Clin Med 1 ( Exam 2 : Arterial Vascular Disease)

Definition Giant Cell (Temporal) Arteritis

•Chronic vasculitis of large and medium sized vessels

•Vascular involvement may be widespread

•Most frequently involves cranial branches of arteries that originate from aortic arch

•Also known as temporal arteritis

EpidemiologyGiant Cell (Temporal) Arteritis

•Age greater than 50 years (peaks at 60-80)

•Risk for blindness

•More common in whites; rare in Hispanics

•More common in Scandinavian descen

•Clustering of illness may occur in families

•Heavy smoking increases risk in women

•F > M

Etiology Giant Cell (Temporal) Arteritis

•Unknown/idiopathic >>presumed to be autoimmune

•T-cells and monocytes "recruited" to vessel wall = inflammatory response

•Association with polymyalgia rheumatica (also autoimmune)

•Infectious etiology has also been speculated

Clinical historyGiant Cell (Temporal) Arteritis

•Onset of symptoms tend to be gradual (may be abrupt)

•Systemic complaints

•New HA occurs in two-thirds (classic HA in temporal regions)

•One-half suffer from jaw claudication

•Aortic aneurysm hx appears to be common

•Extreme scalp tenderness

•Amaurosis fugax

•Temporary vision loss

•Polymyalgia rheumatica sx

Physical ExamGiant Cell (Temporal) Arteritis

Palpate Pulses

•Carotid

•Brachial

•Radial

•Femoral

•Pedal

Temporal artery abnormalities

•Tender or thickened

•Absent temporal pulse

Giant cell arthertitis presenting symptoms

Headache

Scalp tendreness

Thickened temporal arterires

Jaw claudication

Acute visual loss

Weight loss,anorexia ,fever,night sweat

Malaise, depression

Diagnosis Giant Cell (Temporal) Arteritis

Considered in age > 50 years old who has:

•New headaches

•Abrupt onset of visual disturbances

•Symptoms of polymyalgia rheumatica

•Jaw claudication

•Unexplained fever or anemia

•High ESR and/or high serum CRP

Differential diagnosisGiant Cell (Temporal) Arteritis

•Migraine headache

•Takayasu arteritis

•Polymyalgia rheumatica (may co-occur with GCA)

•Trigeminal neuralgia

•Atherosclerotic Disease of Carotid Artery

Workup Giant Cell (Temporal) Arteritis Labs

•CBC w/ diff

•CMP

•Serum Albumin

•Temporal artery biopsy >> diagnostic

•ESR elevated (often > 100mm/hr)

•CRP elevated

Workup Giant Cell (Temporal) Arteritis Imaging

•Angiography

•Doppler

•MRI

Classification criteria Giant Cell (Temporal) Arteritis

•Age (50 at time of onset)

•Localized headache of new onset

•Tenderness or decreased pulse of temporal artery

•ESR > 50 mm/hour

•Biopsy (revealing necrotizing arteritis with mononuclear cells or multinucleated giant cells)

Clinical intervention (Referrals/Consults)Giant Cell (Temporal) Arteritis

•Rheumatologist

•Ophthalmologist

•Vascular surgeon

•Neurologist

Clinical management Giant Cell (Temporal) Arteritis

High dose glucocorticoids

•Prednisone

•Optimal dose for initial treatment uncertain

•*Initial daily dose of Prednisone 40-60 mg of prednisone

Acetylsalicylic Acid (ASA)

Glucocorticoid taperingGiant Cell (Temporal) Arteritis

•Symptoms usually controlled promptly and tapering can begin once disease has been controlled adequately

•After 2-4 weeks of high dose Prednisone

•Is Patient asx and the ESR normal? YES ® taper

•Begin tapering 2.5-5mg/day every 2 weeks to a dose of 20mg/day

•Then decrease dose by 10% every 2 weeks to a dose of 10mg/day

•Then decrease dose by 1mg/day every 4 weeks

•Flares are the rule if tapered too quickly

Prophylaxis of decreased bone densityGiant Cell (Temporal) Arteritis

•SE of high dose/long term steroid use is decreased bone density

•Prevent this decreased bone density with prophylactic tx

Giant Cell (Temporal) Arteritis: •Prophylactic measures

•Obtain a baseline bone density (when patient starts steroids)

•Administer (1500 mg of calcium/800 IU of vitamin D-3 per day)

