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Hearing Impairment Among Soldiers: Special Considerations for Amputees

Chapter 14

HEARING IMPAIRMENT AMONG 

SOLDIERS: SPECIAL CONSIDERATIONS 

FOR AMPUTEES

DEBRA J. WILMINGTON, PhD*; M. SAMANTHA LEWIS, PhD†; PAULA J. MYERS, PhD‡; FREDERICK J. GALLUN, PhD§; 

and STEPHEN A. FAUSTI, PhD¥

INTRODUCTION

TYPES OF HEARING LOSS

DIAGNOSTIC TESTS

TREATMENT AND REHABILITATION

PREVENTION

SUMMARY

*

Research Investigator, National Center for Rehabilitative Auditory Research, Portland VA Medical Center, 3710 SW US Veterans Hospital Road, 

Portland, Oregon 97207; Assistant Professor, Department of Otolaryngology, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, 

Portland, Oregon 97239

†

Research Investigator, National Center for Rehabilitative Auditory Research, Portland VA Medical Center, 3710 SW US Veterans Hospital Road, 

Portland, Oregon 97207; Assistant Professor, Department of Otolaryngology, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, 

Portland, Oregon 97239

‡

Chief, Audiology Section, Department of Audiology and Speech Pathology, James A. Haley Veterans Hospital, 13000 Bruce B. Downs Boulevard, Tampa, 

Florida 33612; formerly, Pediatric Audiologist, All Children’s Hospital, Saint Petersburg, Florida

§

Research Investigator, National Center for Rehabilitative Auditory Research, Portland VA Medical Center, 3710 SW US Veterans Hospital Road, 

Portland, Oregon 97207; Assistant Professor, Department of Otolaryngology, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, 

Portland, Oregon 97239

¥

Director, National Center for Rehabilitative Auditory Research, Portland VA Medical Center, 3710 SW US Veterans Hospital Road, Portland, Oregon 

97207; Professor, Department of Otolaryngology, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, Oregon 97239
382

Care of the Combat Amputee

INTRODUCTION

Injuries to the ear were the single most common 

injury type reported among Marines during Operation Iraqi Freedom (OIF) through 2004, accounting 

for 23% of all injuries.1 One third of soldiers returning 

from Operation Enduring Freedom (OEF) and OIF 

were referred to audiologists for hearing evaluations 

because of exposure to acute acoustic blasts; 72% of 

those sustained hearing loss. Auditory disabilities 

represent one of the most prevalent service-connected disabilities, resulting in over one billion dollars 

in annual compensation. Acute blast trauma and 

resultant traumatic brain injury (TBI) make up 90% 

of the injuries seen at the Department of Veterans 

Affairs (VA) polytrauma rehabilitation centers, and 

an additional 11% to 28% of OEF and OIF troops may 

have mild TBI from blast exposure.2 Polytrauma patients require care for hearing impairment, vestibular 

pathology, vision loss, nerve damage, multiple bone 

fractures, wounds, psychological problems, and amputations.3

 Soldiers with amputations and hearing 

impairment present significant challenges because 

their injuries affect multiple systems, often impairing communication and cognition. In addition, each 

patient has distinctive psychosocial requirements 

that greatly impact pain management, adjustment 

to disability, body image perception, movement 

through the military disability system, and reintegration into the community or back to active-duty 

status.4 Furthermore, sensorineural hearing loss, unlike many other injuries, will continue to progress, 

creating greater impairment for the injured soldier. 

Early identification and treatment of hearing loss 

and vestibular impairment is essential to developing 

treatment strategies, ultimately leading to reduced 

cognitive deficits and improved rehabilitation outcomes and quality of life.5

For service members with limb loss, the types of 

hearing damage sustained are not fundamentally 

different from those that could accompany any other 

type of injury. Hearing loss can result from a blast 

injury, from explosion or weapon firing (acoustic 

trauma), or from ototoxic medications used to treat injuries. The combined effect of trauma, noise exposure, 

and ototoxic agents (such as solvents or medications) 

can also result in hearing loss or vestibular impairment. Complex polytrauma patients commonly 

have hearing and balance deficits, which are often 

initially overlooked. TBI patients with hearing loss 

can also be misdiagnosed as unresponsive.6 Clinical 

complaints from hearing-loss patients rarely occur 

until a communication problem becomes significant, 

indicating reduced audibility within the frequency 

range important for speech understanding (less than 8 

kHz). Also, vestibular problems can be misdiagnosed 

in patients with lower limb amputation because impaired balance may be attributed to the limb loss. It 

is essential that auditory and vestibular deficits be 

identified early for possible intervention and so medical care and rehabilitation can be facilitated. Otologic 

consultation or, at the minimum, an audiometric 

hearing evaluation should be performed on the basis 

of exposure, regardless of symptoms. Damage to the 

outer or middle ear results in a conductive hearing 

loss, which can usually be corrected medically or 

surgically. Inner ear damage can result in permanent 

sensorineural hearing loss. Some otologic symptoms, 

such as tinnitus and hearing loss, may be permanent 

consequences of a blast injury, and their effects on 

quality of life may be substantial.7

TYPES OF HEARING LOSS

Noise-Induced Hearing Loss

Sounds of a sufficient intensity and duration can 

cause temporary or permanent threshold shifts due to 

vascular, metabolic, and chemical changes of the hair 

cells of the cochlea and swelling of the auditory nerve 

endings. The stiffness of hair cell stereocilia can also 

decrease, which reduces the coupling of sound energy.8

Recovery from temporary threshold shifts can occur 

if the noise exposure is not prolonged, although short 

exposures to sounds of sufficient intensity (such as 

explosions) can cause immediate, permanent hearing 

loss. Harmful noise exposure results in cell death by 

necrosis and apoptosis (programmed cell death), and 

eventually leads to the degeneration of the corresponding nerve fiber. Acoustic trauma typically produces a 

unilateral hearing loss without associated middle ear 

damage. The susceptibility to noise-induced hearing 

loss between individuals varies as much as 30 to 50 

dB, possibly due to differences in ear anatomy and 

physiology, prior exposure to noise, and interactions 

with medications.8

Noise-induced hearing loss can occur as a result 

of steady-state or intermittent exposure to loud noise 

or from a single, impulsive exposure to a loud sound, 

such as an explosion (acoustic trauma). Steady-state 

exposure is usually symmetric, leading to bilateral 

sensorineural hearing loss, while some impulse noises, 
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Hearing Impairment Among Soldiers: Special Considerations for Amputees

such as gunshots, can produce an asymmetric loss. 

