severe carotid stenosis [8]. The 2nd European Carotid Surgery Trial (ECST-2): recommends carotid endarterectomy for symptomatic patients with carotid stenosis of 50% or more, based on findings from randomized trials conducted 30 years ago [20].  

The Asymptomatic Carotid Atherosclerosis Study (ACAS) supports using CEA for asymptomatic patients with significant stenosis [21]. CEA addresses symptomatic high-grade stenosis, symptomatic moderate stenosis, and asymptomatic high-grade stenosis of the internal carotid artery. Early intervention reduces the risk of stroke, though the benefits diminish if performed more than two weeks after symptom onset or in cases of large stroke areas, contralateral carotid occlusion, hemodynamic instability, or contralateral laryngeal palsy [17]. The ongoing CREST-2 (Carotid Revascularization, Endarterectomy Versus Stent Trial‐2 trial) aims to provide updated data comparing intensive medical therapy versus surgery in patients with asymptomatic, high-grade internal carotid stenosis [22].  

Providers can screen for asymptomatic carotid stenosis using carotid duplex ultrasonography (CDU) to assess the degree of stenosis by measuring flow velocity [4]. Other imaging modalities like computed tomography angiography (CTA) and contrast-enhanced magnetic resonance angiography (CE-MRA) provide additional insights into plaque morphology, intracranial collateralization, and brain perfusion, helping to determine individual risk profiles when considering surgery [23]. 

Evolving Surgical Methods for Carotid Artery Revascularization: CEA, TFCAS, and TCAR 

The primary methods to address carotid stenosis include Carotid Endarterectomy (CEA), Transfemoral Carotid Artery Stenting (TFCAS), and Transcarotid Artery Revascularization (TCAR) [34]. CEA has long been the gold standard surgical approach, offering effective plaque removal from the carotid arteries [34].  

TFCAS emerged as a less invasive alternative, beneficial for patients with severe stenosis and coexisting conditions [34]. TCAR has gained prominence for high-risk patients due to its lower stroke rates and favorable outcomes [34]. Each method offers distinct advantages, with the choice depending on patient-specific risk factors and anatomical considerations. 

Carotid Endarterectomy (CEA) 

Carotid endarterectomy (CEA) has been the standard operative therapy for carotid artery stenosis in both symptomatic and asymptomatic patients [1][8]. CEA involves removing plaque from the carotid artery via surgical methods to prevent stroke. Analysis of more than 100,000 patients in a cohort study highlights that 75.0% of the patients between 2015 and 2019 underwent CEA, making it the most common carotid revascularization approach [34].  

Transfemoral Carotid Artery Stenting (TFCAS) 

TFCAS accounted for 14.3% of carotid revascularization approaches in the study, reflecting its role as a viable alternative to CEA in high-risk patients [34]. Transfemoral Carotid Artery Stenting (TFCAS) treats carotid artery blockages by using a metallic stent to open a narrowed artery [34]. This procedure serves as an alternative for patients at substantial risk for open surgery and is the preferred treatment for restenosis following Carotid Endarterectomy (CEA). 

Transcarotid Artery Revascularization (TCAR) 

Transcarotid artery revascularization (TCAR) has emerged as a new method for carotid revascularization for high-risk patients [34]. Contemporary data from the Vascular Quality Initiative (VQI) show excellent results for TCAR. In the cohort analyzed from the VQI database during the years 2015-2019, 10.7% of patients underwent TCAR, highlighting its increasing use among patients at substantial risk for stroke, cranial nerve injury, or cardiovascular events [34]. 

TCAR has become the primary carotid revascularization approach in the US for high-risk patients, surpassing both TFCAS and CEA [34].  

While CEA remains the most common overall approach, TCAR reflects advancements in medical devices and surgical techniques, offering safer and more effective options for specific patient groups and underscoring the efficiency of modern carotid revascularization techniques [34]. 

Considerations 

• Symptomatic Ill Patients: Consider carotid angioplasty and stenting (CAS) for patients who are unstable and cannot undergo open surgery. During CAS, the vascular surgeon inserts a small, flexible, mesh-like tube (stent) into the artery under local anesthesia [17]. The surgeon then expands the tube over a balloon to widen the artery’s lumen and improve blood flow. 

• Peri-Procedural Risks: According to the Carotid Revascularization Endarterectomy versus Stenting Trials (CREST), both carotid endarterectomy (CEA) and CAS yield similar outcomes regarding postoperative complications such as restenosis, myocardial infarction, long-term stroke, and/or death [8]. However, the risk of peri-procedural stroke is higher in patients undergoing CAS, whereas the overall risk of myocardial infarction is higher in CEA [24]. 

