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Evaluation and management of middle ear trauma

Evaluation and management of middle ear trauma
Literature review current through: Jan 2024.
This topic last updated: Jan 24, 2024.

INTRODUCTION — The management of blunt or penetrating middle ear trauma will be reviewed here.

The evaluation and management of ear barotrauma and temporal bone fractures are discussed separately. (See "Ear barotrauma" and "Skull fractures in children: Clinical manifestations, diagnosis, and management" and "Skull fractures in adults".)

EPIDEMIOLOGY — Middle ear injury, injury to adjacent inner ear structures, or both occurs in up to one-third of patients with severe head trauma and over one-half of patients with temporal bone basilar skull fractures [1-3]. These injuries include hemotympanum (picture 1), hearing loss, cerebrospinal fluid (CSF) fistula, otic capsule injury, and traumatic perilymphatic fistula [1-5].

Otic capsule injury is four to five times more likely if temporal bone fracture occurs with facial nerve paralysis, CSF otorrhea, or both [4].

Middle ear injury may also occur after direct blunt trauma to the external auditory canal (eg, hand blow to ear ["boxed ears"], fall onto the ear while water or snow skiing, motor vehicle collision, sports injury [eg, wrestling]) or penetrating trauma (eg, Q-tip, matchstick injury, gunshot wound, welding or soldering spark) [3,4,6-11].

Barotrauma with middle ear injury can occur during air travel, scuba diving, or exposure to a blast. (See "Ear barotrauma", section on 'Etiologies'.)

CLINICAL ANATOMY

Middle ear — The middle ear space is an air-filled cavity between the external ear canal and the inner ear (figure 1). The ossicular chain and the facial nerve cross the middle ear space. The boundaries of the middle ear cavity are as follows:

The tympanic membrane, a three-layered membrane, laterally

The otic capsule, containing the cochlea, semicircular canals, and vestibule (saccule and utricle), medially

The bony tegmental wall under the middle cranial fossa, superiorly

The bony jugular wall, encasing the internal jugular vein bulb, inferiorly

The carotid wall, containing the Eustachian tube and tensor tympani muscle, anteriorly

The entrance to the mastoid cavity, called the aditus ad antrum, posteriorly (figure 2)

The posterior aspect of the middle ear space leads into the adjacent air space called the mastoid cavity (figure 2) via the aditus ad antrum. The bony roof of these regions separates them from the middle cranial fossa, which is lined by dura; the bony posterior aspect of the mastoid cavity contains the sigmoid sinus in the posterior cranial fossa. Fractures of the temporal bone into these spaces may result in any of the following:

Cerebrospinal fluid (CSF) middle ear effusion, otorrhea, or rhinorrhea

Hemotympanum (picture 1)

Carotid artery aneurysm, or pseudoaneurysm

Meningitis days to years after the injury

The middle ear space is lined by vascularized, ciliated, pseudostratified, columnar respiratory mucosa. The pressure in the middle ear cavity is equilibrated to ambient pressure by the action of the tensor veli palatini muscle and the salpingopharyngeus muscle located at the orifice of the Eustachian tube (ET). The ET is supported by bone then cartilage, and lined by mucosa, as it travels from the middle ear space into the nasopharynx.

Ossicles — The ossicles (the malleus, the incus, and the stapes) comprise a lever system that amplifies sound by a factor of approximately 1.5. The tympanic membrane has a large surface area compared with the oval window of the inner ear, and thus, it is responsible for amplification of sound by a factor of approximately 20 [12]. Sudden changes in sound intensity can be temporized by the activity of the stapedius muscle and tensor tympani muscle, both of which contract reflexively to dampen sound. Absence of air in the middle ear space, loss of tympanic membrane integrity, or disruption of the ossicular chain compromises the amplification system.

Middle ear injuries, such as those sustained from a slap on the ear or insertion of a Q-tip, may result in mild conductive hearing loss due to tympanic membrane perforation with partial loss of sound amplification (picture 2). Hemotympanum or CSF middle ear effusion caused by temporal bone basilar skull fracture or barotrauma may also dampen tympanic membrane sound conduction (picture 1) [6]. (See "Ear barotrauma".)

