Acoustic trauma

Acoustic trauma is an acute injury of the inner ear and, less often, of the tympanic membrane, produced by a single very intense sound such as a blast, gunshot, firecracker or a sudden burst of loud shouting.声创伤是由爆炸、枪击、爆竹或突然的高声喊叫等单次极强声音引起的内耳急性损伤，鼓膜损伤相对少见。

It is distinguished from chronic noise-induced hearing loss by the impulsive character of the exposure, and it is an otological emergency because treatment started within days can preserve hearing.它与慢性噪声性听力损失的区别在于暴露为脉冲性，属耳科急症，因为数日内开始治疗可保住听力。

Terminology and classification

• The term covers impulsive exposures above roughly 130 to 140 decibels peak sound pressure level, whereas continuous occupational noise acts over years and is classified separately as noise-induced hearing loss.该词涵盖峰值声压级约 130 至 140 分贝以上的脉冲暴露，而持续的职业噪声经年累月作用，另归为噪声性听力损失。
• ICD-10 assigns H83.3 for noise effects on inner ear, and the WHO 2025-01 mapping carries that category to ICD-11 code AB37 with the same title.ICD-10 将其归入内耳噪声效应的 H83.3，WHO 2025-01 映射表将该类别对应到标题相同的 ICD-11 编码 AB37。
• In the ontology it corresponds to MONDO:0013098 for noise-induced hearing loss, and the related susceptibility trait is catalogued as MONDO:0957560.在本体中它对应噪声性听力损失的 MONDO:0013098，相关易感性性状登记为 MONDO:0957560。
• The cardinal phenotypes are HP:0000365 for hearing impairment and HP:0000360 for tinnitus, the two symptoms that define the clinical presentation.核心表型编码为听力受损 HP:0000365 与耳鸣 HP:0000360，二者界定了临床表现。
• Interoperability anchors include MeSH D006316 for hearing loss of noise-induced type and Wikidata Q2230578, while the disorder is absent from Orphanet because it is not a rare disease.互操作锚点包括噪声性听力损失的 MeSH D006316 与 Wikidata Q2230578，该病不属罕见病，故 Orphanet 无条目。
• The older literature separates acute acoustic trauma from chronic noise-induced hearing loss by the presence of a single exposure event, and this distinction drives both coding and compensation claims.较早文献以是否存在单次暴露事件区分急性声创伤与慢性噪声性听力损失，这一区分同时影响编码与赔偿认定。

History

• John Fosbroke described gunner's ear in 1831 among artillerymen, recording deafness and tinnitus after cannon fire and probably the first clinical account of impulsive acoustic injury.John Fosbroke 于 1831 年描述炮手耳，记录炮兵在火炮射击后出现耳聋与耳鸣，这大概是对脉冲声损伤最早的临床记述。
• Thomas Barr coined boilermakers' deafness in 1886, linking the hammering of rivets in shipyards to a characteristic high-frequency hearing loss.Thomas Barr 于 1886 年提出锅炉工耳聋，把船厂铆钉敲击与特征性高频听力损失联系起来。
• Habermann's temporal-bone studies in the 1890s showed degeneration of the organ of Corti in noise-exposed workers, establishing a pathological rather than purely functional basis.Habermann 在 1890 年代的颞骨研究显示噪声暴露工人耳蜗螺旋器退变，确立了病理学而非纯功能性的基础。
• Scanning electron microscopy in the 1970s revealed fusion and disorganisation of stereocilia after impulse noise, and explained why hearing loss can persist with intact hair cells.1970 年代的扫描电镜揭示脉冲噪声后静纤毛融合与排列紊乱，解释了毛细胞仍存而听力持续下降的原因。
• The recognition that oxidative stress and glutamate excitotoxicity continue after the sound has stopped, described from the 1990s, shifted the field towards post-exposure pharmacological rescue.自 1990 年代起认识到氧化应激与谷氨酸兴奋毒性在声音停止后仍持续，使该领域转向暴露后的药物挽救。
• Military experience drove the term blast injury, and improvised explosive devices in Iraq and Afghanistan produced large cohorts with tympanic perforation, tinnitus and permanent threshold shift.军事实践催生了爆震伤一词，伊拉克与阿富汗的简易爆炸装置造成大批鼓膜穿孔、耳鸣与永久性阈移的伤员。
• The understanding of the 4 kHz notch was revised from a pure acoustic resonance artefact to a lesion of the basal cochlea determined by tonotopic vulnerability.对 4 千赫切迹的认识由单纯的声学共振假象修正为耳蜗底转病变，后者由频率拓扑的易损性决定。

