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Leriche syndrome: symptoms and treatment
Last updated: 30.10.2025
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Leriche syndrome is a clinical and anatomical variant of atherosclerotic lesion of the aortic bifurcation and iliac arteries. The classic triad includes intermittent claudication of the gluteal muscles, weakening or absence of femoral pulses, and erectile dysfunction in men. In practice, the spectrum of manifestations is broader: from asymptomatic decreased exercise tolerance to critical ischemia with rest pain, ulcers, and necrosis. This is why today we speak of "aortoiliac occlusive disease" as part of a unified continuum of lower extremity arterial diseases. [1]
The disease develops gradually against the background of atherosclerosis: stenosis and occlusions develop, collateral circulation is restructured, and the muscles and nerve structures of the pelvic girdle and lower extremities are affected. Some patients experience long-term, predominantly exercise-induced pain and fatigue, while others experience symptoms of pelvic organ ischemia (e.g., erectile dysfunction), and a third experience a combination of these symptoms. Early identification and correction of risk factors can slow progression and reduce the incidence of major vascular events. [2]
The Leriche phenotype is important not only for diagnosis but also for the choice of revascularization method. In recent years, endovascular technologies (covered stents, "kissing stents," and covered endovascular reconstruction of the aortic bifurcation - CERAB) have supplanted traditional prosthetic procedures in a significant proportion of patients, although open aortobifemoral bypass remains the benchmark for long-term patency in extensive lesions. [3]
Finally, modern guidelines emphasize that treatment is not simply a matter of "fixing the pipe." The basic principles include tobacco cessation, intensive lipid-lowering therapy, antithrombotic prophylaxis, and supervised structured walking. These measures reduce cardiovascular risk and improve walking as effectively as a number of procedures, and also reduce the frequency of repeat interventions. [4]
Code according to ICD-10 and ICD-11
In ICD-10, Leriche syndrome is coded as an atherosclerotic lesion of the aorta and/or iliofemoral segment. Depending on the location and manifestations, codes from block I70 "Atherosclerosis" are used: I70.0 "Atherosclerosis of the aorta", I70.2 "Atherosclerosis of the arteries of the extremities" (with details by leg and the presence of lameness, ulcers, gangrene), and in case of thrombosis - the section I74.0x "Thrombosis/embolism of the abdominal aorta". For bilateral lesions of the iliac arteries, clarifying positions are used (for example, I70.8 "Atherosclerosis of other arteries") in the absence of a more specific code. [5]
ICD-11 recommends the root code BD40 "Atherosclerotic chronic arterial occlusive disease" with post-coordination: BD40.0 "Atherosclerosis of the arteries of the lower limb," BD40.1 "Atherosclerosis of the aorta," and BD40.3 "Aortic bifurcation syndrome" (aortic bifurcation pathology); side modifiers (right/left/bilateral) are added. This approach more accurately reflects the anatomy of the lesion. [6]
Table 1. Examples of coding for Leriche syndrome
| System | Code | Formulation |
|---|---|---|
| ICD-10 | I70.0 | Atherosclerosis of the aorta (infrarenal segment) |
| ICD-10 | I70.21 / I70.22 | Atherosclerosis of the arteries of the right/left leg with intermittent claudication |
| ICD-10 | I70.8 | Atherosclerosis of other arteries (including iliac) |
| ICD-10 | I74.09 | Abdominal aortic thrombosis/embolism (acute variant) |
| ICD-11 | BD40.0 + side indicator | Atherosclerosis of the arteries of the lower limb |
| ICD-11 | BD40.1 | Atherosclerosis of the aorta |
| ICD-11 | BD40.3 | Lesion of the aortic bifurcation region (Leriche syndrome) |
Epidemiology
Lower extremity arterial disease affects more than 200 million adults worldwide, with the incidence increasing sharply with age: in people over 70, up to 20-25 percent of patients exhibit signs of the disease. The aortoiliac segment is one of the most frequently affected, second only to the superficial femoral artery in prevalence. However, the proportion of asymptomatic forms remains high. [7]