Middle ear injuries, such as more severe ear canal foreign body penetrations or temporal bone fractures, may result in maximum conductive hearing loss (ie, 60 dB) if the ossicular leverage system is disrupted at the incudostapedial joint or if the stapes is subluxed (picture 3) [13]. Alternatively, such injuries can result in sensorineural hearing loss as a result of a cochlear concussion, otic capsule fracture, or internal auditory canal fracture with impingement or laceration of the acoustic nerve (cranial nerve VIII).

Adjacent structures — The following structures are present within and/or adjacent to the middle ear and often sustain injury when middle ear trauma occurs:

Oval window – Sudden changes in pressure, associated with barometric pressure changes, sound waves, or direct cranial injury, may result in trauma to the oval window and may cause a tear in the oval or round window membranes, creating a perilymphatic fistula between the inner ear and middle ear (figure 1). The presence of a perilymphatic fistula is associated with hearing loss and "third window" signs, such as Tullio phenomenon and a positive fistula test [14], which are manifest as follows [5,14-16]:

In Tullio phenomenon, a loud sound presented to the affected ear causes spinning vertigo and nystagmus.

The fistula test is positive when pneumatic otoscopy with positive and negative pressure in the ear canal on the intact tympanic membrane results in spinning vertigo and nystagmus. If movements are large, the semicircular canal may be compromised; if movements are minimal, it may be an oval window fistula [17].

Inner ear (otic capsule) – The inner ear is encased by the bony otic capsule and contains the cochlea, vestibule (saccule and utricle), and semicircular canals. The bone of the otic capsule is denser than the surrounding petrous portion of the temporal bone. When the otic capsule is fractured, damage to the cochlea with permanent sensorineural hearing loss commonly results.

Facial nerve – Usually encased in thin bone, the facial nerve exits the internal auditory canal, crosses the middle ear just superior to the oval window and stapes footplate, and then enters the fallopian canal to exit the mastoid via the stylomastoid foramen. From there, it divides into the branches responsible for activity of the muscles of facial expression. During its temporal bone course, the chorda tympani branch "leaves" the facial nerve to carry special sensory afferent fibers for taste from the anterior two-thirds of the tongue. Injury to the facial nerve results in ipsilateral facial paralysis, which can be either partial or complete. Injury to the chorda tympani results in a loss of taste or a metallic taste to the ipsilateral aspect of the anterior two-thirds of the tongue, which often resolves over time.

EVALUATION — Middle ear trauma is typically identified during clinical evaluation.

Initial stabilization — The patient with suspected middle ear trauma should undergo evaluation and management based upon the patient's mechanism of injury and physical findings. The clinician should evaluate unstable patients and those with a high-risk trauma mechanism (table 1) according to the principles of advanced trauma life support (ATLS) (table 2). Middle ear assessment should be part of the secondary survey in these patients. (See "Trauma management: Approach to the unstable child".)

Important stabilization interventions specific to patients with middle ear trauma include:

Patients with significant facial injury sustained during major trauma warrant cervical spine immobilization until appropriate assessment and diagnostic imaging of the neck are performed. (See "Pediatric cervical spinal motion restriction".)

Protruding aural foreign bodies with bleeding should be left in place until they can be fully assessed and removed under controlled conditions by a specialist and possibly in the operating room. Similarly, a foreign body contained within the canal, the tympanic membrane, or the middle ear should be removed under microscopy by an otolaryngologist after completing their assessment.

Contaminated middle ear wounds are considered tetanus prone and require tetanus prophylaxis, as needed (table 3).

History — Awake and alert patients with a history of closed head injury or direct ear trauma should be asked about the following symptoms:

Ear pain

Hearing loss

Nausea and vomiting

Facial weakness

Vertigo

New-onset otorrhea (purulent, bloody, clear, or sticky) or clear, particularly unilateral, rhinorrhea that is worse with straining (Valsalva) or positioning of the head in a dependent position

Imbalance

Tinnitus (suggesting concomitant inner ear damage), which may manifest as intermittent or continuous, loud or soft, high- or low-pitched

Physical examination

Approach — Blood clots in the ear canal in patients with other signs of middle ear trauma should not be removed until the patient is evaluated by an otolaryngologist. In addition, protruding aural foreign bodies should be left in place until they can be fully assessed and removed under controlled conditions by the specialist and possibly in the operating room.

Examination of the ear requires inspection of the auricle and surrounding area; otoscopy of the external canal, tympanic membrane, and middle ear; and, in patients without obvious tympanic membrane perforation, assessment of tympanic membrane function by pneumatic otoscopy (movie 1). In patients with an intact tympanic membrane, decreased motion or immobility of the tympanic membrane, dullness of landmarks, or an air fluid level suggests fluid in the middle ear.

