Topic of Vascular Claudication

Management of Vascular Claudication

1. MANAGEMENT
OF
CLAUDICATION
By PhongthornTuntivararut
Surgical Residency
Police general hospital, Thailand

3. CLAUDICATION
•Claudication is derived from the Latin word claudicatio
•Means to limp or be lame
•Claudication is pain, tired or weak feeling that occurs in legs,
usually during activity such as walking, and go away a short
time after rest
•Complete relief of symptoms should occur within 5 to 10 min
•It should not be necessary for the patient to sit to obtain relief
Rutherford’s Vascular Surgery 8
th
Ed

4. CLAUDICATION
•Classically, claudication is associated with arterial stenosis or
occlusion
•The symptoms are secondary to inadequate or decreased blood
flow to the muscles affected
•AKA “Arterial claudication” or “Intermittent claudication”
Rutherford’s Vascular Surgery 8
th
Ed

5. CONDITION MIMICKING
ARTERIAL CLAUDICATION
•Differential diagnosis of claudication are musculoskeletal,
neurologic, and venous pathologies
•The most common of which are osteoarthritis, spinal stenosis, and
venous outflow obstruction
•Atypical claudication of nonarterialetiology
•Pain with exertion
•Pain does not stop the patient from walking
•May not involve the calves or other major muscle groups
•Does not resolve within 10 minutes of rest
Rutherford’s Vascular Surgery 8
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Ed

6. Claudication
Arterial condition
Neurologic
condition
Venous condition

7. HISTORY TAKING AND
PHYSICAL EXAMINATION

8. Rutherford’s Vascular Surgery 8
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Ed

9. NEUROGENIC CLAUDICATION
•Caused by lumbar spinal stenosis, nerve root compression
•Whole leg pain, can be associated with tingling and numbness
•Mostly bilateral
•Suddenly pain on standing up or walking
•Relief does not occur promptly once activity has ceased
•Complete symptomatic relief may take 30 to 60 minutes or
longer by sitting, bending forward, or stop walking
•Unable to straighten legs
Rutherford’s Vascular Surgery 8
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Ed

12. VENOUS CLAUDICATION
•The “bursting” thigh pain and “tightness” that develops during
exercise
•Usually seen varicose vein, cyanosis and edematous
•Most commonly unilateral
•Gradual onset after beginning to walk
•Relieve on elevating the leg
Rutherford’s Vascular Surgery 8
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Ed

13. VENOUS CLAUDICATION
•Symptoms are associated with a proximal venous obstruction
resulting in impaired venous outflow
•The pathophysiologyof venous claudication is related to the
high outflow resistance
Rutherford’s Vascular Surgery 8
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Ed

14. PATHOPHYSIOLOGY OF
VENOUS CLAUDICATION
Exercise or other activity
Increase arterial flow to extremities
High venous outflow and pressure
Veins become engorged and tense
Rutherford’s Vascular Surgery 8
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Ed

15. INTERMITTENT CLAUDICATION
•The three major muscle groups of the lower extremity,
depending on the location of the obstruction:
•The buttock, thigh, or calf
•Symptoms may involve one or more of these muscle groups
•Symptoms will often occur in the muscle group immediately
distal to the obstruction
“Peripheral Arterial Disease”
Rutherford’s Vascular Surgery 8
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Ed

16. INTERMITTENT CLAUDICATION
•Gradual onset after walking
•“Claudication distance” is the distance of that patients can walk
until the symptoms aggravated
•One-block Claudication
•Two-block Claudication
•As the process progresses, symptoms occur more frequently
and after shorter distances
Rutherford’s Vascular Surgery 8
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Ed

17. PROGRESSION
Pain only when
doing exercise
(Effort
discomfort)
Pain even
at rest
Limit activity of
daily living
(Shorter walking
distance)
Rutherford’s Vascular Surgery 8
th
Ed

18. Intermittent claudication is one of the
most common symptom of Peripharal
Arterial Disease (PAD), which is caused
by atherosclerosis

