Obstructive subcutaneous sclerosis

　　1. Etiology

　　Since all these patients had varicose veins of the great saphenous vein in the lower leg before onset and all had incomplete function of the superficial and deep venous communicating branches, and even patients without obvious varicose veins also had incomplete conditions of superficial and deep venous communicating branches, incomplete function of the communicating valves may be the initiating factor of the disease.

　　2. Pathogenesis

　　Due to the incomplete function of the valvulars of the superficial and deep venous communicating branches, blood flow from the superficial veins to the deep veins is obstructed, leading to varicose veins of the superficial veins over time; chronic venous congestion may cause phlebitis, which in turn may lead to periphlebitis; involvement of adjacent tissues and small blood vessels may cause microcirculatory disorders and fatty tissue, potentially leading to fatty cell degeneration, necrosis, and the release of fatty acids to exacerbate local inflammatory reactions; hyperplasia of the connective tissue between the fatty lobules may further lead to obstructive sclerosis. Based on the above tissue changes, irregular subcutaneous hard plaques are formed. Compression of the lymphatic vessels can cause lymph leakage; when the papillary capillaries of the dermis are involved, it can cause progressive hyperpigmentation. Since there is no involvement of the deep veins, severe lower leg edema does not occur. Due to the gradual establishment of collateral circulation and the proliferation of small blood vessels to maintain local blood circulation, local tissue nutritional disorders, skin eczema, and necrotic ulcers do not occur.

　　The pathological changes are mainly significant hyperplasia of fibrous connective tissue in the lower dermis and the intervals between the subcutaneous fat lobules, leading to widening of the lobular intervals. The number of fine blood vessels increases, the vessel walls are obviously thickened, the lumen is dilated, filled with an unequal amount of red blood cells, and no thrombosis forms. Scattered lymphocytes are present. The epidermis and fat cells are normal. Modified van Gieson staining and MAB staining show that the hyperplasia is collagen fibers. Elastic fiber staining shows that the affected vessels are veins.

　　A few have progressive hyperpigmentation-like manifestations and lymph fluid leakage after puncturing plaques.

　　Familial progressive hyperpigmentation (FPH) is an autosomal dominant genetic disease that can expand with age, slow down after puberty, has no tendency to heal spontaneously, and sweating is normal. Pigmentation is diffuse brown, deep brown, with interspersed normal skin. It is common on the forehead, cheeks, around the eyes, mouth, neck, trunk, limbs, and on the backs of hands and feet. The mucous membranes of the eyes and mouth may be affected. Sweating is normal, and there are no other defects.

　　The damage initially occurs at the lower 1/3 of the tibia margin on the inner side of the lower leg, with more on the left side than the right. The lesion occurs stealthily within the subcutaneous fatty tissue, forming 1 to 3 hard nodules as large as soybeans or broad beans, which gradually accumulate into hard plaques. The edges are clear, and the skin above is pale red or skin-colored, with mild pain and tenderness. It then slowly develops upwards, with new small nodules appearing at the edge of the original large plaque, causing the area to gradually increase in size, becoming fixed in the subcutaneous tissue. Above it are dilated or cystic veins, which are uneven and hard and soft, with the largest plaque reaching 15×10cm. The lower edge can reach above the medial malleolus, and the upper edge can reach the lower 2/3 of the lower leg, without affecting the lateral side of the lower leg. Prolonged standing or walking can exacerbate local edema, making the plaques hard and tight, with more prominent redness and swelling at the edges, and more obvious local pain and tenderness. However, there are no symptoms such as fever or enlargement of the inguinal lymph nodes. After rest, the edema decreases, but the plaques do not明显 regress significantly. After treatment, most or almost all of the plaques regress, with varying degrees of atrophy of the subcutaneous fatty tissue, thinning of the epidermis, becoming smooth and shiny, and increased pigmentation or slight desquamation. Long-standing lesions have varying degrees of pigmented沉着. Some also develop 1 to 2 nodular erythema-like lesions unrelated to hard plaques. All such patients have mild to moderate varicose veins of the great saphenous vein and its branches, and even if there are varicose veins on both sides, only one lower leg develops hard subcutaneous plaques, and all legs with varicose veins have developed this subcutaneous tissue lesion. Varicose veins occur 1 to 30 years before the subcutaneous tissue lesion.

　　1. For the primary prevention of chronic subcutaneous sclerosis, factories and enterprises with long-term standing work should provide labor protection, such as using elastic stockings or elastic bandages during work, organizing work breaks, etc.

　　2. For patients with mild varicose veins, use elastic bandages or wear elastic stockings, elevate the affected limb.

　　3. Actively treat the primary disease. There was a great saphenous varicose vein in the lower leg before the onset of the disease, pay attention to rest, avoid long-term standing. It is best to prevent early in the morning.

　　Laboratory tests needed for chronic subcutaneous sclerosis include:Urine routine examination, blood routine examination, antistreptolysin O test, erythrocyte sedimentation rate (ESR) determination, serum mucoprotein (SM) determination, venous valve function test, vascular造影 examination, lower limb vascular ultrasound examination. Diagnose the disease through all the laboratory examination results involved.

　　1. What foods should be eaten for chronic subcutaneous sclerosis to be good for the body: Pay attention to light food in diet, and eat the following 10 foods, all have preventive effects. Buckwheat, garlic, oatmeal, eggplant, onion, soybeans, hawthorn, black sesame, apple, sweet potato.

　　2. It is best not to eat the following foods for chronic subcutaneous sclerosis: oily foods. In order to avoid the recurrence of the disease.

　　1. Treatment

　　Compound Danshen Tablets or Danshen Tablets 3-4 tablets, oral administration, 3-4 times a day, or Danshen intravenous drip, if edema is significant, oral administration of amino己ic acid, each time 100g, 3-4 times a day; or nicotinamide 0.1g, 3 times a day.

　　Traditional Chinese Medicine Treatment: Local moxibustion with moxa sticks can also have a good effect on improving blood circulation.

　　2. Prognosis

　　This disease belongs to a benign disease, so the prognosis is still good.