Talk about sudden onset deafness

  Sudden deafness (hereafter referred to as sudden deafness) is a sudden onset of sensory-neural deafness of unknown cause, also known as violent deafness. The etiology of sudden deafness is unknown, and more than 100 causes of the disease have been documented, many of which are rare. According to Mattox (1977), the order of causes of the disease is viral infection, vascular disease, endolymphatic edema, rupture of the vagus membrane, and a combination of these factors.
  Clinical manifestations.
  I. Deafness: The disease is aggressive and hearing loss can occur instantaneously, within hours or days, or suddenly in the morning. In chronic cases, the deafness can gradually worsen and stop progressing only after a few days. Its degree ranges from mild to total deafness. It can be temporary or permanent. It is mostly unilateral, but occasionally occurs bilaterally or sequentially. It may be cochlear deafness or postcochlear deafness.
  II. Tinnitus: Tinnitus occurs mostly before and after deafness, accounting for about 70% of cases. It usually appears a few hours before deafness. It occurs before and after deafness and accounts for about 70%. It usually appears a few hours before deafness, mostly as a buzzing sound, and can last for a month or more.
  Third, vertigo: sudden deafness is accompanied by varying degrees of vertigo, of which about 10% are severe deafness with nausea and vomiting, which can last 4 to 7 days, and mild dizziness can exist for more than 6 weeks. A small number of patients present with vertigo as the main symptom and are easily misdiagnosed as Meniere’s disease. Relief after a few days, without recurrent attacks.
  IV. Ear blockage. 
  V. Nystagmus .
  Diagnosis.
  I. Detailed medical history
  Patients with sudden deafness due to viral infection may clearly provide a history of influenza, cold, upper respiratory tract infection, sore throat, paranasal sinusitis, or contact with a virally infected person, which can occur weeks before the hearing loss. Patients with sudden deafness due to vascular pathology may provide a history of heart disease or hypertension, or they may have a history of diabetes, atherosclerosis, hypercholesterolemia, or other systemic diseases affecting the microvascular system. Patients with ruptured labyrinth membranes tend to have a clear history of exertion or experience of altered air pressure, such as difficult urination, defecation, coughing, sneezing, bending, laughing, etc. or swimming, diving, diving with a ventilator or underwater breathing apparatus, or unusual flight activities.
  Second, whole body examination
  The cardiovascular system, coagulation system, metabolism and immune reactivity of the body should be targeted. Neurological examination should exclude endo-aural tract and cerebellar pontocerebellar horn lesions, vertebrobasilar and cerebral vascular circulation disorders, such as taking endo-aural tract films and cervical spine films, cranial CT scan, fundus and cerebral hemogram.
  Specialized examination
  Otoscopy; audiological examination: pure tone audiometry air bone conduction threshold rises, generally above 50dB. Hearing curve typing is mainly flat, but there are also high-frequency decreasing type, high-frequency steep decreasing type or mild low-frequency decreasing type. Suprathreshold audiometry, speech audiometry, acoustic impedance audiometry, cochlear electrooculography and auditory brainstem response are used to identify cochlear and postcochlear damage and to understand the nature, extent and dynamics of hearing loss; vestibular function examination: should include variable temperature test, positional nystagmus test, fistula test, Romberg test, and nystagmus electrooculography if necessary.
  Treatment.
  I. General treatment.
  Patients should be hospitalized as much as possible, with bed rest and limited water and salt intake.
  II. Hyperbaric oxygen therapy
  The principles of hyperbaric oxygen therapy for sudden deafness are.
  1. Increase the partial pressure of oxygen, increase the amount of physical dissolved oxygen in plasma and the rate of oxygen diffusion in blood. Therefore, tissue hypoxia can be corrected rapidly. In addition, the greater the partial pressure difference of the gas, the faster the rate of diffusion. Therefore, the more hypoxic the site is the more oxygen is diffused to the site under hyperbaric pressure.
  2. In the case of increased partial pressure of oxygen, heart rate slows down, cerebral blood vessels contract, arterial blood pressure decreases, and cerebral blood flow can be reduced by 21%. However, due to the increased blood oxygen content, tissue oxygenation still increases, while vasoconstriction improves or prevents inner ear tissue edema, exudation and hemorrhage. The best time for hyperbaric oxygen therapy is within 48 hours, the sooner the better. However, hyperbaric oxygen therapy should not be abandoned even in patients with a long history of disease. The treatment pressure is 0.15-0.20 MPa and the course of treatment is 2-3 consecutive (i.e. 20-30 sessions).
  III. Vasodilators
  It has been proposed that sudden deafness is often associated with excessive blood coagulation. Heparin has the function of inhibiting the formation of thrombin, inhibiting the activity of thrombin, and preventing the agglutination and destruction of platelets; it also has the function of anti-vascular spasm and reducing the permeability of blood vessels; it can combine with histamine in the body and limit the destruction of cells by histamine. The application of small doses of heparin has been used as a routine treatment for sudden deafness. It can be administered subcutaneously, intramuscularly or intravenously, and the dose varies from person to person. Generally, deep intramuscular injections of 100mg are given once every 8h. Intravenous injection is 50mg once every 4-6 hours. In severe cases, 100-200mg can be added to 5% glucose 1000ml and slowly injected intravenously, the total amount of 24h should not exceed 300mg, and the dose should be adjusted to prolong and maintain the clotting time in 30min (Lee-White test tube method). However, it should be used with caution or contraindicated in patients with bleeding tendency, severe hypertension and liver disease. Dicoumarin, ethyl dicoumarin acetate and acetone benzyl hydroxydicoumarin have similar effects. Low-molecular dextran can reduce blood viscosity, reduce red blood cell agglutination and improve capillary circulation. Available 10% low molecular dextrose 500ml intravenous drip, and then every 6h drip 500ml, a total of 3 days drip.
  IV. Hormonal drugs.
  Early application is more effective, including ACTH, prednisone, prednisolone and dexamethasone, etc. Corticosteroids are effective for nerve damage and virus-induced post-snail deafness. ACTH can make ATP break down into AMP, and circulating AMP can reduce platelet agglutination; ACTH also has the effect of breaking down triglycerides. 40u subcutaneous injection, along with heparin 10,000u subcutaneous injection, 2 or 3 times a week for two weeks, can inhibit or moderate vasculitis.
  V. Nerve-nourishing drugs.
  Drugs such as vitamin A, vitamin B1, vitamin B12, glutamate and energy synergists (ATP, coenzyme A, cytochrome C) should be used early.
  Sixth, physical therapy.
  Microwave therapy has the effect of activating blood circulation and improving microcirculation in the inner ear.