Classic Leriche syndrome is less common than any iliac artery lesion. Estimates vary, but approximately 5-10 percent of patients with lower extremity arterial disease exhibit Leriche's triad: buttock claudication, weakened femoral pulse, and erectile dysfunction. The presence of this triad increases the likelihood of involvement of the infrarenal aorta and common iliac artery. [8]
According to global disease burden reviews, population aging and the prevalence of tobacco smoking and diabetes mellitus support a steady increase in cases by 2030–2050. Women and men are affected at comparable rates, but clinical manifestations and visit rates differ, which is important to consider for screening and routing. [9]
Table 2. Epidemiological landmarks
| Indicator | Grade |
|---|---|
| People with lower extremity arterial disease in the world | >200 million |
| Proportion of persons aged ≥70 years with the disease | up to 20-25% |
| Estimated prevalence of Leriche triad among patients | 5-10% |
| Frequency of asymptomatic course | ≥50% of cases |
Reasons
The main cause is atherosclerosis with the formation of fibrolipid plaques in the infrarenal aorta and iliac arteries. Chronic flow turbulence in the aortic bifurcation zone, smoking, dyslipidemia, and hyperglycemia accelerate lipid infiltration of the intima, inflammation, and wall remodeling. Gradual narrowing of the lumen and thrombosis on the plaque surface lead to clinical manifestations. [10]
Less common causes include inflammation (arteritis), fibromuscular dysplasia, radiation injury, or complications following aortic and iliac artery arthroplasty. In acute cases (sudden ischemia), the cause is thrombotic occlusion due to critical stenosis or embolism in the abdominal aorta. [11]
Risk factors
Key modifiable risk factors include active and passive smoking, dyslipidemia, diabetes, hypertension, chronic kidney disease, physical inactivity, and obesity. Tobacco cessation is the most effective measure for reducing disease progression and the risk of adverse cardiovascular events. [12]
Non-modifiable factors include age, male gender (for the "classical" Leriche), family history, and ethnic and cultural characteristics. The risk is higher in people with a history of cardiovascular disease in the family, as well as in those with a combination of several risk factors. [13]
Table 3. Risk factors and their contribution
| Category | Examples | Comments |
|---|---|---|
| The most powerful | Smoking | Associated with a 2-4-fold increased risk; effects persist for decades |
| Metabolic | Dyslipidemia, diabetes mellitus, obesity | Correction improves prognosis and walking |
| Related | Chronic kidney disease, hypertension | The severity and complications increase |
| Non-modifiable | Age, family history | Require early screening |
Pathogenesis
The underlying mechanisms are atherogenic cascades: endothelial dysfunction, low-density lipoprotein infiltration, an inflammatory response involving macrophages and T cells, and the formation of a necrotic core and fibrous cap. At the aortic bifurcation, low and fluctuating shear stress increases local plaque vulnerability. [14]
As the stenosis progresses, the pressure gradient increases, the perfusion reserve of the gluteal and femoral muscles decreases, and collaterals develop (including through the internal iliac arteries). If these arteries fail, claudication of the buttocks and erectile dysfunction occur due to ischemia of the cavernous tissue and decreased nitric oxide production. [15]
Symptoms
The classic triad: exercise-induced pain and fatigue in the buttocks and thighs, weakened or absent femoral pulse, and decreased erectile function in men. The pain often occurs when walking short distances and forces the patient to stop, while climbing stairs and exposure to cold exacerbate symptoms. [16]
As the condition progresses, pain at rest, forced nighttime dangling of the leg from the bed, trophic ulcers, and necrosis of the toes or heel develop—signs of chronic, limb-threatening ischemia. An "acute scenario" is also distinguished: sudden pain, pallor, coldness, numbness, weakness, and loss of pulse—criteria for acute limb ischemia requiring emergency care. [17]
Table 4. Clinical warning signs requiring urgent attention
| Situation | Signs |
|---|---|
| Acute limb ischemia | "6 P": pain, pallor, coldness, no pulse, paresthesia, paresis |
| Chronic threatening ischemia | Pain at rest, ulcers, necrosis, worse at night |
| Leriche's "Classics" | Buttock lameness, weak femoral pulse, erectile dysfunction |
Classification, forms and stages