In patients with tympanic membrane perforation, pneumatic otoscopy should be deferred to the specialist because it can potentially push air into the otic capsule leading to nystagmus, vertigo, and nausea or vomiting in patients with otic capsule injuries.

In cooperative patients above five to six years of age, Weber and Rinne tuning fork tests permit the bedside assessment of hearing loss (table 4 and figure 3).

Findings of middle ear injury — Middle ear trauma should be suspected in patients with concerning history and the following findings:

Hemotympanum (picture 1)

Amber or clear middle ear effusion

Otorrhea (clear or bloody ear canal drainage)

Hearing deficit by Weber and Rinne tuning fork tests (table 4 and figure 3)

Nystagmus

Ataxia

Retroauricular hematoma (Battle sign) (picture 4)

Battle sign typically appears two days after injury, but may appear within 6 to 12 hours.

In young children and the older patients, certain patterns of ear trauma (eg, bilateral auricular hematomas) or major injuries (eg, basilar skull fractures) that are unexplained by history raise suspicion for physical abuse. A complete physical examination and additional studies are warranted to identify other signs of abuse in these patients. (See 'Child and elder protection' below and "Physical child abuse: Recognition" and "Elder abuse, self-neglect, and related phenomena".)

Facial nerve function — Facial nerve deficit may arise from direct trauma to the middle ear or in association with a basilar skull fracture [18,19]. Facial nerve function is assessed by observing the response to commands for closing the eyes, elevating the brow, and smiling/frowning. Patients with a peripheral facial nerve palsy associated with middle ear trauma may appear to have a facial droop associated with weakness of the forehead or they may appear to have the eye on the weakened side widely opened and the features of the weak side may be softer with absence of the nasolabial crease. These patients should be differentiated from those with stroke, in whom forehead and eyelid strength are preserved. The nasolabial folds and cheeks will be asymmetrical as the teeth are displayed, and the lower lip may appear to be somewhat hugging the teeth on the affected side. Decreased tearing, hyperacusis, loss of taste sensation on the anterior two-thirds of the tongue, and/or a metallic taste can also indicate facial nerve disruption localized to the fallopian canal. (See "The detailed neurologic examination in adults".)

Facial response to a painful stimulus may be helpful in patients who are unable to cooperate or have altered mental status. Early assessment is crucial as a predictor of prognosis, and it directs management steps in the setting of facial nerve weakness or paralysis. After initial examination and stabilization, patients with significant trauma may be sedated or comatose. This situation often complicates further evaluation of facial nerve function.

Ancillary studies — Patients with clinical features suggestive of middle ear trauma warrant the following studies:

Evaluation of any ear or nose drainage for the presence of cerebrospinal fluid (CSF)

Tests of hearing (ie, active, age-appropriate behavioral testing for alert and cooperative patients or passive testing with auditory brainstem response [ABR] for uncooperative or comatose patients)

The ability to hear a whisper and symmetric hearing by report may suffice as an initial screening test in awake patients if pure tone audiometry is not immediately available. However, patients who do not undergo immediate audiometry should be referred to audiology as soon as possible, ideally within 24 hours.

For patients with head trauma and/or who may require operative intervention, we prefer temporal bone computed tomography (CT) without contrast including fine axial and coronal cuts

Evaluation of otorrhea — In patients with middle ear trauma and otorrhea, the clinician must determine if CSF leakage is occurring and assess for clinical features of basilar skull fracture (eg, presence of cranial nerve deficits, hemotympanum (picture 1), periorbital ecchymosis [raccoon eyes] (picture 5), and ecchymosis over the mastoid [Battle sign]) (picture 4). Testing of drainage and advanced neuroimaging to determine the presence of CSF leakage and to locate the source are discussed separately. (See "Skull fractures in children: Clinical manifestations, diagnosis, and management", section on 'Evaluation of CSF leakage' and "Skull fractures in adults", section on 'Basilar skull fracture'.)

Tests of hearing — Early documentation of hearing status helps counsel patients and guide colleagues with emergency as well as delayed decision-making regarding consultation, further testing, and intervention. Bedside hearing testing is extremely helpful to establish the baseline status at presentation and provide information about the possibility of hearing loss and its nature (eg, conductive or sensorineural). The 512 Hz tuning forks tests are simple tests for quick assessment in the patient who can cooperate with the testing.

