This document discusses ischaemia of the lower limbs, including definitions, causes, clinical features, investigations and management. Some key points: - Peripheral vascular disease refers to obstruction or deterioration of arteries other than those supplying the heart or brain. - Causes of acute limb ischaemia include embolism (often from the heart) and thrombosis (due to atherosclerosis, aneurysm, etc.). - Clinical features depend on location and duration of ischaemia, and can include pain, pallor, pulselessness, paralysis. Beyond 6 hours ischemia is usually irreversible. - Investigations include blood tests, imaging like Doppler ultrasound and angiography. Management involves treating the cause, and surgical

1. Ischaemia of Lower Limbs
By
Dr. Shampile
16/11/2017

2. Terminology
• Acute: <14 days
• Acute on chronic: worsening in <14 days
• Chronic: stable for >14 days
• Incomplete: no limb threat
• Complete: limb threatened
• Irreversible: limb non viable

3. Definition
• peripheral vascular disease refers to the
obstruction or deterioration of arteries other
than those supplying the heart and within the
brain.

4. Aetiology-ALI
Embolism- 90% from heart, 9% from great
vessels, 1% other.
• Left atrium in patients in atrial fibrillation
• Mural thrombus after myocardial infarct
• Prosthetic and diseased heart valves
• Aneurysm or atheromatous stenosis
• Tumour, foreign body

5. Aetiology-cont’d
Thrombosis; Atherosclerosis, aneurysm, graft stenosis,
low flow, e.g. hypovolaemia, thrombotic states.
Other
• Trauma ( general or operative)
• Arteritis,
• Congenital anomalies
• Dissecting aneurysm
• Raynaud's Syndrome
• Metabolic (DM)
• Drugs e.g. Acute ischaemia due to intra-arterial
temazepam injection

6. Pathophysiology-ALI
• Sudden interruption of blood supply.
• Emboli tend to lodge at sites of vessel
bifurcation.
• There are two phases of cell injury: ischaemic
injury as tissues are deprived of blood supply
and reperfusion injury if blood flow is
restored

7. Clinical features of limb ischaemia
• Symptoms and signs depend on the site of
occlusion, duration of ischaemia and degree
of collateral circulation.
• Embolus more likely if severe, sudden onset
and potential source identifiable, e.g. atrial
fibrillation.
• Thrombosis usually if less severe (collaterals
present), history of claudication

8. Acute arterial occlusion
• Pain (absent in incomplete ischemia)
• Pallor (present in chronic ischemia)
• Pulselessness (present in chronic ischemia)
• Perishing cold (unreliable)
• Paresthesia (leading to anaesthesia)
• Paralysis (contrasts with venous
occlusion when muscle function is not
affected)

9. • Ischaemia beyond 6 hours is usually
irreversible and results in limb loss.
• No history of claudication

10. EXAMINATION
• Limb is pale with absent pulses; capillary
return is slow.
• After several hours, there is venous
stagnation.
• Altered sensation, and if ischaemia is severe,
paraesthesia with muscle paralysis

11. INVESTIGATIONS
• Bloods: FBC, U&Es, coagulation profile,
thrombophilia screen.
• Imaging: CXR, Doppler or duplex scanning of
blood flow, arteriography to demonstrate the
site of occlusion and plan intervention if limb
viable.
• ECG: Looking for atrial fibrillation.

12. Management
Diagnois
• Is this ischaemia ?
• Is this an embolism or thrombosis ? clinical
features include:
 Rapidity of onset of symptoms
 Features of pre-existing chronic arterial disease
 Potential source of embolus
 State of pedal pulses in contralateral leg
• Is this limb viable ?

13. MANAGEMENT
• Immediate: ABCs, analgesia, heparin
anticoagulation to prevent thrombus
propagation.
• Treat associated cardiac disease
• Surgical: Revascularisation within 6 hours in
order to salvage limb. Operative risk is often
high due to underlying heart disease.
Postoperative anticoagulation is essential

14. MANAGEMENT
Treatment options are:
• Embolic disease - embolectomy or intra-
arterial thrombolysis
• Thrombotic disease - intra-arterial
thrombolysis / angioplasty or bypass surgery
• Amputation ; if non viable limb

15. MANAGEMENT
Emergency embolectomy
• Can be performed under either general or local
anaesthesia
• Display and control arteries with slings
• Transverse artereotomy performed over common
femoral artery
• Fogarty balloon embolectomy catheters used to
retrieve thrombus
• If embolectomy fails - ontable angiogram and consider
Bypass graft or intraoperative thrombolysis

16. MANAGEMENT
• If acute or chronic thrombosis: The limb may
remain viable for a longer time due to
collateral formation, and percutaneous
intervention is an option, e.g. aspiration,
intraarterial thrombolysis with local infusion
of, e.g., t-PA, and angioplasty of underlying
stenoses.