Both steady-state and impulse noise exposure cause 

excessive oxidative stress and the production of free 

radicals (molecules that exist independently in an 

unstable state). To stabilize itself, a free radical takes 

available electrons from adjacent molecules, leaving 

them oxidized and therefore damaged. These changes 

lead to permanent cell damage in the inner ear. In 

addition, concurrent exposure to other agents, such 

as tobacco, solvents, or heavy metals, may have a 

synergistic effect on cell damage.9 Soldiers in tactical 

situations who sustain acute noise-induced hearing 

loss may initially be unaware of it or delay reporting 

it because of the complexity of other injuries they 

have sustained, stress, fatigue, or the shock of the 

explosion.

Ototoxicity

Therapeutic drug regimens for infectious diseases 

and cancer can be ototoxic; nearly 200 prescription 

and over-the-counter drugs are recognized as having 

ototoxic potential and result in auditory or vestibular 

dysfunction. Ototoxicity causes irreversible cochlear 

damage and can occur in 60% to 70% of patients, often exacerbating preexisting hearing loss.10 Clinical 

symptoms of ototoxicity are those commonly associated with hearing loss, such as tinnitus and difficulty 

understanding speech in noise. Hearing loss due to 

ototoxic medications is sensorineural, bilateral, and 

usually initially presents at high frequencies, subsequently progressing to the lower frequencies.11–14 In 

addition, the effects of ototoxic drugs can continue 

well after cessation of therapeutic treatment. Previous noise exposure, almost universal in patients with 

blast injuries, increases the risk of ototoxicity.15 Some 

ototoxic drugs commonly used to treat amputees for 

drug-resistant organisms (eg, gentamicin or vancomycin) can damage the vestibular system, causing 

instability and dizziness (dizziness, which includes 

vertigo, imbalance, and lightheadedness, can manifest with nausea, vomiting, a recurrent tendency to 

stumble or fall, floating feeling, mild unsteadiness, 

or faintness).16

Variations in the behavioral hearing threshold and 

number of frequencies affected suggest that individual susceptibility to ototoxicity is determined by 

multiple biochemical, physiologic, and genetic factors.17 This individual susceptibility makes it difficult 

to determine which patients will experience ototoxic 

hearing changes and when the changes will occur. 

Therefore, high-frequency audiometry is essential 

to accurately identify and monitor ototoxic-induced 

hearing changes.

Audiologic Injury from Blast Exposure

Between 2003 and 2005, 68% of combat injuries in 

Afghanistan and Iraq were caused by explosions.6

When exposed to the blast wave of an explosion, 

the auditory system is vulnerable to both peripheral 

and central damage from the pressure wave itself, 

and from the secondary and tertiary effects of blown 

objects impacting the body and the blown body impacting stationary objects (Figure 14-1). Blast trauma 

usually lasts longer and is more intense than acoustic 

trauma and typically affects both ears. The extent 

of damage from the primary blast injury is usually 

inversely proportional to the distance away from 

the blast. Due to the physics of blast waves, location 

within an environment may change the severity of 

injury, regardless of distance. Gases heated within a 

confined space may also result in a sustained period 

of positive pressure, and therefore prolonged injury. 

In general, closed-space blast injuries result in a 

higher incidence of primary blast injury, greater mortality, and greater injury severity.18 Also, blast waves 

that are directed laterally to the head impact the 

auditory ear canal with a greater amount of energy, 

increasing the likelihood of ear injury. Permanent, 

pure sensorineural hearing loss is the most prevalent 

type of auditory impairment, occurring in 35% to 54% 

of blast injuries.19

One of the hallmark symptoms of unprotected blast 

exposure is injury to the tympanic membrane (TM) 

and, less frequently, to the ossicular chain. A ruptured 

TM indicates that a patient has undergone significant 

blast exposure and that further examination is warranted. The most common otologic complaints immediately following a blast are otalgia, tinnitus, aural 

fullness, dizziness, loudness sensitivity, distorted 

hearing, and hearing impairment. These complaints 

may last several minutes to several days. Hearingrelated complaints may be due to a temporary threshold shift if present less than a month, or considered 

a permanent threshold shift if present over a month. 

Peripheral and central auditory system injury can 

combine to produce complex symptoms. The type 

of acoustic trauma, proximity, orientation of the ear 

to the blast, environment (open or closed space), and 

degree of ear shielding should be noted, when possible, in a patient’s audiological case history.

Primary blast waves can cause concussions or mild 

TBI without a direct blow to the head by producing 

shock wave effects on the brain.20 Concussions can 

cause audiologic symptoms, such as hearing loss, 

dizziness, and central deficits. Computed tomography 

scans and magnetic resonance imaging can detect pathology in the internal auditory canal, membranous 
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Care of the Combat Amputee

labyrinth, and bony labyrinth, and can characterize 

petrous apex lesions. Temporal bone fractures often 

cause loss of audiovestibular function. Auditory 

brain areas in the temporal lobe, corpus collosum, 

and thalamus are vulnerable to damage from exposure to the mechanisms of blast injury. Dizziness and 

sensitivity to sound can be symptoms of vestibular, 

peripheral, and central abnormality; posttraumatic 

stress disorder; concussion; and mild TBI. A thorough, 

multidisciplinary evaluation by specialists in neurology, otolaryngology, audiology, neuropsychology, 

physical therapy, and other related areas can facilitate 

appropriate diagnosis and treatment for patients with 

blast injuries and amputations. Long-term observation is important in all cases of blast-related auditory 

injuries because symptoms may be delayed. Postural 

instability and inner ear dysfunction may be evident 

up to 6 months or longer after blast trauma.21

Outer Ear Injury 

The pinna can be damaged from flying debris and 

bomb fragments. Burns, contaminated debris, and 

purulent otorrhea in the ear canal are also frequently 

Figure 14-1. Blast injuries to the ear.

Drawing: Courtesy of Lynn H. Kitagawa, Veterans Affairs Medical Center, Portland, Oregon.

seen after exposure to blasts.22,23 In addition, blasts 

can cause inner ear damage because of the impulse 

sound, location, and environment, leaving a patient 

with conductive, mixed, or sensorineural hearing 

loss. Alternatively, when the pinna is burned without 

associated noise-induced hearing loss or penetrating 

trauma, normal hearing sensitivity is often preserved. 

Burn patients, who are usually treated with antibiotics, 

are at risk for ototoxic sensorineural hearing loss and 

should be monitored accordingly. 

Middle Ear Injury

Tympanic Membrane Perforation

When the primary shock wave reaches the end of 

the external auditory canal, it stretches and displaces 

the TM medially. Ruptured eardrums indicate that a 

patient has been exposed to peak pressure levels that 

far exceed those needed to produce damage to the 

inner ear, resulting in extensive hearing loss. The ear 

is much more sensitive to rupture pressure than other 

organs, with ruptures occurring in 50% of adults at 5 

lb/in.2 (approximately 185 dB peak pressure level) 
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Hearing Impairment Among Soldiers: Special Considerations for Amputees

depending on the noise spectra and duration.2,24,25

In contrast, pressure gradients of 56 to 76 lb/in2 are 

needed to cause damage to other organs.26 The improvised explosive devices causing injury in OIF and OEF 

produce pressures exceeding 60 lb/in2, reaching peak 

pressure in about 2.5 to 50 milliseconds. 

