Leriche Syndrome

Etiology and pathogenesis in atherosclerosis

The development of Leriche syndrome is inextricably linked with atherosclerotic lesions of the arterial bed. Clinical practice shows that the femoral arteries are most frequently targeted in plaque formation.

The pathogenetic cascade includes:

• Gradual narrowing of the vessel's internal lumen (stenosis).
• Development of severe collateral circulation insufficiency (bypass pathways fail to compensate for blood flow).
• Development of ischemic processes in the tissues of the lower extremities, which morphologically manifests as their atrophy and sclerosis.

The foundation for these changes is a disturbance in the lipid profile. The progression of atherosclerosis is sustained by high levels of atherogenic low-density lipoproteins (LDL) coupled with a decrease in protective, anti-atherogenic high-density lipoproteins (HDL). Correcting this specific metabolic link is one of the key tasks of conservative therapy.

Complications and associated disorders

The course of Leriche syndrome carries the threat of acute vascular catastrophes. The most formidable complication is the onset of secondary thrombosis in the area of the atherosclerotic narrowing. Acute occlusion against the background of an already compromised collateral bed leads to the development of irreversible necrosis — atherosclerotic gangrene of the lower extremities.

When studying peripheral circulatory disorders, it is important to differentiate between ischemia mechanisms. For example, in spastic conditions of peripheral vessels (such as Raynaud's syndrome), the disorders are functional in nature, and the drug prazosin is successfully used to relieve them. In contrast to functional spasm, the obstruction to blood flow in Leriche syndrome is persistent and organic (atherosclerotic) in nature.

Differential diagnosis of vascular pathologies

To make an accurate diagnosis, it is necessary to distinguish lower extremity atherosclerosis from other systemic vascular diseases and compression syndromes.

Nonspecific aortoarteritis (Takayasu's disease, aortic arch syndrome) Unlike Leriche syndrome, this is a chronic inflammatory-allergic disease of unknown etiology affecting the aortic arch and its branches.

• Epidemiology: Females are affected in 90% of cases.
• Clinical presentation: Sharp weakening or complete absence of pulse in the upper extremities, decreased blood pressure in the upper limbs, visual disturbances, and neurological symptoms.
• Morphology: Chronic productive inflammation develops, starting from the outer coat (adventitia). The vasa vasorum vessels are narrowed or obliterated, surrounded by a mononuclear infiltrate with giant cells (a reaction to the breakdown of elastic fibers). The muscular-elastic layer (media) is replaced by fibrous tissue, while the endothelium remains unchanged. The result is fibrous thickening and stenosis (up to obliteration) of the arterial ostia.

Giant mediastinal tumors Tumor masses occupying up to half of the thoracic cavity can cause severe vascular disorders due to external compression, requiring differentiation from true occlusions.

• Symptoms of severe compression: Dyspnea, acrocyanosis, facial puffiness, dilation of chest wall and neck veins, tachycardia, angina attacks, and headache.
• Symptoms of invasion (growth into tissues): Chest deformation, Horner's syndrome, as well as laryngeal and diaphragmatic paresis.

Class and exam questions

What else to study on this topic

• Morphogenesis of the atherosclerotic plaque and the role of LDL/HDL
• Mechanisms of collateral circulation in the lower extremities
• Pharmacodynamics of prazosin in peripheral circulatory disorders (Raynaud's syndrome)
• Pathogenesis and morphology of nonspecific aortoarteritis (Takayasu's disease)
• Topographic anatomy and compression symptoms in giant mediastinal tumors

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.