​Kembara Xtra - Medicine- Carotid Stenosis

​Kembara Xtra - Medicine- Carotid Stenosis 
Introduction 
Atherosclerosis is the most frequent origin of carotid stenosis, but it can also result from intimal fibroplasia, vasculitis, adventitial cysts, or vascular malignancies.
The carotid artery lumen usually narrows as a result of atherosclerotic alterations in the vessel wall. 90% of extracranial carotid lesions and up to 30% of all ischemic strokes are caused by atherosclerotic plaques.
● Carotid stenosis that is "hemodynamically significant" causes a drop in pressure or a decrease in flow. It roughly equates to a stenosis with a diameter reduction of 60–99%.
● Following criteria are used to categorize carotid lesions: - Symptomatology
Asymptomatic patients tend to be homogenous and stable, while symptomatic patients are more likely to have strokes or transient ischemic attacks. High grade stenosis ranges from 80 to 99%.
Low grade: 50% stenosis; Moderate grade: 50-79% stenosis


Prevalence and incidence of disease 

more typical among men and as people get older 
Unknown incidence (many asymptomatic patients go undetected.)
Prevalence

Age 50 years: males 0.2%, women 0%; Age >80 years: men 7.5%, women 5%; Moderate stenosis

Age 50 years: men 0.1%, women 0%; severe stenosis
- Age >80 years: 3.1% men, 0.9% women

Pathophysiology and Etiology 
At the carotid bifurcation, atherosclerosis typically starts around adolescence. The carotid bulb's blood flow patterns are distinctive. Endothelial dysfunction and damage are brought on by hemodynamic abnormalities. Stenosis then develops as a result of plaque formation in the vessel wall.
Although the root reason is not fully understood, there are some risk factors that are usually present. The vessel wall's tensile stress, turbulence, and artery wall shear stress appear to be at play.

Genetics – Increased prevalence in families – Genetically connected factors – Obesity, Diabetes mellitus (DM), race, and hypertension (HTN) – TNFSF4, PPARA, TLR4, ITGA2, and HABP2 were all significantly related with worse carotid plaque in a recent single nucleotide polymorphism research.

Risk factors include male sex, family history, advanced age (>65 years old), coronary artery disease (CAD), peripheral artery disease, aortic aneurysmal disease, and congenital arteriopathies. 
Smoking, diet, dyslipidemia, physical inactivity, obesity, HTN, and diabetes are all modifiable variables.
Chlamydia pneumoniae and cytomegalovirus are potential causes. 


Prevention

 Antihypertensive medication to keep blood pressure under 140/90 mm Hg (systolic blood pressure of 150 mm Hg is preferred in older patients).
Quitting smoking to lower the risk of developing atherosclerosis and having a stroke 
Lipid control: statin therapy-induced reduction of carotid atherosclerotic lesions

Stroke and transient ischemic attack (TIA) are associated conditions. 
Peripheral vascular disease (PVD), CAD/myocardial infarction (MI), hypertension, and diabetes mellitus
• Hyperlipidemia


Diagnosis 

It is not advised to perform a carotid stenosis screening.
However, a workup for this condition may be necessary if there are symptoms that point to a stroke or TIA.

History of a cerebral ischemia event, identification of comorbidities that can be managed and those that cannot, identification of strokes, TIAs, amaurosis fugax (monocular blindness), aphasia, and CAD/MI

Review of systems with an emphasis on the risk factors for stroke (HTN and arrhythmias) and peripheral arterial disease

clinical assessment 
Amaurosis fugax causes transitory ipsilateral blindness due to retinal ischemia. Lateralizing neurologic deficits: contralateral motor and/or sensory deficiency. 
Dysarthria, aphasia (in the case of dominant hemisphere involvement, typically left), and visual field deficiency 
Low sensitivity and specificity for carotid bruit

Aortic valve stenosis, aortic arch atherosclerosis, arrhythmia with cardiogenic embolization, migraine, a brain tumor, metabolic abnormalities, a functional or psychological deficiency, and seizures are among the possible diagnoses.

Diagnostic tests and laboratory results 

Initial examinations (lab, imaging)
Workup for TIA/stroke suspicion may involve the following:
With differential, CBC
ESR (in the case that temporal arteritis is a factor) and a basic metabolic panel 
Fasting lipid profile; glucose/hemoglobin A1c
The first diagnostic test that is advised for asymptomatic patients with carotid stenosis that is known or suspected is duplex ultrasonography.
Duplex ultrasonography (US) has an accuracy of 98% and a sensitivity of 88% in detecting 50% of stenosis.

Tests in the Future & Special Considerations
If a history or physical examination suggests stenosis, proceed to imaging. Other noninvasive imaging methods can enhance duplex results. - CT angiography has a 100% specificity and 88% sensitivity.
 Requires MR angiography, which has a 95% sensitivity and 90% specificity, and requires IV contrast with a risk of future kidney morbidity.
 Analyzes the aortic arch, common carotid artery, and cerebral circulation (intra- and extracranial). If any of the following traits are present, unstable plaque is likely present: 
Thin/ruptured fibrous cap is present.
Has a necrotic core rich in lipids and tends to overstate the degree of stenosis

Other/Diagnostic Procedures
The usual gold standard for diagnosis is cerebral angiography: 
Outlines the aortic arch and proximal vessels' anatomical features. 
The procedure is invasive and comes with a number of risks: - Renal impairment brought on by contrast (1–5% complication rate)
Neurologic problems and thromboembolic-related issues (complication rate: 1-2.6%) - Should only be utilized when other tests are inconclusive
Interpretation of Tests
At the carotid bifurcation, stenosis frequently develops, with plaque formation most frequently occurring at the level of the proximal internal carotid artery: Plaque resides in the intima and inner media, avoiding the outer media and adventitia, and is thickest at the carotid bifurcation.