19. INTERMITTENT CLAUDICATION
•Risk factors for PAD :
•Smoking
•Underlying of DM, HT, DLP and ESRD
•Obesity
•Long-term use of corticosteroid
•Family history of Cardiovascular disease
Rutherford’s Vascular Surgery 8
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Ed

20. SMOKING FACTOR
•The physiologic effects of smoking are incompletely understood
•Nicotine inhalation has been demonstrated to
•Reduce high density lipoprotein (HDL) levels
•Increase platelet aggregation
•Decrease prostacyclin
•Increase levels of thromboxane
•Promote vasoconstriction

21. •Long-term corticosteroid therapy has also been reported to be
associated with a distally accentuated, calcifying peripheral
atherosclerosis, inducing arterial incompressibility
comparable to patients with renal failure or diabetes
EurJ VascEndovascSurg. 2010

22. PATHOPHYSIOLOGY OF
INTERMITTENT CLAUDICATION
•The arteries that supply
blood to your limbs are
damaged, usually as a result
of atherosclerosis
•Atherosclerosis narrows the
arteries and makes them
stiffer and harder
http://www.mayoclinic.org/diseases-conditions/claudication

23. PATHOPHYSIOLOGY OF
INTERMITTENT CLAUDICATION
•The pain sensation results from
•Ischemic neuropathy involving small A delta and C sensory fibers
•Local intramuscular acidosis from anaerobic metabolism
enhanced by the release of substance P
Rutherford’s Vascular Surgery 8
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Ed

24. PATTERNS OF OBSTRUCTION
Inflow
disease
Outflow
disease
Combination
Rutherford’s Vascular Surgery 8
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Ed

25. INFLOW OBSTRUCTION
•Lesions in the suprainguinalvessels
•most commonly the infrarenalaorta and iliac arteries
•Occlusive lesions of the infrarenalaorta or iliac arteries
commonly lead to buttock and thigh claudication
•Bilateral and proximal to the origins of the internal iliac a.
•Vasculogenicerectile dysfunction
Rutherford’s Vascular Surgery 8
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Ed

26. OUTFLOW OBSTRUCTION
•Occlusive lesions in the lower extremity arterial tree below the
inguinal ligament
•Common femoral artery to the pedal vessels
•Superficial femoral artery is the most common lesion
associated with intermittent claudication
Rutherford’s Vascular Surgery 8
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Ed

28. OUTFLOW OBSTRUCTION
•Popliteal and tibialartery occlusions are more commonly
associated with limb-threatening ischemia
•Less collateral vascular pathways beyond these lesions
Rutherford’s Vascular Surgery 8
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Ed

29. COMBINATION OBSTRUCTION
•Symptoms frequently begin in the buttock and thigh and then
involve the calf muscles with continued ambulation
•May appear in reverse order if the distal disease is more severe
•Severe combined inflow-outflow disease may result in limb-
threatening ischemia
Rutherford’s Vascular Surgery 8
th
Ed

30. INTERMITTENT CLAUDICATION
•Symptoms of claudication
associated with PAD
usually manifest in the
muscle groups below the
hemodynamically
significant lesion
Rutherford’s Vascular Surgery 8
th
Ed

31. NATURAL HISTORY OF
PERIPHERAL ARTERY
DISEASE

32. Circulation. 2006;113:1474 –1547

36. INTERMITTENT CLAUDICATION
•The natural history of IC is marked by slow progression to
shorter walking distances, but it rarely reaches the level of CLI
•The risk of major amputation is less than 5% over a 5-year
period
•In a long-term study of 1244 claudicants, only insulin-requiring
diabetes, low initial ABI, and high pack-years of smoking
predicted progression to ischemic rest pain and ischemic
ulceration
J VascSurg34:962–970, 2001

37. •Patients with symptoms of intermittent claudication should
undergo a vascular physical examination, including
measurement of the ABI (Class I, Level of Evidence: B)
•In patients with symptoms of intermittent claudication, the ABI
should be measured after exercise if the resting index is
normal(Class I, Level of Evidence: B)
Circulation. 2006;113:1474 –1547

