The temporal bone is the most complex bone in the human body. It houses many vital structures, including the cochlear and vestibular end organs, the facial nerve, the carotid artery, and the jugular vein. A temporal bone fracture can involve none or all of these structures. Associated trauma to other cranial nerves (other than the facial nerve; ie, VI [abducens], IX [glossopharyngeal], X [vagus] and XI [spinal accessory] can also cause paralysis.
The temporal bone is a very thick and hard structure located in the base of the skull. The base of the skull has multiple foramina, as seen in the images below, creating areas of decreased resistance susceptible to traumatic injury. Therefore, fractures that involve the temporal bone continue along the skull base with a pattern that follows the weakest points of the anatomy.
The spectrum of temporal bone trauma is extremely varied, ranging from minor concussion without functional deficits to severe blunt or penetrating trauma with multifunctional deficits that involve the auditory and vestibular nerves, the facial nerve, and the intracranial contents. The clinical presentations specifically related to temporal bone trauma include facial nerve paralysis (partial or complete), hearing loss (conductive, sensorineural, or mixed), vertigo, dizziness, otorrhagia, cerebrospinal fluid (CSF) otorrhea, tympanic membrane perforation, and hemotympanum and canal laceration.
Temporal bone fracture is a frequent manifestation of head trauma. Most cases of temporal bone fracture involve severe body and/or head trauma. In the adult population, approximately 90% of temporal bone fractures are associated with concurrent intracranial injuries and 9 % with cervical spine injuries.  Therefore, management of the temporal bone trauma may not be the first priority. However, the initial assessment of the temporal bone trauma in the emergency department by the emergency personnel and the trauma team is critically important.
Usually, the otolaryngology-head and neck surgeon is called in for consultation when the patient is fully stable, many hours after the traumatic event. This is why the initial assessment in the emergency room is so important and definitely assists in the posterior management, improving function. This is also why a thorough understanding of the etiology, classification, complications, and treatment of temporal bone fractures is mandatory for healthcare professionals involved in the care of individuals with such injuries.
The head is the most frequently injured part of the body. Head injuries occur in approximately 75% of all motor vehicle accidents. Approximately 30% of head trauma cases result in skull fracture. The ear is the most frequently damaged sense organ. Temporal bone injuries reportedly occur in 14-22% of all skull fractures. Motor vehicle accidents are the cause of 31% of temporal bone fractures. Other causes, in descending order of frequency, are physical assaults, falls, motorcycle accidents, pedestrian injuries, bicycle accidents, and gunshot wounds. Men aged 21-30 years comprise the most commonly involved group. The predisposition in males is based on an increased number of males involved in high-risk activities compared with females, rather than on a weakness in their skull structures. Bilateral temporal bone fractures have an incidence of 8-29%.
Recently, temporal bone fractures related to motor vehicle accidents appear to have decrease, temporal bone fractures related to assaults, particularly in large urban populations, appear to have increased. [2, 3]
The pediatric population comprises 8-22% of the entire population of patients with the diagnosis of temporal bone fractures. Temporal bone fractures in the pediatric population are also associated with a high incidence of intracranial complications, approximately 58%, and with facial nerve paralysis, at 3-9%. [2, 4, 5]
The pediatric population has a very similar proportion of motor vehicle accidents (47%) and falls (40%), as described in the medical literature.  Temporal bone fractures are more common in children younger than 6 years. Approximately 75% of the fractures are longitudinal, and 25% are transverse. The otic capsule is spared in 90% and is involved in 10%.  Intracranial injuries are often with associated hearing loss, which is most likely conductive (56%) followed by sensorineural hearing loss (17%) and mixed hearing loss (10%). However, the facial nerve injury is not frequently affected (3%).  Children are very susceptible to trauma, in particular to falls and other accidents. However, if the injury cannot be explained based on the medical history, consideration should be given to the possibility of a nonaccidental cause.
In 1926, Ulrich was the first to classify temporal bone fractures into longitudinal fractures and transverse fractures.  Ghorayeb and Yeakley, in their study of 150 temporal bone fractures, found that the vast majority of fractures are actually oblique and quite often mixed.  Other classifications are based on otic capsule sparing and otic capsule involvement. An otic capsule sparing fracture runs anterolateral to the otic capsule and is caused by a blow to the temporoparietal region. An otic capsule involvement fracture runs directly into the otic capsule, damaging the cochlea and semicircular canals, and is caused by a blow to the occipital region (see Table 2). The mentioned classifications are useful in predicting otologic sequelae but cannot predict neurological, neuro-otological, or skull base complications.  Despite newer classification systems, Ulrich's original system, due to its simplicity, is still the most commonly used.
The classification models indicated above are arbitrary but indeed useful to predict the pattern of injury. Most temporal bone fractures are completely irregular and not uniform in their pathway, following an oblique or mixed pattern as indicated above. Therefore, rather than the type of fracture, the evaluation of function is the critical issue and is mandatory. The presence or lack of a particular function indicates whether or not the cochlea, middle ear, vestibule, facial nerve, dura, or CNS is damaged, in spite of a demonstrated fracture or the lack thereof.
