For the purposes of this CPG, hazardous noise is defined as impact noise or impulse noise greater than (140dB, ex small caliber gunfire).4 At these levels, Service Members are at elevated risk for acoustic trauma and subsequent hearing loss (HL). Patients exposed to blasts are at risk for both aural and acoustic trauma.5-7 Here we outline acoustic and aural injuries and provide further clinical guidance and importance of treatment and timing.

Hazardous noise may cause injury to the hearing mechanisms in the inner ear. Symptoms of acoustic trauma may include hearing loss, tinnitus (ringing in the ear), aural fullness, recruitment (ear pain with loud noise), difficulty understanding speech, difficulty localizing or finding sound sources, difficulty hearing in a noisy background, and vertigo. Acoustic trauma may result in sensorineural hearing loss (SNHL) that is either temporary (temporary threshold shift, TTS) or permanent (permanent threshold shift, PTS). A TTS resolves over time; audiometric testing should be completed to monitor and confirm whether this was partial or complete resolution of thresholds. While the time frame for hearing recovery is unique in every case, any SNHL that persists beyond eight weeks after injury is most likely permanent and should be considered a PTS. There are no clinical predictors for which patients with TTS will persist, and develop PTS.

The ear, specifically the tympanic membrane (TM), is the most sensitive organ to primary blast injury (PBI). Blast exposures can perforate the TM. Risk of injury is determined by the intensity of the blast, proximity to the source of the blast, as well as factors related to secondary, tertiary, and quaternary blast effects.8 The signs and symptoms of a TM perforation include the signs and symptoms of acoustic trauma listed above as well as pain, bloody ear discharge, dizziness, and conductive hearing loss (CHL) which is the result of a decrease of sound energy transmission through the middle ear to the inner ear. TM perforations heal spontaneously in 80 to 94% of cases.9 The smaller the size of the TM perforation, the greater the likelihood is of spontaneous closure. Most TM perforations that close spontaneously do so within the first eight weeks after injury.10,11 For these reasons, perforation rates in mass casualty situations may be under-reported when limited resources are utilized for more significant polytraumatic cases. TM perforation may likely be included in the non-immediate injuries deferred for later evaluation during which interval spontaneous healing may occur.12

The ossicular chain may be injured because of PBI, with fracture of the ossicles or disarticulation of the chain, both of which can result in CHL with or without SNHL. TM perforations and middle ear injuries may heal with scarring that stiffen the TM or ossicular chain, also resulting in CHL. The combination of a CHL with a SNHL is called a mixed hearing loss.

The temporal bone may also be fractured as a result of higher order blast injury, often associated with secondary or tertiary blast effects.13 Patients with temporal bone fractures may have lacerations in the ear canal, along the TM, or within the middle ear resulting in either bloody otorrhea or hemotypanum (blood behind the TM).12 They may also have SNHL or CHL, depending on the orientation of the fracture. A small number of these fractures (15%) will have an associated cerebral spinal fluid (CSF) leak.14 CSF leaks to the middle ear, mastoid cavity, and/or external auditory canal can become symptomatic as CSF otorrhea (a leak of fluid from the ear canal), CSF rhinorrhea (leak of fluid from the nose, typically unilateral and on the side of the temporal bone fracture), or as CHL from a middle ear CSF effusion. The risk of meningitis within the first seven days post injury ranges from 5-11% but increases to as high as 88% if a persistent leak is left untreated over time; therefore broad spectrum antibiotic prophylaxis and expert consultation are recommended.15-18 Testing otorrhea or rhinorrhea to distinguish between patients with bloody drainage containing CSF from those who have bloody drainage without CSF is insensitive, unless an assay for β2-transferrin (a protein unique to CSF) is obtained. This is unlikely to be available in the deployed setting. There are other, less sensitive, and specific bed-side techniques that can assess for CSF drainage, but assessment for β2-transferrin is considered the gold standard. Spontaneous closure of CSF leaks occurs in greater than 90% of cases and is facilitated by bed rest with the head of bed elevated, anti-strain precautions, and stool softeners. Leaks that fail to spontaneously recover should be considered for lumbar drainage of CSF. Surgical management of CSF leaks should be considered in cases of CSF otorrhea or rhinorrhea that does not close with other measures.19

The facial nerve can be injured in temporal bone fractures.20 Acute management of intratemporal facial nerve injury is to provide objective documentation of facial movement using a standardized grading scale, such as the House-Brackmann grading scale, the Sunnybrook Facial Grading Scale, or another facial nerve standardized grading scale.21,22 Complete immediate paralysis of the face portends more significant injury to the nerve and should be referred for evaluation and possible surgical decompression to optimize outcomes for facial function. If indicated, decompression should occur within two weeks of injury for optimal results -this short window necessities expedited consultation. Delayed onset of facial paralysis after trauma is typically the result of an inflammatory cascade and may result in significant weakness of the motor function approaching complete paralysis; however, this will often recover completely without surgical intervention. Incomplete or complete facial paralysis that preclude eyelid closure should be managed with measures that include eye protection (eye lid taping to ensure complete closure, ophthalmic tear substitutes and protective ointment). For significant facial paresis/paralysis, early administration of steroids should be provided, if not contraindicated, and expeditious referral to an otolaryngologist for management is indicated.23

Dizziness expressed as unsteadiness or vertigo (spinning sensation) following a blast injury can be a result of traumatic brain injury, but is also often caused by injury to the inner ear - specifically benign paroxysmal positional vertigo (BPPV), damage to sensitive neuroepithelial receptors within the inner ear, and perilymphatic fistula.24 Other inner ear abnormalities may cause vertigo such as otic capsule violating temporal bone fractures, secondary infections of the inner ear or vestibular nerves, trauma induced endolymphatic hydrops, and activation of subclinical superior semicircular canal dehiscence.