Etiology and pathogenesis of the disease
The underlying pathology is congenital or acquired insufficiency of the venous wall tissues. This is the primary predisposing factor. Triggers such as prolonged standing, obesity, and pregnancy can initiate the disease. In pregnant women, biologically active substances (relaxin, progesterone) exert a specific relaxing effect on the vascular wall.
The pathogenesis of the disease develops in stages:
- Against the background of congenital predisposition and triggering factors, the vascular lumen begins to increase.
- Deep veins dilate, leading to the failure of their valve apparatus and the occurrence of retrograde blood flow.
- Overstretching and persistent valvular insufficiency of the perforating (communicating) veins develop.
- Reflux (backflow) of blood occurs directly into the superficial system.
- Venous hypertension forms in the subcutaneous veins, leading to nodular dilation, which ultimately results in microcirculatory impairment and the formation of trophic ulcers.
Clinical stages and pathomorphology
Changes affect all structures of the vessel. In areas of maximum dilation, the venous wall thins. In other areas, compensatory thickening is observed due to sclerosis and hypertrophy of smooth muscle elements. The valves themselves undergo deformation and sclerosis, exacerbating blood stasis. This process frequently occurs in combination with phlebothrombosis.
The clinical course is divided into two main stages:
| Grade | Manifestations and symptomatology |
|---|---|
| Initial stage (compensation) | For a long time, it is asymptomatic. Slightly dilated subcutaneous veins appear on the posteromedial surface of the lower leg and the inner thigh. They are soft, easily compressible, and the overlying skin shows no visual changes. |
| Decompensation | Patients complain of a sensation of fullness, heaviness in the legs, and fatigue upon standing. Symptoms completely disappear when the patient assumes a horizontal position. |
Main complications
Progressive CVI inevitably leads to local trophic disorders and inflammatory processes:
- Stasis eczema. As a rule, it is a precursor to more severe skin defects.
- Varicose trophic (venous) ulcers. Most commonly localized in the area of the medial malleolus (medial malleolus). They can reach large sizes and significant depth. The tissues surrounding the ulcer become indurated, and persistent hyperpigmentation (dark spots) appears. Palpation of the affected area causes minimal pain. The main marker is the combination with visible dilation of superficial veins.
- Thrombophlebitis. A dangerous inflammation of the venous wall accompanied by thrombus formation.
Principles of conservative and surgical treatment
Therapeutic tactics depend on the localization of the process and the risk of hemorrhage.
Treatment of lower extremity varicosities:
- Prescription of venotonic agents to improve blood outflow.
- Use of angioprotectors to reduce edema and decrease vascular wall permeability.
- Use of nonsteroidal anti-inflammatory drugs (NSAIDs) and anticoagulants for the prevention of thrombophlebitis.
- In severe progressive cases, surgical intervention is indicated (phlebectomy, resection of altered veins).
Management of esophageal and gastric varices (EGV): In patients with liver cirrhosis for the primary prevention of bleeding in grade II–III EGV, non-selective beta-blockers are used. If medical therapy is ineffective or there is a risk of recurrent bleeding, endoscopic ligation or sclerotherapy is used.
As secondary prevention, patients who have undergone esophageal vein interventions are required to undergo rigorous monitoring via esophagogastroduodenoscopy (EGD). Endoscopy is performed at 3 and 6 months postoperatively, and annually thereafter to assess indications for further treatment.
To remember the pathogenesis of leg varicosities, use the rule of the three "Ds" (or three "Rs" in Russian): Dilation — Retrograde flow — Reflux. First, deep veins dilate, valves fail to close (causing retrograde flow), then communicating veins are affected, and blood is shunted (reflux) into the superficial network.
Class and exam questions
Why do varicosities frequently develop during pregnancy?
In pregnant women, venous pressure in the legs does not rise solely due to mechanical factors. The hormones progesterone and relaxin play an important role, exerting a direct relaxing effect on the vascular wall.
Where do varicose trophic ulcers most commonly form?
Their typical localization is the area of the medial malleolus (medial malleolus). Ulcers can be large and deep, while the skin around them darkens and thickens due to tissue sclerosis.
How are bleeding esophageal varices treated?
Non-selective beta-blockers are prescribed for primary prevention. In the event of bleeding or the threat of recurrence, endoscopic ligation or vein sclerotherapy is performed.
What else to study on this topic
- Topographic anatomy and the valve apparatus of the superficial veins of the lower extremity
- Differential diagnosis of phlebothrombosis and thrombophlebitis
- Surgical treatment techniques: phlebectomy and vein resection
- Endoscopic criteria for evaluating esophageal varices
- Layer-by-layer anatomy of the subcutaneous adipose tissue and fascia of the lower extremities
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