TITLE: Temporal Bone Fracture
SOURCE: Grand Rounds Presentation, UTMB, Dept. of Otolaryngology
DATE: March 31, 2010
RESIDENT PHYSICIAN: Ki-Hong Kevin Ho, MD
FACULTY PHYSICIAN: Tomoko Makishima, MD, PhD
DISCUSSANT: Tomoko Makishima, MD, PhD
SERIES EDITORS: Francis B. Quinn, Jr., MD, MS(ICS)
ARCHIVIST: Melinda Stoner Qui=
nn,
MS(ICS)
"This material was prepared by resident physicians in partial
fulfillment of educational requirements established for the Postgraduate
Training Program of the UTMB Department of Otolaryngology/Head and Neck Sur=
gery
and was not intended for clinical use in its present form. It was prepared =
for
the purpose of stimulating group discussion in a conference setting. No
warranties, either express or implied, are made with respect to its accurac=
y,
completeness, or timeliness. The material does not necessarily reflect the
current or past opinions of members of the UTMB faculty and should not be u=
sed
for purposes of diagnosis or treatment without consulting appropriate
literature sources and informed professional opinion."=
Introduction
Temporal bone fracture is a frequent consultation otolaryngologists face in the emergency setting. Anatomic knowledge of the = many vital structures within the temporal bone is vital to proper diagnosis and = management of such injuries. Appropriate evaluation takes into account the spectrum of severity and the sometimes su= btle symptoms of otologic trauma. Early involvement = of the otolaryngologist/neurotologist in evaluation and management can improve long-term functional outcome.
Incidence and Epidemiology
Temporal bone fractures occur in approximately 1= 4-22% of all skull injuries. Most of these fractures are unilateral, with bilateral fractures reported in 9% to 20%. Children account for 8-22 % of patients wi= th temporal bone fracture.
The primary mechanisms of injury include motor v= ehicle accident (12%–47%), assault (10%–37%), falls (16%–40%), a= nd gunshot wound (3%–33%). With improved automobile safety technology, t= he incidence of fractures resulting from motor vehicle accidents has decreased. On the o= ther hand, increasing rates of violent crimes have led to more temporal bone inj= ury from assault.
Classification
Traditionally temporal bone fracture has been classified into longitudinal fracture (~ 80%) and transverse (~ 20%) based = on several cadaveric studies in the 1940s. Longitudinal fracture results from temporoparietal impact and the most frequent structures involved are the tympanic membrane, the roof of the middle ear, and the anterior portion of = the petrous apex. About 15-20% wi= ll have involvement of the facial nerve, and injury occurs near the geniculate ganglion or in the horizontal portion.&nbs= p; Facial paralysis is often delayed in onset, attributed to edema rath= er than direct interruption of the nerve.&nbs= p; Vestibular involvement and sensorineural deficits are relatively uncommon and are attributed to concussive effects rather than direct trauma= on the vestibular labyrinth and cochlea.
Transverse fracture results from fronto-occipital impact and courses perpendicu= lar to the long axis of the petrous pyramid from the foramen magnum through the posterior fossa, through the petrous pyramid, including the otic capsule, and into the middle cranial fossa. The facial ner= ve is involved in 50% of cases. Otic capsule and internal auditory canal are frequently involved as well.
However, this dichotomous system was deemed by s= ome to be insufficient. It was reported that up to 90% of blunt trauma-induced fractures were more accurately described as mixed or oblique fracture.
More recently, there is also an increasing trend= for categorizing temporal bone fracture into otic capsule sparing (OCS) versus = otic capsule disrupting (OCD) fractures, a system showing better correlation with clinical sequelae. OCS fractures are much more common (>90%) than OCD, a= nd the latter is associated with higher incidence of facial nerve injury (30-5= 0%), SNHL, and CSF leak (2-4 times higher than OCS).
Diagnostic Workup
In addition to gathering an adequate history of =
the
patient and the mechanism of injury, a complete head and neck examination is
necessary. The patient with
multiple systems trauma must proceed according to the ATLS protocol of
emergency resuscitation.
Immobilizations of any cervical spine injuries are immediately perfo=
rmed.
Before the advent of CT scan, the diagnosis of temporal bone fractures were
made on the basis of physical exam alone.&=
nbsp;
Blood in the external ear canal may be more representative of
longitudinal than transverse fractures.&nb=
sp;
Hemotympanum and blood=
in
the external auditory canal are some of&nb=
sp;
the common findings in temporal bone fractures. Evidence of a basilar
skull fracture includes
High resolution CT scan (HRCT) is the most commo= nly used radiographic modality in evaluating the patient with temporal bone trauma. HRCT provides excelle= nt delineation of bony anatomy and allows for evaluation of the facial canal, ossicular ch= ain, otic capsule, carotid canal, and middle cranial fossa.
