Temporal Bone Fractures Treatment & Management

Updated: Nov 21, 2017
  • Author: Antonio Riera March, MD, FACS; Chief Editor: Arlen D Meyers, MD, MBA  more...
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Medical Therapy

Generally, a patient with delayed facial paralysis is managed conservatively with 10-14 days of systemic corticosteroids unless medically contraindicated. A patient with complete paralysis of immediate onset undergoes initial testing with the nerve Hilger stimulator between days 3 and 7. If no loss of stimulability occurs, patients are observed. If the nerve loses stimulability within one week or more than 90% degeneration on ENOG occurs within 2-3 weeks, the threshold for surgical exploration has been reached.



Common complications of temporal bone fractures include hearing loss, CSF fistula, facial nerve paralysis, external auditory canal stenosis, cholesteatoma formation, and vascular injuries. Hearing loss is the most common complication and can be conductive, sensorineural, or mixed type.

Conductive hearing loss

Conductive hearing loss is frequently observed with longitudinal fractures and is caused by hemotympanum, tympanic membrane perforation, or partial or complete ossicular chain disruption. Ossicular chain dislocation is more common than ossicular chain fracture. Tympanic membrane perforations and hemotympanum usually resolve in 3-4 weeks.

Axial and coronal HRCT scans are helpful for diagnosing ossicular chain dislocation. The most common ossicle involved in temporal bone trauma is the incus because it is less stable, having weak attachments to the malleus and stapes. Furthermore, the malleus is anchored by the tensor tympani muscle and its tendon, and the stapes is anchored by the stapedius muscle and its tendon. They contract during trauma and pull the incus medially. This movement is accentuated by the trauma, causing medial dislocation of the incus.

The following chain abnormalities have been identified with temporal bone fractures: [14, 29]

  • Incudostapedial joint separation: The incudostapedial joint is the most common site of traumatic separation. (82%)

  • Incus dislocation (57%)

  • Fracture of the stapes crura (30%)

  • Fixation of the ossicles in the attic (25%)

  • Incudomalleolar joint separation

Other lesions, such as delayed necrosis of the long process of the incus, dislocation of the stapes footplate, and dislocation of the malleus are possible but are not commonly seen.

Most nondisruptive conductive hearing losses resolve spontaneously. If conductive hearing loss is present at greater than 30 dB after 2 months, consider surgical exploration unless the conductive hearing loss is in the only hearing ear. Middle ear exploration/reconstruction in cases of traumatic etiology achieves better functional results compared with middle ear reconstruction for chronic ear infection. [30]

See also the Medscape Drugs & Diseases article Ossiculoplasty.

Sensorineural hearing loss

Sensorineural hearing loss can occur in temporal bone fractures with involvement of the otic capsule (cochlea, vestibule, and semicircular canal) and/or internal auditory canal. Sensorineural hearing loss can also occur with intralabyrinthine bleeding without evidence of temporal bone fracture. Severe-to-profound sensorineural hearing loss most commonly occurs in patients who have transverse fractures with otic capsule involvement. Partial sensorineural loss is also possible. Mild high-frequency loss (5-kHz notch) may occur in longitudinal fractures from cochlear concussion. Blood products and cellular disruption are present on histopathology associated with sensorineural hearing loss.

On physical examination, spontaneous nystagmus observed by the naked eye is an important clinical sign in the acute phase of temporal bone trauma. It is usually related to a transverse temporal bone fracture with damage to the cochlea and semicircular canals.

Before considering cochlear implant, labyrinthitis ossificans must be considered when bilateral severe sensorineural hearing loss is present. Progressive sensorineural hearing loss has also been reported with and without vertigo. When vertigo is present with fluctuating or progressive loss, traumatic endolymphatic hydrops or perilymphatic fistula is the diagnosis. Autoimmune hearing loss may account for some cases of progressive hearing loss.

