Peripheral Vascular Disease Flashcards
Narrowing of arterial lumen —> reduced blood flow to limb
Peripheral Arterial Disease (PAD)
Usually atherosclerotic
Inc risk of CV/Cerebrovascular events (stroke, MI, death)
Continuum of PAD
Asymptomatic stenosis
Chronic arterial insufficiency
Limb-threatening ischemia
Leading cause of M&M for US adults
Atherosclerosis frequently occurs at:
Bifurcations - aortic, iliac, femoral
More than 85% of adults > 50 have some
Major contributing factors for atherosclerosis
HTN
DM
Dyslipidemia
Smoking
Endothelial dysfunction
Inflammatory factors
Immunologic factors
Plaque rupture
Acute v chronic limb ischemia
Acute: SUDDEN decrease in limb perfusion, potential threat to limb
Chronic: patients who present later than 2 weeks after onset of acute event
High risk groups for PAD
Age ≥ 70
Age 50-69 with Hx of smoking or DM
Age 40-49 with DM and at least one other risk factor
Leg symptoms: claudication or ischemic pain at rest
Known atherosclerosis at other sites
Intermittent discomfort (cramping, aching) in defined muscle group, induced by exercise and relieved with rest
Claudication
Common in calf, thigh, or buttock
Due to insufficient blood flow to meet activity demands
Location of claudication and site of stenosis
Buttock/hip —> Aortoiliac
Thigh —> Aortoiliac or common femoral artery
Upper 2/3 of calf —> Superficial femoral artery *** Most common
Lower 1/3 of calf —> Popliteal artery
Foot —> Tibial or peroneal artery
Leriche Syndrome
“ACE”
Absent/dismissed femoral pulses
Claudication (buttock, hip, thigh)
Erectile dysfunction
Ischemic rest pain
Pain in forefoot/toes AGGRAVATED by ELEVATION, relieved by dependency
Non-healing wounds/ulcers
Skin discoloration/gangrene
Pale when elevated, redness when lowered
Physical findings in PAD
Color changes • Pallor with elevation, dependent rubor (redness) Thin, dry, shiny, hairless skin Brittle hypertrophic ridged nails Ulcers Necrosis
Cool to touch, delayed cap refill
Diminished/absent pulses (use handheld Doppler)
Auscultation for bruits
CV assessment (thorough)
Extremity neuro assessment
Ankle-Brachial Index (ABI)
Ratio of the ankle systolic BP divided by highest brachial systolic BP
ABI ≤ 0.9 with exertional symptoms is diagnostic for PAD
Vascular testing in ASYMPTOMATIC PAD
If abnormal or absent pedal pulses, OR
Age ≥ 70 OR
Age 50-69 with Hx of smoking/DM
—> perform ABI
ABI ≤0.9 diagnostic for PAD
ABI 0.91-1.3 = normal
ABI > 1.3 = not PAD but do workup because likely another problem
Arterial duplex Doppler ultrasound
Reflected sound wave frequency is used to determine velocity of blood flow
Accurate, noninvasive, inexpensive
Findings: site and severity of vascular obstruction (%)
Can also be used to asses stent/graft latency
Technically the gold standard for PAD
Vascular imaging - contrast arteriography
• Use prior to intervention and for ongoing surveillance
PAD Management
***Control risk factors and manage Sx Antiplatelet therapy: Aspirin or clopidogrel (Plavix) Smoking cessation Lipid lowering therapy regardless of LDL Control of blood sugar and BP Weight management
For claudication Sx:
Supervised exercise program (30-45 min ≥ 3x/week for 12 weeks)
PAD Revascularization
Endovascular = first line • Percutaneous transluminal angioplasty • Stents • Atherectomy Surgical • Bypass graft (femoral-popliteal = most common, using saphenous vein)
Indications:
Critical limb ischemia
Significant or disabling symptoms unresponsive to lifestyle/pharm therapy
Compartment Syndrom
Complication of revascularization procedures
Tissue swells from repercussion —> increased compartment pressures —> nerves, veins, arteries compressed
Sx: pain out of proportion, pain with passive stretch, paresthesia
Clinical Dx
Management: Immediate surgical consultation (fasciotomy with delayed closure)
The 6 P’s of Acute Arterial Occlusion
Paresthesia
Pain (Located dismally, progresses proximally)
Pallor
Pulselessness (severely diminished or absent)
Poikilothermia - cool nails
Paralysis
Management of Acute Arterial Occlusion