The Weber Test helps determine directionality (figure 3) and is labeled right, left, or non-lateralizing.

Is it equal? Then hearing is symmetric and the result is labeled "non-lateralizing."

Is it unequal? Then to which direction does it go, labeled right or left?

To the injury side, this means that a conductive injury is more likely.

Away from the injury side, this means that a sensorineural injury is more likely.

The Rinne Test is a follow-up to the Weber Test (figure 3) and is recorded as positive, negative, or equivocal:

Is sound louder with air conduction (signifying use of the native sound conduction system, including ear canal, tympanic membrane, ossicles)? This is recorded as a positive test result and means that any conductive hearing loss is likely still less than 40 dB (approximately) or that the hearing loss is sensorineural in nature.

Is the sound louder with bone conduction (signifying transmission across the mastoid bone to the otic capsule)? This is recorded as a negative result and means that a conductive hearing loss is more than 40 dB (approximately). With conductive hearing losses at more than 50 to 60 dB, ossicular disruption is highly suspected.

Can the patient not distinguish whether air or bone conduction is louder? This is recorded as an equivocal test.

Cooperative and alert patients over the age of four years should be further tested with ear-specific pure tone audiometry. Pure tone audiometry provides an objective assessment of hearing and is helpful in determining management and prognosis. The ability to hear a whisper and symmetric hearing by report may suffice as an initial screening test if pure tone audiometry is not immediately available. However, patients who do not undergo immediate audiometry should be referred to audiology as soon as possible, ideally within 24 hours. (See "Hearing loss in children: Screening and evaluation", section on 'Formal audiology'.)

Younger children and comatose patients require audiologic consultation and may be best assessed using auditory brainstem response testing. (See "Hearing loss in children: Screening and evaluation", section on 'Brainstem response'.)

Hearing loss at a sound level ≥40 dB is highly suggestive of serious middle ear injury.

The clinician should not rely solely upon subjective evaluation of the status of the patient's hearing because this approach may miss small tympanic membrane perforations, middle ear fluid, or ossicular discontinuity with the potential for permanent conductive hearing loss. However, when subjective evaluation suggests hearing loss, early audiometry and consultation with an otolaryngologist is paramount.

Computed tomography — Temporal bone computed tomography (CT) without contrast, including fine (0.6 mm) cuts in the axial and coronal planes, should be obtained in patients with the following findings [20]:

Evidence of basilar skull fracture (eg, hemotympanum, periorbital or retroauricular hematoma, or CSF otorrhea or rhinorrhea) (see "Skull fractures in children: Clinical manifestations, diagnosis, and management", section on 'Basilar skull fracture')

Patients with head or middle ear trauma and peripheral facial nerve dysfunction [21]

Blunt or penetrating middle ear canal trauma with hearing loss at ≥40 dB or with vestibular symptoms (ie, Tullio's phenomenon, nystagmus or vertigo)

CT may provide better evaluation of the blood-covered structures in patients with hemotympanum and guide medical and surgical decision making. If it is unclear as to whether a CT scan should be obtained, consultation with an otolaryngologist can facilitate judicious management.

Of note, a routine head or brain CT scan is inadequate to assess serious middle ear trauma because it contains cuts that are too broad (1 mm or larger) to image the otic capsule, ossicles, and facial nerve accurately. Furthermore, the coronal images are usually reconstructions, which provide significantly less detail than the directly-obtained coronal image (image 1 and figure 4 and image 2) [21].

In cases where there is suspicion for associated vascular abnormality, a CT-angiogram or CT-venogram may be indicated [20]. A contrast CT of the temporal bone can hamper visualization because extravasation of contrast into the middle ear space as a result of ongoing bleeding may white-out the mastoid cavity and prevent visualization of fractures or identification of the vascular culprit. Thus, the noncontrast temporal bone CT should be obtained before contrast is given. Depending upon the mechanism of injury, a head CT may also need to be obtained in addition to temporal bone imaging.

Although magnetic resonance imaging can be used preoperatively to evaluate the facial nerve, central nervous system, and cerebrovascular anatomy, it does not add additional information to the evaluation of the bony structures such as the ossicles and the fracture line than temporal bone CT [20].

