1. Approach in Vascular Patient
กิตติพันธุ์ ฤกษ์เกษม PhD, FACA

2. Topic Artery - Limb Ischaemia Venous - Varicose vein - Aneurysm
Leg ulcer

3. Limb Ischaemia Aetiology: most often atherosclerosis > trauma
Most management decisions are based upon
1.Differentiation acute vs chronic
2. Mechanism of occlusion
3.Location of the occlusion
4.Status of limb
5.Fitness of patients

4. 1.Differentiation acute vs chronic

5. What is acute ischaemia?

6. Acute ischaemia Period of onset in minutes or hours
Sudden catastrophic
Less effect in upper extremity and leg affected by chronic ischaemia

7. Acute ischaemia Symptom 5P pain pulselessness paresthesia pallor
paralysis

8. Marble white right foot in acute limb ischaemia

9. What is chronic ischaemia?

10. Chronic ischaemia Symptom of limited circulation over months or years
Slow deterioration of function
Gradually symptom
Life style changes-stop smoking or exercise: remission collateral vv

11. Chronic ischaemia Symptom and sign Claudication rest pain
ulceration/gangrene

12. Why should the effectes of acute arterial ischaemia occlusion be less in someone affected already by symptom of chronic ischaemia or in upper limb?

13. Collateral vessels!!

15. 2. Mechanism of occlusion
Acute iscahemia caused by
Trauma
Non trauma
- embolus
- thrombosis

16. Trauma-fracture tibia

17. Embolus Mobile solid mass Free floating in blood
Capable of occluding a vein or artery distal to its site of origin

18. Composition of embolus
Atheromatous debris or thrombus(clot) (common)

19. Common source of atheromatous or thrombus emboli
Left ventricle wall after MI
Left atrium in atrial fibrillation
Diseased mitral valve or aortic valve
Atheromatous plaques in aorta or iliac vessels
This embolus lodge at the area where arterial tree is smaller than the embolus e.g. bifurcation or pre-existing stenosis

21. Atheromatous debris-blue toe syndrome

22. Thrombosis
Rupture of an atheromatous plaque esp moderate and severe stenosis
Virchow’s triad: abnormality of flow, blood, vessel wall

23. Is it possible to differentiate between thrombosis and embolus as a cause of acute ischaemia??
Sometimes!!!
Previously asymptomatic, preexisting cause with sudden onset of severe ischaemia (normal contralateral pulse) = embolus
Previous claudication and sudden onset of acute ischaemia = thrombosis

24. Chronic ischaemia Progressive narrowing
Cause : Atheromatous disease is the common cause
Other uncommon cause: Aneurysm:
popliteal aneurysm: special nature
Diabetes
Some rare disease
Buerger’s disease
Hyperhomocysteineaemia
Takayasu’s disease

25. 3. Location
Acute occlusion: more proximal, the more extensive ischaemia
Diagnostic location determines the best treatment

26. 3. Location-aorto-iliac disease
Chronic: claudication at buttock, thigh calf, loss of femoral pulse
in men: Leriche syndrome (French surgeon who described distal aortic occlusion and erectile impotence)
Acute: catastrophic for ipsilateral limb, buttock, perineum

27. Distal aorta occlusion

28. Location Common femoral disease
Chronic: thigh and calf claudication, palpable the femoral pulse just below inguinal ligament
Acute: femoral bifurcation is the common site of embolus-typical ischaemic limb

29. Location-superficial femoral disease
Chronic :a very common place for stenosis or occlusion where it passes posteriorly through adductor hiatus (Hunter’s canal)
It can produce calf claudication, but rarely severe in presence of profunda femoris artery
Acute: rare

30. Bilateral occlusion of superficial femoral artery with collateral circulation via profunda

31. Location-popliteal atery dsease
Chronic: calf claudication
Acute: sudden occlusion from thrombus or embolus causes severe ischaemia due to occlusion geniculate arteries

32. Location: crural arterial disease
Occlusion only one out of three vessel can asymptom unless either chronic or acute disease involve all three vessels

33. 4. Status of the limb-acute iscahemia
Determine chance of saving limb vs amputation
Pain: severe pain not response to opiate with tenderness in muscle:often irreversible ischaemia
Paresthesia: range from percentible alternation to numbness. Numbness indicate acute critical ischaemia
Pallor: pale > unfixed mottling ->
fixed mottling (do not blanch on pressure) frequently beyond salvage

34. 4. Status of the limb-acute ischaemia
Pulselessness
Paralysis: stiff of the limb, when patient cannot move ankle joint indicated severe ischaemia

36. 4. Status of the limb –chronic ischaemia
Early calf claudication like angina
i.e.tight, stiff or crushing pain

37. What factors influence claudication distance?
Anything increases work of walking
Excess weight
Walking uphill
Walking against wind
Carry shopping

38. More severe form Very short distance- a few steps
Rest pain first felt in the distal parts such as toes and dorsum of the foot – awake patient need rise from bed and walking around to relieve
Unable to lie flat without pain patient sleep with hanging leg out of beds cause edema and worsen microvascular perfusion

39. Hanging foot

40. Last stage of chronic
Gangrene, clinical depend on the degree of decomposition
Range from ulcer (skin necrosis) to gangrene of toe and foot
Gangrene:
wet gangrene: black, soggy, discoloured green and malodorous requires urgent amputation
Dry gangrene: black hard, brittle, wrinkle rarely odour : may autoamputation or surgery in proper time

41. 5. Fitness of patient Determine investigation and treatment
“ surgeon need to consider the ability of the patient to withstand our effort. Our job should be relieve the symptom of which the patient complain”
Common causes of unfitness
- pre-event unfitness: cardiac e.g. MI, Lung-renal-metabolic disease
- per-event unfitness: dehydration, acidosis, uncontrolled DM
- postevent unfitness: myoglobinaemia, severe acidosis, MI