Hearin= g Loss
More than half of patients with temporal bone tr= auma report some degree of hearing loss. = The type and degree of deficit is related to the force of injury and location of the fracture. Transverse fractures involving the otic capsule and internal auditory canal frequently cause severe sensorineural hearing loss. Longitudinal fractures are more li= kely to cause conductive or mixed hearing loss.= Incudostapedial joint dislocation is the most common ossicular chain injury in temporal bone fracture. Even without temporal bone fractures, concussive injuries to the cochlea or labyrinth can cause hearing loss.
Early audiometric evaluation will frequently sho= w CHL secondary to hemotympanum. It is therefore advised that audiogram should be= repeated about 1-2 months after the injury to allow hemotympanum and middle ear effu= sion to resolve. In the short-term management of CHL, most authors prefer to wait to determine if the loss will resolve spontaneously. However, if earlier neurootologic intervention is planned (eg, facial nerve decompression, CSF leak repair), ossiculoplasty c= an be used as appropriate for concomitant exploration. For patients who experi= ence persistent CHL after the acute recuperative
3 to 4 months, ossicular dislocation or fracture= must be suspected, and exploration with ossiculoplasty is indicated. Patients who have mild to moderate SNHL are usually treated with standard hearing aid amplificatio= n. For unilateral profound SNHL, bone anchored hearing aid has been demonstrat= ed with good outcome. Cochlear implantation has also been shown to have benefits in treating patients with bilateral profound SNHL after temporal bone fracture= s.
Facial Nerve injuries
Facial nerve is injured in approximately 15-20% = of longitudinal fractures and 50% of transverse fractures. Chang and Cass’s review sugg= ests that of longitudinal fractures; 43% had intraneural hematoma or contusion, = 33% had bony impingement, 15% had transaction, and 12% had no identifiable pathology. In contrast, in transverse fractures, 92% had transection and 8% had bony impingement.
Early evaluation and thorough history are crucia= l in evaluating the status of facial nerve.&nbs= p; Particular attention should be given to the time and characteristics= of onset of facial weakness, whether sudden or delayed, and determination of complete versus incomplete paralysis.
The House- Brackmann grading system was designed= to classify the long term degree of facial nerve deficit but is also useful to describe acute facial weakness.
|
=
|
=
Grade |
=
Characteristics |
|
I |
|
Normal facial function |
|
II |
Mild |
Slight synkinesis, no asymmetr=
y,
slight weakness |
|
III |
Moderate |
Complete eye closure, noticeab=
le
synkinesis, no asymmetry at rest, obvious weakness, slight forehead movem=
ent |
|
IV |
Moderately Severe |
Incomplete eye closure, no
asymmetry at rest, no forehead movement |
|
V |
Severe |
Asymmetry at rest, barely
perceptible motion |
|
VI |
Total |
No movement |
ENoG is considered to be the most accurate progn=
ostic
test because it provides quantitative, objective measurement of neural
degeneration. An electrode is
placed near the stylomastoid foramen and a transcutaneous stimulus is
applied. The muscular respons=
e is
then measured using bipolar electrodes placed near the nasolabial groove.
There is general consensus supporting the conser= vative treatment of patients with an incomplete paralysis. In an overview by Chang and Cass, i= t was concluded that surgical treatment was not required in patients who had 1) documented normal facial nerve function after injury regardless of its progression, 2) incomplete paralysis as long as there was no progression to complete paralysis, and 3) less than 95% degeneration by ENoG. Treatment of a complete paralysis = is much more controversial, however. In 1974, Fisch recommended basing the decision for surgery on the ti= me of onset of paresis, the degree of paresis, the degree and evolution of degeneration as measured by ENoG, and the degree and evolution of regeneration. He noted a poor functional outcome in patients presenting with greater than 90% nerve degeneration by ENoG within 6 days of onset of palsy. Chang and Cass suggest that if decompression surgery is anticipated it should be done within a 14 day wind= ow from the time of injury based on animal studies by Yamamoto and Fisch.
After deciding on facial nerve exploration, the suspect location of neural injury and hearing status are the two key factor= s in determining an appropriate approach. Injuries of the facial nerve at or dis= tal to the geniculate ganglion can be approached via the transmastoid procedure. Fractures can be identified laterally upon visualization of the mastoid cortex. Theses fractures can be chased med= ially to the point of injury. If th= ere is no obvious fracture, a facial recess approach will help provide examination= of the nerve from the geniculate ganglion to the second genu. Partial transections of less than = 50% may be repaired with onlay nerve grafts.&n= bsp; If transection exceeds 50%, an interposition nerve graft, such as the greater auricular nerve, should be used in approximation after the epineuri= um is trimmed and the nerve fascicles optimized. Of patients who undergo direct anastomosis or cable graft repair, the majority of patients (82%) will reco= ver to a House Brackmann III or IV, and none have shown to recover to House-Brackmann I or II. If the nerve is found to be intact, decompression of the epineural sheath is performed in proximal and distal fashion until normal nerve is encountered.= In Chang and Cass’s review, about 50% of patients undergoing facial nerve decompression obtain excellent functional outcomes.
