Intermittent Claudication

Article Author:
Shivik Patel
Article Editor:
Scott Surowiec
Updated:
10/27/2018 12:31:40 PM
PubMed Link:
Intermittent Claudication

Introduction

Intermittent claudication (IC) typically refers to lower extremity skeletal muscle pain that occurs during exercise. IC presents when there is insufficient oxygen delivery to meet metabolic requirements of the skeletal muscles. IC is a common manifestation of peripheral arterial disease (PAD), which includes atherosclerotic stenosis of arteries in the extremities. IC is commonly localized to the thigh, hip, buttock and calf muscles. Pain within these muscle groups is reproducibly induced by walking and relieved with rest. The severity of pain can sometimes correlate with the degree of stenosis or blockage in arteries supplying the lower extremities.[1][2][3]

Etiology

The risk factors for developing IC are similar to those for developing atherosclerosis. Modifiable risk factors include: smoking, hypertension, dyslipidemias, obesity, metabolic syndrome, and diabetes mellitus. Non-modifiable risk factors include: age, male gender, family history and congenital predisposition. Investigational risk factors include: alcohol, radiation, C-Reactive Protein, infection, homocysteinemia, lipoprotein(a), reduced adiponectin, and fibrinogen.[4][5]

Epidemiology

In the general population over age 60 IC is present in 5% of men and 2.5% of women. Of all patients with PAD, between 10-35% will have a presentation of “classic” IC. Certain patient groups have a higher incidence of PAD; these include: age greater than 70, smokers and diabetics between ages 50-69, and those with other atherosclerotic cardiovascular diseases.

Pathophysiology

IC occurs due to atherosclerosis-mediated narrowing of lower extremity vessels. Oxidative injury to the inner layer of endothelial cells is the nidus of atherogenesis. The subsequent dysfunction of endothelial cells promotes localized deposition of oxidized-LDL and synthesis of pro-inflammatory factors. This creates a fibro-inflammatory plaque that propagates as macrophages are recruited and become resident foam cells as they phagocytize the oxidized-LDL.  The foam cells form a classic histologic feature called a “fatty-streak”. As the plaque enlarges and matures, surrounding vascular smooth muscles migrate into it, and collagen deposition forms a fibrous cap. The most common location of plaque formation in PAD is in the superficial femoral artery, which may lead to IC symptoms in the calf. Other locations include the aortoilliac bifurcation, producing hip and buttock pain, and the common femoral artery, which can yield thigh or calf claudication.[6]

History and Physical

The typical presentation of IC is a patient with lower extremity pain during ambulation that is relieved with rest. The progression of symptoms is gradual. Physical examination of these patients may show evidence of arterial insufficiency. The affected limb may feel cool and have diminished pulses. The physical examination should include an assessment of femoral, popliteal, dorsalis pedis, and posterior tibial artery pulses. The patient’s presentation should be carefully distinguished from other causes of leg pain like neurogenic pseudoclaudication (spinal stenosis), musculoskeletal pain, and venous claudication associated with leg swelling and varicosities. In general, the presence of strong pedal pulses argues against a diagnosis of IC.

Evaluation

In addition to a full cardiac and respiratory history and physical exam, certain non-invasive and invasive tests can be performed based on the severity of symptoms. All patients should have a baseline lipid profile, Doppler waveform pulse assessment and Ankle-Brachial Indices (ABI). An ABI is a ratio of blood pressure at the ankle compared to the arm. An ABI between 0.9-1.3 is normal. Claudication is common in patients with an ABI between 0.4 and 0.9. ABI less and 0.4 suggests more severe PAD, while an ABI >1.3 is associated with non-compressible calcified arteries. In patients with calcified arteries, commonly diabetics, a Toe-Brachial pressure index (TBI) can be used. The TBI in a healthy patient should be 0.70-0.80. If a symptomatic patient has a normal ABI or TBI, standardized exercise testing can be helpful. In normal patients, the ABI will increase during exercise. In patients with post-exercise ABI drop of >20%, diagnostic imaging and referral to a vascular specialist are warranted. There are three major classification systems for patients with PAD: Wound/Ischemia/Foot Infection (Wifi), Rutherford, and Fontaine. The older Rutherford and Fontaine systems incorporate intermittent claudication as part of their classification. Common imaging modalities include non-invasive duplex vascular ultrasound, minimally invasive CTA and MRA, and formal peripheral angiography. Imagining modalities elucidate the location of the diseased vasculature. Aortoiliac disease is referred to as inflow disease, and typically produces symptoms in the thigh or gluteal musculature. Meanwhile, disease below the inguinal ligament commonly produces claudication affecting the calf muscles. [7][8]

