Angioma is a familiar term among the general public and the majority of clinicians. Although modern medical nomenclature formally refers to the disease as vascular developmental anomalies (hereafter referred to as VA), it is still not well known. VA is a group of common vascular developmental anomalies that occur in the skin and subcutaneous tissues, followed by the oral mucosa and muscles, and some internal organs such as the brain, liver, lungs, and kidneys, with 60% occurring in the head and neck, followed by the extremities and trunk. Classification The names and classification of VA disease groups are confusing, mostly named by appearance and location, such as facial wine spots, strawberry hemangioma, trabecular hemangioma and hepatic cavernous hemangioma. This has caused problems in understanding the nature of the disease, classification, diagnosis and even treatment. In China, even doctors have to explain to patients that these are not tumors, but …… With the in-depth study of this group of diseases, Mulliken and Glowacki classified VA into two major groups, childhood hemangiomas and vascular developmental abnormalities, based on the biological characteristics and histopathological changes of vascular endothelial cells in 1982. The latter was further subdivided into capillary malformations, venous malformations, lymphatic malformations, arteriovenous malformations, and complex malformations according to the type of abnormal vessels. Vascular malformations are classified into high-flow and low-flow vascular malformations according to the level of blood flow in the malformed vessels. This classification method distinguishes lesions in terms of their occurrence, development and hemodynamic changes, and is a direct guide for the diagnosis, treatment and prognostic assessment of VA. According to the above classification method, some of the previously confusing names can be unified into the official names in Table I. Clinical manifestations Childhood hemangiomas originate from residual embryonic angiogenic cells and are characterized by proliferation of vascular endothelial cells and increased cell density, and are classified into proliferative, equilibrium and regressive hemangiomas. They often appear as mosquito-bite red dots on the skin about 2 weeks after birth and grow rapidly, most notably at 3 to 4 months of age. The tumor is usually bright red and protrudes from the skin, resembling a strawberry, and does not shrink or shrink significantly under pressure. The growth of the tumor stops around the age of 1 year and enters a stable phase, which gradually subsides, usually before the age of 5 years, and in some patients it can be delayed until the age of 10-12 years. Overall, more than 80% of children with hemangioma can regress spontaneously without treatment. However, it is not uncommon to see indiscriminate medical treatment and unreasonable overtreatment. Vascular malformations are structural abnormalities caused by genetic mutations during embryonic angiogenesis and angiogenesis. The lesions are present at birth but do not necessarily manifest themselves. The growth rate is synchronized with the body’s development and is slow and continuous, lacking the rapid growth history of hemangiomas, and there is no natural regression process. Venous malformations that are accessible on the surface of the body are soft, shrink under pressure, and return to their original shape with decompression. The lesion increases significantly when it is in a subluxated position and retracts in the opposite direction, i.e., the postural test is positive. The surface of the lesion may be bluish-purple in color and may be surrounded by filling and dilated superficial veins. Lymphatic duct malformations present as a soft to flexible mass due to the lack of mobility of the lymphatic fluid within them and are negative on the postural test. Superficial arteriovenous malformations can be palpated with distinct vascular pulsations and vascular murmurs can be heard. Visceral and deep vascular malformations have different clinical manifestations depending on the location and size of the lesion, and some lesions can only be detected by imaging. In general, vascular malformations may be stable or slowly increasing in size. In some special cases, such as puberty, pregnancy, local inflammation, trauma or surgery, significant growth may be stimulated within a short period of time. The diagnosis of body surface VA can be confirmed by physical examination. Routine physical examination requires attention to the potential extent of the lesion, its color, texture, skin temperature, pulsation or not, and the presence of murmurs. In vivo VA needs to be diagnosed with the help of relevant instruments. Color Doppler (CDI) is a good noninvasive test for diagnosis, treatment guidance and follow-up. Enhanced CT provides a more definitive diagnosis of VA, but not as well as MRI. high-flow lesions appear as a flow-through signal on multiple MRI procedures. Low-flow lesions have significantly higher signal on MRI. Using subcutaneous fat signal as a reference, low-flow lesions are slightly lower on T1WI and slightly higher on T2WI. In addition, MRI can show well the exact anatomical relationship between vascular lesions and their adjacent nerves, muscles, ligaments, and tissues. DSA, on the other hand, is absolutely superior for showing the full picture of arteriovenous malformations and hemodynamic changes. It is important to note that laboratory tests such as the function of locally affected tissues or organs, systemic coagulation and evaluation of cardiac function are also important before deciding on the treatment of a vascular lesion. Treatment The treatment of vascular abnormalities varies depending on the location, size, extent, nature of the lesion, and complications. Many treatment options are available, such as medical treatment, laser irradiation, surgical lesion excision and reconstruction, interventional methods such as direct puncture sclerosis and embolization of the blood supply artery. After a clear diagnosis and assessment of the systemic condition, it is important to determine whether the lesion requires treatment, what treatment modality to use, or an organic combination of several treatments, and to leave the treatment of VA to a team of specialists with extensive experience in interventional, plastic and related vascular surgery. 