Magnetic resonance imaging (MRI) is contraindicated in the setting of a metallic foreign body in the middle ear (with the exception of a known titanium prosthesis). If the patient has a cochlear implant or magnetic osteo-integrated auditory device, the MRI is not necessarily contraindicated. However, removal of the magnetic component may be necessary prior to entry into the MRI suite. Thus, consultation with an otolaryngologist with implantable hearing device experience is imperative prior to obtaining the study. Patients with devices may also need a device integrity check with an experienced audiologist.

INDICATIONS FOR OTOLARYNGOLOGY CONSULTATION OR REFERRAL — The following findings warrant prompt involvement of an otolaryngologist after middle ear trauma once life-threatening conditions are addressed:

Hearing loss ≥40 dB by formal audiometry or subjective decreased perception of normal speech, marked asymmetry, or persisting feelings of fullness in an ear

Basilar skull fracture in conjunction with evaluation by a neurosurgeon

Suspected cerebrospinal fluid (CSF) otorrhea or rhinorrhea

Facial nerve paralysis/paresis

Vestibular symptoms (nausea, vomiting, nystagmus, ataxia)

Foreign body of the ear canal, tympanic membrane, or middle ear

History of surgically implantable hearing device, such as cochlear implant or osteo-integrated auditory device

MANAGEMENT — Treatment recommendations are based upon observational studies and case series [4,5,13,22,23].

Minimal hearing loss — Traumatic tympanic membrane perforation with minimal hearing loss (decreased perception of whisper, minor asymmetry or <40 dB on formal audiometry) and absence of vestibular findings (eg, nystagmus, vomiting, ataxia) or facial nerve weakness is treated as follows:

Water precautions (keeping water out of the ear)

Antibiotic ear drops (eg, ofloxacin otic drops, five drops in the affected ear two times per day for three to five days) for contaminated wounds (eg, external puncture, perforation with water contamination) and canals occluded with blood or drainage in patients with findings of middle ear trauma

Re-examination by the primary care provider in four weeks in conjunction with formal audiometric evaluation by a clinical audiologist to assess for healing of the tympanic membrane and restoration of normal hearing.

Otolaryngological evaluation for patients with persistent perforation or hearing loss longer than four weeks after injury

Traumatic perforation of the tympanic membrane that is less than 25 percent of the total drum surface area will often heal spontaneously within four weeks in the majority of patients [24]. Persistent perforations typically require operative repair.

Although most tympanic membrane perforations have clean margins, those that fold portions of the membrane into the middle ear may develop into cholesteatomas. Recognition of these lesions requires microscopic otoscopy. (See "Cholesteatoma in children".)

Marked hearing loss — We suggest that patients with middle ear trauma and hearing loss (decreased perception of normal speech, marked asymmetry, or ≥40 dB on formal audiometry), vestibular signs (eg, nystagmus, vomiting, ataxia), findings that indicate basilar skull fracture, or facial nerve injury undergo prompt evaluation by an otolaryngologist. Definitive treatment depends upon the specific injury that is identified. (See "Skull fractures in children: Clinical manifestations, diagnosis, and management", section on 'Basilar skull fracture'.)

Additional measures include:

Water precautions (keeping water out of the ear)

Antibiotic ear drops (eg, ofloxacin otic drops, five drops in the affected ear two times per day for three to five days) for contaminated wounds (eg, external puncture, perforation with water contamination) and canals occluded with blood or drainage in patients with findings of middle ear trauma

Definitive treatment consists of:

Ossicle injury – Ossicular disruption, such as footplate subluxation or overtly displaced ossicular discontinuity requires diagnosis and surgical repair within 48 hours of the injury to obtain the best outcomes. Ossicular joint separation without displacement, akin to a sprain, may benefit most from observation to allow the joint time to heal and hearing to recover. Alternatively, surgical treatment involves middle ear exploration under general anesthesia with relocation or replacement of ossicles [13]. Neglected injuries may result in permanent fixation of the ossicles with significant conductive hearing loss, sensorineural loss or mixed hearing loss. Medical and surgical decision-making requires consultation with an experienced otolaryngologist or neuro-otologist.

Facial nerve injury – Immediate facial nerve paralysis after middle ear or head injury warrants urgent consultation with an otolaryngologist and typically requires surgical intervention [4,18,22].