38. EXERCISE TESTING
•Treadmill Exercise is done :
•Two miles per hour
•Five minutes
•Twelvespercentsincline
Rutherford’s Vascular Surgery 8
th
Ed

39. ANKLE BRACHIAL INDEX
•The ankle-brachial index (ABI) is the ratio of the systolic blood
pressure (SBP) measured at the ankle to that measured at the
brachial artery, originally described by Winsor in 1950
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Circulation. 2012;126:2890-2909

41. ANKLE BRACHIAL INDEX
•ABI values more than 1.40 indicate non-compressible arteries
•Normal ABI range of 1.00 to 1.40
•ABI values of 0.91 to 0.99 are considered “borderline”
•Abnormal values is less than 0.90 (Suspected PAD)
•Intermittent claudication usually seen in ABI 0.5 –0.95
Circulation. 2011;124:2020 –2045

42. PULSE VOLUME RECORDING
•Pulse volume recordings are reasonable to establish the initial
lower extremity PAD diagnosis, assess localization and
severity, and follow the status of lower extremity
revascularization procedures (Class IIa, Level of Evidence: B)
Circulation. 2006;113:1474 –1547

43. Circulation. 2006;113:1474 –1547

44. TREATMENT OF
CLAUDICATION

45. TREATMENT OPTION
Risk factor
modification
Exercise therapy
Pharmacologic
treatment
Revascularization

46. TREATMENT OPTION
Risk factor
modification

47. SMOKING CESSATION
•The role of smoking cessation in the treatment of intermittent
claudication is less clear
•Treadmill studies have demonstrated an increase in pain-free
ambulation distancesin some but not all patients
•Reduce their risk of cardiovascular events and limit the
progression of PAD
Rutherford’s Vascular Surgery 8
th
Ed

48. SMOKING CESSATION
•There is a threefold redudedrisk of graft failure in patients
who have undergone revascularization
•Bupropion and other pharmacologic agents have increased
smoking cessation rates
Rutherford’s Vascular Surgery 8
th
Ed

49. SMOKING CESSATION
•Individuals with lower extremity PAD who smoke cigarettes or
use other forms of tobacco should be advised by each of their
clinicians to stop smokingand should be offered
comprehensive smoking cessation interventions, including
behavior modification therapy, nicotine replacement therapy,
or bupropion (Class I, Level of Evidence: B)
Circulation. 2006;113:1474 –1547

50. Circulation. 2011;124:2020 –2045

51. GLYCEMIC CONTROL
•Each incremental 1% increase in HbA1C is associated with a
28% increase in risk for PAD
•Tighter glucose control regimens exhibited only a
nonstatisticallysignificant reduction in cardiovascular events
and had no effect on the incidence of PAD
Rutherford’s Vascular Surgery 8
th
Ed

52. GLYCEMIC CONTROL
•Administration of glucose control therapies to reduce the
hemoglobin A1C to less than 7% can be effective to reduce
microvascularcomplications and potentially improve
cardiovascular outcomes (Class IIa, Level of Evidence: C)
Circulation. 2006;113:1474 –1547

53. BLOOD PRESSURE CONTROL
•Hypertension is associated with a two-to threefold increased
risk of PAD
•Blood pressure goal of
•< 140/90 (nondiabetics)
•< 130/80 (diabetics and individuals with chronic renal disease)
•to reduce the risk of MI, stroke, congestive heart failure, and
cardiovascular death (Class I, Level of Evidence: A)
Circulation. 2006;113:1474 –1547

54. BLOOD PRESSURE CONTROL
•All drugs that are effective at reducing SBP can decrease the
risk of cardiovascular events
•Beta-adrenergic blockers are effective antihypertensive agents
and are not contraindicated in patients with PAD (Class I, Level
of Evidence: A)
•ACE Inhibitors are particularly beneficial, but approve as a
cardioprotectivedrugs
Circulation. 2006;113:1474 –1547