42. Investigation of occlusive disease
Clinical examination: full history
Presence or absence of pulse
Status of the limb
Other test
BUN, CR, electrolyte
CBC, plasma viscosity
Coagulation
EKG, CXR

43. Fixed wave Doppler examination
Ankle brachial pressure index (ABPI)
claudication
< 0.5 critial limb ischaemia
< 0.3 gangrene

45. Treadmill testing Walking incline 10% at speed 3 km/hr
Test of function to allow monitoring disease and the result of therapeutic effort

46. Ultrasound-duplex scan
Composed of
1. B-mode ultrasound reveal the anatomy:aneurysm, occlusive lesion
2. Doppler signal: flow indicate stenosis

47. Duplex scan of SFA stenosis

48. Contrast arteriography
Injection contrast agent make lumen visible
Conventional angiogram: direct intraarterial route
Now we have digital subtraction angiogram(DSA)
CT angiogram: need of arterial puncture
From the picture, what is the diagnosis?

49. Computerised tomographic (CT) angiograhy
Helical CT scan with intra-arterial contrast injection
Look the relation between artery and other structure well
Carotid body tumor

50. Magnetic resonance arteriography(MRA)
without contrast or IV gadolinium
Suitable in patient should not given iodine containing contrast due to renal disease or allergy

51. Aneurysm Pulsatile expansile mass Clinical feature:
invade surrounding tissue cause- pain
rupture
embolisation - ischaemia e.g. claudication, trash foot

52. Ruptured AAA

53. Trash foot-multiple small atheromatous debris

54. Investigation
Ultrasound
CT scan
??? angiogram

55. CT scan “Infrarenal AAA”

56. Angiogram of popliteal aneurysm

57. Venous disease

58. Functional anatomy Superficial venous system devided into 3 parts
Long saphenous vein (LSV)
Short saphenous vein (SSV)
Perforating or communicating vein (PV)

59. Superficial venous system
LSV: medial malleolus to groin
SSV: outer border of foot behind lateral malleolus ascend to middle of the calf 60% to pop V., 20% to LSV and 20% wherelse

60. Superficial venous system
PV connnect superficial and deep vein
> 50 PV in one leg
PV in thigh connect directly between superficial and deep system, in leg connect indirectly via venous plexus

61. Deep venous system
3 artery below knee, there are 2 vein beside of artery from foot up to knee joint
Then pop V beside artery then in thigh
->superficial femoral vein join with profunda femoris vein -> common femoral vein

62. Physiology of venous drainage
Normal: superficial to deep and from distal(foot) to proximal(thigh and heart )
?? At standing position, blood at ankle has to return against gravity to heart over a distance of > 1 metre “how”

63. How 4 factors support this system
Functioning vein valves: resist > 300 mmHg
Functioning foot and calf muscle pumps: weight compress venous plexus in foot and calf muscle compress sinusoidal and deep vein in leg
Residual arterial pressure
Negative intrathoracic pressure
“ however absent valve or damaged valve, the muscle pump cannot work efficiently”

64. Pathophysiology of varicose vein
Abnormal dilated and tortuous superficial vein of the leg
Response to a pathological increase in the vein’s intraluminal pressure
This increases due to higher intraluminal pressure of deep vein (necessary to allow movement of blood out of leg) from deep to superficial system

65. Aetiology
Primary e.g. saphenofemorla valve incompetence

66. Aetiology Secondary mostly due to previous DVT Simple obstruction
Destroying the valves within deep vein
These lead to blood move to superficial system (compensatory mechanism)
** a must to know this, otherwise we may worsen patient with VV surgery**
Primary VV or secondary VV

67. Clinical feature of varicose vein
Cosmetic presentation
Discomfort and pain
Cramps
Swelling
Complication
- thrombophebitis
- haemorrhage
- CVI

68. Patients assessment in VV(1)
History: past Hx of DVT
Examination:
standing position
Area of VV
Brodie Tredelenberg test
Perthes’ test
Continous wave Doppler

69. VV

70. Brodie Tredelenberg test

71. Patients assessment in VV(2)
Radiological evaluation when suspected of previous DVT
Duplex scan
Ascending venography (inject radioopaque in foot and watching it rise in the deep vein)

73. Varicose eczema

74. Chronic leg ulcer

75. Neuropathic ulcer

76. Venous ulcer

77. Arterial ulcer

78. Acute non-traumatic leg pain
Localised to skin
soft tissue, vein
-cellulitis
-lymphagitis
-thrombophlebitis
Pain radiate from back
Exacebate by bending
-lumbosacral N root
compression
Deep pain in whole legThigh, calf 5P
Pain, uniform swelling
No paresis or sensory loss
Emboli source, no IC,N contralat pulse*heparin
DVT,
rupture of baker’s cyst
+ac emboli
- ac thrombosis

79. Chronic non-traumatic leg pain
Pain radiate from back
Exacebate by bending
-lumbosacral N root
compression
Pain in calf, foot
Not radiate to back
claudication
Critical limb ischaemia
Rest pain, gangrene, ulcer

80. History of swelling, DVT Confirm with duplex scan
Varicose vein
History of swelling, DVT
Confirm with duplex scan
Secondary VV
Primary VV
Intervention
Sx, sclerotherapy
Supportive treatment

81. Ulcer
Flat, sloping edge, soft
edge
Punch out
base
Shallow, edema, erythrema
Infection, granulation tissue
Black, dry
Deep to tendon
position
Digit, pressure
Point, heel,
metartarsal head
Above medial
malleolus
Asso DVI
Digit, heel
Ischaemic ulcer
Sensory ulcer
Venous ulcer