•Consider bisphosphonates or hormonal therapy for osteopenia/osteoporosis

Prognosis/patient educationGiant Cell (Temporal) Arteritis

•Many patients tend to run a self-limited course over several months to several years

•Dose can eventually be reduced and discontinued in the majority of patients

•A few may need low dose prednisone for years

•Complications

Blindness

20-50% have recurrence

•Some patients have GCA and PMR at the same time

Definition Aortic Aneurysm

•: arterial dilation

•Diameter of that region is increased > 50% relative to normal aortic diameter

•Normal diameter of the aorta at the level of the renal arteries is approximately 2.0 cm (range 1.4 to 3.0 cm) in most individuals

•Diameter greater than 3.0 cm is generally considered aneurysmal

Most Common types of Aortic Aneurysms

Abdominal (aortic aneurysm) (AAA)

Thoracic

•Ascending (aorta)

•Aortic arch

Descending (aorta

Aneurysm Shapes

Saccular

•bulging on one side

Fusiform

•Bulging on all sides

Pseudoaneurysm

•hematoma that forms as the result of a leaking hole in an artery

ETIOLOGY/PATHOGENESIS/RISK FACTORS Aortic Aneurysm

•Weakening of the aortic wall

breakdown of the extracellular matrix proteins elastin and collagen (help vessels hold their structure/shape)

•Congenital- anatomic defect

•Atherosclerosis

•HTN

•DM

•Smoking

Direct damage to the aorta:

•Trauma

•Arteritis

•Infection

Connective tissue disease

•What disorder do you think is common?

Idiopathic

Risk factors - Aortic Aneurysm

Marfan's syndrome

Marfan's syndrome definition

It is an inherent disorder that affects the connective tissues in the body .Marfan syndrome is cause by proteins in the connective tissue.

Marfan syndrome symptoms

flat feet

curved spine

flexible joint

cystic changes in the lungs

disproportionately longs legs ,arms, toes and fingers

Clinical history Aortic Aneurysm

Occasionally may cause discomfort

More concern is risk of rupture

•severe pain

•massive internal hemorrhage

•without prompt treatment, death occurs rapidly

Pseudoaneurysm

•Communication through a "stalk" from the artery to the "sack"

•Hematoma often develops within the sack

Clinical historyAortic Aneurysm

•Often asx until dissection begins

•Abdominal/chest pain and back pain

"Gnawing, ripping or tearing" abdominal pain

•Compression of nerve roots

•Associated sx:

Anxiety

N/V

Clammy skin

Tachycardia

Other symptoms/findings Aortic Aneurysm

•May be incidental on rad scans

•Palpable, pulsatile abdominal mass

•Groin pain

•Skeletal hip pain

PERTINENT PHYSICAL EXAM FINDINGSAortic Aneurysm

•May be palpable as a pulsatile mass (AAA)

•Bruit may be heard from turbulent blood flow (AAA)

"Gushing noise"

•BP May be elevated followed by a sudden Hypotensive episode

•Persons w/ Marfan syndrome are often males that are tall and "skinny"

Long extremities, fingers

Ruptured or leaking AAA "triad"Aortic Aneurysm

•Abdominal pain

•Hypotension

•Pulsatile abdominal mass

PERTINENT HISTORICAL FINDINGS/CLINICAL sX (Thoracic) Aortic Aneurysm

Aortic Arch Aneurysm

DIFFERENTIAL DIAGNOSISAortic Aneurysm

•Angina Pectoris

•Myocardial infarction

•Pulmonary embolism

•Pancreatitis

•Gastroenteritis

•Mechanical back pain

WorkupAortic Aneurysm Labs

•CBC w/ diff

•CMP

•PT/INR (esp if pending/suspect rupture)

WorkupAortic Aneurysm Imaging

•US is study of choice for unstable AAA

•CXR may reveal widened mediastinum (Thoracic)

•CT scan chest/abd/pelvis

Study of choice in STABLE Thoracic AA

•Angiogram- contrasted imaging of the arterial system

•Angiography is gold standard & is confirmatory

MEDICAL MANAGEMENTAortic Aneurysm

•Strict BP control

•Smoking cessation

•Refer to a vascular surgeon

Decide if surgical candidate

Recommendations about how to follow the patient clinically

Example might be ordering CT q 6 mo to monitor growth

SURGICAL MANAGEMENT Aortic Aneurysm

•Prevent RUPTURE!

