By Bradley Cook,2014-08-23 00:52
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nonatherosclerotic ...

Peripheral vascular diseases


    Section 1 Introduction


     1 intermittent pain

    (1) physical activity : intermittent claudication,

     Cramping or fatigue of major muscle groups in one or both lower extremities that is

    reproducible upon walking a specific distance suggests intermittent claudication, and it is relieved by

    several minutes of rest.

(2) limbs position

    (3) change of tempreture

     2 Continuous pain (rest pain, or pain at rest) (1) arterial pain at rest

    (2) venous pain at rest

    (3) inflammatory or ischemic pain at rest


    1 venous edema

    2 lymphedema


    1 heaviness

    2 abnormal sensation: numbess, tingling, burning,

    3 lose of sensation

     Change of skin temperature

     Changes of skin color

    1 normal and abnormal color

    2 changes of color with pressure

    3 changes of color in physical activity: Buerger test

    4 changes of color in different position

     Changes of shape

    1 shape changes of artery:

     1) pulses decrease or disappear

     2) murmur

     3) form and texture

    2 shape changes of vein


    1 pulsatile mass

    2 non-pulsatile mass

     Skin nutritional changes

1 nutritional dysfunction of skin

    2 ulceration, and gangrene

    3 limbs grow

    Section 2 Thromboangiitis Obliterans

    ( Buerger Disease )

    Thromboangiitis obliterans is a nonatherosclerotic, segmental, inflammatory, vasoocclusive disease

    that affects the small and medium-sized arteries and veins of the upper and lower extremities, cyclic


    more common in males, aged 20-45 years.



    1 external factors: tobacco, cold or humid weather, chronic trauma, infection 2 internal factors: immunologic dysfunction

    exposure to tobacco is essential for both initiation and progression of the disease. Pathology

    1 begin with artery, then vein, from proximal to distal

    2 segmental disease

    3 in active stage, nonsuppurtive inflammation

    4 in end stage, intraluminal thrombosis progressively organizes, new capillary formation, vascular


    5 ischemic change

    Clinical findings

    1 The hands and feet are usually cool.

    2 skin is pale, or cyanosis.

    3 Paresthesias.

    4 pain in limbs, intermittent claudication

    5 changes of nutritional dysfunction

    6 impaired distal pulses in the presence of normal proximal pulses. 7 migratory superficial thrombophlebitis.

    8 painful ulcerations and/or frank gangrene of the digits.

    Clinical stage

    First stage: local ischemic stage

    Second stage: nutritional ischemic stage

    Third stage: necrotic stage


     1 Age younger than 45 years, current (or recent) history of tobacco use

     2 Presence of distal-extremity ischemia

     3 History of migratory superficial thrombophlebitis

     4 Impaired distal pulses.

     5 Exclusion of autoimmune diseases, hypercoagulable states, and diabetes mellitus by laboratory


    General examination

    1 claudication distant and claudication time

    2 skin temperature

    3 Buerger test

    4 tension relief test

    Special examination

    1 Doppler examination

    2 arteriography: formation of distinctive small-vessel collaterals around areas of occlusion known as

    "corkscrew collaterals"

    Differential diagnosis

    1 Atherosclerosis obliterans

    2 Takayasu’s arteritis

    3 Diabetes mellitus


    1 General treatment

    Absolute discontinuation of tobacco use is the only strategy proven to prevent the progression of

    Buerger disease.

    prevent trauma and thermal or chemical injury, avoidance of cold environments, drugs that lead to


    Buerger exercise

2 Medication

    (1) Chinese traditional treatment

    (2) vasodilators, antiplatelet drugs, and anticoagulants (3) antibiotics to treat infected ulcers

3 hypertension oxygen treatment

    4 surgical treatment

     to improve distal arterial flow

    (1) lumber sympathectomy

    (2) vascular reconstructive procedures: bypass transfer, thrombosis Others: Omental transfer

     Arteriovenous transfer

    5 distal limb amputation for nonhealing ulcers, gangrene 1 动脉旁路移植

bypass graft

    Section 3 Arteriosclerosis obliterans

    lower extremity atherosclerosis is a marker for systemic atherosclerotic disease, involving large and

medium arteries, the iliac, femoral, popliteal, and/or infrapopliteal arteries

    advancing age, male sex

    Etiology and pathology

    risk factors: hypertension, abnormal serum lipid levels, cigarette smoking, impaired glucose

    tolerance, and obesity


    Pathology: atherosclerotic plaque

    Clinical manifestation and diagnosis

    Early stage: intermittent claudication, Impaired distal pulses, changes of nutritional dysfunction, the

    limb is perfused via collateral pathways

    Late stage: rest pain

    Loss of pedal pulses is characteristic of disease of the distal popliteal artery or its trifurcation.