55. LIPID LOWERING
•Statinsare indicated for all patients with PAD to achieve a
target LDL < 100 mg/dl (Class I, Level of Evidence: B)
•Target LDL < 70 mg/dl is reasonable for patients with very
high risk of ischemic events. (Class IIa, Level of Evidence: B)
Circulation. 2006;113:1474 –1547

56. Rutherford’s Vascular Surgery 8
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Ed

57. PLATELET AND
THROMBOTIC DRUGS
•Antiplatelet therapy is now widely accepted for the treatment
of cardiovascular disease
•Clopidogrelwas associated with an overall 8.7% reduction in
the risk of stroke, MI, and death
•A relative cardiovascular risk reduction of 24% was found in
the clopidogrelgroup compared with the aspirin group
Rutherford’s Vascular Surgery 8
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Ed

58. Circulation. 2011;124:2020 –2045

59. RECOMMENDATION
•Antiplatelet therapy can be useful to reduce the risk of MI,
stroke, or vascular death in asymptomatic individuals with an
ABI less than or equal to 0.90 (Class IIa, Level of Evidence: C)
•The usefulness of antiplatelet therapy to reduce the risk of MI,
stroke, or vascular death in asymptomatic individuals with
borderline abnormal ABI, defined as 0.91 to 0.99, is not well
established(Class IIb, Level of Evidence: A)
Circulation. 2011;124:2020 –2045

60. TREATMENT OPTION
Exercise therapy

61. EXERCISE THERAPY
•Exercise therapy is the best initial treatment of intermittent
claudication
•Regular aerobic exercise reduces cardiovascular risk by
lowering cholesterol and blood pressure and by improving
glycemic control
Rutherford’s Vascular Surgery 8
th
Ed

62. EXERCISE THERAPY
•Exercise training, in the form of walking
•Minimum of 30 to 50 minutes per session
•Three to five times per week
•Not less than 12 weeks
•(Class I, Level of Evidence: A)
•During each session, the patient should be encouraged to walk
until the limit of lower extremity pain tolerance is reached,
followed by a short period of rest until pain relief is obtained,
then a return to exercise
Circulation. 2006;113:1474 –1547

63. Circulation. 2006;113:1474 –1547

64. EXERCISE THERAPY
•Therefore, although exercise therapy in motivated patients
offers proven benefits, its effectiveness is applicable to only
about one third of patients presenting with intermittent
claudication
Rutherford’s Vascular Surgery 8
th
Ed

65. TREATMENT OPTION
Pharmacologic
treatment

66. PHARMACOLOGIC TREATMENT
•Only two drugs (pentoxifyllineand cilostazol) have achieved
US FDA approval for the treatment of intermittent claudication
•Other drugs :
•Changes in tissue metabolism (naftidrofuryl, levocarnitine)
•Enhanced nitric oxide production (L-arginine)
•Vasodilatoryeffects (statins, buflomedil, prostaglandins, ACE
inhibitors, K-134)
Rutherford’s Vascular Surgery 8
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Ed

67. PENTOXIFYLLINE
•The first drug approved by the FDA for the treatment of
intermittent claudication
•Pentoxifyllineis the methylxanthinederivative that is thought
to improve oxygen delivery
•Pentoxifyllineis also believed to inhibit platelet aggregation
and to increase fibrinogen levels
Rutherford’s Vascular Surgery 8
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Ed

68. •Pentoxifyllineshowed that maximal treadmill walking
distances in patients with claudication were improved by 12%
compared with placebo
•Although walking distances improved, patient discomfort with
walking typically persisted
Am Heart J.1982 Jul;104(1):66-72.

