Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature.

Temporal bone fractures may cause a variety of signs and symptoms. These include hearing loss, vertigo, facial paralysis, cerebrospinal fluid (CSF) otorhinorrhea, tympanic membrane (TM) perforation, hemotympanum, canal wall laceration, and Battle's sign. Adults and children are similarly affected but several series have found that the complication rate is lower in children.

Fractures of the temporal bone are commonly classified based on the relationship of the fracture line to the long axis of the temporal bone. Longitudinal fractures are the most common accounting for 80% of the temporal bone fractures. This fracture extends along the length of the temporal bone. Transverse fractures extend directly across the petrous bone and make up about 10% of temporal bone fractures. Mixed fractures display some characteristics of each.

Longitudinal fractures usually present with classic findings of laceration of the ear canal, tympanic membrane perforation, ossicular disruption, facial paralysis, and hearing loss. The hearing loss is predominately conductive but may have a sensorineural component as well. Facial paralysis occurs in about 10-20% of longitudinal fractures. These fractures result from trauma directed laterally over the temporal area. Conversely, transverse fractures of the temporal bone show hearing loss, hemotympanum, facial paralysis, and vertigo. Facial nerve paralysis occurs about 50% of the time. Transverse fractures result from trauma to the anterior and posterior aspects of the head.

Recently a new classification system was proposed by Ghorayeb and Yeakley at The University of Texas, Houston. They studied 150 temporal bone fractures radiographically using CT scan with three-dimensional reconstruction. Based on their findings they proposed a new classification system. They identified an oblique fracture type that had originally been described by Voss. In their review this was the most common fracture type, occurring in 74.7% of the temporal bone fractures in this series. Other fracture types encountered in this series include transverse, mixed, longitudinal, and fractures confined to the petrous apex. They differentiate the oblique and longitudinal fractures based on the orientation of the fracture line on the external aspect of the temporal bone. The oblique fracture crosses the external canal in a horizontal plane and then extends upward obliquely toward the middle fossa. The fracture misses the otic capsule and may extend toward the petrous apex where the fracture line may extend to the foramen lacerum. Conversely, the longitudinal fracture line is oriented in a more vertical plane.

Histopathologic examination of temporal bone fractures reveals several patterns of injury. As previously mentioned, longitudinal fractures extend anterior to the otic capsule and do not cause direct injury to the otic capsule. In transverse fractures the otic capsule may be completely disrupted leading to complete loss of audiovestibular function. Fractures of the otic capsule do not heal, but may have fibrous union and new bone formation. This lack of healing may lead to infectious complications and the development of labyrinthitis ossificans. This is an important consideration because of the potential for cochlear implantation in patients with bilateral temporal bone fractures and profound deafness. Loss of audiovestibular function results from concussion of the inner ear as well. This may occur in patients with longitudinal fractures or may occur in patients without a temporal bone fracture. As demonstrated experimentally in cats by Schuknecht, high frequency hearing loss may occur from the transfer of vibratory energy to the cochlea. Lindsay described the changes noted in concussion and found the predominate injury to be hemorrhage into the audiovestibular elements. It is thought that hemorrhage induces a hyperplastic inflammatory response which may lead to degeneration of neural elements, fibrosis, and eventual ossification.

The examination of a patient with suspected temporal bone fracture begins with a history and physical exam. Often times the initial assessment occurs in the emergency room where the patient is also being evaluated for other more life threatening injuries as well. History about the mechanism of injury should be obtained along with any audiovestibular symptoms. The physical exam begins with a general examination of the patient. The head and neck should be examined carefully, looking for the signs and symptoms of temporal bone fractures. The facial nerve should be carefully examined and any evidence of weakness documented. When the patient's condition improves audiogram and CT scan of the temporal bones should be performed with further workup directed by any subsequent complications. These complications include hearing loss, vertigo, facial nerve injury, and cerebrospinal fluid otorrhea.