Emergency surgical consultation Anticoagulation: Heparin Thrombolytic therapy - intrarterial Thrombectomy/embolectomy Surgical bypass of obstruction Amputation in 25-30%, long-term survival is poor
Risk factors for Chronic Venous Disease
Age Obesity Smoking Hx of lower extremity trauma Hx of VTE Pregnancy Family Hx of venous disease Standing occupation
Predominant cause of chronic venous disease is
Dysfunction of venous valves —> venous hypertension
Failure of the venous pump
Flow is directly abnormally from deep to superficial system —> local tissue inflammation, fibrosis, and ulceration
Sx of chronic venous disease
(May be asymptomatic) *Aching, heaviness, or burning sensation, worse with standing, relieved by elevation Swelling VIsible varicosities Restless legs Skin hyperpigmentation Ulceration Telangiectasias/reticular veins Stasis dermatitis Edema
Less common signs of Venous insufficiency that look cool
Hemosiderin staining - from pigmented byproduct of hemoglobin
Lipodermatosclerosis - inflammation of layer of fat under the epidermis subcutaneous fibrosis and hardening of skin
• Gross swelling with fibrous band around ankle
Classic but rarely needed gold standard for Dx of venous insufficiency
Venography
Invasive, expensive
Stasis Dermatitis
Commonly on medial ankle
Skin changes: erythema, inflammation, pruritis, scaling, and vehicle formation
Diagnosis is usually clinical
Typically respond to dermatological agents (emollients, barrier creams, topical corticosteroids)
Management of chronic venous disease
Exercise (walking, ankle flexion)
Weigh loss
Elevate legs 30 min 3-4x/day to decrease edema
Compression therapy (20-30 mmHg pressure
• Contraindicated in moderate to severe PAD, cellulitis and acute DVT so confirm Dx
Unsnap Boot
Zinc paste impregnated bandage for wound care in venous ulceration
Medications for chronic venous disease
Diuretics to reduce edema if already on one for other conditions)
Abx for secondary infections (look for lymphangitis)
Radio frequency or laser (non surgical ablative methods)
Sclerotherapy for small surface veins
Surgical: vein stripping if significant, skin grafting for ulcers
Etiology of Aortic Aneurysms
Atherosclerosis = most common
Connective tissue disease
• Marfan’s syndrome, Ehlers-Danlos syndrome
Infection
Trauma (pseudoaneurysms)
Type A vs Type B aortic dissections
Type A: involves arch proximal to left subclavian artery (worse prognosis)
Type B: proximal descending thoracic aorta (usually just beyond left subclavian)
Clinical presentation of aortic dissection
Severe, persistent chest pain (sudden, radiates to back)
Syncope
CVA-like symptoms (hemiplegia, hemiparesis)
Altered mental status
Paresthesia of extremities
Usually hypertensive if conscious (can be hypo if in shock)
Dismissed or unequal peripheral pulses
Neuro deficits
HORNER’S SYNDROME - ptosis, mitosis, anhidrosis
Diagnostic studies for aortic dissection
CT Chest and Abdomen = test of choice
CXR may show widened mediastinum
Management of aortic dissection
EMERGENCY
Immediate control of BP (decrease SBP to 100-120 and pulse pressure)
• Beta-blockers are first line
Urgent surgical intervention (all Type A and +/- Type B)
Abdominal aortic rupture
Associated with high mortality (~50% exsanguinate before reaching hospital, only 50% who get surgery survive)
Sx: Excrutiating abdominal pain that radiates to the back Pulsatile abdominal mass Tenderness Hypotension
Dx: Abdominal ultrasound = study of choice (can also do CT if >5.5cm)
Carotid artery stenosis
May result in cerebral infarction
Sx:
Transient ischemic attacks
Focal neurological Sx
• Amaurosis fugax- transient monocular blindness
•Contralateral weakness/numbness of extremity or face
Physical exam:
Carotid bruit
Absent pupillary light response
Fundoscopic exam - arterial occlusion or ischemic damage to retina
Dx: Carotid duplex ultrasound performed first (sensitive/specific), cerebral angiography is gold standard but rarely performed
Tx: If asymptomatic, controversial; with Sx, revascularization (CEA)