Epidemiology

• Between 20 and 50 per cent of teenagers report exposure to sound levels high enough to cause acute acoustic trauma, according to surveys of recreational noise.据娱乐性噪声调查，20% 至 50% 的青少年报告曾暴露于足以造成急性声创伤的声级。
• Among more than 28 million Americans with some hearing impairment, as many as 10 million have loss attributable in part to excessive noise at work or at leisure.在超过 2800 万有某种听力损害的美国人中，多达 1000 万人的听力损失部分归因于工作或休闲中的过度噪声。
• WHO estimates that over 1 billion young people are at risk from unsafe listening, and that 430 million people worldwide already have disabling hearing loss.WHO 估计超过 10 亿年轻人面临不安全聆听的风险，全球已有 4.3 亿人存在致残性听力损失。
• Hearing loss and tinnitus are the commonest service-connected disabilities among United States veterans, and blast exposure is the leading identified cause.听力损失与耳鸣是美国退伍军人中最常见的服役相关残疾，爆震暴露是首要的可识别原因。
• The risk rises steeply above 85 decibels averaged over eight hours, and the permitted exposure time halves for every three decibel increase under occupational standards.八小时平均声级超过 85 分贝后风险陡增，按职业标准每增加 3 分贝，允许暴露时间减半。
• Male sex, young age, military or construction employment, firearm use and attendance at amplified music events are the best documented risk factors.男性、年轻、军人或建筑从业、枪械使用与参加高分贝音乐活动是证据最充分的危险因素。
• Data sources include WHO global hearing estimates, national occupational noise surveys and military audiology registries, and all three define exposure rather than diagnosis differently.数据来源包括 WHO 全球听力估计、各国职业噪声调查与军队听力学登记，三者对暴露与诊断的定义各不相同。
• Population burden is therefore expressed as attributable risk rather than disease prevalence, because most cases are never separately coded in routine statistics.因此人群负担以归因风险而非疾病患病率表达，因为多数病例在常规统计中从未单独编码。

Pathophysiology

• When sound exceeds about 132 decibels the organ of Corti can be sheared from the basilar membrane, and above roughly 184 decibels the tympanic membrane ruptures.当声音超过约 132 分贝时，螺旋器可自基底膜撕脱，超过约 184 分贝时鼓膜破裂。
• Impulse noise produces mechanical disruption of stereocilia, rupture of hair-cell tight junctions and mixing of endolymph with perilymph, with an immediate rise in auditory threshold.脉冲噪声造成静纤毛机械性断裂、毛细胞紧密连接破裂与内淋巴和外淋巴混合，听阈随即升高。
• Glutamate released in excess at the inner hair cell synapse overstimulates AMPA receptors and causes excitotoxic swelling of auditory nerve dendrites, a process that continues for hours.内毛细胞突触过量释放谷氨酸过度刺激 AMPA 受体，引起听神经树突兴奋毒性水肿，该过程可持续数小时。
• Reactive oxygen and nitrogen species generated during and after exposure damage mitochondrial DNA and membranes, and antioxidants given after the event reduce threshold shift in animal models.暴露期间及之后产生的活性氧与活性氮损伤线粒体 DNA 与膜结构，事件后给予抗氧化剂可减轻动物模型的阈移。
• The basal turn of the cochlea, which encodes 4 to 6 kilohertz, is most vulnerable to impulse injury, which is why the audiogram shows a notch at that frequency.编码 4 至 6 千赫的耳蜗底转最易受脉冲损伤，因此听力图在该频率出现切迹。
• A temporary threshold shift resolves over hours to days, but any sensorineural loss persisting beyond eight weeks is regarded as permanent and is labelled a permanent threshold shift.暂时性阈移在数小时至数日内恢复，而持续超过八周的感觉神经性损失被视为永久性，称为永久性阈移。
• Beyond the cochlea, blast waves can damage the vestibular end organs and cause perilymph fistula, and they may coexist with traumatic brain injury in the same patient.除耳蜗外，爆震波还可损伤前庭终器并造成外淋巴瘘，且在同一患者中可与创伤性脑损伤并存。

