Chapter 59. Temporal Bone Trauma

Essentials of Diagnosis

• History of trauma to ear or foreign body insertion into the ear
• Symptoms of pain and hearing loss
• Bloody otorrhea.

General Considerations

Injuries localized to the external or middle ear include auricular hematoma, external auditory canal abrasion or laceration, tympanic membrane perforation, and ossicular chain dislocation. Local trauma to the tympanic membrane and ossicles can occur by a penetrating injury with objects such as a cotton-tipped applicator, a bobby pin, a pencil, or a hot metal slag during welding. In addition, barotrauma, such as a slap to the ear or a blast injury, can cause a tympanic membrane perforation or ossicular chain dislocation.

Auricular Hematoma

An auricular hematoma may present after a forceful blow to the external ear. It can be recognized as a tender swelling of the pinna that is fluctuant on palpation. The hematoma arises after the perichondrium is sheared off the cartilage of the auricle. This fluid accumulation needs to be drained to prevent chondronecrosis and lead to a misshapen pinna, commonly known as a “cauliflower ear” or “wrestler's ear.” After incision and drainage, a compression dressing is sutured through the pinna to bolster the skin and perichondrium against the auricular cartilage, preventing reaccumulation of the fluid.

External Auditory Canal Abrasion

Injuries to the external auditory canal most commonly occur when a patient is trying to remove his or her own earwax with a cotton-tipped applicator or bobby pin. The injury is usually a simple abrasion or laceration. Treatment consists of using an antimicrobial otic drop to prevent bacterial or fungal superinfection of the area. Alternately, there may be a localized area of blood collection underneath the skin of the external auditory canal, called a bulla. Perforating the tense bulla with a sharp pick often helps to reduce the patient's discomfort. Patients with diabetes have a high risk of developing external otitis from this type of injury because of their poor microcirculation. These patients need to be followed up closely to verify wound healing.

Tympanic Membrane Perforation

A tympanic membrane perforation can occur after the use of a cotton-tipped applicator, a bobby pin, a pencil, or the entry of a hot metal slag into the ear canal during welding. Finally, barotrauma, such as a slap to the ear or a blast injury, can cause a perforation. In all cases, patients usually complain of pain and hearing loss, and the perforation can be diagnosed by otoscopy. It is important to note how much of the tympanic membrane has been perforated. A central perforation does not involve the annulus of the eardrum, whereas a marginal perforation does. In addition, the Weber tuning fork test should be performed to verify that it radiates to the affected ear, and the eyes should be checked for nystagmus. If the Weber test does not radiate to the affected ear and the patient has nystagmus, it is likely that stapes subluxation with sensorineural hearing loss has occurred. This is termed a perilymphatic fistula and requires urgent treatment (see Perilymphatic Fistula, Treatment).

If no evidence of sensorineural hearing loss is found, no specific treatment is required because traumatic tympanic membrane perforations, especially central perforations, typically heal spontaneously. However, strict dry ear precautions should be followed to prevent water from getting into the ear. Instructions to the patient include no swimming and use of a cotton ball thoroughly coated with petrolatum (eg, Vaseline) in the affected ear during bathing. An audiogram should be performed after about 3 months to verify that hearing has returned to normal and that there is no ossicular chain discontinuity. If the perforation has not healed by 3 months, a tympanoplasty will likely need to be performed.

Ossicular Chain Dislocation

Penetrating trauma with objects such as a cotton-tipped applicator, a bobby pin, or a pencil can injure the ossicular chain (after perforating the tympanic membrane). Barotrauma, such as a slap to the ear, a blast injury, or rapid decent in an aircraft, can cause ossicular chain dislocation without tympanic membrane perforation. Ossicular chain dislocation with an intact eardrum manifests as a maximal (60 dB) conductive hearing loss. Ossicular chain dislocation with a perforated eardrum results in lesser degrees of hearing loss. Treatment in any case is middle ear exploration and ossicular chain reconstruction, with tympanoplasty if needed.

Essentials of Diagnosis

• History of blunt head trauma
• Symptoms of hearing loss and possibly vertigo and facial nerve palsy
• Signs include Battle sign, hemotympanum, and bloody otorrhea.

General Considerations

The skull base includes the frontal bone, the sphenoid bone, the temporal bone, and the occipital bone. A fracture in the skull base (otherwise known as a basilar skull fracture) must involve at least one of these bones and may involve all of them. Temporal bone fractures represent roughly 20% of all skull fractures. Risk factors include being male and under 21. The most common causes include motor vehicle accidents, falls, bicycle accidents, seizures, and aggravated assaults. Blunt trauma to the lateral surface of the skull (the squamous portion of the temporal bone) often results in a longitudinal fracture. A blow to the occipital skull may go through the foramen magnum and result in a transverse fracture of the temporal bone (Figure 59–1).