17. MANAGEMENT
Intra-arterial thrombolysis
• Arteriogram and catheter advanced into
thrombus
• Streptokinase 5000u/hr + heparin 250u/hr
• Alternative thrombolytic agents include
Urokinase or tissue plasminogen activator (tPA)
• Repeat arteriogram at 6 -12 hours
• Advance catheter and continue thrombolysis for
48 hours or until clot lysis

18. MANAGEMENT
• Angioplasty of chronic arterial stenosis may be
necessary
• Success 60-70% but needs careful case selection
• Not suitable if severe neuro-sensory deficit
• Thrombolysis can be accelerated by
 Pulse spray through multiple side hole
catheter
Aspiration thrombectomy - debulking thrombus
aspiration
High dose over shorter time

19. MANAGEMENT
• If thrombosis but the limb is not likely to
remain viable for 12–24 hours necessary for
this procedure: Urgent reconstructive surgery
is required,
• if technically possible with autogenous
(saphenous vein) or synthetic (e.g. PTFE or
Dacron) bypass grafting.
• If risk of compartment syndrome, fasciotomy
is required.

20. Vascular Trauma of the Extremity
• Often the extremities are placed at the
bottom of the ‘‘to-do’’ list in patients with life-
threatening multisystem trauma, only to find
an ischemic limb hours later.
• Therefore, a high index of suspicion is
warranted in patients with extremity
fracture/dislocations

21. Vascular Trauma of the Extremity
• Blunt trauma results in a stretch injury and
subsequent occlusion of the artery at the level
of the associated fracture or joint dislocation.
• Penetrating wounds can produce either vessel
transection or a pseudoaneurysm
• Angiography, to discern between vessel spasm
and overt injury, can be performed in the
angiography suite or in the OR.

22. COMPLICATIONS
• From disease: Gangrene, limb loss, death.
• From intra-arterial thrombolysis: Mortality
(1–2%), CVA, major haemorrhage
• Post-treatment: Reperfusion syndrome,
compartment syndrome, rhabdomyolysis,
rethrombosis.

23. PROGNOSIS
• Risk of limb loss is up to 30%; mortality 10%,
with major mortality factor underlying cardiac
disease.

24. Chronic Arterial Insufficiency
• Asymptomatic to gangrenous tissue loss
• Intermittent claudication
• Rest pain
• Dependent rubor
• Ulceration
• Gangrene
• Arterial pulsation diminished or absent
• Arterial bruit
• Slow capillary refilling

25. Chronic vascular insufficiency
• Claudication: crampy aching pain in the calf
muscles appearing with fixed level of exercise
(claudication distance) and relieving promptly
(2-3 mins) on rest
– Boyds 1: pain- walk- relief
– Boyds 2: pain- walk- no relief
– Boyds 3: pain- stop- relief
– Boyds 4: rest pain

26. Chronic vascular insufficiency-cont’d
• Rest pain: cry of the dying nerves; some relief
by “gravity aid”
– A limb with rest pain may appear red due to
accumulation of vasodilator metabolites: sunset
foot sign/ dependent rubor
• Ulceration: arterial ulcers
• Pregangrene: any 2 (rest pain, edema,
hyperaesthesia, colour changes, ulceration)
• Gangrene

27.  Sabiston’s 19th ed

28. Ankle Brachial Pressure Index (ABPI)
• It is cornerstone of diagnosis
• ratio of systolic pressure at the ankle to that in
the arm.
• The highest pressure in the dorsalis pedis,
posterior tibial or peroneal artery serves as
the numerator, with the highest brachial
systolic pressure being the denominator
• Supine position, proper cuff size
• >1.3: Arteriosclerosis

30. ABI-cont’d
• Resting ABPI is normally about 1.0;
• values below 0.9 indicate some degree of
arterial obstruction (claudication),
• less than 0.5 suggests rest pain and
• less than 0.3 indicates imminent necrosis.
• Even normal values may present with
intermittent claudication

31. Site of blockage Clinical features
Aortoiliac Leriche syndrome, buttock-
thigh-calf claudication
Common femoral Thigh & calf claudication
Superficial femoral Calf
Popliteal Calf
Crural Calf