Delayed paralysis of the facial nerve occurring more than one day after injury typically reflects swelling of the nerve within its bony canal and is predominantly managed medically with intravenous glucocorticoid therapy. Studies of operative decompression suggest no improvement in outcome and note the potential risk of iatrogenic facial nerve injury during surgery [4].

Perilymph fistula – Suspected perilymph fistula requires evaluation by the otolaryngologist to determine the need for urgent middle ear exploration and closure of the fistulous connection with the inner ear [5,15,16].

Basilar skull fracture with cerebrospinal fluid (CSF) leakage – The management of basilar skull fracture with CSF leakage is discussed separately. (See "Skull fractures in adults", section on 'Basilar skull fracture' and "Skull fractures in children: Clinical manifestations, diagnosis, and management", section on 'Basilar skull fractures'.)

Cochlear concussion – Cochlear concussion can cause temporary or permanent sensorineural hearing loss and has no specific therapy. Patients with permanent hearing loss should protect the residual hearing as well as the hearing in the unaffected ear from loud noises or excess barometric pressure (eg, SCUBA diving).

Otic capsule injury – Otic capsule disruption usually causes profound sensorineural hearing loss and has no specific therapy [23]. Patients with permanent hearing loss should protect the unaffected ear from loud noises or excess barometric pressure (eg, scuba diving).

Child and elder protection — In cases where child abuse is suspected, involvement of an experienced child protection team is crucial and in many parts of the world (including the United States, United Kingdom, and Australia) reporting to a governmental agency is mandatory. The safety of other children in the home must be ensured by local Child Protective Services. (See "Child abuse: Social and medicolegal issues", section on 'Reporting suspected abuse' and "Physical child abuse: Diagnostic evaluation and management".)

Similarly, suspected elder abuse often requires involvement of social work, law enforcement, and, if available, adult protective services. (See "Elder abuse, self-neglect, and related phenomena".)

DISPOSITION — Patients with simple tympanic membrane perforation and hearing that is normal or shows a deficit of <40 dB by formal audiometry may be discharged to home care with appropriate treatment and follow-up with their primary care provider in four weeks. If audiometry is not urgently available, it should be performed within 24 hours of injury so that ossicle disruption or subluxation, if present, is detected and appropriate surgical consultation and operative intervention can occur. Audiometric studies may be warranted at follow-up to determine progression or improvement, and four weeks is a good first interval. (See 'Minimal hearing loss' above.)

The following conditions warrant hospital admission for observation, operative repair, or both:

Acute basilar skull fracture (especially with cerebrospinal fluid [CSF] leak)

Ossicular disruption

Acute traumatic facial nerve paralysis

Perilymph fistula

Refractory nausea/vomiting may require intravenous fluid management and antiemetics, such as ondansetron

In addition to these conditions and when audiometry is available, patients with hearing loss at ≥40 dB often have an associated condition that warrants hospital admission for definitive otolaryngological evaluation and treatment (See 'Marked hearing loss' above.) For example, ossicular disruption may be associated with a perilymph fistula and persisting, severe, acute nausea and vomiting or nystagmus and gait instability with significant fall risk. The former may be treated with hospitalization for intravenous fluid administration and treatment with non-vestibulo-suppressive antiemetics, such as ondansetron; the latter may require restriction to bedrest until gait symptoms subside.

OUTCOMES — Permanent hearing loss, persistent facial nerve palsy, and cerebrospinal fluid (CSF) fistula with significant risk for meningitis comprise the major long-term complications of middle ear trauma.

Hearing loss – When hearing loss accompanies middle ear trauma, recovery rates vary depending on the type of injury [9,25]. Conductive hearing loss is often reversible (eg, as effusions resolve) and is often amenable to surgical therapy, if indicated. Sensorineural hearing loss is generally permanent. There are no surgical interventions and it may not be amenable to amplification with traditional hearing aids, but cochlear implantation may be considered in the appropriate candidate. Specific outcomes include [26]:

Conductive hearing loss caused by tympanic membrane perforation, hemotympanum, or serous or CSF middle ear effusion will resolve with healing of the tympanic membrane pathology or resolution of the middle ear fluid [27]. Persistent tympanic membrane perforations can be repaired with good results. Persistent middle ear effusion can be alleviated with resultant improved hearing with myringotomy with or without ventilation tube placement. A persistent serous drainage after tube placement is concerning for ongoing CSF leak, which should be evaluated. (See 'Evaluation of otorrhea' above.)