1.Hemangioma Most hemangiomas can spontaneously fade (80% to 90%) and generally do not require treatment. However, hemangiomas occurring in the eyelids, nose and lips are prone to complications such as ulceration due to their greater impact on function and morphology, while the spontaneous regression rate of hemangiomas in these areas is relatively lower and should be treated early and actively. Proliferating hemangiomas respond better to treatment. Before implementing treatment, patients and families should be informed of the occurrence, development and regression of hemangioma, the advantages of the treatment administered, the possible complications and risks, and the choice of patients and families should be respected. Treatment methods mainly include drug therapy (hormone, interferon), laser therapy, cryotherapy, surgical resection, etc. 2.Vascular malformation (1) capillary malformation, which is called capillary hemangioma, erythema and wine spot in the past, is superficially located between epidermis and dermis. Laser is an effective treatment method for surface lesions. 585 nm wavelength flashlamp-pumped pulsed dye laser (FPDL) is commonly used, and the treatment period should start from infancy as early as possible. Patients with FPDL in the hands and upper arms have poorer outcomes than those in the face, neck, and trunk. The overall efficiency is about 50-70%. A small number of patients with ineffective treatment require excisional implant repair. (2) Venous malformations Venous malformations have mostly been treated by surgical focal resection, but it has been proven that in most cases, complete resection cannot be achieved because the malformed vascular mass grows in important areas or is surrounded by normal tissue structures. Forced partial resection of the lesion is often only effective in the short term, and most venous malformations recur in the long term and are even more extensive than before surgery. Interventional treatment of venous malformations is more effective and is known for its minimally invasive and reproducible nature. The ultimate goal is to mechanize the malformed vessel by directly destroying its wall structure. Currently, the treatment of venous malformations is shifting to an interventional-based approach, supplemented by interventional combined with surgical resection. Interventional treatment is divided into 2 methods: direct puncture and arterial route. The body surface venous malformations are mainly treated by percutaneous puncture sclerotherapy, and the sclerosing agents include anhydrous alcohol, sodium cod liver oil acid and pinyamycin iodine oil emulsion. Some venous malformations of internal organs such as hepatic venous malformation (hepatic cavernous hemangioma) are treated by the arterial route by cannulating into the blood supply artery of the venous malformation and injecting vascular sclerosing agent through the catheter, so that it can enter the malformed vascular mass with the blood flow to destroy and embolize the malformed vessels. The sclerosing agent is usually a milder form of Pingyangmycin iodine oil emulsion. (3) Arteriovenous malformation is a high flow rate vascular malformation, mainly composed of blood supply artery, malformed vascular mass and drainage vein. It is divided into resting phase, extended phase and decompensated phase according to the progression of the lesion. Resting arteriovenous malformations are mainly treated with interventional embolization, and some lesions can be treated radically, such as arteriovenous malformations of the kidney and gastrointestinal tract. Embolization can be considered for extended arteriovenous malformations, or embolization + surgery if surgery is appropriate. The use of preoperative adjuvant embolization plus surgical resection is more reasonable for decompensated arteriovenous malformations. In view of the pathological basis of arteriovenous malformation and the abundant collateral circulation, simple ligation of the blood supply artery without removing the malformed vessels often complicates the blood supply of the lesion and increases the difficulty of subsequent treatment, which should be avoided as much as possible. (4) Arteriovenous fistulae Arteriovenous fistulae can be treated surgically, but in some areas surgery is more difficult. Interventional treatment is the preferred treatment for arteriovenous fistulas in all areas and has the advantage of being less invasive and more effective. The method of intervention depends on the location and size of the fistula and the tolerance of the distal tissues and organs to ischemia, mainly by embolization. If the arterial blood supply to the distal tissues needs to be maintained, fistula closure with a membrane stent may also be performed. (5) Lymphangioleiomyomatosis, which used to be called lymphangioleioma, is formed by the dilatation of lymphatic vessels. For small and limited lymphatic duct malformations, they can be left untreated if they do not affect function or are not aesthetically pleasing. Percutaneous sclerotherapy reduces the size of the lymphatic vessels by stimulating the endothelial cells of the lymphatic vessels to produce a sterile inflammatory response, resulting in the proliferation of fibrous tissue and occlusion of the lymphatic vessels. Sclerotherapy is simple, convenient and less destructive to tissues, and can be the first choice of treatment for cystic lymphatic duct malformation. Other types of lymphatic duct malformations are mainly treated surgically, and the lesions should be removed as completely as possible during surgery to avoid recurrence.