Clinical features

• Sudden hearing loss, often unilateral, is the presenting complaint, and it may be accompanied by a sensation of aural fullness and by distortion of loudness.突发听力下降常为单侧，是主要就诊主诉，可伴耳闷胀感与响度重振。
• Tinnitus is present in the majority and is usually high pitched, and recruitment, the painful perception of loud sounds, is common after cochlear injury.多数患者出现耳鸣，通常为高音调，耳蜗损伤后重振即对大声的痛性感受也常见。
• Vertigo, nausea and nystagmus suggest concomitant vestibular involvement, and their presence worsens the short-term prognosis for balance.眩晕、恶心与眼球震颤提示合并前庭受累，其出现使短期平衡预后变差。
• Tympanic membrane perforation, haemotympanum and ossicular disruption indicate a blast injury severe enough to require otoscopy and computed tomography.鼓膜穿孔、鼓室积血与听骨链中断提示爆震伤严重，需行耳镜检查与计算机断层扫描。
• Complications include chronic perforation, cholesteatoma, persistent tinnitus, hyperacusis, sound localisation failure and difficulty hearing in background noise.并发症包括慢性穿孔、胆脂瘤、持续耳鸣、听觉过敏、声源定位障碍与噪声环境下听辨困难。
• Children and young adults are over-represented in recreational cases, while service members and industrial workers dominate occupational and blast cohorts.儿童与青年在娱乐性病例中占比偏高，而军人及产业工人在职业与爆震队列中占主导。
• Bilateral simultaneous injury carries a much greater functional burden, and it should prompt assessment for central auditory involvement and for rehabilitation planning.双耳同时受伤造成更大的功能负担，应促使评估中枢听觉受累并规划康复。

Diagnosis

• Pure-tone audiometry is the cornerstone and typically shows a sensorineural notch at 4 to 6 kilohertz, with recovery at 8 kilohertz.纯音测听是基石，典型表现为 4 至 6 千赫的感觉神经性切迹，8 千赫处回升。
• Otoacoustic emissions are reduced or absent in the affected ear and can detect cochlear damage before the audiogram changes, which matters in early assessment.患耳耳声发射减弱或消失，可在听力图变化前检出耳蜗损伤，对早期评估有重要意义。
• Otoscopy and tympanometry are mandatory after blast exposure to identify perforation, haemotympanum or ossicular discontinuity.爆震暴露后必须行耳镜与鼓室压图检查，以识别穿孔、鼓室积血或听骨链中断。
• The differential diagnosis includes idiopathic sudden sensorineural hearing loss, Meniere disease, vestibular schwannoma, otosclerosis, mumps deafness and functional hearing loss.鉴别诊断包括特发性突发性感音神经性聋、梅尼埃病、前庭神经鞘瘤、耳硬化症、腮腺炎性聋与功能性听力损失。
• Idiopathic sudden deafness is distinguished by the absence of a noise event, and vestibular schwannoma by asymmetric loss with disproportionate speech discrimination and a retrocochlear pattern.特发性突发性聋以缺乏噪声事件区分，前庭神经鞘瘤则以不对称损失伴言语识别率不成比例下降及蜗后型表现区分。
• Magnetic resonance imaging with gadolinium is indicated when asymmetry is out of proportion to the exposure or when vestibular symptoms are progressive.当不对称程度与暴露不相称或前庭症状进行性加重时，应行钆增强磁共振检查。
• Diagnosis is often delayed because patients attribute hearing loss to earwax or infection, and delayed presentation reduces the chance of useful steroid rescue.诊断常被延误，因为患者把听力下降归因于耵聍或感染，而就诊延迟会降低激素挽救的有效机会。