Pathogenesis

Longitudinal fractures involve the squamous portion of the temporal bone, follow the axis of the external auditory canal to the middle ear space, and then course anteriorly along the geniculate ganglion and eustachian tube, ending near the foramen lacerum. In a longitudinal temporal bone fracture, the otic capsule is spared. In contrast, transverse fractures course directly across the petrous pyramid, fracturing the otic capsule, and then extend anteriorly along the eustachian tube and geniculate ganglion. Longitudinal temporal bone fractures and transverse temporal bone fractures represent 80% and 20%, respectively, of temporal bone fractures.

Clinical Findings

Symptoms and Signs

Symptoms include hearing loss, nausea and vomiting, and vertigo. Clinical signs include Battle sign, which is a postauricular ecchymosis resulting from extravasated blood from the postauricular artery or mastoid emissary vein. The “raccoon” sign (periorbital ecchymosis) is associated with basilar skull fractures that involve the middle or anterior cranial fossa. Physical examination may demonstrate an external auditory canal laceration with bony debris within the canal. A hemotympanum is almost always identified. Cerebrospinal fluid (CSF) otorrhea or rhinorrhea may be seen. Tuning fork tests should always be performed on patients with a temporal bone fracture. The Weber tuning fork test radiates to the fractured ear if conductive hearing loss is present and radiates to the contralateral ear if sensorineural hearing loss is present. The presence or absence of facial nerve paralysis should be documented in all patients with temporal bone fractures.

Imaging Studies

After initial resuscitation in the emergency room, computed tomography (CT) scanning of the head is usually the first study performed on patients with head trauma. It is critical to rule out an intracranial hemorrhage, which may require urgent neurosurgical treatment. It is at this point that a temporal bone fracture is usually identified. High-resolution CT scanning of the temporal bone is valuable in delineating the extent of the fracture, but it is not required unless a complication is suspected (eg, otic capsule fracture, facial nerve injury, or CSF leak). Patients with a longitudinal fracture associated with hemotympanum, without nystagmus, without evidence of CSF leak, with a Weber tuning fork test that radiates to the affected ear, and with normal facial nerve function typically do not need a CT scan of the temporal bone. Angiography may be performed if there is significant hemorrhage from the skull base to rule out vascular injury, but this is uncommon.

Special Tests

Audiometry

Audiometry should be performed on all patients with a temporal bone fracture. However, this does not need to be done acutely in most cases. If clinical examination is consistent with conductive hearing loss and there is no evidence of otic capsule fracture, audiometric assessment can be performed several weeks after the injury, permitting time for the hemotympanum to resolve. If the otic capsule is fractured, there is a high likelihood of permanent complete sensorineural hearing loss and there is no treatment available to alter this prognosis. Urgent audiometry may be considered if stapes subluxation into the vestibule has occurred and surgery to repair a perilymph fistula is planned.

Facial Nerve Testing

Facial nerve testing should be performed if a delayed, complete facial palsy occurs. The rationale is to identify patients with >90% degeneration of the facial nerve, because these patients have poorer recovery of the function and may benefit from surgical decompression. The nerve excitability test is performed by placing the two probes of a Hilger nerve stimulator across the stylomastoid foramen and slowly turning up the current until a facial twitch is just barely visible. This is the stimulation threshold of the facial nerve. A 3.5-mA difference between the injured and uninjured sides correlates with a > 90% loss of neural integrity.

Alternately, electroneuronography can be performed by a neurophysiologist. This involves stimulating both facial nerves with equal currents while simultaneously measuring the evoked myogenic potential in the muscles of facial expression. If the amplitude of the ipsilateral evoked potential is < 10% of that from the contralateral side, >90% loss of neural integrity has occurred. Neither of these tests is accurate within 3 days of the injury because it takes about 72 hours for nerve fibers distal to the site of the injury to degenerate. Nonetheless, surgical decompression of delayed facial paralysis remains controversial.

Complications

Conductive Hearing Loss

Conductive hearing loss is most commonly due to hemotympanum, but may also represent a tympanic membrane perforation or ossicular discontinuity. The most common form of ossicular discontinuity after temporal bone trauma is incudostapedial joint dislocation. The second most common is incudomalleolar joint dislocation (Figure 59–2). In addition, ossicular fixation may occur several months after the trauma if new bone formation at the line of the fracture fuses to the ossicular chain.