• Radiation Therapy History: Patients with a history of neck radiation therapy face an increased risk of temporary cranial nerve injury during carotid endarterectomy (CEA), though this does not serve as an absolute contraindication [17]. These patients are also at increased risk of late cerebrovascular events and restenosis following CAS [17]. Performing CEA is more challenging in the radiated neck due to more diffuse plaques, adhesions, scar tissue, and potential wound complications resulting from radiation therapy [17]. 

• Gender Differences in Outcomes: Symptomatic women may be at an increased risk of postoperative complications after CEA compared to men [17][25]. However, outcomes and complications are similar between sexes for asymptomatic patients [17] [25]. 

Complications  

Consider the risks of carotid endarterectomy alongside the potential benefits of the procedure. The morbidity and mortality rates of CEA depend on multiple factors, including: 

• Surgical expertise 

• Degree of carotid artery stenosis 

• Presence of cerebral infarction 

• Coexistent medical conditions including ischemic heart disease 

Reported morbidity rates for CEA have varied from 0 to 20% [26]. In one multicenter study, perioperative morbidity was 2.2%, and mortality was 3.3%, resulting in a combined complication rate of 5.5% in high-risk patients [26]. 

Major Complications 

• Myocardial Infarction 

• Hyperperfusion Syndrome 

• Nerve Injury 

• • Cranial nerves often affected include the hypoglossal, vagus, glossopharyngeal, and facial (marginal mandibular) nerves [27]. 

• Perioperative Stroke 

• Restenosis 

• Death 

Minor Complications 

• Transient Ischemic Attack (TIA) 

• Bleeding 

• Infection 

• Greater Auricular Nerve Injury 

• Dysphagia 

Angiography Risks 

Angiography, often performed as part of the CEA procedure, carries a risk of approximately 1% [28]. The timing of cerebral revascularization after ischemic stroke is critical. Recent studies have demonstrated the safety and effectiveness of performing CEA during the acute phase of stroke: 

• CEA in the acute period post-stroke leads to significant regression of neurological symptoms and is associated with a negligible risk of adverse cardiovascular events [29]. 

• Emergency CEA performed in the first hours after stroke development has shown satisfactory outcomes, due to thorough preoperative preparation [30]. The use of a temporary shunt reduces hemodynamic shock after internal carotid artery occlusion, though this practice is associated with a higher likelihood of hemorrhagic transformation [8]. 

Balancing Benefits and Risks of Carotid Endarterectomy (CEA): Key Considerations and Patient Outcomes 

Consider the potential benefits of carotid endarterectomy (CEA) alongside its risks. Factors such as surgical expertise, the degree of carotid artery stenosis, the presence of cerebral infarction, and coexistent medical conditions like ischemic heart disease influence the morbidity and mortality rates for CEA. Reported morbidity rates vary, with some studies indicating perioperative morbidity of 2.2% and mortality of 3.3% [30] [31]. 

Studies have highlighted the safety and efficacy of performing CEA during the acute phase of stroke, showing significant regression of neurological symptoms with a minimal risk of adverse cardiovascular events. However, performing CEA in proximity to stroke onset increases the risk of hemorrhagic transformation (blood from outside the brain leaks into the brain through a damaged blood-brain barrier) and other adverse outcomes [32] [33].  

A 2021 multicenter study reported a symptomatic hemorrhagic transformation rate of 3.6% and a combined endpoint of adverse outcomes reaching 20.4%, suggesting caution in immediate post-stroke revascularization with CEA [32] [33]. Careful assessment and risk management are essential to optimize patient outcomes when considering CEA. 

Carotid Endarterectomy and Carotid Artery Stenting 

Carotid artery stenting (CAS) is often the preferred treatment for symptomatic carotid occlusion (50-99%) in patients with multiple comorbidities, tracheostomies, or a history of neck radiation or dissection [3]. Despite the increased risk of stroke during the procedure, CAS outcomes are comparable to carotid endarterectomy (CEA) [3]. CAS is under investigation in the ongoing CREST-2 study.  

In the conventional technique, the surgeon creates a longitudinal arteriotomy from the distal common carotid artery (CCA) onto the internal carotid artery (ICA), removes the plaque, and closes the arteriotomy with a patch [35]. In the eversion technique, the surgeon transects the ICA at its origin from the CCA and averts the vessel to expel the plaque [35]. 

