For the purposes of this CPG, Service Members exposed to hazardous noise is impact noise or noise greater than (140dB) are at high risk for acoustic trauma and subsequent Hearing Loss (HL). Patients exposed to blasts are at risk for both aural and acoustic trauma.(3-5)
Hazardous noise causes injury to the hearing mechanisms in the inner ear. The symptoms of acoustic trauma are: hearing loss, tinnitus (ringing in the ear), aural fullness, recruitment (ear pain with loud noise), difficulty localizing sounds, 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 will resolve with time, while the time frame for hearing recovery is unique in every case, any SNHL that persists beyond 8 weeks after injury is most likely permanent and should be considered a PTS. There are no clinical predictors for which patients with a TTS will persist to develop PTS.
The ear, specifically the tympanic membrane (TM), is the most sensitive organ to primary blast injury (PBI). Blasts can perforate the TM. Risk of injury is determined by proximity to the source of the blast, as well as factors related to secondary, tertiary, and quaternary blast effects.6 The signs and symptoms of a TM perforation include the signs and symptoms of SNHL as well as pain, bloody ear discharge, and conductive hearing loss (decreased ability to transmit sound through the middle ear to the inner ear,). TM perforations heal spontaneously in 80 to 94% of cases.7 The smaller the size of the TM perforation, the greater the likelihood is of spontaneous closure. The majority of TM perforations that close spontaneously do so within the first 8 weeks after injury.(8,9) For these reasons, perforation rates in mass casualty situations may be under reported when limited resources are utilized for more significant polytraumatic cases. Because the tympanic membrane may be more at risk for damage than other body systems, it may likely be included in the non-immediate injuries deferred for later evaluation during which interval spontaneous healing may occur.10 The more significant exposures are manifest in the immediate triage and may be the tympanic membrane perforations that are more refractory to spontaneous healing as noticed in the Boston marathon bombing where proximity to blast and significant nonotologic injuries were predictors of perforation.11
The ossicular chain may be injured as a result 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 stiffens the ossicular chain also resulting in CHL. Blasts are noise hazards as well as explosive threats. 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, and these often are associated with secondary or tertiary blast effects.12 Patients with temporal bone fractures may have lacerations in the ear canal or along the TM, resulting in either bloody otorrhea or hemotympanum (blood behind the TM).13 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 These are termed CSF otorrhea (a leak from the auditory canal) or CSF rhinorrhea (a leak from the nose). The risk of meningitis within the first 7 days post injury ranges from 5-11%, but increases to as high as 88% if left untreated over time; therefore broad spectrum antibiotic prophylaxis and expert consultation are recommended.(14-17) Testing otorhinorrhea to distinguish between patients with bloody drainage containing CSF from those who have bloody drainage without CSF is insensitive unless assay for beta2-transferrin (a protein unique to CSF) is obtained, which is unlikely to be available in the deployed setting. Spontaneous closure of CSF leaks occurs in greater than 90% of cases, and is facilitated by bed rest – head of bed elevation - anti-strain precautions and stool softeners. Failures should be considered for lumbar drainage of CSF. Surgical management of CSF leaks should be considered in CSF otorhinorrhea that does not close with other measures.18
The facial nerve can be injured in temporal bone fractures.19 Acute management of intratemporal facial nerve injury is to provide objective documentation of facial movement using the House-Brackmann grading scale.20 Complete immediate paralysis of the face portends more significant injury to the nerve and should be referred for evaluation and possible surgical decompression to improve optimal outcomes for facial function. Significant weakness approaching complete paralysis will often recover completely. Incomplete or complete facial paralyses that preclude eyelid closure should be managed with measures that include eye protection (eye lid taping, ophthalmic tear substitutes and protective ointment). For significant facial pareses/paralyses, early administration of steroids should be provided if not contraindicated, and referral for management by an otolaryngologist is indicated.21
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 rests within the inner ear, perilymphatic fistula, and other.22 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.