Sensorineural Hearing Loss and Vertigo

These complications are found in patients who sustain a transverse temporal bone fracture with otic capsule involvement (Figure 59–3). Pneumolabyrinth (air in the inner ear) is often noted by CT. An audiogram usually demonstrates a complete sensorineural hearing loss in the affected ear. Acutely, clinical examination also reveals nystagmus, which is consistent with a unilateral vestibular deficit. Sensorineural hearing loss can also be sustained without otic capsule fracture if a labyrinthine concussion, traumatic noise exposure, or blast injury occurs. This is thought to involve tearing of the cochlear membranes and/or trauma to the hair cell epithelium due to the rapid acceleration and deceleration forces within the inner ear. These injuries can manifest either as a high-frequency hearing loss, atemporary threshold shift in their hearing that resolves, or a permanent and complete sensorineural hearing loss.

Facial Nerve Injury

Facial nerve palsy occurs in 20% of longitudinal temporal bone fractures and 50% of transverse temporal bone fractures. The most important clinical feature to identify is whether the facial nerve palsy was of delayed or immediate onset. Patients with delayed-onset palsy present to the emergency room with normal facial nerve function that slowly worsens over the next several hours to days. This is thought to represent edema within the facial nerve without disruption of neural integrity. In contrast, immediate facial nerve injury is highly suggestive of facial nerve transection. Unfortunately, it is common to have an undetermined onset time of facial nerve palsy because patients with temporal bone fractures and facial nerve palsy typically have many other life-threatening issues that are being dealt with at the time of the initial evaluation. These patients are often comatose and therefore difficult to examine.

Cerebrospinal Fluid Leak

There is a 2% incidence of CSF leak in all skull fractures and a 20% incidence in temporal bone fractures. CSF leaks usually start within the first 48 hours of the trauma and are noted as clear fluid emanating from the ear or nose. Straining, standing up, or bending over worsens the CSF leak. If clear fluid emanating from the nose or ear is suggestive of a CSF leak, the fluid can be collected and sent for β2 transferrin testing. β2 transferrin is a protein found only in CSF.

Posttraumatic Encephalocele

Posttraumatic encephalocele can result if a large defect in the floor of the middle cranial fossa occurs. Dura and temporal lobe brain can herniate down into the middle ear and mastoid. This can sometimes be visible on otoscopic examination of the ear as a white mass with blood vessels behind the tympanic membrane. A CSF leak can occur in combination with an encephalocele.

Perilymphatic Fistula

A perilymphatic fistula can occur after a fracture of the otic capsule or stapes subluxation of the oval window. It manifests as fluctuating vertigo and sensorineural hearing loss. This entity is fully described later in this chapter.

Treatment

Conductive Hearing Loss

A hemotympanum resolves spontaneously within 34 weeks of the injury with no sequelae. Traumatic tympanic membrane perforations have an excellent chance of healing spontaneously. Within 1 month, 68% are healed; within 3 months, 94% are healed. If the perforation has not healed by 3 months, a paper-patch myringoplasty can be attempted in the office. This should be performed only if the perforation is quite small (<25%) and does not involve the margins of the eardrum and if the middle ear mucosa appears uninfected and dry. The edges of the perforation are freshened with a Rosen needle and a paper patch (cigarette paper or a Steri-Strip) is placed over the perforation.

If the perforation is large or has failed an attempt at paper-patch myringoplasty, the patient should be taken to the operating room for a standard tympanoplasty. The ossicular chain should also be explored to verify that it is intact during this procedure. A patient with a normal tympanic membrane and persistent conductive hearing loss probably has ossicular chain discontinuity. A middle ear exploration should be done through the canal by raising a tympanomeatal flap and carefully inspecting and palpating the ossicles. Ossicular chain reconstruction is based on the site of the injury.

Facial Nerve Paralysis

The treatment of delayed-onset palsy is based on conservative, nonsurgical management. It is expected that 94% to 100% of these patients will have complete and full recovery of their facial nerve function. However, patients with > 90% degeneration of neural integrity have been shown to have poor recovery. Presumably, the nerve is swollen within the bony fallopian canal, compressing itself within this confined space and therefore causing permanent injury to the nerve fibers.

The management of patients with > 90% degeneration is controversial. Although some neurotologists recommend facial nerve exploration and decompression, others recommend watchful waiting. In contrast, there is no controversy about patients with immediate-onset facial palsy. These patients should undergo facial nerve exploration as soon as the patient is medically stabilized. Human studies have not proved that early surgery improves the long-term facial nerve outcome, but animal studies suggest that intervention within 21 days of facial nerve transection is beneficial.

