It is generally accepted that sudden deafness is a sensorineural hearing loss of at least 30 dB on at least three consecutive frequencies that occurs suddenly (within 72 hours), referred to as “sudden deafness”. The etiology of sudden deafness is unclear, mainly due to tumor, trauma, immunity, toxicity, metabolism, and viral infection. There are different etiologies and different pathogenesis, and there are many unknown factors, the most important one being vascular circulation. The blood supply to the inner ear mainly originates from the anterior inferior cerebellar artery, but also directly from the basilar artery and the anterior superior cerebellar artery, which are terminal vessels without collateral circulation, so the local circulation of the cochlea is poorly compensated; the physiological activity of the cochlear auditory hair cells consumes high amounts of oxygen and has a poor ability to tolerate hypoxia, which is more fragile than the vestibular hair cells. Thus various causes of cochlear microcirculatory dysfunction, including microthromboembolism, reduced blood flow, vasospasm, inflammatory swelling of vascular endothelial cells, or changes in ion concentration, may contribute to auditory cell injury. Other pathogenic mechanisms include viral infection, rupture of the vagus membrane, immune-mediated, and abnormal cellular stress. Although some cases of sudden deafness are “self-healing” and do not require special treatment, they can recover naturally with proper rest. However, because of its “deafness” and the “effective time window” for treatment, it is not recommended to wait for its natural recovery, but to treat it as an otologic emergency. The timing of treatment emphasizes the earliest possible time, and the initial treatment methods include pharmacological and non-pharmacological treatments. Here, the emphasis is on corticosteroids and hyperbaric oxygen treatment methods. First, corticosteroids including prednisone, methylprednisolone, succinyl prednisone and dexamethasone act locally in the inner ear and are effective against viral, vascular, syphilitic, autoimmune diseases, endolymphatic effusion (Meniere’s disease) and other causes of hearing impairment. Corticosteroid treatment provides maximum recovery during the first 2 weeks of onset, and is “virtually ineffective” for the next 4 to 6 weeks. The recommended dose of oral prednisone is usually 1 mg/kg/d in a single dose, usually up to 60 mg daily for 10-14 days. 60 mg of prednisone is equivalent to 48 mg of methylprednisolone and 10 mg of dexamethasone. In addition to oral dosing, intravenous systemic dosing is also available. Clinically, there will be some variation in prescriptions by different physicians, but it should be emphasized that early treatment is crucial to ensure an adequate initial dose and to pay attention to the ratio of different doses administered to avoid underdosing and compromising efficacy. Systemic hormone therapy has potential side effects on many organs that need to be taken into account. To minimize the risk of treatment, patients with health problems such as insulin dependence, poorly controlled diabetes, unstable hypertension, tuberculosis, peptic ulcers and prior psychiatric reactions to corticosteroids may not be suitable for systemic corticosteroid therapy. Intra-drum corticosteroids may be used as initial treatment or as “salvage therapy” for patients who fail after 3 months. Dexamethasone and succinyl prednisolone are the hormones commonly used for intra-drum therapy. Although the toxicity of topical administration is less than systemic administration, there are side effects, although rare, such as pain, transient vertigo, infection, persistent tympanic membrane perforation, and possible vasovagal response or syncope during the injection process. Secondly, hyperbaric oxygen therapy is to put the patient into a specially designed sealed chamber in which the oxygen concentration is 100% and the pressure is greater than 1 absolute atmosphere, which can make certain tissues that are sensitive to the lack of cavity – the local oxygen partial pressure of the cochlea is greatly increased, in addition, hyperbaric oxygen has a compound effect on immunity, oxygen transport and hemodynamics, which can reduce hypoxia and edema, and enhance the host response of the body to infection and ischemia. Hyperbaric oxygen was first used to treat sudden deafness in French and German workers as early as 1960. It is generally believed that hyperbaric oxygen therapy is more effective when administered within 2 weeks of the onset of sudden deafness. Hyperbaric oxygen therapy is very unlikely to produce side effects, mainly aural and sinus pneumatic injuries, increased temporary myopia, claustrophobia and oxygen toxicity. However, most studies have not found serious side effects. In foreign countries, hyperbaric oxygen therapy is an expensive and time-consuming treatment; in China, hyperbaric oxygen therapy for sudden deafness is covered by medical insurance and is inexpensive, with a course of 10 sessions at 40 RMB per session, once a day, which is generally recommended for 5-10 sessions in foreign countries, and intermittent treatment until about 3 months after the onset of the disease in China.