32. Atherosclerosis vs Buerger’s
Atherosclerosis Buerger’s (OLIN criteria-2000)
• Old age
• Hypercholesterolemia
• Smoking (4x)
• Diabetes mellitus (3-5x)
• Hypertension
• Pvs history of thromboembolic
phenomena (stroke/ TIA/
amaurois fugax, DVT etc.)
• Large & medium sized elastic
& muscular vessels
• <45 yrs
• Tobacco use (chewing/
smoking)
• Distal extremity ischemia
• Exclusion of autoimmune
disease, hypercoagulability
and DM
• Exclusion of proximal source of
emboli
• Consistent imaging findings
• Medium to small sized vessels

33. CT angiography
Atherosclerosis Buerger’s

34. Other Diseases
• Takayasu arteritis: pulseless disease of asian
young females
• Raynaud phenomenon: pallor followed by
cyanosis & rubor
• Raynaud’s syndrome: peripheral arterial
manifestation of a collagen disease, such as
systemic lupus erythematosus or rheumatoid
arthritis or vibration white finger.
• Raynaud disease: Raynaud phenomenon in a
young female without any other cause

35. Pathogenesis of Atherosclerosis

36. Pathogenesis of Buerger’s Disease
• Cellular, segmental, occlusive inflammatory
thrombi of the vessel wall
• Small to medium sized vessels
• Involves all layers of the vessels
• Integrity of the vessel wall structure is
maintained including internal elastic lamina
• Later on spreads to the adjoining nerve and
vein

37. Pathogenesis of Buerger’s Disease
• Induced by an unknown agent from smoking
& tobacco chewing, nicotine patch
• Rickettsia infection
• Increased antiendothelial antibodies
• Impaired relaxation of the peripheral vessels
• HLA-A9, HLA-54, HLA-B5
• Increased sensitivity to type 1 & type III
collagen

38. Assessment
• Disappearing pulse: decreased pulse pressure
on exercise: pulse disappears on exercise
• Allen’s test: positive in young patient with foot
ulceration: Buerger’s Disease
• doppler: harmless, defines level

39. Investigations
• ECG: rule out embolic phenomenon
• Angio(Arterio)graphy: (convntional/ MR/ CT)
– Buerger’s (TAO): corkscrew collaterals, tree root/ spider leg appearance
– Atherosclerosis (ASO): level of obstruction

40. Other investigations
General
• FBC
• U/E
• Lipid profile
• ECG
• ESR
• CRP
• Homocystine
• PT/ aPTT/ INR, Protein C/S/
Factor V leiden, Antithrombin
III/ Lupus anticoag
• Carotid duplex

41. Buerger’s Disease specific treatments
• Prostaglandins (limaprost/iloprost) : antiplatelets
& vasodilators
– Increase cutaneous & muscular blood supply
• Bosentan: endothelin antagonist
• Epidural anaesthesia
• Hyperbaric Oxygen therapy
• Genetic therapy by VEGF gene intramuscular
transfer
• Stem cell & VEGF injections intramuscularly
• Debridement

42. Buerger’s: Surgeries
• Lumbar Sympathectomy-
open or endoscopic,
remove 2nd -4th lumbar
sympathetic ganglia
• Amputation
• Chemical Sympathectomy

44. Atherosclerosis: specific T/T
Endovascular Surgical
• Self expandable metallic
stents
• Balloon expandable stents
• Endarterectomy
• Bypass:
– Aortobifemoral
– Axillobifemoral
– Femorofemoral
– Obturator bypass
– Axillopopliteal
– Thoracofemoral
– Infrainguinal

45. REFERENCES
• Beard J D Gaines P A. Management of the acutely
ischaemic leg. Curr Pract Surg 1995; 7: 123-130.
• Beattie D K Davies A H. Management of the
acutely ischaemic limb. Br J Hosp Med 1996; 55:
204-208.
• Earnshaw J J. Thrombolysis in acute limb
ischaemia. Ann R Coll Surg Eng 1994; 76: 216-
222.
• Golledge J Galland R B. Lower limb intra-arterial
thrombolysis. Postgrad Med J 1995; 71: 146-150.

46. REFERENCES
• Carroll PR, McAninch JW, Klosterman P, Greenblatt M
(1984) Renovascular trauma: risk assessment, surgical
management, and outcome. J Trauma 30:547
• Courcy PA, Brotman S, Oster-Grantie ML, et al. (1984)
Superior mesenteric artery and vein injuries from blunt
abdominal trauma. J Trauma 24:843
• Dajee H, Richardson IW, Iype MO (1979) Seatbelt aorta:
acute dissection and thrombosis of the abdominal aorta.
Surgery 85:263
• Feliciano DV (1998) Approach to major abdominal vascular
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