Mixed hearing loss

Mixed conductive and sensorineural hearing loss may be difficult to detect in the presence of severe sensorineural hearing loss. Surgical correction is considered when gain from correction of the conductive component is desired.


These conditions are difficult to assess during the acute injury phase because of associated neurologic trauma and/or life threatening injuries. Therefore, the incidence of vertigo has been estimated on a wide spectrum to comprise 24-78% of cases. Spontaneous nystagmus observed by the naked eye is an important clinical sign in the acute phase of temporal bone trauma. It is usually related to a transverse temporal bone fracture with damage to the cochlea and semicircular canals. The spontaneous nystagmus in this instance is a severe one, horizontal or horizonto-rotatory, third degree, and beating to the opposite ear. It represents a peripheral vertigo and it is suppressed or diminished by fixation (nystagmus in central vertigo can have a vertical direction, horizontal, horizonto-rotatory, or a changing direction, and its intensity can be enhanced by fixation).

The accompanying vertigo is also severe, with a spinning sensation, and can be associated with nausea and vomiting. Once the acute phase has passed, the spontaneous nystagmus and vertigo resolve within 3-6 months. At this time, the ENG reveals absent vestibular responses in the affected labyrinth. Spontaneous nystagmus, horizontal or horizonto-rotatory, of lesser degree, not easily seen by the naked eye, can also occur in longitudinal fractures and in general is less severe and intense than that seen in transverse fractures. Also, posttraumatic vertigo is usually found in concussive injuries to the labyrinth associated with temporal bone trauma that does not involve the otic capsule or vestibular apparatus. Note that these injuries may not be observed radiographically, nor does the incidence of vertigo or its intensity and duration correlate well with the severity of the temporal bone injury.

Posttraumatic benign paroxysmal positional vertigo

Posttraumatic benign paroxysmal positional vertigo (BPPV) is common. BPPV is defined by a latent onset of postural related nystagmus and fatiguing which is nonreproducible. In BPPV, a geotropic rotatory nystagmus is elicited with the Dix-Hallpike maneuver. After positioning the injured ear down, a latency period of 10 seconds occurs before the nystagmus is seen. The elicited nystagmus is fixed, horizontal, or horizonto-rotatory and, after a few seconds, fatigues. With repetition, the nystagmus is not reproducible at a point; contrarily, central positional vertigo is a changing-direction nystagmus that has no latency period, is nonfatiguing, and is easily reproducible. Postural vertigo of central etiology could be related to injury or hemorrhage in the brainstem, resulting in dysfunction of the vestibular nuclei.

In both benign paroxysmal positional vertigo and central postural vertigo, the spontaneous nystagmus and vertigo usually resolve over 3-6 months and the remaining symptoms by 10-12 months; however, these symptoms may persist in elderly patients. A combination of both central and peripheral causes are highly possible in the pathophysiology of vertigo after head and temporal bone trauma. Vestibular rehabilitation or canal repositioning may be of value, in particular in BPPV.

Perilymphatic fistula

Perilymphatic fistula may also cause paroxysmal vertigo. The onset of fistula and its symptoms may be delayed. This diagnosis is considered when fluctuating hearing loss and vertigo are present in the near posttraumatic period. A fistula test in the ear canal should not be performed in the acute setting to avoid further trauma or complications. CT images with fractures involving the footplate and round window are compatible with perilymphatic fistula. [31] .Medical treatment initially consists of bed rest, head elevation, and stool softeners. Surgical exploration may be indicated in persistent perilymphatic fistulas.

Traumatic endolymphatic hydrops

Traumatic endolymphatic hydrops as a cause of posttraumatic vertigo has the following etiologies: bony labyrinthine fistula, direct membranous labyrinth injury, injury to the endolymphatic drainage system, or surgical trauma. The onset of traumatic hydrops may be delayed for months or years.