The exploration of posttraumatic facial nerve palsy is based on two routes. If the patient has normal hearing, a combined middle fossa-transmastoid facial nerve exploration is performed (Figure 59–4). This includes a subtemporal craniotomy with delineation of the facial nerve within the internal auditory canal from the porus acousticus internus to the geniculate ganglion. A mastoidectomy is also performed to explore the facial nerve from the middle ear to the stylomastoid foramen. If the patient has a complete sensorineural hearing loss, a translabyrinthine facial nerve exploration and repair can be undertaken (Figure 59–5). This approach allows for complete exposure of the facial nerve from the porous acousticus to the stylomastoid foramen completely through the mastoid.

Injuries are most commonly located in the area of the geniculate ganglion. If an intraneural hematoma is identified, the epineurium should be carefully opened and the hematoma evacuated. If bony fragments are impinging upon the nerve, these can be carefully removed as well. If there is an obvious fracture of the facial nerve, the two ends of the facial nerve should be freshened and anastomosed. If the segment of missing nerve is too long to be easily anastomosed without tension, an interposition nerve graft should be used from the greater auricular or sural nerve. If no pathology is visualized, the act of opening the bony canal of the facial nerve should allow adequate decompression and permit swelling of the nerve without impingement. The epineurium does not need to be incised.

Cerebrospinal Fluid Leak and Encephalocele

Eighty percent of posttraumatic CSF leaks close spontaneously after 7 days, and the risk of meningitis is quite low (3%) within this time period. Thus, medical treatment is attempted initially. This includes head elevation, stool softeners, acetazolamide (to decrease CSF production), and the placement of a lumbar drain. Patients with intracranial hemorrhage who have undergone craniotomy often already have an intraventricular drain in place, in which case a lumbar drain is not needed. Short-term antibiotics have been shown to be useful in preventing meningitis. The most common organisms that cause meningitis in this situation are Pneumococcus, Staphylococcus, Streptococcus, and Haemophilus influenzae. If the CSF leak persists for more than 7–10 days, the risk of meningitis increases dramatically (>20%) and surgical repair of the CSF leak should be performed. This situation is most common in patients who sustain a transverse temporal bone fracture with CSF leaking through the otic capsule. Otic capsule bone does not heal with new bone formation but by fibrous union, and this is often not strong enough to contain CSF.

An encephalocele should always be surgically repaired. If the patient has normal hearing, the repair of either a persistent CSF leak or an encephalocele is via a combined middle fossa craniotomy-transmastoid approach with dural repair and skull base reconstruction. In a patient with no useful hearing, obliteration of the ear with an abdominal fat graft, plugging of the eustachian tube, and closure of the ear canal can be performed through the mastoid alone.

Essentials of Diagnosis

• Usually caused by a gunshot wound
• Significant soft-tissue deficit
• High likelihood of facial nerve palsy and vascular injury.

General Considerations

Penetrating trauma, predominantly from gunshot wounds, is much more damaging to the temporal bone than is blunt trauma. There is often significant injury to the external auditory canal, which requires local debridement of bone fragments and soft tissue, as well as stenting with Merocel wicks (a type of expandable, nonabsorbable sponge) to prevent stenosis. If stenosis does occur after several months, a canaloplasty may be required. Soft tissue loss may require regional or free-flap reconstruction. Tympanic membrane perforation, ossicular discontinuity, and labyrinthine fracture are also common entities with a gunshot wound to the temporal bone. Epithelial elements can be introduced into the mastoid or middle ear cavities and not be detected as a cholesteatoma until years later.

Vascular Injury

The most important aspect of penetrating trauma to the temporal bone is the potential for injury to the internal carotid artery, internal jugular vein, or dural sinuses. Vascular injury is found in 32% of patients with penetrating trauma to the temporal bone; therefore, these injuries should be considered as penetrating trauma to Zone III of the neck and treated accordingly. Angiography should be performed on all patients, with embolization or balloon occlusion used to control bleeding from the skull base. If the hemorrhage continues or there is evidence of major vessel injury on an angiogram, surgical exploration may be required. In the event that internal carotid artery laceration is found, Fogarty catheters can be used temporarily to control bleeding.

Facial Nerve Injury

The rate of facial nerve paralysis with penetrating trauma to the temporal bone is 36%. Facial nerve injury most commonly occurs in the tympanic and mastoid segments. Essentially all of these injuries are of immediate onset and occur because of nerve transection. Facial nerve electrophysiologic testing with a Hilger stimulator can be used to identify facial nerve trauma in a comatose patient. Facial nerve repair needs to be undertaken as soon as the patient is medically stable.