Conductive and sensorineural hearing loss can result from temporal bone fractures. Classically, conductive loss is associated with longitudinal fractures, and sensorineural loss with transverse fractures. But each may have components of both. The etiology of the conductive hearing loss may result from tympanic membrane perforation, hemotympanum, and ossicular disruption. Persistent conductive hearing loss suggests an ossicular disruption. Middle ear injury with ossicular derangement was initially reported at the time of autopsy by Keleman, and was noted by Thornburn in 1956. Shortly thereafter Hough described this as well, and later published his experience with 31 patients. He found that the most commonly damaged ossicle is the incus. This is thought to result from its relative lack of support compared to the other ossicles; and its location between the other two ossicles, which subjects it to torsional forces. Treatment of these injuries requires middle ear exploration and appropriate ossicular reconstruction.

Sensorineural hearing loss may result from disruption of the membranous labyrinth or concussion. Treatment options for traumatic sensorineural hearing loss are limited. For the majority of patients the only option is rehabilitative. This consists of hearing aids and cochlear implantation for patients with profound bilateral hearing loss.

Another sequelae of temporal bone fractures is vertigo. The incidence varies between different studies with a incidence of 78% by Tuohimaa, while Griffiths reports only 24%. The mechanism of the vertigo may vary and can result from a variety of causes which may be central or peripheral. Central causes are related to injury to the brainstem and result from dysfunction of the vestibular nuclei. There are a number of peripheral causes, the most common being benign positional vertigo. Patients that have associated vertigo with a fluctuating hearing loss should be suspected of having a perilymph fistula. Disruption of the labyrinth may lead to a unilateral weakness that causes vertigo. Another cause of vertigo that has been reported is endolymphatic hydrops. Rivzi describes a patient who sustained a transverse temporal bone fracture that left the otic capsule intact. This patient developed Meniere's-type symptoms and several months later died of unrelated causes. On examination of the temporal bones the fracture line was noted to cross the vestibular aqueduct. Since the majority of these patients' symptoms resolve within 12 months, initial treatment is conservative. Patients who have persistent incapacitating symptoms may require vestibular nerve section or labyrinthectomy.

Temporal bone fractures may result in facial nerve paralysis. Approximately 20% of longitudinal fractures and 50% of transverse fractures result in a facial palsy. This derives from edema, intraneural hemorrhage, bony fragment impingement and dehiscence of the nerve. In a review of 15 cases of longitudinal temporal bone fractures at Baylor, Coker et al found the perigeniculate region to be the most common site of injury. This injury occurred there about 93.3% of the time. Surgical findings noted neural edema present in 93%, intraneural hemorrhage in 40%, bony fragment impingement in 33%, and one patient with dehiscent geniculate ganglion and dehiscent proximal tympanic segment. In this same review, three patients with transverse temporal bone fractures underwent surgical exploration and they were noted to have injury to the labyrinthine and tympanic segments of the facial nerve.

The evaluation of patients' facial paralysis from temporal bone fractures begins with early diagnosis. Patients with complete paralysis should be followed up with electrical testing. Several tests are available, with nerve excitability test, ENOG, and EMG being the most commonly used. Audiogram is also important since hearing status influences the choice of surgical approach. Initial treatment is conservative, consisting of eye protection and steroids. Facial nerve exploration and decompression is indicated for patients who show significant neural degeneration. For patients with serviceable hearing, decompression by a middle cranial fossa/transmastoid approach is best. For those without hearing a translabyrinthine/transmastoid approach is used.

CSF otorrhea may result from temporal bone fractures, although the incidence is relatively low. In a review of 1,185 patients with skull fractures Raaf found that 3.6% presented with CSF otorrhea. Of these, 97% closed spontaneously. Of the patients with otorrhea 7.8% developed meningitis, with one patient dying. Patients with longitudinal fractures usually develop CSF leaks from the tegmen where the fracture line perforates the dura. Transverse fractures are more likely to cross the vestibule and leakage may occur through the defect. Also, since the TM may be intact they are more likely to present with CSF otorhinorrhea. In most cases identification of the fluid is obvious. In questionable cases the most specific test available is electrophoretic identification of the B2 fraction of transferrin, which is specific for CSF. For persistent leaks localization may be attempted with CT scan with metrizamide.