Treatment / Management

The guiding principle of treatment for IC is that few patients, around 1-2%, with claudication ever progress to limb threatening ischemia. Under this pretense, initial aggressive treatment strategies are discouraged. Most patient with IC can be treated with medical management. Medical management includes smoking cessation, antiplatelet agents, statin therapy, blood pressure modification, glucose control, structured walking programs and cilostazol. Structured walking programs improve pain-free walking distance better than pharmacologic therapy alone. It is important to note that continued smoking with walking therapy restricts improvement in these patients. A three-month trial of smoking cessation, ambulation and cilostazol is typically prescribed. Headaches are the most common side-effect of cilostazol and may warrant a dose-reduction. Patients undergoing medical management should have frequent follow-ups to assess their symptom relief. Most patients are instructed to walk at least three ten-minute walks daily. Any patient with intermittent claudication or PAD should also be evaluated for coexisting cardiac disease. If symptoms are worsening despite medical treatment, or if symptoms are considered disabling or lifestyle-limiting, intervention may be considered. Other considerations for invasive procedures may include: atherosclerotic lesion characteristics and patient prognosis. Intervention may initially involve minimally-invasive endovascular angioplasty, stenting or atherectomy. Percutaneous techniques are typically performed via the femoral artery with insertion of a sheath with wires and catheters to the diseased region. Lesions that are multifocal, long or heavily calcified may not be amenable to endovascular repair. In these cases, intervention may ultimately require endarterectomy or a conduit bypass. The conduit can either be and autogenous vein or a prosthetic material. In 2007 the Society for Vascular Surgery developed the Trans-Atlantic Inter-Society Consensus (TASC II) guidelines that can aid physicians in determining whether endovascular or open surgery should be pursued in a patient. The classification identifies lesions as A, B, C or D based on location, number, length and severity of the stenosis. The complications of any surgical intervention should also be considered -- these include vessel or graft conduit thrombosis, in-stent stenosis or fracture, and infection. [3][9][10]

Differential Diagnosis

  • Sciatica
  • Atheroembolic disease
  • Venous insufficiency
  • Vasculitis

Complications

  • Lack of exercise endurance
  • Prolonged wound healing
  • Impotence
  • Blue toe syndrome
  • Ischemic leg

Consultations

Vascular surgery

Interventional radiologist

Deterrence and Patient Education

  • Discontinue smoking
  • Maintain healthy weight
  • Exercise
  • Eat a healthy diet

Enhancing Healthcare Team Outcomes

The treatment of intermittent claudication is surrounded with controversy. The past belief that exercise therapy alone could improve the disease and symptoms is now known to have many shortcomings. The older studies were never standardized, did not use adequate measures of outcomes and were heterogeneous- meaning that the patient population was not controlled and the type of exercise was not controlled. While the debate rages, experts agree that prevention of claudication is perhaps the best way to manage the disease. The pharmacist and nurse is in the ideal position to educate the patient on the risks of smoking and lack of exercise. Patients with intermittent claudication must be told to eat a healthy diet, control the blood sugars and hypertension, lower the levels of cholesterol and glucose and participate in an exercise program. There is ample evidence showing that undertaking these measures improves quality of life and reduces the burden of many medical disorders.[11][12][13](Level II)

Outcomes

The latest data suggest that in patients with intermittent claudication, endovascular surgery, open surgery, and exercise therapy are superior to medical management in terms of walking distance and symptom relief. (Level V) However, there are no good long-term studies to determine which of the procedures is more effective. The data on exercise therapy alone are conflicting and only of short-term duration. What is also not known is how many additional endovascular procedures will be required in the future to keep the patient symptom free. Whether any of these treatments can improve claudication over the long term still remains to be seen. [14][15][16]