1. Peripheral vascular diseases
Dr Seyed Mostafa Shiryazdi
Associate professor of surgery

2. 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.

3. (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

4. Edema
1 venous edema
2 lymphedema
Paresthesias
1 heaviness
2 abnormal sensation: numbess, tingling, burning,
3 lose of sensation

5. 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

6. Changes of shape
1 shape changes of artery:
1) pulses decrease or disappear
2) murmur
3) form and texture
2 shape changes of vein

7. Mass
1 pulsatile mass
2 non-pulsatile mass
Skin nutritional changes
1 nutritional dysfunction of skin
2 ulceration, and gangrene
3 limbs grow

8. 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 years.

9. 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.

10. 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

11. 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

12. 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.

13. Clinical stage First stage: local ischemic stage
Second stage: nutritional ischemic stage
Third stage: necrotic stage

15. 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

16. General examination 1 claudication distant and claudication time
2 skin temperature
3 Buerger test
4 tension relief test

17. Special examination 1 Doppler examination
2 arteriography: formation of distinctive small-vessel collaterals around areas of occlusion known as "corkscrew collaterals"

18. Differential diagnosis
1 Atherosclerosis obliterans
2 Takayasu’s arteritis
3 Diabetes mellitus

19. 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

20. 2 Medication
(1) Chinese traditional treatment
(2) vasodilators, antiplatelet drugs, and anticoagulants
(3) antibiotics to treat infected ulcers

21. 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

22. 图1　动脉旁路移植
bypass graft

23. 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

24. Etiology and pathology
risk factors: hypertension, abnormal serum lipid levels, cigarette smoking, impaired glucose tolerance, and obesity
Mechanism
Pathology: atherosclerotic plaque

25. 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

26. 1 general examination: ECG
2 noninvasive examination: Doppler
3 X-ray
4 arteriography, MRA (Magnetic resonance angiography), DSA

27. Differentiation of Arteriosclerosis obliterans and thromboangiitis Obliterans
age
>45
<45
superficial thrombophlebitis no
common
Hypertension, coronary heart disease
uncommon

28. Involving vessels
large and medium arteries
the small and medium-sized arteries and veins
Change of other arteries
common no
Calcification of involving arteries
Can be found
arteriography
Extensive irregular stenosis and segmental occlusion
Segmental occlusion, others are normal

29. Treatment 1 nonoperative treatment 2 surgical treatment
(1) percutaneous transluminal angioplasty
(2) endarterectomy
(3) vascular bypass surgery

30. Section 4 Arterial embolism
acute arterial occlusion
Etiology and pathology

31. Clinical Manifestation
Pain
Paresthesias
Paralysis
Pulselessness
Pallor, coolness
Other general symptoms

32. Examination and diagnosis
1 skin temperature
2 Doppler examination
3 arteriography

33. 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

34. Complication of operation
the possibility of reperfusion complications such as compartment syndrome or myopathic-metabolic-nephrotic syndrome

35. 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

36. 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

38. Dynamics of blood flow 1 muscular pump
2 negative pressure in thoracic cavity
3 valve function

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

40. 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.

41. 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.

42. 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.

43. 1 Trendelenburg test
2 Perthes test
3 Pratt test
4 others: Doppler, angiography

46. Differentiated diagnosis
1 primary lower extremity deep vein valve insufficiency
2 sequela of deep vein thrombosis
3 arteriovenous fistula

47. Treatment
Treatment is indicated whenever venous reflux produces secondary skin or subcutaneous tissue changes, symptomatic varicose veins

48. 1 Nonoperative treatment: compression stockings, keeping the legs elevated
2 Injection sclerotherapy
3 Operation: Vein ligation, stab evulsion technique, communicating veins ligation

49. complications 1 Superficial thrombophlebitis 2 ulceration
3 Varicose veins bleeding

50. 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

51. Examination
1 angiography
2 venous pressure
3 noninvasive examination

52. Treatment
Reconstruction of deep venous valves

53. Section 8 Deep venous thrombosis
formation of thrombi, ---chronic venous insufficiency
Etiology and pathophysiology
Virchow triad (venous stasis, hypercoagulability, endothelial trauma)

54. 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

55. Examination and diagnosis
Prevention and treatment
1 nonoperative treatment
2 operation
Complications and sequela