The Fontaine and Rutherford scales (for chronic ischemia) and the Rutherford scale for acute limb ischemia are used in clinical assessment of severity. They correlate with management: exercise and medications for claudication, and revascularization for rest pain and tissue damage. [18]
From an anatomical perspective, the TASC II (AD) consensus is used for aortoiliac lesions: short stenoses (A) are best treated endovascularly, while extended bilateral occlusions (D) have historically been referred to open surgery, but with technological advances the boundaries are shifting. [19]
Table 5. Correspondence between the stages of chronic ischemia
| Fontaine scale | Rutherford scale | Clinic |
|---|---|---|
| I | 0 | Asymptomatic |
| IIa | 1-2 | Mild to moderate lameness |
| IIb | 3 | Severe lameness |
| III | 4 | Pain at rest |
| IV | 5-6 | Ulcers/gangrene |
Complications and consequences
Without treatment, the risks increase: deterioration of walking and quality of life, chronic limb-threatening ischemia, ulcer infections, and amputations. Iliac segment disease is a marker of systemic atherosclerosis, leading to increased rates of heart attacks and strokes; cardiovascular risk management is the primary goal. [20]
After interventions, restenosis, stent or bypass thrombosis, and internal iliac artery steal syndrome with worsening gluteal claudication and erectile dysfunction are possible; proper choice of technique (preservation of internal iliac artery flow) reduces these risks. [21]
When to see a doctor
Immediately - if signs of acute ischemia appear (sudden severe pain at rest, paleness and coldness of the limb, numbness, weakness, no pulse). Losing time reduces the chances of saving the limb. [22]
In the coming days, progressive lameness, night pain, trophic skin changes, non-healing wounds on the feet, decreased femoral pulse, and the development of erectile dysfunction combined with gluteal lameness are indications for further examination and selection of a treatment strategy. [23]
Diagnostics
Step 1. Clinical hypothesis. Questioning and examination: assessment of walking distance, Leriche's "classics", condition of the skin of the feet, pulses on the femoral, popliteal and pedal arteries. [24]
Step 2. Hemodynamic confirmation. Measurement of the ankle-brachial pressure index at rest. A value ≤0.90 is a sign of disease; ≥1.40 indicates "non-compressible" arteries, in which case the toe-brachial pressure index and absolute pressure on the toe are measured. If the index is normal and the patient presents with typical complaints, a walk test is performed and the measurement repeated. [25]
Step 3. Localization of the lesion. Segmental pressures, Doppler waves, and pulse-volume curves help pinpoint the level of stenosis. Vascular ultrasound reveals the velocity and spectrum of flow in the common and external iliac arteries and at the aortic bifurcation. [26]
Step 4. Angiographic verification during intervention planning. Computed tomography angiography or magnetic resonance angiography for mapping the length and calcification of lesions, and the anatomy of the internal iliac arteries. Digital subtraction angiography is both the “gold standard” and an access point for endovascular treatment. [27]
Step 5. Critical ischemia assessment. For ulcers and necrosis, toe pressure, transcutaneous oxygen tension, and/or skin perfusion pressure are assessed. Toe pressure values less than 30 mmHg and transcutaneous oxygen tension less than 25–30 mmHg indicate a low probability of healing without revascularization. [28]
Table 6. Threshold values for non-invasive tests
| Indicator | Norm/pathology | Comment |
|---|---|---|
| Ankle-brachial index | ≤0.90 - pathology; ≥1.40 - "stiff" arteries | If the value is normal and there are complaints, perform a walking test. |
| Finger-brachial index | Used for "stiff" arteries | Microcirculation assessment |
| Pressure on the finger | <30 mmHg - poor healing potential | Criteria for planning revascularization |
| Transcutaneous O₂ tension | <25-30 mmHg - unfavorable | Useful for ulcers/necrosis |
Differential diagnosis
Vascular claudication must be distinguished from neurogenic claudication (lumbar canal stenosis), arthrogenic claudication (coxarthrosis, gonarthrosis), and compression of the internal iliac arteries in other conditions. Neurogenic pain is relieved by leaning forward or sitting, while vascular claudication resolves upon standing, regardless of posture. [29]
