Acoustic trauma (AT) is characterized by severe hearing loss in the after long-term exposure to elevated noise levels or after a singular traumatic acoustic event, for example an explosion. An episode of AT is often preceded and accompanied by tinnitus. AT caused hearing loss is irreversible but can be prevented entirely by proper acoustic protection measures and avoiding noisy environments. Treatment of AT must focus on the preservation of remaining hearing function mainly by avoiding further noise exposure and on the prescription of adequate hearing aids.
The main symptom for an acoustic trauma (AT) is progressive hearing loss, oftentimes accompanied by tinnitus, which may also be chronic. Hearing loss due to AT typically starts at high-pitched frequencies and spreads to lower frequencies later. The following consensus criteria provide a both a qualitative and quantitative guideline for AT caused hearing loss symptoms : high-frequency losses are typically smaller than 75 dB, whereas low-frequency losses are seldom greater than 40 dB. Hearing loss is always greater for sound frequencies greater than 3-5 kHz than for the frequency range between 0.5 and 2 kHz. AT often presents with a hearing loss notch in the sound spectrum located around 4 kHz. Hearing loss will always progress unless noise exposure is stopped. In stable noise exposure, AT caused hearing loss stabilizes after about a decade with a slower rate of progression in later stages, is irreversible, always sensorineural and almost always bilateral.
Patients will first present with tinnitus, have problems following nearby conversations and feel as if their ear was congested after noise exposure. Furthermore, patients will gradually find it increasingly challenging to engage in conversations. AT is often ignored in early stages. If left untreated, AT can have severe impacts on the mental health of patients and their social lives. In such cases, depressions, social isolation, anxiety, paranoia, and poor self-esteem have been reported     as well as relationship problems   and business-related angst .
The first step in building an AT diagnosis is a thorough understanding of the patient's lifestyle and history. Crucial factors are the patient's (former) professional occupation(s), which may involve permanent noise exposure in selected industry jobs or in the music industry  and the patient's pastime habits and hobbies, which may include listening to loud music or watching TV at a high volume. Weapon aficionados and soldiers as well as veterans may have developed AT during service . If the patient has recently witnessed an exceptionally loud event in immediate proximity, the patient may suffer from acute AT.
The next step is a routine examination of the ear, in particular of the tympanic membrane and of the external auditory canals to rule out other aural conditions conducive to hearing loss. A neurologic examination may also be advisable in selected cases.
The only irrefutable way to diagnose AT is a detailed audiometric test. Pure-tone audiometry (PTA) in the standard octave intervals should be performed with a special focus on the interval around 3 kHz. Furthermore, speech reception thresholds should be measured for each ear. In order to rule out suspected pseudohypoacusis in selected patients, more objective tests like cortical evoked response audiometry (CERA) or brainstem electric response audiometry (BERA) should be taken into consideration  .
AT cannot be cured. The earlier treatment starts, the better the odds to prevent further hearing loss .
Hearing loss can be compensated by fitting appropriate hearing aids. Further progression of AT can be efficiently tackled by protective earplugs and are usually provided by employers. In severe cases of hearing loss, a patient should be advised to learn sign language. Progression of AT should be carefully monitored with regular audiometric checks. Patients should be encouraged to monitor their daily noise exposure with appropriate devices and avoid sounds louder than 85 dB.
Intravenous infusions of Sermion or Cavinton after an acute AT have been reported to relieve acute tinnitus symptoms . Administration of magnesium has been implicated to have a preserving effect on remaining hearing functions and also provides an efficient relief of tinnitus symptoms in humans . Combinations of hyperbaric oxygenation therapies with administration of corticoids have also provided promising treatment results in acute AT . Experimental treatments with the cell-permeable c-Jun N-terminal kinases (JNK) ligand AM-111 and stem cells may also be viable method of choice in the future  .
AT related hearing loss is irreversible. The only way to prevent further hearing loss is to avoid further noise exposure. If protective measures are insufficient or omitted by the patient, further hearing loss may lead to the compulsive use of hearing aids or the necessity to learn sign language.
AT is caused by either long-term noise exposure both in professional and in private life over 85 dB or by excessively loud blasts. Continuous exposure to 100 dB can lead to a hearing loss of up to 19 dB on the timescale of four decades.
Unprotected use of everyday devices, for instance e.g. leaf blowers, lawn mowers, chain saws and motorcycles, may also lead to slowly progressive AT, rock concerts have been shown to be able to cause AT both in musicians and concert attendees .
AT is on the decline in industrialized countries, since working people at risk are getting increasingly aware of the fact that noise protection is imperative in their jobs . AT is most prevalent in developing countries. Males are more prone to suffer from AT than females. It is not clear, if this observation is due to increased noise sensitivity or to increased noise exposure for men in their daily lives. AT susceptibility is independent of age . In the US, 5-10 million people are estimated to be at an increased risk of acquiring AT because of their lifestyle .
Pathological changes in AT can be inferred from experiments with animals, which get exposed to loud noises. Anatomic changes typically involve distortions of the stereocilia of the inner and outer hair cells and the rupture of the Reissner membane. In the immediate aftermath of the noise pulse, edema of the stria vascularis may develop. AT can also invoke an immune reaction in the form of a cochlear inflammation and substantial recruitment of leukocytes to the inner ear .
High amplitude sound waves have a destructive effect on the stereocilia of hair cells that can lead to a partial to complete loss of the hair cell mechanoexcitability and also to stereocilia loss conducive to hair cell apoptosis  and hair cell phagocytosis by epithelial supporting cells .
AT is entirely preventable. Raising awareness in the general public about detrimental side effects of loud noise in pastime activities and providing adequate sound protection for workers at risk are paramount to achieve declining statistics in new AT cases. Quantitative noise measurements can be carried out to reliably assess noise levels everywhere and at any time.
Acoustic trauma is a condition of irreversible hearing loss mainly caused by lifestyle factors. It often presents with tinnitus symptoms and could be entirely prevented with adequate noise protection. Acute tinnitus symptoms can be efficiently tackled but hearing loss typically persists. Treatment efficiency in acute acoustic trauma is highest if patients seek professional help immediately. Patients should be strongly advised to protect their ears from noises louder than 85 dB at all times. Hearing aids may be necessary to ease symptoms. In extreme cases, sign language classes should be advised.
Acoustic trauma occurs either after prolonged exposure to loud sounds or after traumatic events like explosions or gunshots. If you hear a permanent ringing in your ear or find it increasingly harder to understand conversations, you should seek professional help. You should avoid loud noises at all times to prevent further hearing loss. Doctors may advise you to wear hearing aids or learn sign language.