The etiology of sudden deafness is unknown; more than 100 causes of the disease have been documented, many of which are rare. According to Mattox (1977), the order of causes of this disease is viral infection, vascular disease, endolymphatic edema, rupture of the vagus membrane, and a combination of these factors.
(i) Deafness
The disease is aggressive and hearing loss can occur instantaneously, within hours or days, or with sudden deafness on rising in the morning. In chronic cases, the deafness may gradually increase 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 before and after deafness, accounting for about 70% of cases. It usually appears a few hours before deafness and is mostly a buzzing sound that can last for a month or more. Some patients may emphasize the tinnitus and ignore the hearing loss.
(iii) Vertigo
About 2/5 days 1/2 sudden deafness is accompanied by varying degrees of vertigo, of which about 10% are severe deafness with nausea and vomiting that can last 4-7 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. It relieves after a few days and does not recur.
(iv) Ear blockage
The blocked ear sensation usually precedes deafness.
(v) Nystagmus
If vertigo is present, spontaneous nystagmus may be present. Liu Hongying, Department of Otolaryngology, Second Affiliated Hospital of Shandong University of Traditional Chinese Medicine
(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, etc., 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.
(II) Systemic 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. Wang Shuchun et al. performed cerebral hemogram examination on 104 patients with sudden deafness and found that the cerebrovascular functional status of patients with sudden deafness was worse than that of normal subjects.
(C) Laboratory examination
It includes blood picture, blood sedimentation, clotting time, prothrombin time, platelet count, etc. Serological examination isolates virus and antibody titer measurement, and also considers blood glucose, lipids, blood nitrogen and serum syphilis test.
(iv) Otoscopy
The tympanic membrane is often normal and may also be slightly red.
(E) Hearing examination
The pure tone audiometry air bone conduction threshold rises, usually 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, cochlea electrographic examination and auditory brainstem response are used to identify cochlear and postcochlear damage and to understand the nature, extent and dynamics of hearing loss.
(F) Vestibular function examination
It should include variable temperature test, positional nystagmus test, fistula test, Romberg test, and nystagmography if necessary. Yagi et al. reported 51 cases of sudden deafness, and positional nystagmus was performed on 50 sides at the initial diagnosis, and positional nystagmus was seen in 38 cases. 48 cases were examined by nystagmography, and horizontal nystagmus was seen in 30 cases. The diagnosis of sudden deafness can be made based on the above history, symptoms and various examinations. However, the etiologic diagnosis and differential diagnosis should be made as much as possible in order to provide early and reasonable treatment. In particular, it should be differentiated from eustachian tube stenosis, Ménière’s disease, and auditory neuroma.
(I) Eustachian tube stenosis
Many patients with sudden deafness present with low-frequency hearing loss, and these patients have initial symptoms of dullness and low-pitched tinnitus, similar to eustachian tube stenosis, and complain of a lighter sensation after ventilation. Therefore, sudden deafness can be misdiagnosed as eustachian tube stenosis and delay treatment. It should also be noted that the two diseases can occur together.
(ii) Meniere’s disease
Patients with sudden deafness are often associated with vertigo, but not repeatedly, with only one episode leading to the end of deafness; there is no dynamic change in low and mid-frequency hearing thresholds; and the positive rate of resonance phenomena is low. Although both may have terminal vestibular disorders, sudden deafness is sometimes associated with directional exchange nystagmus, with spontaneous nystagmus seen within 3 days of onset in the fast phase of vagal excitation toward the affected side, followed by a shift to paralytic nystagmus in the fast phase toward the healthy side. Resonance is almost always present in Ménière’s disease.
(iii) Auditory neuroma
Reviewing the literature, auditory neuromas presenting as sudden deafness are more common than generally recognized. Berg reported that 17 of 133 cases of auditory neuromas presented primarily as sudden deafness, and that four recovered auditory function before auditory neuroma resection, suggesting that patients with sudden deafness, even if they recover, must be excluded from the possibility of pontocerebellar horn tumors. Treatment principles for sudden deafness: Once sudden deafness is present, it should be treated urgently.
(I) General treatment
Patients should be hospitalized as much as possible, with bed rest and limited water and salt intake.
(II) 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.
(iii) Vasodilators
They are mainly used for sudden deafness caused by vascular lesions. Niacin is given orally, intramuscularly or intravenously. 1~2mg of histamine phosphate is added to 250ml of saline or 500ml of 5% glucose in a sedative drip (pay attention to the drip rate and patient’s reaction). Also used 0.1% procaine 250-500ml intravenous drip. ye also use poppy bases 60mg dissolved in 10% glucose 500ml intravenous drip, once a day, 10 times for a course, 3-5 days apart to start the second course, generally 3 courses. Or Ginkgo biloba preparations such as Jinadu, Ginkgo Damo, etc., Danshen injection treatment.