In patients with diabetes who experience foot pain at rest, it is important to differentiate ischemic pain from neuropathic pain. In cases of erectile dysfunction and buttock claudication, a vascular origin and damage to the internal/common iliac arteries are considered. An acute scenario requires ruling out embolism/thrombosis and immediately initiating anticoagulation and revascularization. [30]
Table 7. Vascular versus neurogenic claudication
| Sign | Vascular | Neurogenic |
|---|---|---|
| Distance | Stable | Variable |
| Relief | Stop | Sitting/forward leaning |
| Pulse on the thigh | Weakened/not | Saved |
| Walking test + index | Falls | It doesn't change |
Treatment
Basic therapy begins on the day of diagnosis. All patients are prescribed intensive lipid lowering with highly effective statins (with the addition of a PCSK9 inhibitor if necessary), blood pressure and glycemic control, and complete tobacco cessation with a support program. Smoking is the leading modifiable factor: cessation reduces disease progression, increases walking distance, and reduces the risk of heart attack, stroke, and amputation. Cardiovascular prevention is the foundation upon which further management is built. [31]
The antithrombotic strategy in symptomatic patients typically includes aspirin or clopidogrel. To reduce major cardiovascular and end-stage events in some high-risk patients, a combination of low-dose rivaroxaban and aspirin is justified, as demonstrated in large studies and reflected in the 2024 guidelines. After revascularization, this combination reduces the risk of acute limb ischemia and reinterventions. The choice of regimen is individualized, taking into account bleeding. [32]
The number one non-pharmacological "cure" remains structured, supervised walking, with gradually increasing intervals until moderate pain occurs, and repeated after a short rest. Meta-analyses show significant increases in treadmill distance and 6-minute walk distance after just 12 weeks, and programs can be adapted for home use with remote monitoring. Regular walking improves function as well as a number of treatments for isolated claudication and increases the effectiveness of any intervention. [33]
Symptomatic pharmacotherapy for claudication includes cilostazol, which increases walking distance and maximum walking distance; headache is the most common adverse reaction. The drug is not used in heart failure; the decision is made on an individual basis. Some studies indicate moderate improvement with statins as a means of increasing muscle endurance, but walking remains the preferred treatment. [34]
The choice of revascularization depends on the anatomy, symptoms, and comorbidities. For limited stenoses and short occlusions, endovascular tactics are preferred: balloon angioplasty with stenting, including "kissing stent" techniques at the iliac artery orifices. For extended bilateral aortic bifurcation lesions, CERAB-covered stent-graft reconstruction is widely used, which approaches open surgery in terms of long-term secondary patency while being less invasive. [35]
Open surgery remains the benchmark for long-term primary patency in extensive TASC II CD lesions: aortobifemoral bypass grafting (ABBG) provides five-year primary patency rates of approximately 85-90 percent in experienced hands. However, the "price" is a major operation with the risk of cardiorespiratory complications; therefore, extra-anatomical bypass grafts (axillofemoral and femoral-femoral) are considered in high-risk patients. The choice is always a balance between longevity and surgical risk. [36]
When planning reconstruction, it is important to maintain perfusion of the internal iliac artery on at least one side to reduce the risk of gluteal claudication and erectile dysfunction. Modern endovascular techniques allow this to be achieved through selective implantation and separation of scaffolds at the bifurcation. The choice of approach (retrograde femoral, brachial) and embolic protection are determined by the anatomy and experience of the team. [37]
Following revascularization, key elements include maintaining antithrombotic therapy, strict lipid and blood pressure control, a walking program, and noninvasive monitoring (pulse, ankle-brachial index, and, if necessary, duplex monitoring of stents/bypass grafts). Early detection of restenosis increases the chances of minimally invasive correction. Behavioral support for tobacco cessation critically reduces the risk of loss of patency. [38]