TM perforation is the most common injury to the 

middle ear, occurring during the positive phase of a 

blast. Typically, TM ruptures occur in the pars tensa, 

vary in appearance from linear tears to subtotal defects, and may have a protective effect because they 

reduce sound energy transmission to the inner ear.23

TM rupture is also a clinical indicator that a patient 

has undergone a significant exposure, and it has 

been recommended as a diagnostic tool for determining whether or not a blast survivor has sustained 

life-threatening injuries. It may also be used as a 

potential marker for concussive injury.22 However, 

the absence of TBI should not be assumed when TMs 

are intact.27

Clinical reports of TM rupture associated with ear 

infections range from 4% to 79% for explosion casualties.1,28–30 Most TMs heal without surgical intervention, except in cases of resultant middle ear infection 

or when blast causes total TM perforation. 

When the overpressure of a primary blast wave 

ruptures the eardrum, it sends small fragments of 

the squamous epithelium into the middle ear cavity. 

These cells may still be viable and grow into cholesteatomas that can infect or erode ossicles. Cholesteatomas usually present with conductive hearing 

loss and dizziness. Muscle weakness on the affected 

side can also occur. Careful surgical debridement is 

recommended for treatment, as is close follow up 

(10%–20% of cholesteatomas recur). Complications 

of cholesteatoma can include nerve damage and 

deafness.

Ossicular Disruption

The ossicles attach to the TM and transmit its 

vibrations to the cochlea, where the vibrations are 

converted into neural impulses via tiny hair cells. 

Overpressure can cause ossicle distortion and fracture. Ossicular damage is rare, usually occurring only 

with more severe blast trauma. Blasts that cause inner 

ear damage but spare the ossicular bones have been 

reported. A study of individuals exposed to blasts 

by explosive devices reported that ossicular damage 

occurred in 16% of patients, while 79% experienced 

TM perforations.31 Injury to the middle ear structures 

usually results in relatively minor conductive hearing 

loss, compared to the extensive sensorineural hearing loss that can accompany exposure to impulsive 

pressure waves. In addition, ossicular-chain disruption may absorb some of the incoming energy of the 

blast wave, sparing the sensory structures of the inner 

ear. In a small study of patients with ossicular-chain 

disruptions, subjects regained much of their hearing 

at the lower frequencies following surgical repair of 

the ossicles.32

Inner Ear Injury

Cochlear Injury

The cochlea at the Organ of Corti is less resilient than 

the ossicles. This delicate system is overwhelmed by 

the amplification of blast and sound waves, causing 

loss of structural integrity with damage of the inner 

and outer hair cells. The result is the development of 

conductive and sensorineural hearing loss33 because 

the basilar membrane displacement tears and mechanically injures the sensory cells in the cochlea. Inner ear 

damage following explosions results from the combination of the blast wave and the subsequent impulse 

sound. Signs of otologic injury are usually present at 

the time of the blast and should be suspected in anyone 

presenting with hearing loss, tinnitus, otalgia, vertigo, 

bleeding from the external ear canal, TM rupture, or 

mucopurulent otorrhea. Immediately following a blast, 

casualties may experience temporary hearing loss and 

tinnitus; some may sustain permanent damage to the 

Organ of Corti.7 Disruption of the oval or round window can cause permanent hearing loss.22

The risk of acoustic trauma exists at sound pressure 

levels exceeding 140 dB. In a blast injury, pressure levels may exceed 160 dB, subjecting the ear to both the 

pressure effect and the acoustic wave. The structures of 

the inner ear are exposed to mechanical forces exceeding the elastic compliance of the tissue. At lower sound 

pressure levels, the effects are thought to be conveyed 

via metabolic disturbances in the inner ear, which lead 

to subsequent sensory and neuronal damage.34 Exposure to blasts in excess of 200 dB results in substantial 

TM and ossicular damage, but sensorineural hearing 

loss can be variable, with most losses having a recoverable temporary threshold shift. In general, sustained 

high-intensity noise causes more sensorineural damage than a single high-intensity blast.32

Pure sensorineural hearing loss is the most prevalent type of auditory impairment following blast injury.19 Recent literature suggests that 35% to 100% of 

blast victims present with hearing loss.7,33,35–37 Walter 

Reed Army Medical Center reported that 64% of blast 

injured patients seen in 2005 had ongoing hearing 

loss.6 The audiometric configuration and degree of 
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Care of the Combat Amputee

the hearing loss varied from normal hearing (typical 

of those who had shielding during the blast, such as 

headphones or earplugs), to high-frequency hearing 

loss at one or more frequencies (most likely presentation), to flat configurations from mild to severe hearing 

loss (primarily conductive or sensorineural), and in 

rare cases, profound deafness. Initial presentation can 

be mixed hearing loss (conductive element of TM perforation and mucosal lacerations of the middle ear and 

the sensorineural element due to mechanical injury). 

Although patients who have noise-induced hearing 

loss usually present with a 4 kHz “noise notch,” or a 

decrease in hearing sensitivity around 4 kHz, those 

with blast injuries have a sloping high-frequency hearing loss that often affects frequencies below 8 kHz.

Vestibular Injury

Labyrinthine Damage

To maintain balance and postural stability, the vestibular system in the inner ear provides the brain with 

information about head movement via communication 

with the sensory organs (semicircular canals and otolith organs) and the eye, neck, arm, and leg muscles. 

Nerve connections from the semicircular canals and 

otoliths send information about head movement to 

the brain, resulting in eye movements that keep vision 

stable when the head moves. Similarly, nerve connections from the vestibular sensory organs to the brain 

send information to the neck, trunk, arms, and legs, 

resulting in posture changes that maintain balance. 

For the soldier with blast injury and amputation, it 

is possible that vestibular pathology, visual impairment, central pathology, certain medications, and 

proprioceptive changes all contribute to dizziness. The 

incidence of dizziness with mild head injuries ranges 

from 15% to 78%,38,39 and is most often due to pathologies affecting the peripheral vestibular system, central 

nervous system (CNS), or cervical structures. In one of 

the few long-term studies on untreated patients with 

mild head trauma, vertigo persisted in 59% of patients 

after 5 years of recovery.40 Compensation results from 

changes that occur within the CNS, rather than from 

changes in the peripheral vestibular system.41 Following blast trauma, 27% of soldiers with amputation 

reported experiencing dizziness, and 18% reported 

experiencing vertigo.16

A primary care physician should rule out nonvestibular causes (orthostatic hypotension, postconcussive 

syndrome, TBI, ototoxic drugs, and visual impairment) 

of dizziness and an audiologist, otolaryngologist, and 

physical therapist can determine if dizziness is related 

to otovestibular pathology, such as peripheral disequilibrium, vertigo, or posttraumatic Ménière’s disease. 