Management

• High-dose systemic corticosteroids are started as soon as possible and are most effective when begun within 72 hours of the injury.应尽早开始大剂量全身糖皮质激素，在损伤后 72 小时内开始效果最好。
• Hyperbaric oxygen therapy combined with corticosteroids is used for acute acoustic trauma, and the combination has been reported effective when initiated within three days.高压氧联合糖皮质激素用于急性声创伤，据报告在三天内开始治疗有效。
• Intratympanic steroid injection is offered when systemic steroids are contraindicated or when hearing fails to improve after initial therapy.当全身激素禁忌或初始治疗后听力无改善时，可行鼓室内激素注射。
• Blast injury with perforation requires avoidance of water entry, antibiotic cover when infected and delayed myringoplasty after the ear has stabilised.伴穿孔的爆震伤需避免耳内进水、感染时使用抗生素，并在耳部稳定后延期行鼓膜修补。
• Hearing protection with correctly fitted earplugs or earmuffs and avoidance of further impulse noise are the core secondary prevention measures.正确佩戴耳塞或耳罩并进行听力防护、避免再次脉冲噪声暴露是核心的二级预防措施。
• Tinnitus is managed with cognitive behavioural therapy, sound therapy and hearing aids when hearing loss coexists, and these measures reduce distress rather than the sound itself.耳鸣采用认知行为治疗、声治疗，合并听力损失时使用助听器，这些措施减轻的是困扰而非耳鸣本身。
• Prognosis depends on the magnitude of the initial threshold shift, and recovery is good when the shift is under 30 decibels and treatment begins within three days.预后取决于初始阈移的幅度，阈移低于 30 分贝且治疗在三天内开始时恢复较好。
• Permanent loss is managed with hearing aids, assistive listening devices and, in profound bilateral cases, cochlear implantation.永久性损失以助听器、辅助聆听设备处理，双耳深度损失者可行人工耳蜗植入。

Research and controversies

• No drug has been approved for the prevention of noise-induced hearing loss, and candidates such as N-acetylcysteine, D-methionine and JNK inhibitors remain investigational.尚无药物获批用于预防噪声性听力损失，N-乙酰半胱氨酸、D-甲硫氨酸与 JNK 抑制剂等候选药物仍处研究阶段。
• The benefit of hyperbaric oxygen is debated because trials are small, heterogeneous in timing and often combine oxygen with steroids, so its independent effect is unresolved.高压氧的获益存在争议，因为试验规模小、时机不一且常与激素联合，其独立效应尚未确定。
• Occupational exposure limits differ between jurisdictions, with the United States using 85 decibels over eight hours and some European states applying 80 decibels, which produces divergent compensation outcomes.各地职业暴露限值不同，美国采用八小时 85 分贝，部分欧洲国家采用 80 分贝，导致赔偿结果分歧。
• Whether recreational listening through personal audio players causes permanent injury remains contested, because exposure estimates rely on self-report and dosimetry is rarely performed.通过个人音频设备进行的娱乐性聆听是否造成永久损伤仍有争议，因为暴露估计依赖自我报告，很少进行剂量测量。
• Repair research focuses on hair-cell regeneration with ATOH1 gene delivery and on synapse-protective agents that target the ribbon synapse, and none has reached clinical approval.修复研究聚焦于以 ATOH1 基因递送实现毛细胞再生，以及靶向带状突触的突触保护剂，尚无一项进入临床获批。