In the community, parks and roads, we can often see this scene: an old man walking a short distance, stopping, rubbing his legs, resting for a while and then continuing to walk, walking almost the same distance, stopping to rest again, and so on. Many people may not realize that this is a manifestation of intermittent claudication, a common geriatric condition.
Understanding intermittent claudication
Intermittent claudication is not an independent disease; it is a typical symptom of lower extremity atherosclerotic occlusive disease; nor is lower extremity atherosclerotic occlusive disease an isolated disease; it is part of a systemic peripheral arterial occlusive lesion. Tian Wen, Department of Vascular Surgery, Shanghai Changhai Hospital
Existing clinical studies confirm that more than 90% of patients with symptoms of intermittent claudication also have severe coronary artery disease. The pathological basis for these vascular lesions is atherosclerosis. In fact, atherosclerotic lesions may begin in childhood, but symptoms generally rarely appear before the age of 60.
Risk factors for atherosclerosis include: advanced age, smoking, hypertension, hyperlipidemia, family history and inflammatory mediators. Western studies have shown that approximately 20% of the elderly have atherosclerotic-occlusive lesions of the lower extremities. Depending on the severity of the patient’s symptoms, the lesions are generally classified into four stages. (1) mild complaint stage: only feeling of decreased skin temperature and coldness in the affected limb, or mild numbness, and easy fatigue after activity; (2) intermittent claudication stage; (3) resting pain stage; and (4) tissue necrosis stage.
Intermittent claudication is an intermediate stage in the development of lower extremity atherosclerosis occlusive disease, and about 30% of patients will have this typical symptom, which is equivalent to the significance of “metastatic right lower abdominal pain” for the diagnosis of appendicitis. The third and fourth stages of lower extremity atherosclerosis are the severe limb ischemia stages, which require surgical treatment and are collectively referred to as severe limb ischemia (CLI).
Symptom characteristics, examination and diagnosis
Diagnosis of lower extremity atherosclerosis-occlusive disease is usually clear based on medical history, physical examination, and noninvasive tests, and the severity of the lesion can be measured. However, CT imaging (CTA), magnetic resonance artery imaging (MRA) or angiography of the lower extremity arteries are required to know specifically the stenosis of the lower extremity arteries.
Symptoms Intermittent claudication is characterized by soreness and pain in an associated muscle group of the lower extremity after exercise, mostly in the lower leg, sometimes in the upper thigh or buttocks. The pain is usually spasmodic, and a few patients experience a feeling of heaviness in the leg after exercise, and in severe cases, they may fall. Other conditions, such as degenerative lesions of the vertebral body caused by a herniated disc resulting in nerve root or spinal cord compression, can present similarly to intermittent claudication.
The symptoms of intermittent claudication usually come on after walking a certain distance and disappear completely after rest (<10-15 minutes), which is the point of differentiation from other diseases causing claudication.
Any exercise that requires increased energy expenditure, such as climbing stairs and walking on inclined surfaces, reduces the walking distance in patients with lower extremity atherosclerotic occlusive disease. The extent of symptoms present correlates with the extent of the lesion, with involvement of the muscle usually one plane below the arterial occluded segment (e.g., abnormalities of the gastrocnemius are usually the result of occlusion of the superficial femoral artery, whereas lesions of the femoral or gluteal muscles indicate lesions in their proximal segments). Usually, gastrocnemius lesions are the most common site of atherosclerotic occlusive disease of the main iliac arteries.
History and examination The history of lower extremity atherosclerosis-occlusive disease includes ischemic manifestations such as coldness, intermittent claudication, pain, and skin breakdown in the lower extremities. Examination may reveal diminished or absent pulsations in the dorsalis pedis and posterior tibial arteries, and noninvasive examination may evaluate the lesions by ankle-brachial index and arterial ultrasound.
In patients with mild claudication, the dorsalis pedis artery pulsation is palpable at rest but disappears after exercise. For lower extremity arteries, the most basic noninvasive vascular examination method is the resting ankle-brachial index (ABI). Clinical symptoms are closely related to the ABI, which is usually 0.4 to 0.8 in patients with claudication and less than 0.4 in patients with resting pain and tissue necrosis, but in those with calcified arteries (mostly diabetic patients), the ankle-brachial index may appear falsely elevated due to the presence of rigid intimal plaque, which prevents normal vasoconstriction under the compression of the cuff. Therefore, this needs to be taken into account in patients with significant symptoms but a normal ankle-brachial index.
Principles and methods of non-surgical treatment
Principles of treatment The goals of treatment for arterial occlusive disease of the lower extremities are threefold: relief of ischemic symptoms, delay of disease progression, and improvement of long-term survival. In general, mild intermittent claudication is not a major problem and only requires non-surgical treatment to delay disease progression. However, when patients present with skin flushing, low toe artery pressure, and low ABI, they are prone to develop CLI and require early revascularization.
Non-surgical treatment For patients with intermittent claudication, the non-surgical treatment is a comprehensive process, including control of risk factors, adherence to exercise, improvement of lifestyle habits, medication and other measures.