TM injury can be complicated by a perilymph fistula, 

an often under-diagnosed condition in which a tear 

between the membranes of the inner and middle ear 

causes a perilymph leak that produces vertiginous 

symptoms.39 Labyrinthine damage may also occur 

after blast injuries, resulting in complaints of vertigo. 

Although blast injury often affects vestibular function, it is less common and the symptoms less defined 

than other auditory damage sustained during an explosion. Vestibular testing can typically determine the 

presence of a vestibular pathology, yet the cause of the 

vestibular disorder may remain unknown. In general, 

vestibular damage can occur to one or both ears, and 

may affect the sensory organs (semicircular canals or 

otoliths), the vestibular nerve, or its connections. The 

most common causes of vestibular disorders include 

benign paroxysmal positioning vertigo (BPPV), Ménière’s disease, labyrinthitis, vestibular neuritis, and 

ototoxicity.

Head trauma as a result of blast injury is one of the 

most frequent causes of BPPV.21 BPPV is characterized 

by brief (a few seconds to a minute), severe vertigo associated with changing head positions, such as looking 

up or rolling over in bed. Ménière’s disease (or endolymphatic hydrops) results from an increase in the fluid 

of the inner ear and can be traumatically induced. It is 

characterized by attacks of vertigo, ringing or roaring 

in the ears, a feeling of pressure or fullness in the ear, 

and hearing loss. Attacks typically last several hours, 

but can vary in length and frequency. 

Some acoustic trauma and dizziness studies also 

suggest that noise exposure may result in vestibular 

disturbance.42 Asymmetric exposure to extremely 

intense (140 dB or above) sounds leads to a greater 

likelihood of producing vertigo. Finally, ototoxicity can cause temporary or permanent balance loss, 

hearing loss, or both. Individuals who lose unilateral 

peripheral vestibular information must depend on 

other components of the sensory system (visual and 

proprioception), further complicating the rehabilitation process for patients with visual field deficits and 

lower limb loss, particularly if they have uncompensated unilateral peripheral vestibular loss or bilateral 

vestibular loss.41

Central Vestibular Damage 

Otologic effects of blast injuries can include centrally 

mediated symptoms. TBI as a result of the primary 

blast wave or subsequent blow to the head may lead 

to central vestibular pathology, peripheral vestibular 

pathology, or both. Central vestibular trauma may be 

due to postconcussive syndrome or cerebral or brainstem injuries.43,44 Central vestibular pathology is less 

common than peripheral pathology in patients follow-
387

Hearing Impairment Among Soldiers: Special Considerations for Amputees

ing head injury45 and blast exposure.37 In some cases, 

there may be evidence of both central and peripheral 

vestibular dysfunction.45

Central Auditory System Damage

While the presence of a ruptured TM is an obvious 

physical finding of blast exposure, the most detrimental effects of a blast may be less obvious and harder 

to treat. It is likely that patients with amputations 

resulting from blast exposure were either hit by flying 

objects (secondary damage) or were picked up by the 

blast wave and thrown into a stationary object, such 

as a vehicle or a wall (tertiary damage). In either case, 

there is a significant chance that the brain was also 

impacted. It is not known what proportion of those 

exposed to blasts sustained damage to the central auditory system; however, it has been well established 

that when an impact causes the brain to move to the 

extent that it impacts bone, contusions (hemorrhage 

and edema) occur, and the auditory processing areas of 

the temporal lobe are most commonly impacted.46 Additionally, shearing, stretching, and angular forces of 

blast waves cause swelling and disconnection of axons 

in the central auditory system.46 Damage to the CNS 

after an explosion has been increasingly attributed 

to the direct effects of the blast.22 Inhalation of toxic 

chemicals (including materials such as paint and some 

industrial organic chemicals) may also affect the CNS 

and may present as vertigo or unsteadiness.42

There are a significant number of people who have 

normal hearing sensitivity following blast exposure, 

yet still complain of hearing difficulty. Central auditory dysfunction may contribute to these complaints, 

but diagnosis and treatment is challenging because the 

link between neural structures and function in central 

auditory processing (CAP) disorders has not been fully 

discerned. The lower brainstem nuclei, such as the inferior colliculus, are involved with comparing stimuli 

arriving from the ears (“binaural” processing). For 

this reason, only sensitivity to binaural relationships 

is affected by unilateral brainstem damage (bilateral 

lower brainstem damage is generally fatal). The thalamic nuclei in the upper brainstem can be damaged 

by shearing or stretching forces, resulting in deficits 

in determining the location or duration of sounds. 

Binaural “unmasking” refers to the ability to determine time and level differences at each ear to improve 

detection of speech and other important sounds in 

noisy environments. Essentially, listeners can “cancel 

out” noise coming from a location that differs from 

that of the signal to be detected.47 Although exactly 

where such binaural unmasking occurs is still a matter 

of debate, it is possible that the binaural information 

extracted by the early brainstem is used for binaural 

unmasking operations that actually occur at the level 

of the auditory cortex.

At the cortical level, bilateral damage to the superior 

temporal gyrus (primary auditory cortex) can result in 

immediate and ongoing insensitivity to all sounds. The 

extent to which attentional and behavioral processes 

underlie these deficits is not yet well understood.48 In 

addition to “cortical deafness,” which often recovers 

over time, there are a number of additional processing 

deficits associated with damage to auditory cortical 

areas that may impact speech comprehension, appreciation and discrimination of music, and identification 

and discrimination of environmental sounds. These 

diverse “agnosias” may stem from difficulties analyzing spectrotemporal patterns in sounds.49

Providing clinical data that relates specific damage 

to discrete behavioral deficits will provide a better understanding for a clinician and corroborative evidence 

for the spectrotemporal processing pathways that are 

being uncovered in animal studies. The relevance of 

diagnosing clinical disorders using animal models 

of cortical processing will likely only be appreciated 

when clinical and animal data are merged. Current 

trends suggest that the same basic units of analysis that 

exist in the mammalian cortices of cats and primates 

correlate with human perception of speech, music, and 

environmental sounds. If such a relationship could be 

clearly established, it would be possible to develop a 

set of standardized diagnostic tests that specifically 

target the perception of patterns in frequency, time, 

level, and spatial position. A more detailed discussion 

of diagnostic testing has been provided below.

