Arteriovenous malformation (AVM) is a high-flow vascular malformation that can occur in all parts of the body, with the highest incidence occurring intracranially. Soft tissue arteriovenous malformation, also known as trabecular hemangioma, is also more prevalent in the head and neck. The vascular structure is characterized by a large number of microscopic arteriovenous fistulas (short-circuiting) of the nutrient arteries in direct communication with the refluxing veins without a normal capillary bed in between. The pathogenesis of arteriovenous malformations remains unclear, but it is generally believed to originate from unresolved primitive arteriovenous traffic or can result from trauma. The vast majority of AVMs are disseminated, but it also occurs in certain rare hereditary syndromic vascular diseases, such as Parkes Weber syndrome and hereditary hemorrhagic telangiectasia (HHT), and studies of the families of these syndromes have revealed a number of genetic mutations associated with vascular development Mutations in genes associated with vascular development, such as RASA1, Endoglin, and ALK-1, have been revealed in families with these syndromes. All of these genes have been associated with angiogenesis, angiogenesis and vascular plasticity. AVM has a flushed appearance with localized skin temperature and sweating. Pulsation is palpable at the nutrient arteries, and a persistent murmur is audible. Imaging methods include ultrasound, MRI, CTA and DSA, of which DSA is the gold standard for the diagnosis of AVM and can be performed concurrently with treatment. The course of AVM can be divided into quiescent, dilated, destructive and decompensated stages according to the manifestation of disease progression. AVM is more likely to progress in adolescence, which is related to rapid development and hormone levels in adolescence. AVM can lead to local hypertrophy and deformation, tissue destruction, ulceration and infection, and can occur due to trauma or spontaneous rupture with uncontrollable bleeding and even fatal. Severe AVMs can lead to high-flow heart failure and eventually lead to patient death. Therefore, effective measures need to be taken as early as possible to treat AVM and control the progression of the disease to prevent it from progressing to the point of being untreatable or even unmanageable and to obtain better long-term results. AVM has unclear boundaries and often involves multiple tissue levels and anatomical sites, and its treatment is challenging and requires multidisciplinary combined treatment. Treatment methods include interventional embolization, percutaneous percutaneous embolization, sclerotherapy, surgical resection, copper needle or wire placement, and a combination of these methods. It is necessary to choose the appropriate treatment method according to the patient’s specific situation. The following are images of the appearance and imaging of AVM.