Venous malformation (VM) (formerly known as cavernous hemangioma or venous hemangioma) is second only to infantile hemangioma in the incidence of vascular disease of the head and neck. Among the vascular malformations of the head and neck, venous malformations are the most common. Previous inconsistencies in nomenclature have led to confusion between venous malformations and vascular tumors, resulting in some inappropriate treatment. In 1982, Mulliken and Glowacki classified vascular diseases into two main categories: infantile hemangiomas and vascular malformations, based on history, clinical presentation, and histologic features. Infantile hemangiomas present as endothelial cell proliferation, whereas vascular malformations are mature endothelial cells with no tendency to proliferate. Venous malformations are vascular malformations in which the lesion consists of a number of dilated venous sinuses of varying size, which histologically appear as spongy, thin-walled lacunae of varying size. Vascular malformations also include lymphatic malformations, capillary malformations (formerly known as “wine stains”), arteriovenous malformations (formerly known as “trabecular hemangiomas”), and mixed vascular malformations. Based on hemodynamic characteristics, venous malformations are low-flow vascular malformations. The hemodynamic classification facilitates the selection of the correct treatment. Low-flow vascular malformations such as venous malformations and lymphatic malformations are mainly treated by percutaneous sclerotherapy, whereas arteriovenous malformations are treated by arterial interventional embolization. It should be noted that a significant number of lesions called “cavernous hemangiomas” located in the bone or muscle are in fact venous malformations. 1.Clinical manifestations: Venous malformations are congenital diseases, but they can be asymptomatic at birth and are not detected until several years later. Most venous malformations are superficial, soft and compressible, without pulsation, and the skin on the surface of the swelling may be bluish. In deeper lesions, signs are usually unremarkable. Venous malformation lesions are stable, and trauma and hormonal environmental changes can stimulate rapid enlargement of the mass. Venous malformations do not resolve on their own, and there is no gender difference in their incidence. Venous malformations of the head and neck can occur within the soft tissues or within the bone. The soft tissue sites of venous malformations are, in order of preference, the cheek, mandible, sublingual space, tongue, and periorbital area. Intraosseous venous malformations are more prevalent in the frontoparietal region in the cerebral cranium and in the mandible in the facial cranium. Venous malformations are usually asymptomatic but can cause cosmetic damage, abnormal bone development, localized wasting coagulation and bleeding tendencies. Intramuscular and deeply located venous malformations often present with morning pain. Large venous malformations in the head and neck can compress the airway and interfere with breathing and eating, and those located in the orbit can damage the optic nerve. The venous malformation in the midline region of the face should be paid special attention to whether it is complicated by intracranial venous anomalies and extracranial communication. 2.Auxiliary examination: Ultrasound shows heterogeneous hypoechoic cavity and venous stone is the characteristic manifestation of venous malformation. MRI showed characteristic features. medium signal in T1W and significant high signal in T2W, with varying degrees of enhancement of the lesion after enhancement. The “grape bunch”-like structures within the lesion are typical, and sometimes round, low-signal venous stones are seen within the lesion. Venous stones and bony invasion can be defined by X-ray and CT. Percutaneous transluminal angiography provides good visualization of the lesion and its hemodynamic features. Patients with venous malformations with airway involvement on MRI require laryngoscopy to assess the extent of endotracheal involvement and risk of tracheotomy. Treatment of venous malformations includes sclerotherapy, electrochemical therapy, laser and surgical resection. Anti-angiogenic drugs are not effective for venous malformations. Irregular diagnoses such as “cavernous hemangioma” often lead to inappropriate medication or even radiation therapy. Surgery often recurs or causes unacceptable functional and cosmetic damage due to excessive surgical trauma, with unsatisfactory results. Sclerotherapy with direct percutaneous puncture can shrink or cure the lesion and is now the treatment of choice in the majority of vascular disease treatment