•Aneurysms >5.5 cm (5 cm in good operative candidates) often surgically repaired

•Symptomatic PTs with any size aneurysm often candidates for surgery

•U/S every 6 months for aneurysm 4-4.5cm

•U/S annually for aneurysms 3-4 cm

•Thoracic aneurysm surgery more complex with greater risks

Surgery may be delayed until absolutely necessary

Surgical candidates Aortic Aneurysm : •Open surgical repair vs. endovascular

Open repair

•Low or average risk of operative complications

•Direct visualization

Endovascular repair

•High risk of complications from open operations

•Minimally invasive

•Access usually through femoral arteries

Screening/Health Maintenance Aortic Aneurysm

•1-time screening with ultrasonography

•Men aged 65 to 75 yo

•Men aged 65 to 75 years who have ever smoked

aortic disssection

•Tear in the inner wall of the aorta (intima) causes blood to flow into the middle layer (media) and force the layers apart

ETIOLOGY/ PATHOGENESIS/RISK FACTORS Aortic Dissection

•Associated w/ HTN and connective tissue disorders (Marfans)

•Trauma to chest

•Post operative complication of cardiothoracic surgery

•M > F [4 : 1]

•Smokers

•Atherosclerosis

•Existing aneurysm

•Idiopathic

•MC in those 50-60

Stanford Typing SystemAortic Dissection:•Most simplified classification system EVER!

•Stanford Type A (proximal)

Involves the Ascending aorta

•Stanford Type B (distal)

•Does NOT involve the ascending aorta

Stanford Type A (proximal)

Debakey I = 60%

Debakey = 10-15%

Stanford Type B (distal)

Debakey = 25-30%

PERTINENT HISTORICAL FINDINGS/CLINICAL SxAortic Dissection

•Most commonly in the aortic arch or L subclavian

•Always include in differential of chest pain

•Typically c/o severe sharp, "tearing" (ripping) sensation in the chest or back

Be suspicious of dissection in high risk patients c/o pain radiating to the back

•Pain may migrate as the dissection extends

•Stanford Type A-chest pain anteriorly—may hear new murmur in aortic area

•Stanford Type B-may see pain between scapular areas/back pain.

•Neck or jaw pain may occur with involvement of aortic arch

PERTINENT PHYSICAL EXAM FINDINGS Aortic Dissection

•Peripheral extremity pulses may be decreased

•Elevated BP in most cases (may see decreased BP)

•Difference in pulse amplitude (strength)

•Unequal BP in upper extremities (UE)

•Aortic valve or ascending is affected >> new aortic regurgitation murmur

DIFFERENTIAL DIAGNOSISAortic Dissection

•Aortic embolism

•Acute MI

•Angina Pectoris

•Pulmonary embolism

•Pancreatitis

•Gastroenteritis

•Mechanical back pain

Workup Aortic Dissection

•Widened mediastinum on CXR

•Transesophageal echocardiography (TEE) esp if AKI or contrast allergy

•CT scan Chest, Abd, Pelvis with IV Contrast when TEE cannot be quickly performed

•Sonography SPEED protocol

What is the gold standard Test for Aortic dissection?

•Aortic angiography (MRI) is gold standard

Not universally available

Expensive

Workup - Speed Protocol Aortic Dissection

•SPEED

Sonographic Protocol for the Emergent Evaluation of (Aortic) Dissections

Combines TTE and abdominal aorta US

Abdominal aorta 6"

Xiphoid to bifurcation (iliacs)

•Designed for patients too unstable to leave the ER for imaging

MEDICAL MANAGEMENTAortic Dissection

•Acute dissection suspected

•Labetalol and sodium nitroprusside IV typically used to aggressively lower BP

•Lowest level that adequately supports cerebral, cardiac and renal perfusion

•Goal is systolic BP 100-120mmHg within 20 mins

MEDICAL MANAGEMENT Aortic Dissection

•Hypotensive

•IVF and vasopressors

•Dopamine/Dobutamine

•Epinephrine/Norepinephrine

MEDICAL MANAGEMENT Aortic Dissection:

•Patients with a dissection that does not threaten organs may be observed with strict BP control