Cerebrospinal fluid fistula

CSF fistula may occur as a result of a dural tear after any type of temporal bone fracture (17%). [14, 32] The leak almost always closes within 4 weeks. The average duration of the leak is approximately 4 days. Longitudinal fractures tend to leak more severely, and this occurs through the middle cranial fossa. Transverse fractures cause leaks through the posterior cranial fossa. The most common sites of fistula are the tegmen tympani and tegmen mastoideum when the leak originates in the middle cranial fossa. Most CSF leaks are obvious by their clear, watery appearance in the immediate posttrauma period. CSF leak may be delayed after the initial trauma in approximately 28% of the cases. CT scanning can assist in the identification of the site of the CSF leak after temporal bone trauma. Coronal and sagittal CT image reconstructions will assist in identifying the location and site of the dural defect. [31] MRI of the brain with contrast can help in the identification of patients with encephaloceles. [31] Pneumatoceles and brain herniations are rare. Pneumatoceles may resolve but will occasionally expand.

CSF contains decreased potassium and protein and elevated glucose concentration levels. Qualitative testing of the fluid for glucose is helpful but lacks specificity. Quantitative testing for potassium, protein, and glucose is more precise. The halo test performed by using a filter paper may be helpful (as the paper separates CSF from blood). Nevertheless, if available, beta2- transferrin assay is the most accurate diagnostic test for CSF.

Otorrhea through a canal laceration or tympanic membrane laceration is usually the presenting symptom, or rhinorrhea may be the only symptom. The rate of flow is increased with exertion or learning forward. CSF can also be observed in the middle ear behind an intact tympanic membrane after the blood is resorbed.

The use of antibiotics in the presence of CSF fistula is controversial. In studies before 1970, MacGee and colleagues reported that 16% of patients who receive prophylactic antibiotics developed meningitis. [33] Rathmore found no difference in the rate of meningitis with or without prophylactic antibiotics. [34] Demetriades and colleagues found that the incidence of meningitis and other co-infections was higher in the group that did not receive prophylaxis. [35] Villalobos et al combined 12 studies (1970-1996) of 1241 subjects and concluded that antibiotic prophylaxis does not appear to decrease the risk of meningitis. [36] To date, no clear answers exist, although the literature generally seems to support prophylactic use of antibiotics in patients with CSF fistulas, particularly in the presence of open laceration or co-infection.

CSF leaks tend to close spontaneously with elevation of the head, bed rest, stool softeners, and cessation of sneezing, straining, and nose blowing. Intermittent lumbar punctures or indwelling lumbar drains may help if the leak persists. However, surgical exploration may be indicated for CSF fistulas that last longer than 14 days.

Radiography is necessary before surgical repair is considered. The usefulness of HRCT and CT cisternography in localizing the site of CSF leaks is debatable, and if the fistula is inactive at the time the localizing technique is used, the CSF leak will not be detected. HRCT scanning alone shows bony defects in 70% of patients with fistulas and is the most specific test. MRI may be the next step. If the fracture is seen but the site of the fistula is not identified, CT cisternography with intrathecal contrast agent (Omnipaque) is the next diagnostic procedure of choice. However, if the bony defect cannot be demonstrated with HRCT scanning, CT cisternography rarely depicts the site of leakage. Intrathecal fluorescein can be used when other tests have failed to detect the site of leakage. [30]

The method of surgical closure of CSF fistulas after temporal bone fractures depends on the location of the fistula, hearing status of both ears, presence of brain herniation through the tegmen, and patency of the external canal.


The risk of meningitis is low (5-11%) in patients with leaks that last less than 7 days. [14, 37] The incidence increases to 33-54% in leaks that last greater than 7 days. This incidence increases with time and is usually related to the duration of the CSF leakage. The risk of meningitis increases in patients who have temporal bone fractures with CSF fistula, open lacerations, and co-infections. Brodie and Thompson found a 20% incidence of meningitis with concurrent infection and 3% incidence in the absence of concurrent infection. [32]  Streptococcuspneumoniae and Haemophilus influenzae are the most common infecting organisms. The incidence of meningitis in patients with posttraumatic CSF fistula treated with prophylactic antibiotics was 2.1%. In those patients who did not receive prophylactic antibiotics, the incidence was significantly higher (8.7%).