Tinnitus

Damage to hearing due to excessive noise exposure 

in acoustic trauma is frequently accompanied by tinnitus. Noise-induced tinnitus can be characterized by 

a high-pitched buzzing or ringing sound that lasts 

longer than 5 minutes and may produce annoyance, 

behavioral changes, and depression.50,51 Damage to 

neural networks, association pathways, associated 

cortical regions, the limbic system, and the prefrontal 

cortex may be involved in the generation of tinnitus.52

Tinnitus symptoms resulting from blast or impulse 

noise exposure often resolve over time. Persistent 

symptoms can occur in some tinnitus patients, many 

of whom report disability equal to or greater than that 

associated with hearing loss.50 Although tinnitus is a 

symptom associated with many forms of hearing loss, 

it can also be a symptom of other health problems, such 

as stress, use of certain medications, allergies, tumors, 

metabolic factors, and vascular disease (especially that 

involving vessels in the jaw and neck).
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Care of the Combat Amputee

DIAGNOSTIC TESTS

It is often difficult to assess for otovestibular injury 

in a polytrauma patient in a timely manner because 

of consciousness level, contraindications to testing (cspine precaution, ventilator use, bed rest orders, pain), 

and multiple priority appointments at other clinics. 

Testing protocols are commonly modified based on 

the complexity of an injury. For example, many polytrauma patients have burns or severe injuries to their 

skulls, so some testing equipment, such as earphones 

or bone conduction headsets, is contraindicated. There 

is currently no standard method for diagnosing otologic, otovestibular, and CAP disorders in patients with 

blast injury and amputation. When possible, the following protocol is recommended until ongoing clinical 

research identifies factors to aid in the development of 

more sensitive tests to assess blast-injury amputees for 

peripheral, central, and otovestibular pathology.

Patient Questionnaires

Polytrauma patients should complete case history 

and standardized questionnaires that assess the impact 

of hearing loss, tinnitus, and dizziness. The audiologic 

case history questionnaire should elicit information 

about a patient’s medical history, including cognitive 

functioning, visual history before and after the blast, 

audiologic history before and after the blast (including 

exposure to potentially damaging noise), and tinnitus 

history (if applicable). Patients should also be asked to 

provide detailed information about the blast exposure, 

describing the nature of the blast, proximity to the blast, 

use of hearing protection, and loss of consciousness at 

the time of injury. The Hearing Handicap Inventory 

for Adults consists of two subscales and assesses the 

emotional and social consequences of hearing loss.53

The Tinnitus Handicap Inventory is used to assess selfperceived handicap related to tinnitus, and the Dizziness 

Handicap Inventory assesses handicap by quantifying 

the functional, emotional, and physical effects of dizziness and unsteadiness.54,55 Screenings for posttraumatic 

stress disorder and mild TBI should be administered 

when appropriate. TBI screening was created for VA 

clinicians to screen all OEF and OIF veterans receiving 

medical care within the Veterans Health Administration. 

The screening allows clinicians to offer further evaluation and treatment to those who test positive.

Comprehensive Audiometric Evaluation

Otoscopy should be performed prior to audiometric 

evaluation. If otoscopy reveals occluding or impacted 

cerumen or otherwise abnormal pathology, patients 

should be referred to an otolaryngologist. Monaural 

air- and bone-conduction thresholds should be measured in each ear to determine the type and degree of 

peripheral hearing impairment. Because many patients 

with blast-related limb loss may be taking ototoxic 

medications, air-conduction hearing thresholds should 

be measured at frequencies up to 12,000 Hz, or to the 

frequency limits of the individual’s hearing.56 Monaural speech-recognition testing, including reception 

thresholds for speech and speech intelligibility for 

one-syllable words, should be conducted in quiet. To 

further rule out or confirm the presence of conductive 

or retrocochlear pathology, immittance audiometry, 

including tympanometry, ipsilateral and contralateral 

acoustic reflex thresholds, and contralateral acoustic 

reflex decay should be completed in each ear. If pure 

tone testing reveals conductive or mixed hearing loss 

or if tympanometry results are abnormal, the patient 

should be referred to an otolaryngologist for evaluation. Otoacoustic emissions should be used to confirm 

other test findings. Additionally, auditory brainstem 

response testing and auditory steady-state response 

testing should be considered when a patient is unable 

to undergo conventional behavioral audiometry.

Ototoxic Monitoring Protocol

For patients on ototoxic medications, comprehensive baseline testing should supply information 

about pretreatment hearing levels. Baseline measures 

will provide a reference for comparison to determine 

if hearing levels have changed. This testing should 

be done as soon as possible after patients have been 

identified as needing ototoxic medication. For patients 

treated with aminoglycoside antibiotics, baseline testing should occur prior to the start of medication or 

within 72 hours of the first dose administered. Patients 

receiving loop diuretics should be seen sooner than 72 

hours after the first dose. For patients receiving cisplatin or carboplatin, baseline testing should be evaluated 

within 24 hours of the first dose.

Minimum baseline evaluation should consist of 

bilateral pure tone air-conduction thresholds from 250 

to 8,000 Hz. This should include the half octaves of 

3,000 and 6,000 Hz. Whenever possible, high-frequency 

thresholds above 8,000 Hz should be tested (9,000, 

10,000, 11,200, 12,500, 14,000, 16,000, 18,000, and 20,000 

Hz). Intrasession reliability should also be evaluated 

by retesting some frequencies to measure for consistent 

results. A reliable test should show responses that are 

within or equal to 5 dB HL. If hearing loss is present 

from 250 to 4,000 Hz, bone conduction should also be 
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Hearing Impairment Among Soldiers: Special Considerations for Amputees

performed. Testing should be as thorough as possible; 

however, if a patient is too sick for a comprehensive 

evaluation, testing may need to be modified or may 

need to occur over multiple sessions. If a patient is 

unable to complete behavioral testing, electrophysiological testing may be performed.

Ototoxicity monitoring is based on a patient’s drug 

therapy schedules. For patients receiving aminoglycosides, otoscopy and pure tone air conduction tests in 

the normal and high-frequency ranges should occur at 

least once a week. Cisplatin patients should be monitored within 24 hours preceding each dose. For ototoxic 

medication monitoring, speech audiometry, bone conduction, and immittance testing should be performed 

if there is a change in hearing. If a change in hearing 

occurs, a retest should take place within 24 hours to 

confirm threshold change. Reevaluation should occur 

at approximately 3 and 6 months after treatment to assess any residual effects of drug treatment. If a decrease 

in hearing threshold is noted, weekly tests should take 

place until changes cease.

Ototoxic monitoring protocols at military facilities 

and VA hospitals must institute best practice policies 

for situations in which baseline measures are not available, concomitant medications are being used, septic 

patients require immediate therapy, and when bedside 

testing must be made available for patients that cannot be transferred for testing. In addition, ototoxicity 

monitoring should include patient counseling and 

education.