Longitudinal fractures comprise 80% of all temporal bone fractures. They are frequently caused by a lateral force over the mastoid or temporal squama, usually produced by temporal or parietal blows. The fracture line parallels the long axis of the petrous pyramid. It starts in the pars squamosa (mastoid or external auditory canal), as seen in the images below, and extends through the posterosuperior bony external canal, continues across the roof of the middle ear space anterior to the labyrinth, and ends anteromedially in the middle cranial fossa in close proximity to the foramen lacerum and ovale.
The most common course of the fracture is anterior and extralabyrinthine; however, although rare, intralabyrinthine extension is possible.  Again, bilateral temporal bone fractures are present in 8-29% of all fractures, according to the medical literature. 
Signs and symptoms include bleeding into the ear canal from skin and tympanic membrane laceration, hemotympanum, external auditory canal fractures, ossicular chain disruption that produces conductive hearing loss, and facial nerve paralysis. Twenty percent of longitudinal fractures injure the facial nerve and cause paralysis. The injury site is usually the horizontal segment of the nerve distal to the geniculate ganglion. CSF otorhinorrhea is common but usually temporary. Sensorineural hearing loss may occur as a result of concussive damage. Vertigo occurs but is not related to the severity of the fracture.
Transverse fractures comprise 20% of all temporal bone fractures. They are usually caused by a frontal or parietal blow but may result from an occipital blow. The fracture line runs at a right angle to the long axis of the petrous pyramid and starts in the middle cranial fossa (close to the foramen lacerum and spinosum). It then crosses the petrous pyramid transversely and ends at the foramen magnum. It may also extend through the internal auditory canal and injure the nerves directly. The pathways of the transverse temporal bone fracture lines are depicted in the image below.
Cochlear and vestibular structures are usually destroyed, producing a profound sensorineural hearing loss and severe ablative vertigo. The intensity of the vertigo will decrease after 7-10 days and then continues to decrease steadily over the following 1-2 months, leaving only an unsteady feeling that lasts approximately 3-6 months, until compensation finally occurs. Intense nystagmus (third degree) is present since the initial fracture, with the fast component beating away from the fracture site. The nystagmus is easily seen by the naked eye. Nystagmus also decreases progressively in intensity (third degree, second degree, first degree) and then finally disappears. The image below depicts right temporal bone transverse fracture with severe spontaneous nystagmus.
Rarely, a mixed hearing loss may occur. Facial nerve injury occurs in 50% of transverse fractures. The injury site is anywhere from the internal auditory canal to the horizontal segment distal to the geniculate ganglion. Pneumolabyrinth may be noted. 
Histopathology reveals hair cell loss, ganglion cell loss, and supporting cell loss. In rare cases, labyrinthitis ossificans occurs secondary to the trauma or subsequent infection. This must be kept in mind when one considers the placement of cochlear implants after a temporal bone fracture.
Oblique or mixed fractures
These patterns, which extend both longitudinally and transversely, are common. According to some authors, these patterns occur more often than isolated transverse or longitudinal fractures. [13, 14, 15] . A range of 62-90% of temporal bone fractures were designed as a mixed pattern in medical literature. [2, 3, 16]
Table 1. Longitudinal and Transverse Fractures (Open Table in a new window)
|Feature||Longitudinal Fractures||Transverse Fractures|
|Incidence||Approximately 80%||Approximately 20%|
|Mechanism||Temporal or parietal trauma||Frontal or occipital trauma|
|Tympanic membrane perforation||Common||Rare|
|Facial nerve damage||20% (most often temporary and frequently delayed in onset)||50% (severe, usually permanent, and immediate in onset)|
|Hearing loss||Common (conductive type and possibly high tone neurosensorial secondary to concomitant inner ear concussion)||Common (severe sensorineural or mixed)|
|Hemotympanum||Common (associated with otorrhagia)||Possible (not associated with otorrhagia)|
|Nystagmus||Common (usually spontaneous, usually less intense [first or second degree] or positional; nystagmus absence also possible)||Common (intense [third degree], spontaneous, fast component beating to the opposite ear, long lasting; positional nystagmus also possible before and after compensation period)|
|Vertigo||Common (less intense, and/or positional; absence is also possible)||Common (intense, usually associated in the acute phase with nausea and possibly vomiting)|
Table 2. Otic Capsule–Sparing and Otic Capsule–Disrupting Fractures (Open Table in a new window)
|Feature||Otic Capsule Sparing||Otic Capsule Disrupting|
|Incidence||Approximately 95%||Approximately 5%|
|Mechanism||Temporal or parietal trauma||Occipital trauma|
|Line of fracture||Anterolateral to the otic capsule||Through the otic capsule|
|CSF leak||Middle cranial fossa (tegmen mastoideum, tegmen tympani, middle ear, and external auditory canal or eustachian tube)||Posterior cranial fossa (middle ear, eustachian tube)|
|Ossicular chain involvement||Common||Rare|
|Hearing loss||Conductive or mixed||Sensorineural|
|Facial paralysis||Less common||Common|
Stab and gunshot wounds are the most common penetrating wounds. Most of the patients involved are male and young. Gunshot wounds medial to the geniculate ganglion are usually fatal. The otic capsule may act as a missile deflector, protecting the brain. Associated injuries of cranial nerves (other than the seventh) can occur, as well as intracerebral damage and arterial or venous injury. These account for the most severe temporal bone injuries. Usually the timing of the facial paralysis and its injury location are well known, the result of direct observation or CT findings.