69. PENTOXIFYLLINE
•Pentoxifylline(400 mg 3 times per day) may be considered as
second-line alternative therapy to cilostazolto improve
walking distance in patients with intermittent claudication
(Class IIb, Level of Evidence: A)
•The clinical effectivenessof pentoxifyllineas therapy for
claudication is marginal and not well established (Class IIb,
Level of Evidence: C)
Circulation. 2006;113:1474 –1547

70. CILOSTAZOL
•Phosphodiesterase-III inhibitor increases cyclic adenosine
monophosphate (cAMP)
•Physiologic effects :
•Inhibition of smooth muscle cell contraction
•Inhibition of platelet aggregation
•Cilostazolis also thought to decrease smooth muscle cell
proliferation, a process that has been implicated in coronary
artery restenosis after percutaneous transluminalangioplasty
Rutherford’s Vascular Surgery 8
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Ed

71. CILOSTAZOL
•Cilostazolhas a beneficial effect on lipid concentrations
•Decrease in serum triglycerides
•Increase in HDL
•Although the precise mechanismby which cilostazolimproves
the symptoms of intermittent claudication is unknown
Rutherford’s Vascular Surgery 8
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Ed

72. •Compared with placebo, Cilostazolimproves maximal walking
distance by 40% to 60% after 12 to 24 weeks of therapy
•Cilostazol, 100 mg or 50 mg, twice a day
VascEndovascular Surg2002;36:83-91

73. •Cilostazolwas associated with greater improvements in
community-based walking ability and health-related quality of
life (HQL)in patients
•Questionnaires assessing walking ability and HQL provide
important patient-based information about clinical outcomes of
claudication therapy
J Am Geriatr Soc 2002;50:1939–46

74. CILOSTAZOL
•Cilostazol(100 mg orally 2 times per day) is effective improve
symptoms and increase walking distance in patients with lower
extremity PAD and intermittent claudication (in the absence of
heart failure) (Class I, Level of Evidence: A)
•A therapeutic trial of cilostazolshould be considered in all
patients with lifestyle-limiting claudication (in the absence of
heart failure) (Class I, Level of Evidence: A)
Circulation. 2006;113:1474 –1547

75. CILOSTAZOL
•Cilostazolhas a moderate but notable adverse effect profile
that includes headache, diarrhea, and gastrointestinal
discomfort
•Contraindication : Congestive Heart Failure
•Cilostazolis a phosphodiesterase-3 inhibitor capable of
exacerbating ventricular dysfunction
•Metabolized by the liver via the cytochrome-P450 pathway
•CYP 3A4 and CYP 2C19
Rutherford’s Vascular Surgery 8
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Ed

76. TREATMENT OPTION
Revascularization

77. REVASCULARIZATION
•Decision making regarding revascularization is based first on
symptom status and the patient’s condition
•Revascularization is recommended only in cases of severe
claudication, and only after medical therapy has failed
Rutherford’s Vascular Surgery 8
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Ed

78. REVASCULARIZATION
•The majority of claudicantsare stable pattern of disease or have
an improvement with risk factor modification and exercise
•There are 20% to 30% require operation within 5 yearsas a
result of disease progression
•Risk for mortality and limb loss is 5% and 1% respectively

79. •Walking study consisted of a randomized trial to determine
outcome differences in patients with intermittent claudication
treated with angioplasty and stents versus medical
management (daily low-dose aspirin, lifestyle modification)
after 2 years
•There are no difference in maximal walking distance, treadmill
distance until onset of claudication, and QoLmeasures
between the two groups
J VascSurg26:551–557, 1997

80. REVASCULARIZATION
•Indications for surgical reconstruction
•Disabling claudication (lifestyle-limiting disability)
•Ischemic rest pain
•Tissue loss
Rutherford’s Vascular Surgery 8
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Ed

81. •Supervised exercise therapy has also been compared with primary
stenting revascularization for disabling claudication due to aortoiliac
occlusive disease
•At 6-month follow-up, the peak walking time was greatest for
supervised exercise, intermediate for stenting, and least with
pharmacologic therapy
•Supervised exercise shows the better outcome than stenting(P < .04)
Circulation. 2012 Jan 3;125(1):130-9

82. THANK YOU
FOR YOUR ATTENTION