Assessment of the Vestibular System 

If a patient reports problems with dizziness or unsteadiness, a multisensory balance evaluation is indicatied. The comprehensive balance evaluation should 

include a vestibular, visual, somatosensory, and brain 

integration system assesment. Clinicians working 

with soldiers with blast trauma and amputation need 

to consider several causes of postural instability, including TBI, orthostatic hypotension, cervical vertigo, 

visual deficits, possible side effects of ototoxic drugs, 

and vestibular pathology. Vertigo is often related to 

a vestibular balance disorder; however, imbalance 

and lightheadedness may or may not be related to 

inner ear damage. Some other causes of imbalance or 

lightheadedness include neurological impairments, 

vascular flow or pressure changes, cardiac problems, 

certain medications, or systemic disorders, such as 

diabetes. Screening tests typically administered by 

physical therapists during the vestibular portion of 

the blast evaluation include a cervical range-of-motion 

and cervicalgia assessment, oculomotor evaluation, 

postural stability tests, gait assessments, and vertebral artery tests to assess for potential vertebral 

insufficiency and vascular causes of dizziness. The 

passive dynamic visual acuity test and head thrust 

test performed bilaterally assess the vestibular ocular 

reflex. Contraindications to these screenings include 

cervical instability, fractures preventing cervical rangeof-motion assessments, and use of medical equipment 

that precludes communication, such as a jugular line or 

ventilator.16 Screening tests are not sensitive enough to 

detect all vestibular abnormalities and do not provide 

quantitative data to determine the presence or absence 

of vestibular lesions.

Patients showing signs of vestibular pathology 

should be further evaluated to determine if dizziness 

or balance problems are related to a vestibular disorder. Vestibular tests can help characterize the deficits a 

patient has and guide the development of appropriate 

rehabilitative techniques. Videonystagmography is a 

battery of tests that evaluates the horizontal semicircular canals (one of the inner ear balance organs), its 

nerve connections, and the eye movement systems. 

Because the vestibular system is connected to the eye 

muscles, vestibular function is measured by recording 

eye movement. If electrodes are used, the test battery 

is typically called electronystagmography. The videonystagmography test can identify an inner ear balance disorder that can occur in one or both ears and 

is related to the horizontal semicircular canal and its 

nerve. The Dix-Hallpike maneuver, often performed 

as part of the videonystagmography/electronystagmography test battery, can determine if the symptoms 

of vertigo are related to BPPV and can identify which 

semicircular canal is involved.

Vestibular-evoked myogenic potentials assess the 

saccule (one of the otolith organs) and its nerve connections to the neck muscles to evaluate vestibular 

function. The rotary chair test evaluates the horizontal 

semicircular canals and their connection to the eye 

muscles and is used to monitor vestibular loss in patients on ototoxic medications. Finally, computerized 

dynamic posturography evaluates a patient’s ability to 

integrate vestibular, visual, and somatosensory cues to 

maintain balance. This test is helpful for patients with 

lower extremity issues (eg, amputation, paralysis, etc) 

to monitor their risk of falls and retrain them for better 

stability and balance.

More recent best practices have begun to incorporate the computerized dynamic visual acuity test 

and the subjective visual vertical test during off-axis 

rotation to assess utricle function in the blast-injured 

population. The computerized dynamic visual acuity 

test measures visual acuity during head movement 

to assess vestibular deficits.57,58 Monitoring an amputee with vestibular symptoms is essential and can 
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Care of the Combat Amputee

a patient’s ability to recognize degraded speech 

stimuli. Many audiologists use a speech-in-noise 

test to assess this component of central auditory 

processing. An example of such an assessment is the 

Quick Speech-in-Noise Test.62 This test can be used 

with patients that have either normal or impaired 

hearing.

Binaural Interaction Tests 

Binaural interaction assessments, such as the 

masking-level difference test, evaluate binaural 

processes depending on intensity or time difference 

of acoustic stimuli. In the masking-level difference 

test, binaural thresholds for pure tones (typically 

500 Hz) or speech are determined in the presence of 

binaural masking noise. The tone or speech signal 

is presented in-phase to the ears and the noise is 

presented either in-phase or out-of-phase between 

the ears. Normal binaural processing is associated 

with an improved detection threshold for the outof-phase noise. A 500-Hz masking-level difference 

test is clinically available and can be used for this 

assessment.63

Electrophysiologic Tests

Electrophysiologic tests measure electrical potentials that reflect activity generated by the CNS in 

response to auditory stimulation. The middle-latency 

response and the late-latency response have been 

shown to assess central auditory dysfunction. Putative neural generators for the middle-latency response 

include the auditory thalamocortical pathways, the 

mesencephalic reticular formation, and the inferior 

colliculus. The middle-latency response consists of 

a series of positive and negative peaks that fall in 

the latency range of 10 to 80 milliseconds after onset 

of the stimulus. Putative neural generators for the 

late-latency response, on the other hand, include 

thalamic projections into the auditory cortex, the 

primary auditory cortex, the supratemporal plane, 

the tempoparietal association cortex, and the lateral 

frontal cortex. In general, an averaged late-latency 

response wave is composed of contributions from 

multiple structures and can reflect brain functions 

such as attention, cognition, discrimination, and 

integration. The recorded wave consists of a series 

of positive and negative peaks that occur from 70 to 

500 milliseconds after onset of the stimulus. These 

electrophysiologic tests, in conjunction with the auditory brainstem response, can help pinpoint where in 

the auditory system deficits might exist.

CAP assessment is controversial and complex, 

be accomplished by outcome questionnaires, physical screens, repeating tests that had initial positive 

findings, and assessing and modifying management 

strategies on an ongoing basis.

Assessment of Central Auditory Processing Disorders

Deficits in CAP refer to “difficulties in the perceptual processing of auditory information in the CNS,” 

as demonstrated by poor performance in one or more 

of the following skills: (a) auditory performance in the 

presence of competing acoustic signals (eg, dichotic 

listening); (b) temporal aspects of audition (eg, temporal integration, temporal discrimination, temporal 

ordering, temporal masking); (c) auditory pattern 

recognition; (d) auditory discrimination; (e) auditory 

performance with degraded acoustic signals; and (f) 

sound localization and lateralization.10 Unfortunately, 

central deficits can be mistaken for posttraumatic stress 

disorder, mental health issues, and cognitive deficits, 

and therefore may be overlooked. With the increased 

incidence of TBI, CAP function must be assessed to 

ensure that remediation strategies can be devised and 

implemented. Currently, no standard CAP assessment 

protocol exists. A CAP test battery should be chosen 

for a given patient based on specificity, reliability, and 

validity. Tests should be selected that measure different central processes, and both verbal and nonverbal 

stimuli should be used. Some potential test measures 

an audiologist may include in a CAP assessment battery are provided below. 