CEA involves accessing the carotid sheath via a longitudinal incision along the medial border of the sternocleidomastoid muscle (SCM), isolating and controlling the distal CCA, its bifurcation, and the ICA and external carotid artery (ECA) [35]. Surgeons must decide whether to use a shunt to maintain cerebral perfusion through the ICA.  

Clinical Significance 

The primary purpose of carotid endarterectomy (CEA) is to prevent stroke. The benefit of CEA is dependent on achieving low morbidity and mortality rates. CEA treats symptomatic high-grade stenosis, symptomatic moderate stenosis, and asymptomatic high-grade stenosis of the internal carotid artery [17]. 

Implications for Current Practice 

The benefit of endarterectomy lies in its ability to reduce the substantial stroke risk in treated patients [1][3]. The combined stroke and death risk of CEA ranges from 2% to 4%, with higher rates in symptomatic patients compared to asymptomatic ones. [1][3] These findings highlight the crucial role of CEA in stroke prevention for patients with significant carotid stenosis. 

Two Case Studies: Carotid Endarterectomy (CEA) for Extracranial Carotid Disease  

Neurologic dysfunction from microemboli can manifest as sudden or transient symptoms, including unilateral motor and sensory loss, aphasia, or dysarthria, often termed Transient Ischemic Attack (TIA). Most TIAs are brief, lasting only minutes, and by convention, the limit for a TIA is 24 hours.  

Persistent symptoms beyond this period indicate a stroke or cerebrovascular accident (CVA). An embolus to the ophthalmic artery can cause temporary or permanent vision loss, known as amaurosis fugax. 

Atherosclerotic lesions in the internal carotid artery can develop along the carotid bulb wall, opposite the external carotid artery origin. The bulb’s enlargement creates an area of low wall shear stress, promoting atherogenic particle interaction with the vessel walls and localized plaque formation at the bifurcation. This localized atheroma’s accessibility facilitates effective plaque removal reducing stroke risk. Without treatment, 26% of patients with TIAs and over 70% with severe stenosis will develop permanent neurological impairment within two years. Plaque removal can reduce this risk to 9%. 

Patient Case Study: Carotid Endarterectomy with Nerve Block Technique 

Patient Profile: 

• Age/Gender: 70-year-old female 

• Medical History: Severe stenosis of the right internal carotid artery, previous history of stroke 

Clinical Presentation and Diagnosis 

A 70-year-old female with severe stenosis of the right internal carotid artery arrived for evaluation and treatment. Due to her age and history of stroke, the surgical team opted for carotid endarterectomy (CEA) under regional anesthesia to allow for continuous neurological monitoring during the procedure. 

Nerve Block Technique: The surgical team positioned the patient supine with her neck extended and rotated away from the blocked side. Using a high-frequency linear ultrasound transducer, the surgeon visualized the cervical plexus along the posterior border of the sternocleidomastoid muscle. Using ultrasound guidance, the clinician inserted a 22-gauge, 50 mm needle in-plane. After confirming negative aspiration and correct needle placement, the clinician incrementally injected 10 mL of 0.25% bupivacaine around the cervical plexus, while monitoring for signs of intravascular or intrathecal injection. 

Procedure: The surgeon performed the carotid endarterectomy to remove the atherosclerotic plaque. Throughout the procedure, regional anesthesia allowed the surgical team to monitor the patient’s neurological status. 

Outcome: The procedure was successful with no immediate complications. The patient remained stable and showed no signs of post-operative neurological deterioration. 

Patient Case Study: Carotid Endarterectomy in an 81-Year-Old Male with Change in Mental Status  

Patient Profile: 

• Age/Gender: 81-year-old male 

• Medical History: Ischemic stroke, hypertension, hyperlipidemia, hypothyroidism, chronic kidney disease, previous ischemic strokes in 2003 and 2007 with residual right-sided weakness, on aspirin/dipyridamole for stroke prevention. 

Clinical Presentation 

An 81-year-old right-handed man presented to the Emergency Department with symptoms of dizziness, nausea, dysarthria, and a change in mental status. His history included two prior ischemic strokes, hypertension, hyperlipidemia, hypothyroidism, and chronic kidney disease. 

Initial Examination: 

• Vital Signs: Afebrile, BP 162/81 mmHg, HR 77 bpm, O2 sat 98% on room air 

• Neurological Examination: Alert and oriented to person but disoriented to location and time. Noted poor memory, fair concentration, mild dysarthria, nonfluent aphasia, poor knowledge, and limited judgment. The pupils appeared round and reacted to light, with extraocular movements intact. No facial weakness or pronator drift, and motor and sensory examinations were nonfocal. Reflexes were symmetrical, and coordination was normal. 