Homogenous (stable) plaques hardly ever bleed or ulcerate, according to plaque histology:
 Deposition of fibrous tissue and fatty streaks
Heterogenous (unstable) plaques may bleed or ulcerate due to diffuse intimal thickening.
 The presence of cholesterol crystals, necrotic debris, and macrophages that are lipid-loaded Ulcerated plaques are soft, gelatinous clots made up of red and white blood cells, platelets, and fibrin.

Management 
The main treatments for both asymptomatic and symptomatic carotid stenosis are quitting smoking, blood pressure management, antiplatelet medicine, and statin medication.

Treatment 

 Patients should be counseled to stop smoking and offered smoking cessation intervention to lower the risk of atherosclerosis development and stroke. Lifestyle modifications: food control and weight loss, exercise of 30 minutes per day at least five days per week.

 Managing HTN with antihypertensive medications to keep blood pressure under 140/90 mm Hg, or 150/90 mm Hg in elderly patients. Tighter blood pressure control may prevent cerebrovascular incidents in carefully chosen individuals, however this is questionable.

Medication: Antihypertensive therapy (140/90 mm Hg or, in the elderly, 150/90 mm Hg 
Exercise, quitting smoking, and a healthy diet are beneficial therapeutic add-ons.
The risk is decreased in people with diabetes when a comprehensive program includes tight management of HTN with ACEI or ARB medication. Statin initiation is advised; consider moderate- to high-intensity statin therapy for anti-inflammatory effect. It is unknown whether rigorous glucose-lowering medication helps prevent strokes.
Aspirin: 75 to 325 mg/day If the patient has a sustained TIA or ischemic stroke, antiplatelet therapy with aspirin alone (75 to 325 mg/day), clopidogrel alone (75 mg/day), or aspirin plus extended-release dipyridamole (25 and 200 mg BID, respectively) is recommended. Combining clopidogrel and aspirin within three months after the TIA or CVA is not advised.

Motives for the Referral 
Order imaging and get in touch with neurology if you have recent stroke symptoms.
If the carotid stenosis is known and the patient is a candidate for surgery, some experts advise duplex imaging every six months.

Carotid endarterectomy (CEA) is of some benefit in patients with 50–69% symptomatic stenosis, highly beneficial for those with 70–99% stenosis without near-occlusion, and ineffective in patients with carotid near-occlusion. Surgical Procedures Symptomatic carotid stenosis (history of ischemia ipsilateral to stenosis) - Patients with a minimum 5-year life expectancy are advised to undergo CEA. Predicted perioperative stroke or death rates must be less than 6%.
– All individuals with CEA are advised to take aspirin (81 to 325 mg/day) as part of their treatment.
Prior to surgery, aspirin should be taken daily for at least three months, but it can be continued permanently.
– Similar long-term results are seen with carotid artery stenting (CAS) as with CEA. When contemplating a carotid intervention, age should be taken into account.
CAS has a similar mortality risk in the young and the elderly, but the elderly have a higher risk of unfavorable cerebrovascular events. In spite of higher mortality, CEA is linked to similar neurologic outcomes in both young and old people.
 In some patients with neck anatomy that is unfavorable for vascular surgery and those with concomitant diseases that significantly raise the risk of anesthesia and surgery, CAS is recommended.
For 30 days following CAS, dual antiplatelet therapy using aspirin (81 to 325 mg/day) and clopidogrel (75 mg/day) is advised.

Patients who have no symptoms: If surgery is offered as a management option for asymptomatic carotid stenosis, CEA is preferable over CAS. Increased risks of periprocedural stroke and periprocedural death are possible with CAS. - With modern medical management, the benefit of surgical therapy over medical therapy has diminished. With the available literature, it is impossible to make an evidence-based recommendation for or against surgical therapy.


Admissions
Any patient exhibiting acute symptoms of carotid stenosis should be admitted to the hospital for additional diagnostic testing and the necessary treatment.
Rapid evaluation for TIA-compatible symptoms should be acquired in an inpatient or emergency department (ED) environment.
Discharge requirements include ambulation, appropriate PO intake, and neurological integrity 24 to 48 hours after CEA.

Patient Follow-Up Monitoring
Duplex every 6 to 12 months; Duplex at 2 to 6 weeks following surgery; Reoperative CEA or CAS is reasonable in cases of fast progressing restenosis.
Patients who have any of the following conditions are at high risk of readmission after CEA: renal failure, heart failure, diabetes, and age >80 years; as a result, comprehensive medical care and stringent follow-up are advised.
A heart-healthy diet without trans fats and low in saturated fat


Complications 

Untreated TIA/stroke: 1.68 percent annual risk of ipsilateral stroke 
Perioperative (within 30 days) - Postoperative (state after CEA)
 MI - Late (>30 days postoperative), cranial nerve damage, bleeding, hemodynamic instability
 False aneurysm and recurrent stenosis at the surgery site