bubble_chart Overview

Sudden deafness, also known as idiopathic deafness or sudden deafness, refers to the unexplained sudden onset of tinnitus and deafness in the absence of prior symptoms, with hearing rapidly deteriorating to its peak within hours or days. It mostly affects one ear, with a higher incidence in adults aged 40-60. Bilateral cases account for 1%, and it is more common in males, with a higher occurrence in spring and autumn. According to Byl's statistics (1977), the incidence rate is 10.7 per 100,000. Data from Beijing Tongren Hospital's audiology clinic shows it accounts for 4.8% of initial sensorineural deafness cases. Recent domestic and international literature suggests a gradual increase in the prevalence of this condition.

bubble_chart Etiology

Before the onset of the disease, emotional stimuli such as anger, depression, and sadness, as well as triggers like fatigue, alcohol consumption, pregnancy, and changes in environmental air pressure and temperature, are often observed. According to literature reports from the past decade, there are no fewer than 200 types of disease causes. Morrison (1976) estimated that central sexually transmitted diseases account for 50%, retrocochlear lesions for 17%, trauma for 10%, and idiopathic cases for 23%. The idiopathic sexually transmitted disease causes are detailed below:

1. **Viral Infections** Most patients have a history of upper respiratory tract infection within one month before onset. Reports indicate that the incidence of sudden deafness in upper respiratory tract infections ranges from 8% to 30%. Serological and viral isolation methods have confirmed that viruses such as mumps virus, measles virus, influenza and parainfluenza viruses, and adenovirus type III can cause viral endolymphatic labyrinthitis, while herpes zoster virus can cause viral neuronitis and ganglionitis. The routes of viral entry into the inner ear are: ① Through the bloodstream into the inner ear. ② From the subarachnoid space via the cochlear aqueduct into the inner ear. ③ Diffusion through the middle ear mucosa into the inner ear. After infection, the virus proliferates extensively, adhering to red blood cells, causing sluggish blood flow and a hypercoagulable state. Additionally, the virus can induce vascular membrane edema, making vascular embolism highly likely, leading to impaired inner ear blood supply and cell necrosis.

2. **Inner Ear Vascular Lesions** In patients with diabetes, hypertension, arteriosclerosis, and cardiovascular diseases, the inner ear vascular matrix is more prone to spasms and thrombosis. This explains why factors such as fatigue and anxiety often trigger the condition. In recent years, observations of sudden deafness patients regarding blood lipids, cholesterol, and rheograms have not identified significant correlations with the disease. Wright (1975) reported a case of sudden deafness following cardiopulmonary bypass surgery, while Zhong Naichuan (1980) reported two cases of polycythemia-induced sudden deafness in the northwestern plateau, serving as examples of sudden deafness caused by inner ear vascular embolism.

3. **Inner Ear Window Membrane Rupture** Actions such as sneezing, nose blowing, vomiting, sexual intercourse, and diving can cause a sudden increase in venous pressure and cerebrospinal fluid pressure. Besides rupturing the cochlear and vestibular window membranes, these actions can also lead to ruptures of the vestibular membrane, tectorial membrane, and endolymphatic sac. Individuals with potential congenital inner ear malformations are more susceptible. This can result in ionic imbalance in the lymph fluid and cellular toxicity. Excessive endolymph in Ménière's disease can also cause cochlear window rupture, leading to sudden deafness.

bubble_chart Pathological Changes

Schuknecht (1962) observed the histological changes in the temporal bones of four cases of sudden deafness, and Saito's animal experiments (1986) also found that the pathological changes of sudden deafness manifested as labyrinthine membrane-like damage, primarily affecting the outer hair cells, with the basal turn of the cochlea being the most severely affected. Perivascular edema was present, neuroepithelial cells were necrotic, and the spiral organ could disappear. The saccule and utricle might also be involved, but the damage to the semicircular canals was relatively mild.

bubble_chart Clinical Manifestations

Symptoms often occur in the evening or upon waking. Initially, patients experience low-frequency or high-frequency tinnitus in one ear, followed by sudden hearing loss within hours. The progression from partial to complete deafness may take hours or days. Half of the patients experience vertigo, often feeling a spinning sensation on the affected side, with severe cases accompanied by nausea and vomiting. The degree of deafness is usually proportional to the severity of vertigo. Vertigo typically subsides within a week, and about one-third of patients may gradually recover their hearing within 1–2 weeks. If hearing does not recover within a month, it often results in permanent sensorineural deafness.