Laboratory Studies: 

• WBC Count: 12,600/μL 

• Platelet Count: 155,000/μL 

• Electrolytes: Sodium 141 mEq/L, Potassium 4.3 mEq/L 

• Glucose: 123 mg/dL 

• Serum Creatinine: 1.50 mg/dL 

Imaging: 

• CT scan: No acute findings 

• CTA: Remote infarct in the left parietal lobe, diminished flow in distal left MCA branches, severe atherosclerosis and stenosis of the proximal ICA, PTA supplying mid and distal basilar artery. 

• MRI: Subacute infarcts in the posterior left temporal and frontal lobes, right occipital lobe, and bilateral cerebellar hemispheres. 

Hospital Course 

Two days after admission, the patient became nonverbal and somnolent, with a motor examination revealing right-sided hemiplegia. A repeat MRI showed new areas of restricted diffusion in the left frontoparietal region, brain stem, bilateral superior cerebellar, and occipital regions, indicating emboli from the atherosclerotic left ICA reaching the posterior fossa via the PTA. 

Intervention: The medical team transferred the patient to the neuroscience intensive care unit, setting a systolic blood pressure goal of 180-200 mmHg. A carotid duplex ultrasound confirmed 80% to 99% stenosis of the proximal left ICA. One week after admission, the surgical team performed a left carotid endarterectomy and used a bovine patch for angioplasty. 

Outcome: The procedure was successful with no complications. The patient’s neurological status improved, and he transitioned to a skilled nursing facility for rehabilitation without experiencing a recurrence of ischemic stroke. 

Post-Endarterectomy Home Care Instructions 

Ensuring patients adhere to proper home care instructions post-carotid endarterectomy is vital for a smooth recovery. During the first few days after surgery, patients should engage in quiet activities such as reading or watching television to avoid unnecessary strain. 

Patients must take their prescribed medications to aid in recovery and prevent complications. It is crucial to perform a daily inspection of the incision site, monitoring for signs of infection, including redness, swelling, drainage, or warmth. The wound must remain dry until the healthcare provider permits showering, and patients should avoid scrubbing the incision area. 

When shaving around the incision, patients should use an electric razor to prevent accidental cuts. Inform patients that temporary loss of sensation along the jawline, incision line, and earlobe is a normal postoperative occurrence, with sensation returning within 6 to 12 months [37]. 

Patients should increase their activity level but avoid strenuous activities for at least 7 to 10 days following surgery [36]. They must refrain from lifting objects heavier than 10 pounds for 2 to 3 weeks to prevent undue stress on their healing body [36]. They should not drive until their healthcare provider grants clearance, which occurs 1 to 2 weeks post-surgery. 

Patients should consult their healthcare provider to determine an appropriate timeline for returning to work based on their recovery progress. Adhering to these guidelines will help ensure a safe and effective recovery process. 

Conclusion

Extracranial carotid disease, often presenting with symptoms caused by embolization, is a significant contributor to strokes in Europe and North America. Atherosclerotic lesions at the bifurcation of the carotid artery are responsible for 80% of emboli leading to these strokes. Carotid endarterectomy (CEA) addresses these lesions, reducing stroke risk by removing the plaque and restoring normal blood flow. Studies have shown that without treatment, 26% of patients with transient ischemic attacks (TIAs) and over 70% with severe stenosis will develop permanent neurological impairment within two years. CEA can reduce this risk to 9%. 

Carotid endarterectomy (CEA) stands as the preferred treatment for both symptomatic and asymptomatic carotid stenosis. The procedure, which involves plaque removal from the common and internal carotid arteries, has evolved since its inception in the early 1950s, leading to improved survival rates and reduced stroke risks. While carotid angioplasty and stenting offer alternative treatments for patients with restenosis post-CEA, CEA’s effectiveness in preventing strokes in high-grade stenosis cases is well-documented.  

Understanding the anatomy and physiology of the carotid arteries, along with the pathophysiology of carotid artery disease, is crucial for optimizing treatment strategies and improving patient outcomes. Providers must weigh the risks of CEA, such as myocardial infarction, hyperperfusion syndrome, nerve injury, perioperative stroke, restenosis, and death, against its benefits. However, with careful patient selection and advancements in surgical techniques and monitoring, CEA continues to be a critical intervention in managing carotid artery disease and preventing strokes. 

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