The human ear functions as a biological pressure transducer. Noise exposure is a significant global health issue, with approximately 5% of hearing loss in the worldwide population attributed to noise-induced hearing loss (NIHL). Perception of loudness varies based on individual sensitivity to noise and is influenced by the below-mentioned 3 key aspects of sound.
Sound pressure level (acoustic pressure level): This logarithmic measure quantifies the effective pressure of sound relative to a reference level, expressed in decibels (dB). Examples are provided below.
Party balloon rupture or jet engine: 150 dB.
Loudest human voice: 135 dB.
Typical pain threshold: 120 dB.
Hearing damage from long-term exposure (not necessarily continuous): 85 dB.
Frequency content.
Duration of sound.
Most individuals with normal hearing are particularly sensitive to sounds in the 2 to 4 kHz range, which corresponds to high-intensity impulse noises such as blasts. Human voices have fundamental frequencies, which represent the lowest frequency of a periodic waveform or the pitch in music, ranging from 90 to 155 Hz for males and 165 to 255 Hz for females. The sensitivity of the human ear varies based on perceived loudness at different frequencies.
A lesser-known subtype of NIHL is acute acoustic trauma (AAT), defined by sudden sensorineural hearing loss resulting from exposure to intense impulse noise, such as blasts or gunshots. This occurs when noise levels exceed the elastic limits of the auditory system, typically exceeding 140 dB for less than 0.2 seconds. In contrast, NIHL generally develops after prolonged exposure—lasting several minutes to hours—to intense sounds in the 100 to 120 dBA range, commonly found in workplaces or combat zones. AAT and NIHL often occur concurrently.
AAT often results from mechanical and metabolic injuries to the auditory system, causing symptoms such as hearing loss, tinnitus, otalgia, ear fluttering, pain, vertigo, and hyperacusis. Characteristic audiometric findings can be observed following AAT, and prompt recognition and referral to otolaryngology may help prevent permanent hearing impairment. Despite its distinct history and audiometric profile, AAT has not garnered as much research attention in the literature as NIHL. Additionally, patient awareness and urgency in seeking treatment for AAT are often low. Many individuals underreport AAT or continue to expose themselves to further trauma due to their responsibilities and circumstances, particularly in military settings. A retrospective study revealed that relatively few patients report symptoms immediately after the trauma, with most incidents occurring in military environments.
AAT may damage both the middle and inner ear, leading to issues such as tympanic membrane perforation, disruption of the ossicular chain, and direct injuries to the cochlear or vestibular apparatus from blunt force or ballistic trauma. The resulting hearing loss can be conductive, mixed, or sensorineural, though it is most commonly sensorineural. Accompanying symptoms may include vertigo, tinnitus, and pain. The extent of hearing impairment depends on factors such as noise intensity, duration of exposure, the adequacy of hearing protection used, and the individual’s genetic susceptibility.
Sensorineural hearing loss may be accompanied by a diminished sensitivity to specific frequencies, subtle difficulties in hearing in noisy environments, and bothersome sensations of ear ringing or fluttering. A classic presentation following AAT might involve a patient with an intact tympanic membrane but decreased hearing thresholds above 3 kHz after a blast, as intense weapon noise typically falls within the 2 to 5 kHz range. The sensory cells of the cochlea are particularly susceptible following AAT, with the initial structural change often being damage to the stereocilia bundle.
Sensorineural hearing loss can be either temporary or permanent. Individuals with this condition may no longer hear low-level sounds, while high-level sounds might still be perceived as equally loud by those with normal hearing. This phenomenon can be explained by the following 2 theories.
Loudness recruitment: An abnormally rapid increase in loudness.
Softness imperception: Soft sounds perceived by individuals with sensorineural hearing loss are louder than the faintest sounds heard by those with normal hearing.
Many insights regarding AAT can be drawn from similar clinical scenarios, such as sudden-onset sensorineural hearing loss and ototoxicity from chemotherapeutic agents. Both conditions share common mechanisms involving the development of reactive oxygen and nitrogen species, free radicals, and oxidative stress.
The most effective initial step in preserving hearing for patients exposed to AAT is hearing protection. Hearing protection devices (HPDs) can significantly reduce noise levels at these frequencies. HPDs can be classified as either passive or active. Both military and civilian leaders and clinicians strongly recommend using HPDs to prevent temporary threshold shifts and permanent hearing loss.
Passive Hearing Protection Devices
Passive HPDs rely on physical barriers without embedded electronics and function in 2 ways, as mentioned below.
Noise level–dependent HPDs:
These HPDs, such as solid earplugs, provide attenuation that varies with noise intensity.
Noise level–independent HPDs:
Provide consistent noise reduction across different frequencies and intensities.
Feature a narrow inner channel along the earplug’s length, causing acoustic impedance to increase nonlinearly with external sound.
Nonlinear HPDs reduce harmful impulse noise while allowing speech and softer sounds to remain audible for communication and safety.
Active Hearing Protection Devices
Active HPDs work differently, using noise reduction algorithms within electronic devices to cancel noise actively. These devices optimize the signal-to-noise ratio to enhance the desired result, such as speech and communication amid noisy environments. These devices combine passive components, such as physical barriers, with active elements, such as preamplifiers and microphones. Some models also feature external signal processors, operating switches, and volume controls for added functionality.
Active HPDs feature directional microphones that enhance communication and hearing protection. However, they can impair sound localization, particularly from behind—referred to as a soldier’s “6” in combat. The impact of blast-type noises varies based on proximity, device type, and whether the environment is open or enclosed. Diagnosing hearing loss from AAT requires audiological evaluation and access to high-quality equipment. Advances in technology, such as smartphone screening apps and audiometric headsets, may enhance future diagnostic capabilities.
Patients with suspected AAT presenting with symptoms such as acute tinnitus, muffled hearing, or ear fullness should undergo a comprehensive head and neck examination, including a detailed otologic evaluation, ideally with otomicroscopy. Audiometric testing is the primary diagnostic tool and should be performed if hearing loss persists beyond 72 hours. Cortical evoked response audiometry may be indicated for patients suspected of exaggerating their hearing loss.
Further noise exposure should be avoided, especially if vertigo accompanies the hearing loss, to prevent risks during activities like driving or operating heavy machinery. Absolute indications for otolaryngology referral include suspected temporal bone fracture, tympanic membrane perforation, persistent clear or discolored ear drainage that does not resolve within a few days, facial nerve paralysis, and hearing loss in a patient with a single functional ear.
The most significant challenges in AAT include the following:
Accurate diagnosis
Delays in seeking medical care (underreporting)
Repeat acoustic trauma
Blast-type noise
Concomitant prolonged noise exposure
Management of AAT should be personalized and initiated promptly. Treatment outcomes and prognosis vary, and patients should be informed that hearing recovery remains unpredictable, regardless of intervention.
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