(iv) Heparin
It has been proposed that sudden deafness is often accompanied by excessive blood coagulation. Heparin has the function of inhibiting the formation of thrombin from prothrombin, 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 drug in the treatment of 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 into 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 method). However, it should be used with caution or contraindicated for patients with bleeding tendency, severe hypertension and liver disease. Dicoumarin, dicoumarin ethyl acetate and acetone benzyl hydroxy dicoumarin also have similar effects.
(E) Low molecular dextran
It 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.
(F) Hormonal drugs
Some people believe that early application is more effective, including ACTH, prednisone, prednisolone and dexamethasone. Corticosteroids are effective for nerve damage and viral-induced post-snail deafness. ACTH can break down ATP into AMP, and circulating AMP can reduce platelet agglutination; ACTH also has the effect of breaking down triglycerides. 40u subcutaneously, along with heparin 10,000u subcutaneously, 2 or 3 times a week for two weeks, can inhibit or moderate vasculitis.
(vii) Urografin
Urografin is a water-soluble sulfone-containing contrast agent. It does not cross the blood-brain barrier when administered intravenously, and thus may not cross the blood-cochlear barrier. Its therapeutic effect on sudden deafness may be that its molecule fills the defect in the capillary wall, restores the damaged blood-cochlear barrier, restores the activity of Na+, K+, and ATPase, and thus re-establishes the cochlear potential, resulting in improved hearing. The Department of Otolaryngology of Shanghai Sixth People’s Hospital treated 35 cases of sudden deafness with pantothenic glucosamine by intravenous injection of 60% pantothenic glucosamine or by adding it to 5% glucose solution as intravenous drip. Danshen injection was applied at the same time. There were 17 cases with significant effect, 7 cases with progress and 11 cases with no effect. The iodine allergy test must be done before using the drug.
(H) Mixed oxygen therapy
Carbon dioxide is an effective vasodilator, and cerebral blood flow can be increased by 30% to 70% after inhalation of carbon dioxide. Animal experiments show that cerebral blood flow increases after 10min, 20min and 30min inhalation, and arterial oxygen supply increases, confirming that 5% CO2 plus 95% O2 mixed oxygen is beneficial to improve cerebral oxygen metabolism. Murata et al. reported that the partial pressure of exolymphatic oxygen increased from 5.04 kPa (37.8 mmHg) to 18.16 kPa (136.2 mHg) after inhalation of 5% CO2-95% for 29 to 21 min. Carbon dioxide also promotes oxygen separation from hemoglobin, which facilitates oxygen transport to the local hypoxic area. Ma Weili et al. treated 34 cases of sudden deafness with mixed oxygen by 30 min per hour for 7 h per day for 3 days, and those who needed to continue treatment for 4 h per day. 71% efficiency. After stopping the treatment, vasodilators were applied to consolidate the effect.
(ix) Hyperbaric oxygen therapy
Li Zhengyan et al. concluded that the principle of hyperbaric oxygen therapy for sudden deafness is
①Increase the partial pressure of oxygen, increase the amount of physical dissolved oxygen in plasma and blood oxygen diffusion rate. 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 that site under hyperbaric pressure.
②In 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, tissue oxygenation still increases due to increased blood oxygen levels, while vasoconstriction improves or prevents inner ear tissue edema, exudation and hemorrhage. They treated 100 cases of sudden deafness with this method with an efficiency of 78%.
(x) Stellate ganglion block
Stellate ganglion block is used to cause reflex dilatation of the capillaries in the inner ear, thus improving inner ear circulation. Wu Runsheng reported that 28 cases of sudden deafness were treated with stellate ganglion closure with an efficiency of 75%.
(XI) Physiotherapy
Microwave therapy has the effect of activating blood circulation and improving microcirculation in the inner ear. Wu Runsheng treated 15 cases of sudden deafness with salvia injection and internal use of Ge Gen Tang and microwave therapy, with an efficiency of 80%. Prevention and recuperation
1. Patients with sudden deafness should rest at home and avoid exposure to noise or excessive sound. Keeping the home environment neat and tidy and the patient in a relaxed mood will be conducive to recovery.
2.Prevent colds, some patients with sudden deafness may be indirectly related to colds, so preventing colds can reduce a morbidity factor.
3. Don’t overexert yourself, do not overexert yourself, and do not overexert yourself. This disease mostly occurs in middle-aged people, so middle-aged people should pay more attention to this point.
4, emotional stability, avoid anger and ecstasy, because these can cause the imbalance of neurohumoral regulation in the human body, resulting in blood circulation disorders in the ear and deafness.