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| REVIEW ARTICLE |
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| Year : 2022 | Volume
: 5
| Issue : 3 | Page : 68-74 |
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Arterial claudication
Pierre Abraham1, Simon Lecoq1, Jeanne Hersant2, Samir Henni2
1 Department of Vascular Medicine; Department of Sports Medicine, Hospital and University of Angers, Angers, France
2 Department of Vascular Medicine, Hospital and University of Angers, Angers, France
| Date of Submission | 07-Jul-2022 |
| Date of Decision | 23-Jul-2022 |
| Date of Acceptance | 08-Aug-2022 |
| Date of Web Publication | 10-Nov-2022 |
Correspondence Address:
Dr. Pierre Abraham
Department of Vascular Medicine; Department of Sports Medicine, Hospital and University of Angers, Angers
France
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/2589-9686.360872
Arterial claudication is generally the revealing form of clinically symptomatic lower extremity artery disease. It is defined as a pain of limb muscles that occurs during exercise and is relieved within 10 min when exercise is lowered or stopped. Atherosclerosis is the first underlying cause of arterial intermittent claudication. As such, the occurrence of arterial claudication is a severe medical event sharing almost similar the long-term morbidity and mortality risk as other arterial events such as stroke or myocardial infarction. Comorbid (both vascular and nonvascular) affections must be actively searched. Surgery is generally indicated only when medical treatment and training have failed to improve symptoms. This paper shortly reviews the cause, presentation, diagnostic algorithm, and treatments of arterial claudication.
Keywords: atherosclerosis, diagnosis, lower extremity arterial disease, lower limb ischemia, peripheral artery disease, treatment
How to cite this article:
Abraham P, Lecoq S, Hersant J, Henni S. Arterial claudication. Vasc Invest Ther 2022;5:68-74 |
| Introduction | |  |
Arterial intermittent claudication (AIC) is a specific form of intermittent claudication resulting from impaired inflow to the exercising lower limb muscles and one of the first causes of referral to vascular medicine physicians or surgeons. Etymologically, claudication refers to the alteration of walking pattern associated with the pain that occurs during exercise. In fact, pain in AIC does not result “stricto-sensus” to the mismatch of blood flow supply and blood flow requirement of exercising muscles, but rather from the mismatch between oxygen requirement and oxygen delivery by impaired blood flow due to lower extremity arterial disease (LEAD).[1] Most patients with AIC report discomfort or pain at the calf level but may also experience pain at the lower back, buttock, thigh, or foot depending on the localization of the arterial lesions. Typically, pain is absent at rest, occurs for an individual level of exercise level, and is relieved within 10 min when exercise is stopped. Nevertheless, exertional leg symptoms other than intermittent claudication are common in LEAD.[2] The level of exercise at which pain occurs depends on the severity of arterial lesions and on the presence or absence of comorbid conditions that may worsen the tolerance to exercise.[3] Thereby athletes may suffer AIC from minor lesions that shall remain asymptomatic during usual daily life activities as can be observed in endofibrosis.[4] Inversely, severe atherosclerotic lesions may remain asymptomatic in sedentary or very inactive subjects, or the presence of collateral circulation.[5] Last, lesions of similar severity shall result in more severe walking impairment in case of comorbid conditions (exercise-induced hypoxemia, anemia).[3]
| Epidemiology | | |
The prevalence of LEAD and AIC depends on the diagnostic criteria used for the diagnosis[6],[7],[8] and is likely increasing in the worlds even in middle age subjects[9] In 19748, adults between 40 and 69 years of age, the age-adjusted prevalence of intermittent claudication was 1.1% for men and 1.2% for women and increased by age.[10] It is highly sensitive to the risk factors of the exposed population,[11] but increases with aging.[12],[13]
| Risk Factors | | |
Atherosclerosis being the major cause of AIC, risk factors for AIC include smoking, obesity diabetes, or chronic immune-inflammatory arterial diseases.[14],[15] These are important to consider because some are modifiable with lifestyle changes and prevention. Diabetes mellitus, hypertension, and dyslipidemias are important risk factors too and their treatments reduce the risk an evolution of atherosclerosis and AIC. Last, the prevalence of AIC increases with age and shows a male dominance as does atherosclerosis. The pathophysiology of atherosclerosis has been largely described elsewhere and will not be recalled here. Numerous biological factors (among which: C-reactive protein, infection, homocysteinemia, lipoprotein (a), reduced adiponectin, and fibrinogen) have been studied and are associated with the presence, severity, or evolution of AIC but are not typically used in routine.[16],[17],[18],[19],[20],[21],[22],[23],[24],[25] Last, specific factors associated with nonatherosclerotic arterial lesions, such as radiations (postradic disease),[26] long-lasting high-level endurance training (endofibrosis),[27],[28] ABCC6 mutation (pseudoxanthoma elasticum),[29] may also be considered in unusual or specific clinical situations.