Gunshot wounds to the temporal bone often result in profound sensorineural hearing loss, CSF leak, and facial nerve disruption, which is found in approximately 50% of the patients and requires repair by interposition nerve grafting.
Patients with temporal bone fractures usually have multiple traumatic injuries.  Intracranial and maxillofacial injuries can be associated with severe trauma capable of producing temporal bone fracture. Other associated injuries not related to the head and neck, are also possible, such as, abdominal, thoracic and orthopedic injuries.
In the initial evaluation, the application of Advanced Trauma Life Support protocols is imperative in the assessment and management of these patients. Therefore, stabilization must be accomplished first. Airway management, evaluation of neurological status, hemorrhage, open fractures, and abdominal and chest injuries may delay early diagnosis and treatment of temporal bone injuries. The cervical spine should be evaluated and stabilized before the head is manipulated.
As mentioned in the beginning of this article, otolaryngologists are typically not members of the initial team who treat a patient with a head injury. Therefore, neurosurgeons, neurologists, and emergency physicians should be trained to assess the 2 most important aspects of temporal bone fractures: status of the external canal (checking for blood or CSF) and status of the facial nerve.
The physical examination of the patient with temporal bone trauma should include a complete neuro-otologic examination, as well as a complete nose and throat examination. Look for the impact site on the skull. Examine the patient's eyes for nystagmus, indicate the direction and degree. Severe nystagmus (third degree) often occurs in patients with transverse fractures. Central vertigo may have vertical or direction-changing characteristics that fail to suppress with fixation. On the contrary, peripheral vertigo is horizontal or horizonto-rotatory and suppresses with fixation.
If the patient's condition permits, test the hearing with tuning forks, comparing the bone conduction to air conduction (Weber and Rinne tests). Bedside masking can be done by rubbing a piece of paper against the opposite auricle. Complete vestibular audiometric testing can be performed later because it is not usually necessary in the acute phase. Complete audiological evaluation is mandatory prior to any otologic intervention.
The Battle sign (ecchymosis of the postauricular skin) and the raccoon sign (ecchymosis of the periorbital area) may be noted in either type of fracture.
The auricles are inspected for lacerations and hematomas. Lacerations are closed after cleaning and debridement of exposed cartilage. Hematomas are drained and pressure bolsters placed to prevent reaccumulation of blood.
Taking aseptic precautions, examine the external canal for blood, CSF, or the presence of brain herniation. Observe for external canal lacerations, step deformities, and tympanic membrane lacerations/perforations. Canal fractures typically occur along the scutum and roof of the external auditory canal. Check for hemotympanum.
Do not lavage the ear canal and do not use packing in the canal unless bleeding is difficult to control because either may introduce infection into the cochlea and labyrinth, as well as into the brain and meninges. If profuse hemorrhage cannot be controlled with packing, the patient is taken to the operating room for carotid ligation or to the angiography suite for balloon occlusion.
Severely traumatized ear canals are at high-risk for stenosis or cholesteatoma formation. These patients should be monitored closely for the development of these complications. Early intervention at the first sign of stenosis can prevent a problem that is difficult to treat when the stenosis is mature.
Examine the mandible and mid face for fractures. If the patient is conscious, determine if he or she has vertigo. Examine the facial nerve. Checking for paralysis and determining whether it is of immediate or delayed onset is crucial. This may be difficult to determine if the patient is intubated or comatose or if muscle relaxants have been administered. Painful stimuli may elicit a grimace response, even in comatose patients.
In the patient with facial paralysis or CSF fistula, an audiogram is required before surgical repair because the patient's hearing status dictates the surgical approach.
A prospective study by Montava et al of temporal bone fracture sequelae (39 patients, 45 fractures) found that presentations included the following: balance problems (44%), hypacusis (56%), tinnitus (56%), and facial paralysis (15%). Cochleovestibular sequelae were described as disabling in 75-80% of patients. 
A study by Schell and Kitsko found that in children with temporal bone fracture–related hearing loss, the majority of those in whom the otic capsule was spared suffered only mild hearing loss and recovered normal hearing levels after a mean of 6 weeks, while 75% of those in whom the fracture disrupted the otic capsule suffered severe hearing loss. The study involved 58 children, with most hearing losses in otic capsule–sparing fractures being conductive and all classifiable hearing losses in otic capsule–disrupting fractures being mixed.