In patients with persistent pure conductive hearing loss related to ossicular disruption or stapes footplate subluxation, surgical repair or hearing aids are likely to fully or partially restore lost hearing. Ossicular disruption can be treated by ossiculoplasty; however, complete restoration cannot be guaranteed. Alternatively, ossicular joint separation without displacement may resolve over a period of weeks to months as the fibrous attachments contract during healing. Hearing losses <40 dB are less likely to benefit from surgical intervention.

Sensorineural hearing loss in association with otic capsule disruption is usually severe to profound and is not improved by surgery or hearing aids. Injuries (unilateral or bilateral) resulting in profound hearing loss would qualify a patient for consideration for cochlear implantation as therapy.

Cochlear concussion results in temporary or permanent sensorineural hearing loss. When hearing loss is persistent, it varies from an isolated sensorineural deficit at <40 dB to profound hearing loss.

Sensorineural hearing loss in association with otic capsule disruption is usually severe to profound and is not improved by surgery or hearing aids. Bilateral injuries resulting in profound hearing loss would qualify a patient for consideration for cochlear implantation as therapy.

For patients who have sustained a perilymphatic fistula, sensorineural hearing loss usually persists, but vestibular symptoms typically resolve spontaneously within 48 hours [28]. Patients with prolonged vertigo caused by middle ear trauma often benefit with full recovery after surgical repair.

Traumatic facial nerve injuries – Outcomes for traumatic facial nerve paralysis vary dramatically depending upon the mechanism of injury, time at diagnosis, medical treatment steps taken and surgical treatment steps required [4,29]:

Injuries that present with initial facial movement and are later complicated by the development of facial nerve paralysis tend toward full functional recoveries. However, bone shards clearly visualized as embedded in the nerve on CT scanning can be removed with similar good outcomes.

Post-injury edema can often be managed with intravenous steroids. Functional recovery is good in most patients who by electroneurography (ENG) continue to have no more than 90 percent degeneration and is unlikely to warrant surgical intervention. Debate remains regarding the benefit of nerve decompression if there is greater than 90 percent degeneration between days 3 and 14 after injury.

A clear impaction (eg, bone shard in nerve) or transection injury (eg, gunshot wound) with nerve tissue loss usually presents with immediate and complete facial nerve paralysis [4]. In this event, it is unlikely that the nerve will regain function and highly likely that a nerve repair or a facial nerve reinnervation procedure will be necessary.

The best opportunity for the surgeon to identify the remnants of the nerve (even if only to tag them for future repair) is during the initial wound exploration with cleaning and wound closure. It is helpful to consult your otolaryngology (facial plastics) expert or your plastic surgeon early in this type of injury for optimal recommendations [30,31]. End-to-end nerve repairs are the most likely to recover acceptable function. Delayed repairs or those requiring grafts are less likely to have desirable outcomes.

Reinnervation procedures via interposition nerve grafting are complicated by synkinesis, wherein there is lack of organization to the reinnervation process and multiple motor units fire simultaneously. In the case of repair of facial nerve injury delayed by years, results are less predictable and the restoration of function using the nerve itself is less successful due to motor unit atrophy caused by the prolonged lack of nutritive footplate signaling. Nerve/muscle tissue transfer procedures are more successful but remain limited by the donor nerve/muscle group placement (eg, gracilis muscle to cross facial jump graft) and donor nerve function (ie, hypoglossal or trigeminal jump graft).

Delayed facial nerve paralysis in the setting of basilar skull fracture of the temporal bones is associated with normal or near normal recovery in most patients by three months. Recovery may take as long as one year in some patients [4].

Traumatic CSF fistula – Observational evidence suggests that the risk of meningitis is significantly increased in patients with a CSF leak after a middle ear injury, especially those patients whose drainage lasts longer than seven days. In a case series of 122 patients, most of whom had otorrhea, the risk of meningitis was 3 percent among patients who experienced spontaneous resolution of the leak within seven days [4]. The frequency of meningitis increased to 22 percent in patients with CSF leakage beyond seven days. Prophylactic antibiotics did not appear to prevent meningitis unless obvious local infection was present. However, an adequate course of antibiotics was administered in only 22 percent of patients in this case series [4].

