Etiology and pathomorphology
The leading role in the development of the disease is played by the neuro-reflex factor and autosensitization. The pathological process usually starts in the small vessels of the lower extremities, but in some cases, the upper extremities are also involved.
The essence of the pathology lies in the progressive narrowing of the lumen with subsequent thrombus formation. Changes in the vascular wall follow a consistent pattern:
- Initial stage: endothelial detachment occurs, and capillary angiomatosis develops in the tunica intima.
- Subsequent changes: the tunica media hypertrophies, and the wall is abundantly infiltrated with lymphoid-histiocytic cells.
- Morphological features: unlike other pathologies, the muscular layer of the artery remains intact, while the internal elastic membrane thickens.
Similar changes affect the veins, and hypertrophy of arteriovenous anastomoses is additionally noted.
Clinical stages of endarteritis
The course of the disease is usually divided into several successive stages, each with its own characteristic features.
- Initial (preclinical) stage: Manifests as transient mild pain, aching, and coldness in the first toe or heel. Hair loss on the outer surface of the lower leg can be visually observed. Patients rarely consult a doctor, and the pathology is often detected accidentally during routine medical check-ups.
- Progression stage: Chills, paresthesia (the feeling of 'pins and needles'), numbness, and causeless leg fatigue appear. The main marker is intermittent claudication (heaviness and pain in the calf muscles when walking). Due to spasm, the pulse in the arteries of the foot may transiently disappear. Heat intolerance, general hyperhidrosis of the feet, fungal nail infections, and paronychia join the clinical picture.
- Stage of pronounced insufficiency: Pain becomes constant, sharply increasing at night and causing insomnia. Intermittent claudication forces the patient to stop frequently and for long periods. The skin of the feet acquires a purplish-cyanotic tint, and the toes become atrophic ('empty toe' sign).
- Pregangrenous stage: The foot swells, and the nails become coarse and brittle. Deep painful cracks appear on the sole and between the toes, while sharply painful trophic ulcers and small areas of necrosis develop on the toes themselves. The pedal pulse is not palpable, it is often absent behind the knee, but is preserved in the femoral artery. Any minor trauma or hypothermia can trigger gangrene.
- Gangrene stage: Pain increases, becoming unbearable at night due to ischemic neuritis (ischemia of the nerves themselves). Palpation causes sharp pain. As soon as the tissues completely necrose (nerve endings die), the pain syndrome disappears.
Thromboangiitis obliterans (Buerger's disease)
Buerger's disease is a specific, aggressive form of thromboangiitis obliterans. It predominantly affects young men aged under 30–35 years and is characterized by a progressive, remittent course.
Key differences and pathogenesis:
- It begins with a pronounced allergic component (fever, blood count changes, general sensitization).
- Combined lesions develop: against the background of arterial ischemia, migratory thrombophlebitis occurs (veins are also affected).
- The process is systemic in nature (focal or diffuse lesion). Eventually, the vessels not only of the extremities but also of the skin, muscles, bones, central nervous system, and internal organs are affected.
- It is characterized by rapid progression with frequent progression to wet gangrene.
Diagnostics and treatment principles
The leading instrumental method is angiography. The main diagnostic sign of endarteritis, which distinguishes it from atherosclerosis, is smooth vessel walls with uniform narrowing of their lumen at the periphery.
Conservative treatment:
- Medical therapy: anti-inflammatory, analgesic, and vasodilating drugs are used. Desensitizing (antiallergic) agents, ganglionic blockers, and hormonal drugs (e.g., hexestrol) play an important role.
- Physiotherapy: UHF therapy, diadynamic currents (Bernard currents), drug electrophoresis.
- Rehabilitation: sanatorium-resort treatment is indicated.
Surgical treatment: If conservative measures are ineffective, operations on the sympathetic nervous system are performed — thoracic or lumbar sympathectomy. In the event of limb gangrene, amputation becomes the only option.
Briefly: answers to topical questions
Which vascular beds are affected in the generalized form of Buerger's disease in addition to the vessels of the extremities?
In the generalized form of Buerger's disease, in addition to the vessels of the extremities, there is a systemic lesion of the vessels of the skin, muscles, bones, central nervous system, and internal organs. At the end stage of the disease, the pathological process is diffuse or focal, involving the following structures:
- Skin — systemic vascular lesion of the skin integument.
- Muscles — lesion of the vascular bed of muscle tissue.
- Bones — involvement of bone vessels.
- CNS — lesion of the central nervous system vessels.
- Internal organs — lesion of visceral vessels.
By caliber in these beds, small-caliber arteries, microcirculatory vessels, and veins are predominantly affected.
Class and exam questions
Why does a patient stop feeling pain during complete tissue necrosis in gangrene?
Pain disappears due to the complete death of nerve endings in necrotic tissues. Until this moment, pain is caused by ischemic neuritis and is extremely intense.
Which pulse remains palpable in a patient even in the late stages of endarteritis?
As a rule, patients retain a confident pulsation in the femoral artery for a long time, while the pulse disappears on the foot and in the popliteal fossa.
How to distinguish endarteritis from atherosclerosis on an angiogram?
In thromboangiitis obliterans, the arterial walls on the angiogram remain smooth, and lumen narrowing occurs uniformly.
What else to study on this topic
- Mechanism of development of capillary angiomatosis of the tunica intima
- Technique for performing thoracic and lumbar sympathectomy
- Pathogenesis of migratory thrombophlebitis in Buerger's disease
- Ganglionic blocking drugs in the treatment of vascular pathologies
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