Etiology】 Hemangioma is formed by the proliferation of vascular network during embryonic period. There are two main theories to explain the proliferation of hemangioma: 1) Increased estrogen level and specific estrogen receptors in the tumor; 2) Mast cell theory: Gwaki proposed that mast cells can directly stimulate endothelial cell proliferation, and indeed mast cells have increased in the tumor tissue of children with hemangioma. The histological features of hemangioma during the regression period are: fibrous degeneration, fatty infiltration, occlusion of the vascular lumen and reduction of mast cells. 70% to 80% of capillary hemangiomas and 5% to 50% of capillary spongiform mixed tumors regress spontaneously within one to three years after birth. Vascular malformations and certain types of hemangiomas, such as orange-red spots, do not recede for life. The key is that hemangiomas that do not regress are proliferative in nature. Therefore, for this hot spot, we focus more on biochemical measurements of the proliferative phase of hemangiomas, such as urinary basic fibroblast growth factor and an8iogenic factor. Clinical manifestations and classification】 Our traditional classification of hemangioma is as follows 1. capillary hemangioma: 2. neonatal nevus (epidermal capillary hemangioma) 3. intradermal capillary hemangioma: orange-red spot (bright flesh spot) 4. wine spot 5. spider nevus 6. strawberry capillary hemangioma 7. senile hemangioma 8. sclerosing hemangioma 9. granulomatous hemangioma 10. cavernous hemangioma 11. trapezius hemangioma 12. The diagnosis of erythroderma and strawberry capillary hemangioma can be established from the clinical presentation. The diagnosis can be established from clinical manifestations. The diagnosis of subcutaneous cavernous hemangioma and strawberry hemangioma with atypical symptoms can be confirmed by aspiration of blood through fine needle aspiration, or angiography if necessary, to clarify the site of small arteriovenous fistula. Strawberry hemangioma in children should be allowed to heal by itself as much as possible. It takes a long time for cavernous hemangioma to subside, such as parotid cavernous hemangioma takes 5-10 years, but it is better to wait and surgery is easy to cause facial nerve damage. Cryotherapy (CO z dry ice or liquid nitrogen) is suitable for treating small capillary hemangioma, but in clinical practice, it is often found that it can lead to demented skin scars. 2.Laser irradiation Chin-doped diamond pomegranate laser (Nd-YAG) has stronger penetrating ability to tissues and more absorbing ability to blue, violet, red and other color tissues, so it has better efficacy in the treatment of hemangioma, among which small, <3cm or surface capillary hemangioma, the effect is better, and it can also occur that the irradiated area leaves scarring. 3.Radiation therapy x-ray, radium and radionuclide were once carried out in many medical units in China as one of the main treatment means, but the effect of this therapy is not sure and it is more harmful, and skin deformation and even skin cancer occur after many years, so it should be abandoned. 4.Limb bandage compression therapy Applicable to limb venous malformation. 5.Sclerotherapy injection Injection of sclerosing agent in the tumor to cause fibrosis until it disappears, the sclerosing agents used now are sodium cod liver oil acid, urea and pinyamycin. 6.Hormone therapy is especially suitable for cavernous hemangioma with rapid facial growth, giant cavernous hemangioma and Kasabach-Merritt syndrome. Hormone therapy can be divided into two types, one is local injection of dexamethasone 5-10mg into the hemangioma body, adding 1% procaine 2-4m1 and pure ethanol 0.1-0.55m1, and injecting into the tumor body by partitioning, generally once a week, 5 times for a course of treatment. Most of the tumors are mechanized and shrunken, and may even disappear completely. The use of oral high-dose corticosteroids was first proposed by Zarem and Ed8eton (1967) and has been recognized as the method of choice for the rapid growth phase of hemangiomas. The first is the shock phase, i.e., 40 mg of oral prednisone every N (6-7k8 weight children) for 7 times, then 20 mg every 2d for 2 weeks or 7 times, followed by l0 mg every 2d for 2 weeks or 7 times, 5 mg every 2d for 2 weeks or 7 times, and then the maintenance phase, 25 mg of oral prednisone every 2d for 60-90d. In about 30% of hemangiomas, when the dose is reduced to lomg or 5mg every 2d, the hemangioma may increase again, then the dose should be increased to 15-20mg every 2d for 2 weeks, and then to the maintenance dose. The whole course of treatment should be 3 months. Long-term use of hormones in children can lead to complications, as in the case of organ transplantation, leukemia and kidney disease, and clinicians should take this into account. 7.Interventional embolization therapy For progressive growth of hemangioma, if there are clear vascular feeding branches, the blood vessels can be occluded through interventional therapy by injecting mucoadhesive, which is clinically effective, such as giant hemangioma of the liver. 8.Interferon therapy This is a recent new approach to the treatment of progressive growth hemangioma. 1989 White first used interferon (A1) to treat pulmonary hemangioma lesions successfully, followed by similar reports. Progressive hemangioma lesions, especially Kasabach-Merritt syndrome, are very dangerous and often have a mortality rate of >40%. It has been successfully treated with a single hormonal therapy. Friesel (1987) suggested that the in vitro mechanism of action of AI is to antagonize the action of endothelial cells, smooth muscle cells and fibroblasts, and also to inhibit vascular growth factor. As for the side effects, fever, eosinophilia, anorexia, diarrhea and recurrent infections were observed.