Temporal bone injuries are usually associated with severe head trauma. Maintenance of the patient's vital functions is critically important, and temporal bone fractures are often overlooked initially. Emergency doctors must worry about more essential functions than balance or conductive hearing loss when patients are bleeding heavily.

After clearing the airway, stabilizing hemodynamic status, and placing the cervical spine into a collar, however, the emergency physician should evaluate the patient's consciousness and motor and sensory functions, consult a neurosurgeon, and request an otolaryngologic evaluation.1 Any clinical sign that makes doctors think of a temporal fracture should lead them to request a CT examination (see table). X-ray sensitivity is too low to be considered useful in such cases, owing to superimposition of surrounding bony structures. MR should be reserved for workup in later stages of the disease, when soft-tissue injuries are in question. It is difficult to use with intubated, hemodynamically unstable patients and does not visualize bone pathology satisfactorily.

Patients with suspected head trauma should receive a CT brain scan in the emergency unit or in close proximity to it. This examination will more or less cover the area of temporal bone at the border of the middle and posterior cranial fossa. Technical requirements for imaging brain tissue, however, differ enormously from those needed to visualize the temporal bone. Even if this initial CT scanning reveals pathology in the temporal region, the patient will still need referring for further CT examination, using thin sections with a high-resolution bone algorithm. Whether the scanner is sequential or spiral, single- or multidetector, does not necessarily influence diagnosis and patient management.

We use a CT scanner with an increment of 0.3 mm, 4 x 5-mm slice thickness, pitch of 0.8, rotation time of one second (120 kV, 250 mAs), and a high-resolution bone algorithm. Axial slices suffice most of the time. Multiplanar reconstruction, especially of the coronal plane, can be helpful in ossicular injury and in assessment of the outer auditory canal or epitympanum roof.

Greater availability of workstations in hospitals and rapid software development have contributed to a rise in requests for 3D reconstructions of the skull base and virtual endoscopic views of the tympanic cavity. Two different techniques can be applied here:

- Surface rendering uses information of superficial structures only. It involves rapid data processing but lacks information about deeper structures.

- Perspective volume rendering uses all voxels in the region of interest. It produces cross-sections of a volume block but poses a bigger challenge to computer equipment.

Regardless of the technique chosen, these reconstructions do nothing more than aid understanding of anatomy and pathology as well as help with interdisciplinary communication or teaching.2 Findings may be masked by artifacts. Special difficulties emerge in cases with hematotympanum, for example, in which the normally high contrast between air and ossicles is absent.

Fractures are generally described on imaging as hypodense lines traversing the bone. They must be differentiated from other hypodense lines (Figure 1).3 These include vessel canals, peri- and endolymphatic duct, nerves (branches from cranial nerves VIII to X), extrinsic sutures (petro-occipital, temporo-occipital, occipitomastoid), and intrinsic fissures (tympanosquamous, tympanomastoid, and petrotympanic). Assessment of symmetry, anatomical location, and the line's borders can help with differential diagnosis. Vessel borders are smooth, while the borders of sutures or fissures are serrated. Only fractures tend to exhibit irregular borders. Sutures and fissures are also filled with hyaline cartilage in children. They consequently appear larger in pediatric patients and should not be misinterpreted as ruptures.

ANATOMICAL MARKERS

The sense of hearing and balance are embedded within the temporal bone, between the middle and posterior cranial fossa. They are carried by cranial nerve VIII with its cochlear and vestibular part.4 The ear is subdivided into an outer, middle, and inner part. The outer ear comprises the auricle and the cartilaginous and osseous outer auditory canal. This canal is separated from the middle ear by the tympanic membrane and is directly accessible for inspection. The temporomandibular joint lies underneath the outer auditory canal.

The middle ear consists of the tympanic cavity and pneumatized cells, mainly in the mastoid process and squamous part. It is aerated via the eustachian tube from the nasopharynx and also contains the ossicles. The malleus head and the body and short process of the incus together resemble an ice cream cone on axial images. Stirrup-shaped stapes connect the incus to the oval window of the labyrinth.

The internal carotid artery, jugular bulb, and tympanic segment of the facial canal and inner ear lie adjacent to the middle ear (anteriorly, inferiorly, and medially, respectively). These structures are all vulnerable. The labyrinthine segment of the facial canal runs from the inner auditory canal anteriolaterally, bends backward at the geniculate ganglion, where it lies horizontally in the medial wall of the tympanic cavity, and courses downward through the mastoid to exit at the stylomastoid foramen.

Sound waves induce the tympanic membrane to swing, and this motion is transmitted into the fluid-filled labyrinth of the inner ear via the stapes footplate. Deflection of hair cells' cilia within the cochlea-like waves, resembling the movement of algae in the sea, creates a proper stimulus for the cochlear nerve. Similarly, head movements lead to movement of fluid within the semicircular canals, which then deflect sensory cells and evoke reactions in the vestibular nerve. The cochlear and vestibular nerves run parallel through the inner auditory canal, traversing the cerebellopontine angle to enter the brain stem.

IDENTIFYING FRACTURES

We differentiate fractures as either longitudinal or transverse, a characterization held over from the plain-film radiography era. Cross-sectional imaging could doubtless show that oblique and squamous fractures are not only possible as well, but also occur frequently.5

Patients who have suffered blunt temporoparietal trauma risk developing a longitudinal fracture, running parallel to the long axis of the petrous pyramid. These fractures are three to four times more common than transverse fractures, and they remain outside the labyrinth. Patients with longitudinal fractures are consequently likely to have a better outcome, assuming they survive their other intracranial injuries.