Facial nerve paralysis

Facial nerve injuries are more common after transverse fractures of the temporal bone. About 50% of patients with transverse fractures have associated facial nerve paralysis, whereas 20% of patients with longitudinal fractures have associated facial nerve paralysis. The higher incidence of longitudinal (80%) versus transverse fractures (20%) makes facial nerve injuries after longitudinal fractures a more common occurrence. The site of injury of the facial nerve in temporal bone fractures is in the perigeniculate region 82-93% of the time.

In longitudinal fractures, the middle ear is almost always involved, although the otic capsule is spared. The most common site of facial nerve involvement is the horizontal segment of the intratympanic portion. The injury is usually caused by compression and ischemia, rather than disruption. Multiple sites are involved in 20% of cases, usually in the mastoid portion. Onset may be immediate or delayed and partial or complete.

In transverse fractures, otic capsule injury is present. Facial nerve paralysis is usually immediate in onset and complete. Frequently, the nerve is avulsed or severed by the comminuted bone fragments. The usual location of injury is anywhere from the internal auditory meatus to the horizontal segment distal to the geniculate ganglion.

Surgery for facial nerve paralysis can involve decompression of the nerve, nerve anastomosis, nerve grafting, and nerve rerouting, depending on the intraoperative findings. [31]

However, treatment of facial nerve paralysis in temporal bone fractures is controversial, including with regard to the decision to operate, the timing of the operation, and the preferred surgical approach to the injured segment. [38] Furthermore, while some practitioners advocate limited exploration of the facial nerve based on clinical and radiographic information, Fisch advocates total facial nerve exploration and decompression by a middle fossa and transmastoid approach. In patients who have total sensorineural hearing loss, Fisch suggests a translabyrinthine approach.  

Initial evaluation in the emergency department is extremely important because patients with delayed-onset paralysis almost always recover. Therefore, delay in onset is the most important predictive factor for nerve recovery. Those patients with immediate paralysis of an incomplete nature also almost always recover. Incomplete paralysis implies a functional nonsevered facial nerve with good prognosis. Electrodiagnostic testing is usually unnecessary, and these patients should be treated conservatively. Determining whether immediate paralysis is partial may be difficult in the emergency department or ICU. Middle ear and mastoid infection can cause a partially denervated nerve to become totally denervated.

Immediate complete paralysis is usually the result of a severed nerve. Recovery rates are lower for immediate-onset paralysis, a fact that generates the main controversy. Turner treated 30 patients with complete paralysis conservatively and reported good recovery in 63%. [39] Maiman and associates treated 21 patients with complete traumatic facial paralysis and reported full recovery in 52% and partial recovery in 43%. [40] When these recovery rates are compared with the expected recovery rate of 55% with facial nerve decompression, decompression surgery does not appear to be indicated. Determining if the facial nerve is severed is difficult and sometimes impossible without surgical exploration.

Generally, surgery for facial nerve paralysis is selected in patients with complete, immediate nerve paralysis and/or in patients with clear progression of loss of function, with nerve degeneration detected with the assistance of electrodiagnostic studies. Surgery should be performed in the case of 90% nerve degeneration detected by ENOG, whether the paralysis is immediate or delayed. Electrodiagnostic studies help the clinician to differentiate “degeneration” and “percentage of degeneration” on the traumatized side as compared with the normal side.