centers. Sclerotherapy is particularly effective in patients with venous malformations complaining of pain and limited lesions, and pain relief can be obtained even with residual lesions after treatment. Diffuse venous malformations are relatively ineffective, and treatment is aimed at symptom relief rather than complete cure. Sclerotherapy may seem simple to perform, but it can lead to serious complications and should be performed by an experienced specialist. Patients should be informed in detail about the risks prior to treatment. Commonly used sclerosing agents include anhydrous ethanol, sodium cod liver oil acid, sodium tetradecyl sulfate, polydocanol, aminoethanol, pinyamycin and cyclophosphamide. Anhydrous ethanol is becoming an important choice for the treatment of venous malformations because of its strong aggressive properties, remarkable efficacy and low recurrence rate. Anhydrous ethanol can denature proteins, precipitate protoplasm, and permanently close the lesion, which is the most effective sclerosing agent clinically proven so far, and the destroyed endothelial cells cannot be regenerated. Several scholars have reported that anhydrous ethanol can completely cure some patients with venous malformations, with a treatment efficiency of 74-91%. However, complications due to anhydrous ethanol cannot be ignored, including tissue necrosis, peripheral nerve injury, central nervous system depression, hypoglycemia, hypertension, hemolysis, pulmonary embolism, pulmonary vasospasm, and cardiopulmonary failure. Because of these potential complications, sclerotherapy with anhydrous ethanol should only be performed by well-trained and experienced specialists. The hospital must be well equipped with anesthesia and ICU. The patient’s vital signs are closely monitored during the treatment. Regardless of the type of lesion, the serum concentration of ethanol is directly related to the dosage. Therefore, the dose must never exceed 1 ml/kg body weight. Sodium cod liver oil acid, sodium tetradecyl sulfate, polydocanol and aminoethanol have no neurodestructive effect. As with anhydrous ethanol, treatment should be precisely positioned; accidental entry into the artery will cause severe tissue necrosis. There is a growing interest in mixing sclerosing agents with air to make foam dosage forms. Foam dosage forms can achieve better efficacy than liquid embolic agents, probably because of the longer retention time of the foam in the lesion. Compared to anhydrous ethanol, these sclerosing agents also destroy endothelial cells, leading to thrombosis and fibrosis; however, thrombus formation is slower and the chances of recanalization and recurrence are higher. In 1977, Yura et al. first applied them to the sclerotherapy of lymphatic duct malformations with good results. It is becoming more and more widely used in the treatment of this type of disease because of its safety and effectiveness. Subsequently, several antineoplastic drugs were introduced to the treatment of venous malformations. However, compared with lymphatic malformations, the retention time of antineoplastic drugs in the lesions of venous malformations is short, and it is difficult to completely eliminate the lesions by applying antineoplastic drugs alone, and the toxicity caused by the accumulation of drug doses should be noted in repeated treatments. Small doses of anhydrous ethanol are used to embolize the reflux vein of the lesion and prolong the retention time of the subsequently injected Pingyangmycin in the venous malformation lesion in order to give full play to its sclerosing effect. In addition to the high safety profile of this therapy, the efficacy was satisfactory, with a treatment efficiency of 97.6% (206/211). Among them, 51.2% (108/211) patients had disappearance or near normal appearance of the swelling. Swelling was evident after sclerotherapy and could last for several days to weeks. Therefore, in patients with large lesions with airway involvement, a thorough evaluation of the airway is required prior to sclerotherapy to ensure that the airway remains open after treatment. Other non-surgical treatments include electrochemical therapy and laser therapy. Electrochemical treatment has been phased out due to its poor efficacy, tendency to relapse and the obvious scarring residue on the skin. Laser treatment is only indicated for superficially located skin and mucosal venous malformations and is not effective for deeper lesions. It should be emphasized that in addition to sclerotherapy, surgical revision remains an irreplaceable treatment option for patients with venous malformations with poor sclerotherapy results and significant secondary skeletal deformities in order to improve their appearance.