Damage to the middle meningeal artery, which runs within grooves situated medially on the squamous part of the temporal bone, can lead to life-threatening epidural hemorrhage. Ossicular chain disruption, consisting of dislocation or fracture leading to conductive hearing loss, is common (Figure 2).6 The incus is heavier than both the malleus and stapes and has less ligamentous support, making it the most vulnerable of the three structures. Immediate transection of the facial nerve (cranial nerve VII) is less of a problem. Hemorrhage or traction may cause late onset of facial paralysis, in which the greater petrosal nerve exits the main branch at the geniculate ganglion. This type of nerve injury is the mildest and usually heals fully within two to three weeks.

Longitudinal fractures may sometimes extend into the sphenoid bone or occur contralaterally. Transverse fractures, on the other hand, tend to happen after blunt frontal or occipital head trauma. These fractures run perpendicular to the long axis of the petrous pyramid and are highly likely to transect either the vestibulocochlear nerve or the facial nerve (or both) near the fundus. Immediate surgical repair is generally required in these cases (Figure 3). Because delayed onset of paralysis has a better prognosis than immediate paralysis, assessment of facial movement in the emergency unit helps in estimating potential future recovery.5

Patients with transverse fractures can also suffer from abnormal communication between the inner and middle ear, resulting in a perilymphatic fistula.7 Symptoms resemble those of Meniere's disease, with fluctuating sensorineural hearing loss, vertigo, tinnitus, and headache.

Indirect fracture signs, such as incorrectly located air or soft-tissue densities, can provide additional diagnostic assistance. Observation of air in the normally fluid-filled labyrinth is a clear indication of communication abnormalities between the inner and middle ear, with the potential for severe damage to hearing and balance (Figure 4).

Air-fluid levels in the tympanic cavity or mastoid cells are always pathologic. CT is unable to further differentiate the nature of densities between inflammatory secretions, blood, perilymphatic, or cerebrospinal fluid, and alternative direct and indirect fracture signs must be sought. An intact tympanic membrane will bulge into the outer auditory canal. Fluid will leave the middle ear via the eustachian tube, causing nasal discharge if the pressure is high enough. Ruptured tympanic membranes will allow otorrhea. Careful clinical inspection can help to assess the nature of the fluid. Differential diagnosis of an abscess is of theoretical interest only in trauma patients with mastoid soft-tissue emphysema.

LATER COMPLICATIONS

Transverse fractures to the temporal bone often involve the labyrinth. This may be due to hemorrhage or disruption of the membranous labyrinth. The latter condition can lead to loss of hair cells and the risk of developing a hyperplastic inflammatory reaction, producing an intracochlear fibrotic scar.8 CT may anticipate this reaction and scar formation if the patient continues to suffer from sensorineural hearing loss. Heavily T2-weighted thin-slice MR visualizes the same condition as intralabyrinthine signal loss and pathologic contrast uptake. Doctors must decide rapidly what therapeutic approach to take. Delay may result in development of labyrinthitis ossificans, which makes cochlear implantation difficult and less successful.

Meningitis can develop from the perilymphatic fistulae, and therefore this is an indication for surgical repair. The temporal bone does not tend to form calluses, so fractures rarely heal. The dura mater, sometimes accompanied by brain, can bulge into the defect in severe cases, causing meningoceles or meningoencephaloceles. Post-traumatic cholesteatomas can also form when squamous cells gain access to mastoid cells and then spread within pneumatized cells.

References

1. Alvi A, Bereliani A. Trauma to the temporal bone: diagnosis and management of complications. J Cranio Maxillofac Trauma 1996;2:36-48.

2. Rodt T, Bartling S, Schmict AM. Virtual endoscopy of the middle ear: experimental and clinical results of a standardised approach using multi-slice helical computed tomography. Europ Radiol 2002;12:1684-1692.

3. Swartz JD. Temporal bone trauma. Sem US, CT, MR 2001;22:219-228.

4. Curtin HD, Som PM, Bergeron RT. Temporal bone embryology and anatomy. In: Som PM, Curtin HD, eds. Head and neck imaging, 3rd ed. St Louis: Mosby, 1996:1300-1318.

5. Davis RE, Telischi FF. Traumatic facial nerve injuries. J Cranio Maxillofac Trauma 1995;1:30-41.

6. Meriot Ph, Veillon F, Garcia JF, et al. CT appearance of ossicular injuries. Radiographics 1997;17:1445-1454.

7. Kim SH, Kazahaya K, Handler SD. Traumatic perilymphatic fistulas in children: etiology, diagnosis and management. Int J Ped Otorhinolaryngology 2001;60:147-153.

8. Morgan WE, Coker NJ, Jenkins HA. Histopathology of temporal bone fractures: implications for cochlear implantation. Laryngoscope 1994;104:426-432.

PROF. ROBINSON is a senior radiologist at Helsinki University Central Hospital and University Hospital in Vienna. DR. PEKKOLA is a radiology resident at Helsinki University Central Hospital, and PROF. BAUMGARTNER is an otorhinolaryngological surgeon at University Hospital in Vienna.

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CLINICAL SIGNS OF TEMPORAL BONE FRACTURE THAT INDICATE CT EXAMINATION

Sensorineural or conductive hearing loss

Vertigo, nystagmus, tinnitus

Facial nerve paralysis

Cerebrospinal fluid leak (ear or nose)

Hematotympanum

Soft-tissue emphysema

Mastoid ecchymosis