| History and Physical Examination | | |
Atherosclerotic, the major cause of AIC, generally results in a progressive narrowing of the arterial lumen, except in case of plaque rupture or thrombosis. In the early evolution of lesions, moderately active or sedentary subjects with LEAD mild-to-moderate lesions will remain asymptomatic for years before claudication occurs while walking, probably explaining why claudication mostly appears in patients in their sixties. A history of AIC will include analysis of the personal and familial history of risk factors and the presence of comorbid conditions. Symptoms and their localization are optimally described using standard questionnaires such as the Edinburg[30] or San-Diego[31] questionnaires and help define whether symptoms are of vascular type. Similarly, the evaluation of self-reported walking impairment with the WIQ or Walking Estimated-Limitation Calculated by History questionnaires[32],[33],[34],[35],[36] [Figure 1] and of quality of life[37],[38] can be standardized with self-completed tools that can participate in the evaluation the clinical severity and guide treatment options.[39] | Figure 1: Example of the filling of a WELCH questionnaire. Each of the first three items is scored from 0 points (impossible) to 7 points (3 h or more). The evaluation of usual speed is scored a coefficient of 1 (much slower) to 5 (faster). The WELCH score is the sum of points minus one, multiplied by the coefficient found in item 4. Here, the WELCH score is 6 ([4 + 2 + 1] − 1) × 1 = 6. WELCH: Walking Estimated-Limitation Calculated by History
Click here to view |
Last, detecting symptoms of cardiac or cerebral-associated arterial lesions are essential because atherosclerosis is a systemic disease.
Physical examination should include palpation of arterial pulses and auscultation searching for a bruit (including at the carotid level). Although essential, pulse palpation in AIC has a poor sensitivity at rest particularly if AIC appears only for moderate-to-high level of exercise or if the lesions are located on branches (internal iliac or profunda femoris arteries) and the presence of normal pulses should not be used to argue against the arterial origin of pain. Muscle palpation and osteoarticular passive mobilization at rest are strictly nonpainful. Facing proximal claudication, the presence of sensitive or motor deficits might guide to the presence of a lumbar spine stenosis. Classical signs associated with severe LEAD such as ulcers, pallor, decrease of limb temperature, or hair loss, are generally absent at rest when LEAD is only responsible for AIC.
| Primary Care Investigation | | |
The technical requirements for measuring lower limb pressures (a sphygmomanometer and a hand-held pocket Doppler) are so simple, that measurement of the ankle to brachial index (ratio of ankle to the highest of the two arms systolic arterial pressure) should be systematically used by primary care physicians to argue for the presence of LEAD.[40] Attention must be paid to the conditions of the recording and specifically to respect a strict lying position otherwise ankle-brachial index (ABI) may be overestimated [Table 1] and [Figure 2]. | Figure 2: Example of Doppler recording with ABI calculation in a diabetic patient. As shown, velocimetry profiles are normal but ABI is high due to arterial stiffness. Thereby, toe pressure was also performed with photoplethysmography confirming normal results. ABI: Ankle-brachial index
Click here to view |
In case of severe claudication, a normal ABI (results between 0.90 and 1.30) makes an arterial origin of symptoms unlikely but in AIC occurring only during significant heavy-load exercise (as in claudication in athletes), ABI will generally be normal at rest. Limits to the use or interpretation of ABI must be kept in mind, such as cardiac arrhythmia, artery calcification (that are frequent in the presence of renal disease or diabetes),[41] inability to tolerate the strict lying position leading to overestimation of ankle values (heart and respiratory failure), or localizations of lesions on branches that are not in the measurement axis (internal iliac or profunda femoris arteries).