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Ruptured eardrum (The Basics)")

SUMMARY AND RECOMMENDATIONS

Epidemiology – Middle ear injury may occur after head injury and blunt or penetrating trauma to the ear. Damage may involve the ossicles, facial nerve, oval window, and/or inner ear (figure 1). (See 'Epidemiology' above and 'Clinical anatomy' above.)

Initial stabilization – The patient with suspected middle ear trauma should undergo evaluation and management based on the patient's mechanism of injury and physical findings. The clinician should evaluate unstable patients and those with a high risk trauma mechanism (table 1) according to the principles of advanced trauma life support (ATLS) (table 2). Middle ear assessment should be part of the secondary survey in these patients. The immediate functional status of the facial nerve should also be observed and documented as part of the secondary survey. (See 'Physical examination' above.)

Evaluation – Clinical findings identify middle ear trauma and guide ancillary studies and treatment.

History – Historical features that suggest serious trauma to the middle or inner ear include hearing loss, facial weakness, vertigo, nausea and vomiting, otorrhea, and/or ataxia. (See 'History' above.)

Physical examination – Blood clots in the ear canal should not be removed until the patient is evaluated by an otolaryngologist (ENT surgeon). In addition, protruding aural foreign bodies should be left in place until they can be fully assessed and removed under controlled conditions by an otolaryngologist. Additionally, use of imaging modality (eg, magnetic resonance imaging [MRI]) may be affected by the material content of the foreign body. (See 'Physical examination' above.)

Concerning findings on physical examination include otorrhea, rhinorrhea, hemotympanum (picture 1), post-traumatic serous middle ear effusion, facial nerve weakness, abnormal Rinne and Weber tuning forks tests, nystagmus, or Battle sign (ecchymosis over the mastoid/occiput). (See 'Facial nerve function' above and 'Findings of middle ear injury' above.)

Patients with clinical features suggestive of middle ear trauma warrant the following studies (see 'Ancillary studies' above):

-Evaluation of any ear drainage for the presence of cerebrospinal fluid (CSF)

-Tests of hearing

-For patients with head trauma, temporal bone computed tomography without contrast including fine axial and coronal cuts

Indications for specialty consultation – Patients with the following findings after middle ear trauma warrant prompt evaluation by an otolaryngologist once life-threatening conditions are addressed (see 'Indications for otolaryngology consultation or referral' above):

Hearing loss ≥40 dB if formal audiometry is available, or a subjectively decreased ability to hear a whisper or asymmetric appreciation of sounds between the two ears

Basilar skull fracture in conjunction with a neurosurgeon (see "Skull fractures in children: Clinical manifestations, diagnosis, and management", section on 'Basilar skull fracture')

Otorrhea or rhinorrhea

Facial nerve paralysis

Vestibular symptoms (nausea, vomiting, nystagmus, ataxia)

History of surgically implantable hearing device

Management – Management is determined by the degree of hearing loss:

Minimal hearing loss and isolated tympanic membrane perforation – Patients with small isolated tympanic membrane perforation <25 percent in size and minimal hearing loss (<40 dB, decreased perception of whisper or minor asymmetry) may be managed with water precautions (keeping water out of the ear), antibiotic otic drops (for contaminated wounds), recommendation for audiometry within 24 hours if not previously obtained, and follow-up with their primary care provider and audiologist (if loss was present) in four weeks to ensure that the perforation is closed and hearing deficit has resolved. (See 'Minimal hearing loss' above.)

Marked hearing loss, vestibular injury, basilar skull fracture, or facial nerve injury – Patients with middle ear trauma and hearing loss ≥40 dB, vestibular signs (eg, nystagmus, vomiting, ataxia), findings that indicate basilar skull fracture, or facial nerve injury should undergo emergency evaluation by an otolaryngologist whenever possible, but at least within 48 hours of injury. Definitive treatment depends upon the specific injury that is identified. (See 'Marked hearing loss' above.)

Child and elder protection – In young children and older adults, certain patterns of ear trauma (eg, bilateral auricular hematomas) or major injuries (eg, basilar skull fractures) that are unexplained by history may indicate physical abuse. In cases where child abuse is suspected, involvement of an experienced child protection team is crucial and in many parts of the world (including the United States, United Kingdom, and Australia) reporting to a governmental agency is mandatory. (See 'Evaluation' above and 'Child and elder protection' above.)

ACKNOWLEDGMENT — The editorial staff at UpToDate would like to acknowledge Steven D Handler, MD, MBE, who contributed to earlier versions of this topic review.

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References

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