Temporal Bone Fractures Treatment & Management

  • Author: Antonio Riera March, MD, FACS; Chief Editor: Arlen D Meyers, MD, MBA   more...
 
Updated: Jun 23, 2010
 

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.

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Complications

Common complications of temporal bone fractures include hearing loss, CSF fistula, facial nerve paralysis, external auditory canal stenosis, cholesteatoma formation, and vascular injuries.

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:[10, 17]

  • 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.

Sensorineural hearing loss

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.

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.

Vertigo/nystagmus

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. 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%).[10, 18] 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. Pneumatoceles and brain herniations are rare. Pneumatoceles may resolve but 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.[19] Rathmore found no difference in the rate of meningitis with or without prophylactic antibiotics.[20] Demetriades and colleagues found that the incidence of meningitis and other co-infections was higher in the group that did not receive prophylaxis.[21] 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.[22] 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. HRCT 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, CT cisternography rarely depicts the site of leakage. 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.

Meningitis

The risk of meningitis is low (5-11%) in patients with leaks that last less than 7 days.[10, 23] The incidence increases to 33-54% in leaks that last greater than 7 days. 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.[18] 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.

The controversies regarding facial nerve paralysis involve the decision to operate, the timing of the operation, and the preferred surgical approach to the injured segment. 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%.[24] Maiman and associates treated 21 patients with complete traumatic facial paralysis and reported full recovery in 52% and partial recovery in 43%.[25] 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.

The decision to operate is made with the assistance of the electrodiagnostic studies. Generally, surgery should be performed in the case of "nerve degeneration," whether the paralysis is immediate or delayed. The electrodiagnostic studies help the clinician to differentiate degeneration and percentage of degeneration on the traumatized side as compared with the normal side.

The most common electrical tests are the maximum stimulation test (MST), the nerve excitability test (NET), electroneuronography (ENOG), and electromyography (EMG).

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.
  • 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.
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Contributor Information and Disclosures
Author

Antonio Riera March, MD, FACS  Associate Professor, Department of Otolaryngology-Head and Neck Surgery, University of Puerto Rico School of Medicine

Antonio Riera March, MD, FACS is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Cleft Palate/Craniofacial Association, American College of Surgeons, and Society for Ear, Nose and Throat Advances in Children

Disclosure: Nothing to disclose.

Coauthor(s)

Sarah Connell, MD  Fellow, Department of Otolaryngology, Head and Neck Surgery, University of Miami, Jackson Memorial Hospital

Sarah Connell, MD is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American Cleft Palate/Craniofacial Association, and Triological Society

Disclosure: Nothing to disclose.

Peter C Belafsky, MD, MPH, PhD  Assistant Professor, Department of Otolaryngology, University of California at Davis

Peter C Belafsky, MD, MPH, PhD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery

Disclosure: Nothing to disclose.

Specialty Editor Board

Jack A Shohet, MD  President, Shohet Ear Associates Medical Group, Inc; Associate Clinical Professor, Department of Otolaryngology-Head and Neck Surgery, University of California, Irvine, School of Medicine

Jack A Shohet, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Medical Association, American Neurotology Society, American Tinnitus Association, and California Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Peter S Roland, MD  Professor, Department of Neurological Surgery, Professor and Chairman, Department of Otolaryngology-Head and Neck Surgery, Director of Clinical Center for Auditory, Vestibular and Facial Nerve Disorders, Chief of Pediatric Otology, University of Texas Southwestern Medical Center; Adjunct Professor of Communicative Disorders, University of Texas School of Human Development

Peter S Roland, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Otolaryngic Allergy, American Academy of Otolaryngology-Head and Neck Surgery, American Auditory Society, American Laryngological Rhinological and Otological Society, American Neurotology Society, American Otological Society, North American Skull Base Society, and Society of University Otolaryngologists-Head and Neck Surgeons

Disclosure: Alcon Labs Honoraria Speaking and teaching; Advanced Bionics Honoraria Board membership; Cochlear Corp Honoraria Board membership; Med El Corp travel grants Consulting; Foresight Consulting fee Consulting