    the dorsalis pedis pulse, the posterior tibial pulse

1 general examination: ECG

    2 noninvasive examination: Doppler

    3 X-ray

    4 arteriography, MRA (Magnetic resonance angiography), DSA

Differentiation of Arteriosclerosis obliterans and thromboangiitis Obliterans


    1 nonoperative treatment

    2 surgical treatment

    (1) percutaneous transluminal angioplasty

    (2) endarterectomy

    (3) vascular bypass surgery

    Section 4 Arterial embolism

    acute arterial occlusion

    Etiology and pathology

Clinical Manifestation





    Pallor, coolness

    Other general symptoms

Examination and diagnosis

    1 skin temperature

2 Doppler examination

    3 arteriography


    The usual immediate management of acute arterial occlusion is immediate heparin anticoagulation and rapid surgical thromboembolectomy.

    1 nonoperative treatment

    2 surgical therapy: direct thromboembolectomy, Fogarty cancal thromboembolectomy Complication of operation

    the possibility of reperfusion complications such as compartment syndrome or

    myopathic-metabolic-nephrotic syndrome

    Section 5 Introduction of venous diseases

     the lower extremities:

    1 superficial veins, include the lesser and greater saphenous veins and their tributaries. These include the lateral and medial femoral cutaneous branches, the external circumflex iliac vein, the superficial epigastric vein, and the internal pudendal vein

    2 deep veins, include the anterior tibial, posterior tibial, peroneal, popliteal, deep femoral, superficial femoral, and iliac veins.

    3 muscular vein

    4 perforating or communicating veins

Dynamics of blood flow

    1 muscular pump

    2 negative pressure in thoracic cavity

    3 valve function


    Most varicose disease is caused by elevated superficial venous pressures, but some people have an inborn weakness of vein walls

    Section 6 Simple lower extremity varicose veins

    normal veins have dilated under the influence of increased venous pressure. allow venous blood to escape from its normal flow path and flow in a retrograde direction down into an already congested leg.

Etiology and pathophysiology

    Prolonged standing leads to increased hydrostatic pressures that can cause chronic venous distention and secondary valvular incompetence anywhere within the superficial venous system. If proximal junctional valves become incompetent, high pressure passes from the deep veins into the superficial veins and the condition rapidly progresses to become irreversible. Clinical manifestation and diagnosis

    Symptoms: uncomfortable, annoying, or cosmetically disfiguring, pain, soreness, burning, aching, throbbing, cramping, muscle fatigue

    Signs: dilated vessels, mild swelling. inflammatory dermatitis, recurrent or chronic cellulitis,

    cutaneous infarction, ulceration, and even malignant degeneration.

1 Trendelenburg test

    2 Perthes test

    3 Pratt test

    4 others: Doppler, angiography

Differentiated diagnosis

    1 primary lower extremity deep vein valve insufficiency 2 sequela of deep vein thrombosis

    3 arteriovenous fistula


    Treatment is indicated whenever venous reflux produces secondary skin or subcutaneous tissue

    changes, symptomatic varicose veins

1 Nonoperative treatment: compression stockings, keeping the legs elevated

    2 Injection sclerotherapy

    3 Operation: Vein ligation, stab evulsion technique, communicating veins ligation


    1 Superficial thrombophlebitis

    2 ulceration

    3 Varicose veins bleeding

    Section 7 primary lower extremity deep vein valve insufficiency

Etiology and pathophysiology

     Congenital absence of or damage to venous valves in the superficial and communicating


    Clinical finding and diagnosis

    Mild, moderate, severe


    1 angiography

    2 venous pressure

    3 noninvasive examination


    Reconstruction of deep venous valves

    Section 8 Deep venous thrombosis

    formation of thrombi, ---chronic venous insufficiency

Etiology and pathophysiology

    Virchow triad (venous stasis, hypercoagulability, endothelial trauma)

    Clinical finding and types

    1 upper extremity deep venous thrombosis 2 inferior vena cava or superior vena cava thrombosis 3 lower extremity deep venous thrombosis Examination and diagnosis

    Prevention and treatment

    1 nonoperative treatment

    2 operation

    Complications and sequela

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