In patients with ulcers and necrosis, the goals are infection control, foot offloading, local perfusion assessment, and timely, targeted revascularization based on the "wound and anatomical targeting concept" of global guidelines. A team approach (vascular surgeon, interventional specialist, cardiologist, diabetologist, podiatrist) improves limb salvage and survival. [39]
Finally, in patients unsuitable for reconstruction and with intractable pain or a non-viable limb, palliative care is considered, including adequate pain relief and, unfortunately, sometimes amputation followed by rehabilitation and prosthetics. In such cases, secondary event prevention (heart and brain) and treatment of comorbidities are important. [40]
Table 8. Comparison of revascularization strategies in Leriche
| Approach | Pros | Cons | Who is it suitable for? |
|---|---|---|---|
| Endovascular stenting (including kissing stents) | Less trauma, faster recovery | Lower long-term primary patency in extensive lesions | Local/moderate lesions, high surgical risk |
| CERAB (covered stent grafts) | High secondary patency, good bifurcation geometry | Requires experience, material consumption | Extended bilateral lesions in high-risk patients |
| Aorto-bifemoral bypass grafting | The standard of durability | The larger the surgery, the higher the risk of early complications. | Young/fit patients with TASC CD |
| Extraanatomical shunts | Bypassing high-risk laparotomy | Lower long-term patency | Very high risk patients |
Table 9. Antithrombotic regimens for symptomatic disease
| Situation | Mode (example) | Expected effect |
|---|---|---|
| Symptomatic disease without recent revascularization | Acetylsalicylic acid or clopidogrel | Reduction in cardiovascular events |
| High risk of systemic and limb events | Low-dose rivaroxaban + acetylsalicylic acid | Additional reduction in MACE/MALE in patients with moderate bleeding risk |
| After revascularization | Low-dose rivaroxaban + acetylsalicylic acid | Less acute limb ischemia and reinterventions |
Prevention
Quitting smoking and controlling lipids, blood pressure, and sugar levels are measures that reduce the risk of heart attack, stroke, and amputation more than any local interventions. Regular walking and strength training of the lower extremities improve functional endurance and tolerance to procedures. Individualized weight and nutrition goals complement this strategy. [41]
Screening for the ankle-brachial pressure index is indicated for individuals with complaints or high risk; asymptomatic screening for low-risk individuals is not recommended. For a normal index and typical complaints, a walk test and extended physiological assessment (digital pressures, transcutaneous oxygen tension) are useful. [42]
Forecast
Without basic therapy, progression leads to deterioration of walking and increased cardiovascular risk. With comprehensive prevention and exercise, most patients at the "claudication" stage live active lives, and many avoid surgery. In extensive lesions, revascularization provides long-term symptom control, with open bypasses having a longer lifespan and endovascular techniques having a better safety profile. [43]
In chronic limb-threatening ischemia, timely targeted reconstruction significantly improves the chances of wound healing and limb preservation; delayed treatment worsens outcomes. Decisions are made multidisciplinary. [44]
FAQ
Is this definitely a vascular claudication, not a back/joint issue?
If the pain goes away simply by stopping walking, and the hip pulse is weakened, there's a high probability of a vascular cause; if in doubt, a walking test and blood pressure testing can help. [45]
When is surgery unavoidable?
Pain at rest, ulcers, necrosis, or severe lameness that is unresponsive to basic therapy and walking are indications for revascularization (endovascular or open). The choice depends on anatomy and risk. [46]
Which is better: stents or "major" surgery?
Endovascular techniques are less traumatic and suitable for many, especially the elderly and those with comorbidities; open bypass surgery is more durable for extended lesions in "prepared" patients. The decision is made jointly after angiography. [47]
Are long-term blood thinning injections necessary?
Most patients require antiplatelet agents; a combination of low-dose rivaroxaban and aspirin reduces the risk of limb and systemic events in some patients, especially after revascularization. The balance between benefit and bleeding risk is discussed individually. [48]
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