Since the majority of these leaks close spontaneously management is conservative. Several studies have failed to show any benefit from prophylactic antibiotics, and, while it remains controversial, they are probably not indicated. Initial management includes elevating the head and avoiding elevations of intracranial pressure. If this fails to resolve the leak the next step in management is insertion of lumbar drain. Leaks that persist, despite these measures, require surgical closure. While the period of waiting is controversial, surgical closure should be considered for leaks that have persisted for two weeks despite conservative therapy. The surgical approach is based on the suspected location and status of hearing. If the patient has good hearing and the defect is suspected in the tegmen, a middle fossa approach may be used. For patients with no hearing, obliteration via a translabyrinthine approach may be used.

In a review of 82 temporal bone fractures in 75 patients Ghorayeb et al presented several other more unusual complications of temporal bone fractures. These include abducens nerve palsy which may be bilateral or unilateral, trigeminal paralysis, and aseptic sigmoid sinus thrombosis. In their review the incidence of abducens palsy was 6.67%. The abducens nerve has the longest intracranial course of any cranial nerve and is intimately associated with the facial nerve and the trigeminal nerve. It appears the nerve is most vulnerable as it enters Dorello's canal at the end of the petrous apex. Because of the complex anatomy of this nerve the exact mechanism of injury is unclear and may result from stretching and contusion alone. Patients present with an inability to abduct the eye. Many of these injuries are partial and may recover. Treatment consists of alternately patching one eye and if the injury fails to recover, corrective surgery may be attempted.

Ghorayeb et al found an incidence of trigeminal paralysis in 2.67% of the cases. This injury also occurs near the end of the petrous apex where the trigeminal ganglion sits in Meckel's Cave. Patients present with hypesthesias and paresthesia in the trigeminal distribution. They may also have weakness of the muscles of mastication. No therapy is available for this injury.

Sigmoid sinus thrombosis was found in one patient in this series. Patients may be asymptomatic or symptoms of increased intracranial pressure may occur. These include headache and retinal changes. The diagnosis is made with CT scan which shows occlusion of the sigmoid sinus with soft tissue. Clinically the diagnosis is made with the Tobey-Ayer Test, which consists of measuring changes in the CSF pressure with compression and release of the jugular veins. For septic sigmoid thrombophlebitis the treatment of choice is exploration of the sinus via a mastoid approach. For aseptic sigmoid sinus thrombosis Ghorayeb et al caution against exploration in debilitated patients, but advocate exploration as part of any other ear procedure. The patient presented in this review underwent facial nerve decompression and at that time the sinus was explored.

Another rare complication of temporal bone fractures is cholesteatoma formation. This occurs in fractures that involve the external canal. With the disruption of the bony external canal small amounts of epithelium may be trapped. Many years later these patients may present with large and extensive cholesteatomas.

Due to the complex anatomy, temporal bone fractures may cause a variety of disorders. Often the patients have sustained other more life threatening injuries that take precedence over the evaluation of temporal bone fracture. Early identification of the fracture, along with careful observation in the recovery period, is necessary for proper treatment.

Case Presentation

A 21-year-old black male presented to the Emergency Room after suffering blunt trauma to the head. He reportedly was hit with a vase in the right temporal area and lost consciousness at the scene. He complained of decreased hearing and bleeding from the right ear, but denied any vertigo. Physical exam of the right ear revealed a posterior external canal wall laceration and a hemotympanum. The facial nerve was intact. CT scan of the head and temporal bone was obtained which revealed a longitudinal fracture of the right temporal bone. He was admitted to the Neurosurgery Service for observation. On the second day of hospitalization he developed a complete right facial paralysis and he was transferred to the Otolaryngology Service. Audiogram showed a mild conductive hearing loss in the right ear, and acoustic reflexes showed a probe effect in the right ear. He was started on steroids and received local care for the right eye. He was followed daily with nerve excitability tests with the side to side difference remaining less than 2mA. On the seventh day after the onset of the paralysis, nerve excitability testing revealed a greater than 3.5 mA difference between sides. ENOG revealed greater than 95% degeneration of the facial nerve. He subsequently underwent a combined middle cranial fossa/transmastoid exploration and decompression of the facial nerve. At the time of surgery a bony spicule was found impinging on the facial nerve at the geniculate ganglion. The facial nerve was intact but edematous in the labyrinthine and tympanic segments. The postoperative course was uneventful and the patient was discharged to home on the sixth postoperative day.

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