Auditory Temporal Processing and Patterning Tests

Auditory temporal processing and patterning tests 

are designed to assess a patient’s ability to analyze 

acoustic events over time. An example of such a test 

is the Gaps-in-Noise Test.59

Dichotic Speech Tests 

Dichotic speech tests are designed to assess a patient’s ability to either separate or integrate different 

auditory stimuli presented to the ears simultaneously. 

One such test, the Dichotic Digits Test, requires a 

patient to listen to numbers presented to both ears 

simultaneously and indicate what was heard in each 

ear.60 This test has demonstrated sensitivity to CNS 

pathology while remaining relatively resistant to mildto-moderate high-frequency cochlear hearing loss.61 

Monaural Low-Redundancy Speech Tests

Monaural low-redundancy speech tests assess 
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Hearing Impairment Among Soldiers: Special Considerations for Amputees

especially with the polytrauma population, because 

variables such as motivation, attention, cooperation, 

cognition, neuronal loss, noise toxicity, metabolic and 

circulatory changes, working memory, and other comorbid factors can confound test interpretations and 

cause misdiagnosis. Because CAP deficits can be mistaken for myriad other disorders, it is essential that 

this assessment be done as part of a comprehensive 

team approach. An audiologist should work closely 

with professionals in mental health, neuropsychiatry, 

speech-language pathology, physical and occupational therapy, and other related specialties.

Tinnitus Evaluation

Patients presenting with complaints of tinnitus 

should undergo evaluation to assess symptoms and 

to identify treatment options. The Tinnitus-Impact 

Screening Interview and the Tinnitus Handicap 

Inventory questionnaire should be completed to 

determine the severity of symptoms. Sound tolerance measures can determine the presence of 

hyperacusis, or reduced loudness tolerance.64 In 

addition, psychoacoustic measures, such as loudness and pitch matching,65 allow for full characterization of a patient’s tinnitus if it is problematic 

and requires treatment. An assessment of tinnitus 

maskability, or the minimum masking level necessary to render the patient’s tinnitus inaudible, has 

been shown to correlate with treatment efficacy.66

Finally, if measures of otoacoustic emissions have 

not already been performed, they should be done at 

this time to provide objective evidence of cochlear 

dysfunction (even if normal pure tone thresholds), 

and to provide frequency-specific information, 

which may be associated with the frequency region 

of the tinnitus.67

Reevaluation

The long-term effect of blast exposure on peripheral and central auditory functioning is not yet 

known and needs to be investigated more fully. The 

current recommendation, therefore, is to reassess 

patients in 6 months (or sooner if indicated) and 

annually thereafter.

TREATMENT AND REHABILITATION

Treatment and rehabilitation of auditory and vestibular injury in the amputee often require a multidisciplinary approach, focusing on otolaryngology, 

neurology, audiology, occupational therapy, and physical therapy. The type of auditory deficit present in a 

patient will determine treatment options, including 

medical and surgical interventions, technological considerations, and auditory training and counseling. Audiologists must make special considerations for service 

members with severe injuries to their extremities as a 

result of blast exposure. Those with concurrent hearing 

impairment must adjust to life with prosthetic limbs as 

well as prosthetic hearing aids and assistive listening 

devices.68 Additionally, many soldiers with amputation have concurrent TBI and require accommodating 

rehabilitative approaches. Providers may need to give 

examples to go with new ideas and concepts, reduce 

visual and auditory distractions, and give step-by-step 

directions to reduce confusion. It is also important to 

demonstrate and explain information in more than 

one modality. Brain injury can cause cognitive impairments, such as problems with orientation, attention, 

concentration, perception, comprehension, learning, 

thought organization, executive function, problem 

solving, and memory. Additionally, up to 28% of all 

blast-exposed soldiers have significant eye injuries. 

Visual field deficits must be taken into consideration 

when providing aural rehabilitation and amplification 

device instructions. Furthermore, behavioral issues, 

including aggression, agitation, mental trauma, and 

adjustment to disabilities may interfere with treatment 

plans at early stages of recovery.3

Audiologists must be knowledgeable about managing problems specific to a patient’s amputation and 

work with the treatment team to reduce this impact. 

For example, upper limb amputees that require hearing aids need to learn how to independently place 

an aid using a prosthesis. These challenges become 

compounded if an individual also has a TBI, vision 

loss, or loss of more than one limb. It is imperative 

that an audiologist actively participates as part of the 

rehabilitation team.

Peripheral Hearing Loss

Hearing aids deliver an amplified signal to the ear 

and are recommended when their use can significantly improve a patient’s ability to communicate. When 

effective medical treatment can be implemented to restore normal hearing, or when hearing-aid use would 

exacerbate a disease or interfere with treatment, 

amplification is not used. Hearing aids are classified 

by their style, size and placement, or technological 

features. The most important developments in hearing aids in the past decade have been the introduction of digital programmable hearing aids, ranging 
392

Care of the Combat Amputee

treatment. Depending on diagnostic test results, 

vestibular treatment options can include vestibular 

rehabilitation therapy; physical therapy; canalith 

repositioning therapy; change in activity levels, 

medication, and diet; treatment for underlying disease that may be contributing to the balance disorder; 

and surgery. 

Vestibular rehabilitation therapy is the treatment 

of choice for many types of vestibular disorders. 

Vestibular rehabilitation therapy is exercise therapy 

that includes head and eye movement and balance 

and walking tasks that are designed to help the 

brain compensate for vestibular problems. Vestibular rehabilitation therapy, postural stability training, 

and gait training are usually provided by a physical 

therapist. 

Canalith repositioning therapy is the preferred 

treatment for BPPV. The goal of canalith repositioning 

therapy is to move the displaced particles (otoconia) 

through the semicircular canal and back to the vestibule that houses the otolith organs. This is achieved 

by placing the patient in a series of head positions and 

observing eye movement. It may be performed by an 

audiologist, otolaryngologist, or physical therapist.

Central Auditory Processing Deficits

Treatment options for CAP deficits are currently 

under investigation by the research community. 

Current clinical guidelines recommend a two-step 

approach that includes auditory training and general management.10 Auditory training is designed to 

capitalize on the plasticity of the auditory system by 

altering the neural encoding of sound and subsequent 

timing of brainstem responses. Studies have linked 

the neurophysiologic changes seen after training to 

perceptual changes.70–72 Subjects can learn to interpret 

sounds as speech that could not be discriminated before training. It is recommended that training occur 

soon after injury to maximize the plasticity of the brain, 

and training should be patient specific and focused on 

the deficit areas noted on the CAP assessment. General management strategies include environmental 

tactics, like the use of an FM system, and teaching 

compensatory strategies. These treatment options 

may be provided by a speech-language pathologist, 

an audiologist, and an occupational and physical 

therapist. Specific remediation activities (deficit 

specific), such as phonological awareness and discrimination training (speech-to-print skills), auditory closure, and prosody training, can be provided 

by a speech-language pathologist. Speechreading 

and auditory training exercises can be provided 

by an audiologist, and occupational and physical 

in size from completely in the ear canal to behind 

the ear, and the increasing popularity of directional 

microphones. Directional microphones provide the 

greatest amount of amplification for signals arriving 

from the front, where speech typically emanates, 

and places nulls (areas of reduced amplification) for 

signals from the sides and back, which are the usual 

locations for noise sources.