•MUST be completely asymptomatic

•At discretion of CT specialist

Cardiologist specializing in vascular repair

•Beta blocker often used as first line

MEDICAL MANAGEMENT Aortic Dissection:

•Tx choice often depends on location

•Stanford type A (ascending aortic) dissection

Immediate Open surgical mgmt superior to medical mgmt

•Uncomplicated Stanford type B (distal aortic)

Medical mgmt preferred over surgical intervention

Repair if evidence of rupture or vessel occlusion

SURGICAL MANAGEMENT Aortic Dissection

•Objective is often to resect (remove) the most severely damaged segments of the aorta, and prevent entry of blood into the false lumen

>>>>>>>>Graft inserted post resection

Definition Peripheral Artery Disease (PAD)

•Atherosclerotic disease leading to peripheral artery obstruction

•PAD regarded as a coronary heart disease risk equivalent

Epidemiology Peripheral Artery Disease (PAD)

•Age ≥70 years

•Age 50-69 years with a history of smoking or diabetes

•Age 40-49 with diabetes and at least one other risk factor for atherosclerosis

•Known atherosclerosis at other sites (coronary, carotid, or renal artery disease)

•Å Family history

•Smoking

•HTN

•HLD

•M > F

•AA > Caucasian

Etiology Peripheral Artery Disease (PAD)

•Risk factors

Similar to those for development of coronary atherosclerosis

•Most often affects the popliteal artery

•Atherosclerotic disease >>>obstruction of peripheral arteries

•Associated Conditions

Leriche syndrome ® aortoiliac occlusion

•BLE claudication

•PLUS impotence

•PLUS lower extremity muscular atrophy

•CAD

Clinical history Peripheral Artery Disease (PAD)

•Progressive severity

•asymptomatic

•intermittent claudication

•pain at rest

•nonhealing wounds

•ulceration

•gangrene and threatened limb

Physical Exam Peripheral Artery Disease (PAD)

•Questions related to history of

•Walking impairment

•Extremity pain

•Presence of non-healing wounds

•Claudication?

•Intermittent claudication?

•Lower extremity pain (predominant symptom)

•Intermittent claudication

•Atypical leg pain or constant pain in forefoot aggravated by elevation and relieved by dependency (rest pain)

Level of obstruction for PDA

Aorta 25-30% >>>> buttock ,hip, thigh

Femoral Artery or branches >>>> Thigh calf

Popliteal artery 80-90% >>>>Calf, ankle, foot

Tibial and peroneal artery 40-50 % >>> Foot

Claudication score

Score 0 = None pain

During rest or early exercice

Score 1 =Mild pain level

Onset of pain -just noticebale

Score2 =Moderate pain=

More than mild pain but tolerable

Score 3 =Severe pain = Severe pain -barely tolerable

Score 4= Maximun

Maximal Pain have to stop

Physical ExamPeripheral Artery Disease (PAD)

•Cardiovascular exam

Auscultation for bruits

*Check pulses and ABI if needed

•Neurologic exam

•Abdominal exam

+/- bruit

**Ischemic wound with fibrotic tissue mixed with eschar

Physical exam Peripheral Artery Disease (PAD)

Presence of ischemic ulcers

•Usually on the foot

Derm changes

•Pale or red skin

•Dry, shiny and hairless in severe disease

•Cool to touch

•Decreased or absence pulses

•Extremity appearance - derm changes

•Nails may become brittle, hypertrophic, ridged

•Compare color and trophic changes between extremities

Physical ExamPeripheral Artery Disease (PAD)

Blue toe syndrome

•Manifestation of peripheral embolization of atheromatous material from proximal arterial sources (aorta)

•Pedal pulses are often normal

•**30-year old with history of type 1 DM and severe peripheral vascular disease (presented with foot pain and discoloration)

Ankle brachial indexPeripheral Artery Disease (PAD)

Greater than 1.4

Differential diagnosis Peripheral Artery Disease (PAD)

•Arterial aneurysm

•Deep Vein Thrombosis (DVT)

•Popliteal artery entrapment

•Chronic compartment syndrome

•Neurospinal disease

•Diabetic neuropathy

WorkupPeripheral Artery Disease (PAD)

•A history of risk factors or symptoms of PAD, in combination with physical exam findings, are sufficient to establish diagnosis