Although not well established, surgical decompression done in the initial 14 days leads to the best response with respect to facial nerve function. If performed up to 3 months after the initial trauma, it can improve nerve function in approximately 50% of patients. In patients with otic capsule temporal bone fractures who still have serviceable hearing capacity, a middle fossa/transmastoid/supralabyrinthine approach is taken. In patients with otic capsule involvement with profound sensorineural hearing loss or anacusis, the translabyrinthine route is the best approach to directly access the entire intratemporal facial nerve course. In otic capsule sparing with conductive hearing loss and a well-aerated mastoid, a transmastoid/supralabyrinthine approach for exploration and management of the facial nerve is recommended. If this approach is still not adequate for good exposure of the nerve, the alternative is a combined transmastoid/middle cranial fossa approach. [31]

Unusual complications of temporal bone fractures

Paralysis of cranial nerves IX (glossopharyngeal), X (vagus) and XI (spinal accessory)

These cranial nerves can be affected at the jugular foramen in petrous apex fractures. The treatment is conservative

Paralysis of cranial nerve VI (abducens)

This condition usually occurs in the area of the Meckel cave and the Dorello canal. Recovery within 6 months is usual. Alternate eye patching may be the only treatment necessary.

Paralysis of cranial nerve V (trigeminal)

This condition usually occurs in the area of Meckel cave. Treatment is conservative. Mastication muscles may be involved.

Intratemporal carotid artery injury [30, 41]

This type of injury is rare; however, it can be severe and even life threatening. If a fracture of the carotid canal is noted using CT scanning, a carotid artery injury is a possibility, and a stable patient will require CT angiography or MR angiography to assess the possibility of vascular complications.  If a patient has significant bleeding, the carotid artery into the skull base is involved. Significant or massive bleeding can be seen from the external auditory canal, nose, and oral cavity and is associated with rapid deterioration of neurologic status. In such cases, bleeding can be partially controlled by applying pressure on the ear canal, nose, or both. Immediate IV fluid resuscitation is necessary in these patients, as well as preparation for control of the airway with possible intubation. Once the carotid artery injury is inspected and the patient is adequately stabilized, the patient should be taken for angiography, balloon occlusion, or carotid ligation. Balloon occlusion appears to be more effective than ligation in resolving the massive bleeding than ligation. [31]

Carotid cavernous fistula

This is a delayed vascular complication of temporal bone fracture. It is suspected by a pulsatile or nonpulsatile exophthalmus, chemosis, and a bruit detected in the affected area. [30, 42]

Sigmoid sinus thrombosis

This condition occurs but is rare. Sigmoid sinus thrombosis is usually aseptic and nonsymptomatic. It may cause elevated CSF pressure and septicemia if infection is present. Diagnosis is made by means of MRI, magnetic resonance angiography, magnetic resonance venography, or angiography. The Griesinger sign (mastoid emissary vein thrombosis due to thrombus extension) may be noted. Treatment may require exploration of the sinus and ligation of the jugular veins in the neck.

Posttraumatic cholesteatoma

This is a late complication of temporal bone fracture and is caused by skin entrapment in the cranial vault or temporal bone. It can grow undetected for years and become extremely invasive, owing to its size. Treatment is surgical.

Classic Eagle syndrome

This condition may follow tonsillectomy. It consists of pain in the throat with foreign body sensation associated with difficult and painful swallowing. Referred otalgia is common. Traumatic fracture of an ossified styloid and stylohyoid ligament can cause pressure on the external or internal carotid artery and pain may be referred to the cheek or eye, producing atypical pain. Diagnosis is somewhat difficult after trauma and is made by means of palpation and CT scanning. Relief of symptoms by intraoral anesthetic injection may help the diagnosis. Treatment is surgical.

Sympathetic cochleolabyrinthitis

This is a rare complication of temporal bone fracture. The condition is clinically significant because of the potential for hearing loss in the sole ear with hearing. Etiology may be related to the initiation of autoimmune inner ear damage with development of autoantibodies directed against inner ear proteins, as seen in polyarteritis nodosa. Cochlear fracture may release inner ear antibodies and cause host sensitization. Diagnosis is difficult and requires a high index of clinical suspicion. Results of Western blot assays for anticochlear antibodies may or may not be positive. Treatment includes immunosuppression.