Essentials of Diagnosis

• History of head trauma or previous stapedectomy
• Fluctuating hearing loss and episodic vertigo worse with straining

General Considerations

The most common cause of a perilymph fistula is when a long thin object (eg, pencil, bobby pin, Q-tip) is jammed into the ear canal, pushing the stapes into the vestibule. Barotrauma during scuba diving, a rapid descent in an airplane, an explosion, or straining during a difficult childbirth may also cause a perilymphatic fistula. A postsurgical perilymphatic fistula is also a well-recognized entity. It can occur after stapedectomy if the oval window fails to seal appropriately. Poor surgical technique while performing a mastoidectomy can lead to an iatrogenic lateral canal fistula. In addition, an expanding cholesteatoma can erode into the lateral semicircular canal or cochlea, causing a fistula. Finally, patients may present with a congenital perilymphatic fistula. These patients typically have stapes footplate anomalies or other temporal bone anomalies that are identified on CT scan. The superior semicircular canal dehiscence syndrome may be identified by CT scan, with a fistula from the superior canal into the intracranial space.

Clinical Findings

Symptoms and Signs

While much has been written about chronic perilymphatic fistula as a cause of chronic, episodic vertigo, most of this literature was written prior to modern imaging techniques. Most commonly, patients with a perilymphatic fistula present with acute onset of hearing loss, disequilibrium, and vertigo, after some inciting trauma or event. Symptoms may worsen with a Valsalva maneuver, such as coughing, sneezing, or straining. Occasionally, an altitude change, such as going up and down in an airplane or in an elevator, can precipitate symptoms. Patients may complain of Tullio phenomenon, whereby loud noises precipitate a vertiginous attack. Clinically, the fistula test can be performed by insufflating air into the external auditory canal and observing the patient for evidence of nystagmus. This test is very insensitive and is positive in only about 50% of patients with a fistula. Also, it is nonspecific because many patients without a fistula experience disequilibrium during this test.

Laboratory Findings

None

Imaging Studies

Modern CT techniques are quite good at detecting subluxaton of the stapes into or out of the vestibule. As well, perilymph leakage out of the vestibule can be noted as a soft tissue density material around the oval window niche.

Special Tests

Audiometry typically will demonstrate a mixed hearing loss. Vestibular testing may demonstrate a unilateral deficit. Nystagmus elicited by straining can be documented using electronystagmography monitoring and then evaluated. An abnormally low VEMP (vestibular evoked myogenic potential) threshold is often associated with superior semicircular canal dehiscence syndrome.

The only definitive way to make the diagnosis of a perilymphatic fistula is surgical exploration with visualization of the leak. Even this evaluation is not necessarily definitive since it is difficult to verify that small amounts of clear fluid within the middle ear cavity represent a perilymphatic leak and not serous transudate from the middle ear mucosa. Fluid suggestive of perilymph can be sampled on an absorbable gelatin sponge (eg, Gelfoam pledget) and sent for β2 transferrin testing. β2 transferrin is a protein found only in CSF and perilymph; it is not found in other fluids of the body. Although the test result is not immediately available, it may be useful when following up these patients postoperatively.

Differential Diagnosis

The differential diagnosis includes all causes of hearing loss and dysequilibrium, most notably Meniere disease and bacterial labyrinthitis.

Complications

Complete sensorineural hearing loss and unilateral vestibular deficit can occur if the inner ear becomes inflamed (labyrinthitis). Since there is a fistula from the middle ear space to the inner ear, an episode of acute otitis media is worrisome because bacteria in the middle ear can easily enter the inner ear and CSF. This may lead to meningitis.

Treatment

When the suspicion for a perilymph fistula is high, an urgent middle ear exploration is usually performed. This is done by a transcanal approach with elevation of the tympanomeatal flap and careful examination of the oval and round windows. If the stapes has been subluxed, it can usually be repositioned in the correct location and held in place with Gelfoam pledgets until it heals properly. If a defect is noted, a graft of fascia, perichondrium, or vein should be laid over the defect. If needed, ossicular chain reconstruction may be performed simultaneously as long as the prosthesis is supported laterally (ie, clipped onto the incus) so it will not push down into the vestibule over time.

When the suspicion for a perilymph fistula is low, treatment is based on conservative therapy. The patient should be at bed rest with head elevated. Patients are placed on stool softeners and serial audiograms should be obtained to follow up for evidence of disease progression. If symptoms persist or the sensorineural hearing loss worsens, surgical treatment may be considered. One option is to simply draw blood from the patient's arm and inject it through the eardrum into the middle ear space. This blood seal may help allow a fistula to heal.