| Additional Nonradiological Investigations | | |
When ABI is normal at rest, its measurement after exercise is essential.[42] ABI will decrease after exercise in proportion to the maximal workload performed. Then, in normal individuals, ABI will remain mostly unchanged after walking but will decrease significantly in athletes following heavy-load exercise. Thereby postexercise ABI will be considered useful after walking tests,[43] but values as low as 0.50–0.65 can be found normal after maximal heavy-load cycle exercise in athletes.[44],[45] Ultrasound imaging is the most powerful and largely used investigation for patients with AIC. It determines the presence and location of arterial lesions, can complete the investigation of cerebral and renal arteries in case of lower limb lesions, and detect the presence of arterial aneurysms. Other tests such as postexercise magnetic resonance imaging,[46],[47] near infrared spectroscopy,[48],[49],[50] exercise transcutaneous oximetry [Figure 3][51],[52] are of interest and are used in secondary care specialized units but are hardly accessible in routine practice. They can be of interest if claudication is a debatable of doubtful arterial origin. Blood tests searching for unknown risk factors (glycemic and fatty acid investigations), renal cardiac or cerebral complications (urea creatinine) must be part of the initial and follow-up investigations | Figure 3: Representation of exercise oximetry results expressed in DROP: Limb changes from rest minus chest changes from rest) in a patient with bilateral occlusion of hypogastric arteries (upper panel) ad isolated right femoropopliteal occlusion (lower panel). The walking period (“phase d'effort”) is the gray area. Note that in the lower figure, the recovery period was extended to 15 min due to the very slow recovery of regional flow impairment on the left calf. DROP: Decrease from rest of oxygen pressure
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| Noninvasive Treatments | | |
Patients with intermittent claudication must first be treated with medical interventions, including lifestyle changes to improve risk factors (sedentary, smoking, pharmacological control of risk factors (dyslipidemia and diabetes mellitus), and prevention of LEAD aggravation with a triad of antiplatelet/anticoagulant drugs, ACE inhibitors, and cholesterol-lowering agents (mostly statins).[53] Cilostazol was proved effective in improving walking capacity but is of no benefit on LEAD evolution.[54] In debilitating AIC, structured supervised walking programs improve walking capacity better than pharmacologic therapy alone and may even have better results on long-term prognosis than revascularization.[55],[56] In the absence of complications (aneurysms, ulcers, etc…), failure to improve symptoms of claudication or increase the walking capacity to a level that is acceptable for a physically active patient should be the sole reason leading to invasive investigations and revascularization.
| Radiological Investigations and Revascularizations | | |
We believe that lower limb angiography, computed tomography, or magnetic resonance angiography [Figure 4] should not be done until noninvasive treatments have failed to sufficiently improve AIC and a revascularization has been proposed. Imaging modalities depend on the patient status, the location of the lesions, the accessibility to the techniques, the advantage and limits of each approach, and overall, whether revascularization is proposed through and endovascular or surgical approach. The advantage and limits of each revascularization technique will not be discussed here and depend on the location, number, length, and severity of the stenosis.[57],[58],[59] | Figure 4: Angioscan imaging of the iliac vessels in a patient complaining lower back and right buttock pain when walking. Here, the patient presents a complete occlusion of the right (D) internal iliac artery, while the left (G) side is patent
Click here to view |
| Conclusion | | |
AIC is a severe disease with a high risk of morbidity[60] and mortality[61],[62],[63],[64],[65],[66] underlying the importance of secondary medical prevention. Morbidity includes the evolution of LEAD, occurrence of arterial complication in other vascular territories (infraction, stroke), and complications of medical or surgical treatments (statin intolerance, graft infection, or angioplasty thrombosis). Education of the patients through a multidisciplinary approach is mandatory.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1]
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