bubble_chart Diagnosis

Based on a history of no previous tinnitus or deafness, sudden onset of tinnitus and deafness that rapidly peaks in severity, with half of the cases accompanied by vertigo, diagnosis is generally straightforward. However, differentiation from Ménière's disease is sometimes necessary. In the early stages of Ménière's disease, hearing loss is minimal, exhibits a fluctuating hearing curve, and typically does not exceed 60dB, whereas in the former condition, hearing loss often exceeds 60dB. This condition presents four types of hearing curves: high-frequency, low-frequency, mixed high-and-low frequency, and total deafness. Flat-type curves account for 70% of cases, and recruitment phenomenon is observed in 60%. Vestibular function impairment is less common, with 80% of cases showing normal function. To rule out acoustic neuroma, X-ray imaging of the internal auditory canal or CT scanning of the cerebellopontine angle should be performed. Additionally, a comprehensive systemic examination is necessary to exclude conditions such as hypertension, diabetes, syphilis, and blood disorders. If feasible, viral isolation tests should be conducted within three weeks of symptom onset.

bubble_chart Treatment Measures

1. Acute phase (early stage): For those with severe vertigo, sedatives and antiemetics such as diazepam, chlorpromazine, or scopolamine should be used. Prostaglandin E₁ 60μg, which has the effect of dilating peripheral small blood vessels and inhibiting platelet aggregation, along with ATP 80mg, can be dissolved in 250ml of low-molecular-weight dextran and administered intravenously over 90 minutes. Dexamethasone 5–10mg may also be added for intravenous drip.
2. Vasodilators: Since most cases are caused by vascular embolism or spasms leading to insufficient blood supply, large doses of vasodilators should be used. For example, Salvia 16–18g dissolved in 500ml of low-molecular-weight dextran, or 654-2 30–40mg dissolved in 500ml of 5% glucose solution, or histamine 2.75mg dissolved in 500ml of normal saline, administered intravenously. Morimitsuo (1976) advocated the use of 10ml of 60% contrast agent meglumine diatrizoate for daily intravenous injection, with 30 injections constituting one course. An iodine allergy test should be performed first; if negative, an initial dose of 2ml is administered, and if no reaction occurs, 10ml can be used. It is said that sudden deafness is caused by damage to the blood-cochlear barrier, and meglumine diatrizoate molecules can fill the gaps in this barrier, reactivating the sodium pump and restoring the cochlear CM potential, with an efficacy rate of 52–86%.
3. Hyperbaric oxygen therapy: Hyperbaric oxygen chamber therapy can be used to increase blood oxygen partial pressure and enhance cellular metabolism. Alternatively, inhalation of 95% pure oxygen and 5% carbon dioxide may yield better results.
4. Anticoagulant and thrombolytic drugs: Anticoagulants such as heparin 200mg intramuscularly twice daily may be used, though some scholars oppose their use. Ahylysantinfarctase can reduce plasma fibrinogen concentration and decrease platelet adhesion, dissolving acute thrombi. The dosage is 0.5U per dose, dissolved in 250ml of 5% glucose saline, administered intravenously once daily. Dipyridamole 75mg can be taken orally three times daily. This drug selectively inhibits viral RNA and DNA synthesis, suppressing viral proliferation, and is effective for cases caused by viral infections. As it may also inhibit adenosine metabolism and increase intracellular cAMP levels, it has additional effects of inhibiting platelet aggregation and reducing adhesion.
5. Others: Neurotrophic drugs such as vitamin B1, vitamin B12, citicoline, energy mixtures, and Chinese medicinals can be tried. In the early stage, cervical stellate ganglion block may also be attempted.
6. Surgical treatment: If the medical history suggests round window membrane rupture, or if the only hearing ear is affected with no signs of recovery, surgical exploration may be considered. If tympanic exploration reveals window membrane rupture, fascia membrane repair can be performed.

bubble_chart Prognosis

Currently, there are many treatment methods available domestically, with efficacy rates mostly around 75%. Some reports indicate that nearly one-third of untreated patients can recover spontaneously. For patients with hearing loss exceeding 90 dB, severe high-frequency hearing loss, age over 40, absence of stapedius reflex, or accompanied by severe vertigo, hearing recovery is often unsatisfactory. Additionally, the prognosis is poor for those with a disease course exceeding one month.