The control of risk factors includes the following: quit smoking, including reducing the inhalation of second-hand smoke; actively treat hypertension, hyperlipidemia and diabetes, and maintain blood pressure, lipids and blood glucose within normal levels.
Exercise is the foundation of treatment for patients with intermittent claudication. Walk consistently at a normal moderate pace for at least 30 minutes a day, resting at each walking distance until the maximum pain is tolerated, and repeat the cycle at the same intervals after recovery. This can be effective in improving lower extremity symptoms and increasing walking distance. Exercise can also increase a sense of well-being, reduce weight, and improve cardiovascular function.
Also, drinking more water, controlling total daily calories, and reducing the intake of animal fats, foods high in cholesterol, salt, and sugar are effective measures to improve atherosclerosis and reduce the occurrence of vascular events.
The most direct and effective drug for the treatment of intermittent claudication is cilostazol. This drug is a type 3 phosphodiesterase inhibitor that inhibits platelet aggregation, dilates blood vessels, and improves lipid levels. The more common use is 50 mg orally twice daily. Dosage adjustments can be made based on the patient’s condition during specific applications. In addition, since patients with intermittent claudication are usually accompanied by other vascular pathologies, some drugs targeting cardiovascular and cerebrovascular vessels are also relevant to reduce cardiovascular events and prolong survival in patients, including antiplatelet agents, beta-blockers, statins, and angiotensin-converting enzyme inhibitors. It is worth mentioning that because of its effectiveness in reducing cardiovascular events and its relatively low cost, aspirin is recommended for all patients at a dose of 100 mg daily for life (in the absence of prior use of this or similar medications).
It is important to emphasize that exercise is the most effective and convenient and economical of all non-surgical treatment measures. Medications cannot replace the role of exercise. Studies have shown that exercise has a longer lasting effect on improving walking distance than cilostazol. Therefore, the role of exercise cannot be overemphasized in patient education.
Patients with intermittent claudication should be treated with
① Pay attention to the identification of whether the claudication is vascular or not, and the need to exclude walking problems caused by lumbar spine and other problems.
② Surgery is generally not required, and it is most important to adhere to walking exercises. Advise to drink more water, quit smoking, and control blood pressure, blood sugar, and blood lipids. Cilostazol can be used as an adjuvant drug.
③ Intermittent claudication with a distance of less than 200 meters is feasible for intracranial therapeutic intervention; with lower limb skin flushing, claudication distance less than 30 meters, and ABI less than 0.4 requires active consideration of surgical treatment; development of resting pain, skin breakdown, and gangrene of the toes requires immediate consideration of surgery.
④ Surgical intervention includes bypass surgery and endoluminal intervention, and endoluminal intervention is recommended to be preferred.
⑤ Acute lower extremity ischemia needs to be treated at the first time to a hospital with vascular surgery.
⑥ Vascular diseases are systemic diseases, and patients with intermittent claudication usually have cardiovascular and cerebrovascular diseases. Attention should be paid to the detection and control of vascular lesions in other areas to increase patients’ life expectancy.
Conditions requiring surgical intervention
Patients with mild intermittent claudication without lower extremity resting pain or ulcers usually do not have severe lesions and do not require surgical intervention. However, moderate or severe intermittent claudication (claudication distance less than 200 meters) can have a greater impact on the quality of life of patients, and if there is no improvement with regular non-surgical treatment, surgical treatment should be considered. Particularly when patients present with skin flushing, short-distance claudication (less than 30 m), and a significant decrease in ABI (down to about 0.4 or lower), a high degree of vigilance is required. About 25% of such patients will progress to CLI within one year, and surgical intervention should be actively considered. If the disease progresses to the point of resting pain, skin breakdown or gangrene of the fingertips, then normal life is seriously affected and the risk of amputation is high, and immediate surgical intervention is required.
Current surgical interventions include both vascular bypass surgery (i.e., bypass) and endoluminal interventions. Vascular bypass surgery is a traditional surgical procedure to restore the distal blood supply through autologous or artificial vessels, which is relatively more invasive. Interventional endoluminal technology reopens the occluded vessel through balloon dilation and stenting, which is relatively less invasive and has the opportunity for multiple procedures, and is recommended as the preferred treatment for lower extremity atherosclerosis occlusive disease.
It is important to note that if a patient suddenly develops loss of arterial pulsation, pallor, pain, numbness, and abnormal sensation in the lower extremities, it indicates acute lower extremity ischemia, which means that an arterial embolism has occurred, and the risk of amputation and death is extremely high, and the patient needs to be sent to a hospital with vascular surgery for treatment at the first time. During the course of acute arterial embolism, pain, loss of sensation, loss of motor function, and skin swelling and rupture will occur sequentially in the affected limb, which is a process associated with sequential nerve-muscle-skin necrosis. For patients with acute arterial embolism, time is limb and life. Before referral, medical institutions in a position to do so can immediately administer low-molecular heparin subcutaneously, followed by immediate transport to a hospital with vascular surgery for treatment; at the same time, the relevant physicians can be contacted during the transfer to save time in preparation for treatment upon arrival. If a family member rewarms the patient’s cooled lower extremities, this needs to be stopped in time, as cellular oxygen consumption increases with temperature, exacerbating the progression of the disease.