When selecting a hearing aid for today’s polytrauma patient, there are multiple factors to consider. 

For instance, some returning soldiers with hearing 

impairment have body-image issues stemming from 

multiple scars, burns, and amputation requiring prosthetic limbs, and may prefer a completely in-the-canal 

hearing aid versus a larger style. Additionally, it is 

important to consider possible alternatives when it 

is difficult or impossible for the patient to manually 

insert the hearing aid. This is especially true if the 

patient has lost or significantly impaired one or both 

upper limbs. The use of remote control options to adjust the volume and program settings (for quiet and 

noisy environments, telecoil or frequency modulation 

[FM] use) is likely to be a good option for these patients. Automatic hearing aids that adjust to different 

acoustic environments without human intervention 

are also available as needed, especially for those with 

significant cognitive impairment.

Unfortunately, traditional hearing aids, even those 

equipped with directional-microphone technology, 

may provide only limited improvement in speech 

perception in everyday listening environments where 

there is noise and reverberation. One well-recognized 

technology to improve speech perception in listeners 

with hearing loss is FM systems. With an FM system, 

the speaker’s voice is picked up by a wireless microphone and the signal is transmitted via FM radio waves 

to the receiver. The close proximity of the FM microphone minimizes the negative effects of reverberation, 

distance, and noise on speech perception.69

In addition to FM technology, a host of other assistive listening devices could be considered for this 

patient population. Some of these options include 

captioning for television viewing, teletext or volumecontrol telephones, and alerting devices that employ 

flash-visual or vibrotactile signals to warn of acoustical environmental events. Many of these devices are 

available at no cost to the veteran through the VA or 

the state in which the veteran resides.

Vestibular Problems

Treatment of vestibular problems should be specific to the patient and to the deficit, and physicians 

and physical therapists should collaborate on patient 
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Hearing Impairment Among Soldiers: Special Considerations for Amputees

therapists can use cross-modality activities to improve interhemispheric transfer of information.

Tinnitus 

The majority of patients who present with tinnitus 

following blast exposure experience a resolution of 

symptoms over time and do not require any audiologic 

intervention.19 Of the approximately 20% of tinnitus 

patients that have clinically significant symptoms, 

rehabilitation needs vary from simple education about 

the condition to counseling and treatment.19 Because 

no treatment has been effective in directly reducing 

tinnitus symptoms, the goal of treatment is to lessen 

their impact.9 Tinnitus treatments include medication, 

masking therapy, Tinnitus Retraining Therapy, Neuromonics Tinnitus Treatment and other sound therapy 

and directed counseling, psychological therapy (such 

as cognitive-behavioral therapy), and hearing aids.50

The type of intervention for tinnitus patients can vary 

significantly, and clinical management methods do not 

adhere to any standards at this time.67

PREVENTION

Because of the many types of ear injuries incurred by 

soldiers, multiple strategies must be employed to prevent 

hearing loss in this population. Physical barriers to sound, 

pressure, and debris, such as headphones and earplugs, 

prevent injury to the external and middle ear. In addition, 

monitoring hearing thresholds while patients are receiving ototoxic medications provides early identification of 

hearing loss, allowing for possible changes in treatment. 

Finally, systemic compounds for otoprotection may prevent damage at the cellular level. The optimal treatment 

for soldiers may be a combination of all these approaches 

to ultimately minimize hearing impairment.

Hearing Conservation

Headphones and hearing protectors offer significant 

shielding and protection from otologic injury by protecting the ear from excessive noise, flying debris, and the 

pressure wave associated with a blast. Technological advances have enabled hearing protectants to be equipped 

with microphones so users can maintain hearing sensitivity. For those wearing hearing protection, the risk of 

hearing loss is minimized and the incidence of ruptured 

TM is significantly reduced. In several blast incidents, 

soldiers using hearing protection did not sustain ear 

injuries, whereas those without ear protection suffered 

ear damage and hearing loss.73,74 Military personnel 

assigned to light armored vehicles as commanders, 

gunners, and drivers wear protective helmets, but 

personnel in the rear of these vehicles do not generally 

wear protection and are therefore most susceptible to 

ear blast injuries.1 Greater than 20% of the blast-injured 

soldiers traveling in light armored vehicles in various 

military conflicts presented with ear injury, mostly 

ruptured TMs.1 In contrast, eye injuries are extremely 

uncommon for these soldiers, presumably due to the 

ballistic eye protection soldiers wear when traveling in 

light armored vehicles.1 It is essential to adopt hearing 

protection standards to shield service members at risk 

for blast or excessive noise exposure.

Otoprotectants

Otoprotective agents may be capable of preventing 

noise-induced and ototoxic hearing loss by reducing 

the damaging effects of noise or medications on the hair 

cells of the cochlea. In addition, some otoprotectants 

may be able to rescue damaged cells once injury has 

occurred, thereby minimizing hearing loss. There have 

been numerous studies of various compounds used to 

protect hearing, including antioxidants that scavenge free 

radicals, agents that increase blood flow, and drugs that 

block cell-death- pathway–signaling factors. Despite the 

potential of these compounds, the translation of animal 

studies of otoprotectants to clinical treatment has been 

limited. Clinical trials are needed to delineate the effects 

of these protective compounds. Effective preventative 

therapies may ultimately require a combination of compounds that employ multiple mechanisms to combat cell 

damage in the inner ear.

SUMMARY

The escalating use of explosive devices in warfare, 

combined with the excessive noise of ballistic weapons, has created an unprecedented number of hearing 

impairments among soldiers, many of whom also sustain amputations, further complicating rehabilitation 

efforts. A comprehensive interdisciplinary evaluation 

of peripheral, central, and vestibular components of 

the auditory system must be completed in polytrauma 

patients to ensure that all injury is accurately diagnosed 

and appropriate rehabilitation can be devised. Furthermore, the implementation of hearing conservation 

strategies—including physical ear protection, preventative therapy with otoprotectants, and implementation 

of early detection and monitoring programs—may sig-
394

Care of the Combat Amputee

nificantly reduce the number of patients with disabling 

hearing impairments. Effective treatment and hearing 

loss protection programs can also reduce the potential 

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