Peripheral vascular diseases Dr Seyed Mostafa Shiryazdi Associate professor of surgery

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Transcript Peripheral vascular diseases Dr Seyed Mostafa Shiryazdi Associate professor of surgery

Peripheral vascular diseases
Dr Seyed Mostafa Shiryazdi
Associate professor of surgery
Section 1 Introduction
Pain
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
Edema
• 1 venous edema
• 2 lymphedema
Paresthesias
• 1 heaviness
• 2 abnormal sensation: numbess,
tingling, burning,
• 3 lose of sensation
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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:
4 changes of color in different position :
Buerger test
Changes of shape
• 1 shape changes of artery:
1) pulses decrease or disappear
2) murmur
3) form and texture
• 2 shape changes of vein
Mass
• 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 upset.
• more common in males, aged 20-45 years.
etiology
unclear
• 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
distal to proximal.
• 2 segmental disease
• 3 in active stage, nonsuppurtive
inflammation
• 4 in end stage, intraluminal thrombosis
progressively organizes, new capillary
formation, vascular fibrosis
• 5 ischemic change
Clinical findings
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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
Diagnosis
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 tests
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
Treatment
• 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 vasoconstriction
• Buerger exercise
• 2 Medication
• (1) Chinese traditional treatment
• (2) vasodilators, antiplatelet drugs, and
anticoagulants
• (3) antibiotics to treat infected ulcers
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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
图1
• bypass graft
动脉旁路移植
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
• Mechanism
• 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
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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
Arteriosclerosis
obliterans
Thromboangiitis
Obliterans
age
>45
<45
superficial
thrombophlebitis
no
common
Hypertension,
coronary heart
disease
common
uncommon
Involving vessels large and
medium
arteries
the small and
medium-sized
arteries and
veins
Change of other
arteries
no
common
Calcification of Can be found
involving arteries
arteriography
no
Extensive
Segmental
irregular stenosis occlusion, others
and segmental
are normal
occlusion
Treatment
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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
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Pain
Paresthesias
Paralysis
Pulselessness
Pallor, coolness
Other general symptoms
Examination and diagnosis
• 1 skin temperature
• 2 Doppler examination
• 3 arteriography
Treatment
• 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-metabolicnephrotic 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
Pathophysiology
• 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.
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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
• 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
complications
• 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 systems
• Clinical finding and diagnosis
• Mild, moderate, severe
Examination
• 1 angiography
• 2 venous pressure
• 3 noninvasive examination
Treatment
• 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