Christopher L Slack, MD  Private Practice in Otolaryngology and Facial Plastic Surgery, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders

Christopher L Slack, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Arlen D Meyers, MD, MBA  Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine

Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Head and Neck Society

Disclosure: Covidien Corp Consulting fee Consulting; US Tobacco Corporation Unrestricted gift Unknown; Axis Three Corporation Ownership interest Consulting; Omni Biosciences Ownership interest Consulting; Sentegra Ownership interest Board membership; Medvoy Ownership interest Management position; Cerescan Imaging Consulting; Headwatersmb Consulting fee Consulting; Venturequest Royalty Consulting

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Mark L Belafsky, MD, FACS, to the development and writing of this article.

The author wishes to acknowledge Joan Flaherty, RN, for her editorial assistance.

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Internal aspect of the skull base: arcuate eminence (AE), cochlea (C), foramen magnum (FM), internal auditory canal (IAC), foramen lacerum (L), foramen ovale (O), foramen rotundum (R), foramen spinosum (SP), sigmoid sinus (SS), transverse sinus (TS), vestibular system (V).
External aspect of the skull base: carotid canal (C), condyle (CO), foramen magnum (FM), jugular foramen (J), foramen lacerum (L), foramen ovale (O), pterygoid plates (P), styloid foramen (S), foramen spinosum (SP).
Internal aspect of the skull base that represents, in black and blue colors, the pathway of the longitudinal temporal bone fracture lines.
Internal aspect of the skull base that represents, in black and red colors, the pathways of the transverse temporal bone fracture lines.
Axial high-resolution CT of the right temporal bone that represents a longitudinal fracture line that extends from the roof of the external auditory canal to the middle ear cavity.
Right temporal bone transverse fracture with severe spontaneous nystagmus (third degree) manifesting immediately after trauma. The fast component beats away from the fracture site in all directions of the gaze; the intensity of the spontaneous nystagmus is represented by the different lengths of black arrows. This type of nystagmus is usually seen by the naked eye. According to Alexander's law, the nystagmus increases when the eyes are turned in the direction of the quick component and decreases when the eyes are turned in the direction of the slow component.
Internal aspect of the skull base depicting, in green color, a mixed temporal bone fracture line with both a longitudinal pattern (circle) and a transverse pattern (rectangle).
Table 1. Longitudinal and Transverse Fractures
FeatureLongitudinal FracturesTransverse Fractures
IncidenceApproximately 80%Approximately 20%
MechanismTemporal or parietal traumaFrontal or occipital trauma
CSF otorrheaCommonOccasional
Tympanic membrane perforationCommonRare
Facial nerve damage20% (most often temporary and frequently delayed in onset)50% (severe, usually permanent, and immediate in onset)
Hearing lossCommon (conductive type and possibly high tone neurosensorial secondary to concomitant inner ear concussion)Common (severe sensorineural or mixed)
HemotympanumCommon (associated with otorrhagia)Possible (not associated with otorrhagia)
NystagmusCommon (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)
OtorrhagiaCommonRare
VertigoCommon (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
FeatureOtic Capsule SparingOtic Capsule Disrupting
IncidenceApproximately 95%Approximately 5%
MechanismTemporal or parietal traumaOccipital trauma
Line of fractureAnterolateral to the otic capsuleThrough the otic capsule
Pathway
  • Squamosa portion of temporal bone
  • Posterosuperior wall of the external auditory canal and tympanic membrane commonly involved
  • Also, mastoid air cells and middle ear
  • Foramen magnum, petrous pyramid, and otic capsule
  • Also jugular foramen, internal auditory canal, and foramen lacerum
  • Tympanic membrane and external auditory canal not usually affected
CSF leakMiddle cranial fossa (tegmen mastoideum, tegmen tympani, middle ear, and external auditory canal or eustachian tube)Posterior cranial fossa (middle ear, eustachian tube)
Ossicular chain involvementCommonRare
Hearing lossConductive or mixedSensorineural
Facial paralysisLess commonCommon
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