•For atypical symptoms, or an equivocal pulse exam

•Ankle-brachial index (ABI) is diagnostic if ≤0.9

•ABI Calculation

•Right ABI = Highest Pressure in Right Foot

Highest Pressure in right or left arm

•Left ABI = Highest Pressure in Left Foot

Highest Pressure in right or left arm

WorkupPeripheral Artery Disease (PAD) : •Vascular imaging indication AND •Arteriography

•Identify appropriate targets for intervention

•Surveillance following intervention

•Findings low velocity flow through the artery

Workup - plain film imagingPeripheral Artery Disease (PAD)

•Image (A) X-ray shows calcification of below knee popliteal artery just before it branches into anterior tibial artery laterally and tibioperoneal trunk medially

•Image (B) Magnification view shows branch point (arrow)

•

Clinical managementPeripheral Artery Disease (PAD)

•PCP

•Medical specialists

•Vascular surgeon

•Plastic surgery

•Podiatrist (foot care)

Clinical interventionPeripheral Artery Disease (PAD)

•Cardiovascular risk factor modification

•Management of HLD, DM, HTN according to guidelines

Clinical intervention/revascularizationPeripheral Artery Disease (PAD)

Surgical intervention

•Bypass grafts

•Amputation

•Thromboendarterectomy

Endovascular techniques

•Angioplasty

•Stenting

Clinical pharmacotherapeutics Peripheral Artery Disease (PAD)

•Antiplatelet agents

•ASA

•Clopidogrel (Plavix)

•Medical management of underlying disease

Prognosis Peripheral Artery Disease (PAD)

•Treatable condition if recognized early and appropriately managed

•Complications can be minimized

Osteomyelitis

Loss of limb

CV even

DefinitionSubclavian Steal

•Rare condition resulting in syncope or other neurologic deficit

•Occurs secondary to a proximal stenotic lesion or occlusion in the subclavian artery

•Condition where an artery takes or "steals" blood that's supposed to the brain but is now going to the arm

Epidemiology/risk factorsSubclavian Steal

•M > F (2:1)

•L side > R side (3x)

•18% of people with PAD also have subclavian steal

•

•Risk factors

•Atherosclerosis

•Increasing age

•Hyperlipidemia

•Hypertension

•Smoking

•Diabetes

•Other risk factors

•Surgery to fix coarctation of the aorta

•Congenital defect of aortic arch

•Compression of the subclavian artery

•MC in athletes

•Thoracic outlet syndrome (TOS)

Etiology/pathophysiologySubclavian Steal

•Blood supply to the affected arm is increased through exercise

•To compensate for the increased O2 demand in the arm blood is drawn from collateral circulation resulting in reversed blood flow in the ipsilateral vertebral artery (occasionally from the internal thoracic artery)

•Atherosclerosis is MCCC

•Other causes

•AVM

•Aortic dissection

•Takayasu arteritis

•Fibromuscular dysplasia

•

Clinical history Subclavian Steal

•Usually occurs during exercise or even when turning head suddenly to the side

•Blurry vision

•Dizziness ® syncope

•+/- vertigo

•Pain, numbness, tingling or tiredness in your arm

•Hearing loss

•Clumsy muscle movement (ataxia)

Physical examSubclavian Steal

•Best if assessed with activity or exercised

•Different BP in UE

•> 15mmHg

•Difference in radial pulses

•Diplopia

Differential diagnosis Subclavian Steal

•UE PAD

•Posterior circulation stroke

•Aortic stenosis

•Diabetic Neuropathy

workupSubclavian Steal

Labs :

•What you order is typically driven by CC or how they presented

Imaging :

•Duplex US

•CXR

•Definitive (diagnostic)

•CTA or MRA

Clinical interventionSubclavian Steal

•Symptomatic

•Surgical intervention

•Endovascular - connect subclavian to another artery to use as bypass

•Angioplasty and stenting

•Atherectomy

•Endarterectomy

Clinical pharmacotherapeutics Subclavian Steal

•Non-surgical patients

•Anticoagulant or antiplatelets

•Treatment of

•Atherosclerotic disease

•HTN

Prognosis/patient educationSubclavian Steal

•Prevention/Risk reduction

•Prevent atherosclerosis

•Maintain healthy body weight

•Daily exercise (30 minutes daily)

•Avoid tobacco products)

•Low fat diet

•Control cholesterol/BP and DM

•Although relatively benign it is a marker of atherosclerosis

•Think of it as a "warning" sign