Injuries medial to the geniculate ganglion may be approached in several ways, depending on the status of hearing. For patients in whom hearing is not useful, a transmastoid-translabyrinthine approach is reserved. The entire intratemporal course of= the facial nerve can be seen after translabyrinthine skeletonization of the internal auditory canal.
For patients with intact hearing, a transmastoid= -supralabrinythine approach or a middle cranial fossa approach is considered. Following complete mastoidectomy, = the superior semicircular canal is skeletonized, thus allowing exposure of the labyrinthine portion of the facial nerve.&= nbsp; If there are any concerns regarding adequate exposure or if grafting= of the meatal portion is anticipated, the middle fossa approach is more suitable. The middle fossa ap= proach is usually preceded by a mastoidectomy to aid in the identification of the internal auditory canal. The superior portion of the temporal bone is then exposed via an extradural craniotomy approach.
CSF Otorrhea
Blunt trauma to the skull may produce fractures = in the temporal bone with tearing of dura and foramina causing acute leakage. Fractures may also produce defects= in the bony tegmen plate, predisposing one to encephaloceles or meningoceles w= ith resultant delayed CSF leakage. As described previously, fractures involving the otic capsule are associated w= ith higher incidence of CSF leak. CSF otorrhea in temporal bone fractures usual= ly occurs within minutes of the accident but may be delayed in its presentatio= n if it is draining through the nasopharynx.&nb= sp; After trauma, CSF otorrhea is typically serosanginous and can be mistaken for blood byproducts. The fluid should be sent for beta-2-tranferrin, as this protein is highly speci= fic to the CSF. Measurements of g= lucose and protein in the fluid have fallen out of favor for CSF identification. <= span style=3D'mso-spacerun:yes'> A high resolution CT scan can demon= strate the course of the fracture line and give information as to the likely site = of CSF fistula. Contrast cisternography may increase the sensitivity of detect= ing CSF leak when it is active.
Management of cerebrospinal fluid leak begins wi= th conservative measures including head elevation, bed rest with head elevatio= n, stool softeners, avoidance of nose blowing/sneezing and other forms of straining, and, in selected patients, placement of a lumbar drain. Spontane= ous resolution with this conservative management occurred in 95% to 100% of patients. In spontaneously recovering leaks, closure occurred in the first 7 days in 78%, with an additional 17% closing between 8 and 14 days. The use = of prophylactic antibiotics remains controversial, although leak persists more than 7 days has been correlated with a higher incidence of meningitis. Surg= ical repair is recommended for those cases that persist 7-10 days after an injur= y. Tegmen defects may be multiple rather than single, and identifying only one defect= may not be sufficient for achieving definitive repair. Because surgical repair by way of a mastoidectomy approach alone can be inadequate if there are multiple tegmen defects, a middle fossa approach alone or in combination with a transmastoid approach should be considered in most cases.
Vascular injury
Carotid injury is uncommon (1-4%) in temporal bo= ne trauma A recent article by Dempewolf describe 44 of 127 (35%) temporal bone fracture patients had carotid canal fractures whereas only 5 of 127 (4%) had carotid artery inju= ry. Both CT temporal bone and CT maxillofacial have been shown to be very sensi= tive in detecting carotid canal fracture, with a negative predictive value > 100%. CT angiography and MRA have been used more frequently than standard angiography when CT scan demonstrates evidence of vascular injury. Physical exam has not been shown to be very sensitive as only 2 of 5 patients in the Dempewolf series displayed physical findings of vascular injury (epistaxis, focal neurologic deficit).
Vertigo
Vertigo after temporal bone trauma may be second= ary to either vestibular concussion in OCS or vestibular destruction in OCD settin= g. It is usually self-limiting and resolves within 6 to 12 months from central adaptation. Perilymph fistula after otic capsule injury can also cause vert= igo and SNHL. Another cause of vertigo after temporal bone fracture is posttraumati= c endolymphatic hydrops. These patients present with aural fullness, tinnitus, fluctuating hearing loss, and vertigo similar to patients who have Meniere’s dise= ase. Brief vertigo episodes may be attributed to benign positional paroxysmal vertigo. It is presumably caused by traumatic displacement of otoconia from= the vestibule into the ampulla of the posterior semicircular canal. Treatment of BPPV includes standard rehabilitation and repositioning maneuvers.
Other complications
Some of the late rare complications after tempor= al bone injury include meningocele, encephalocele, meningitis, and cholesteato= ma. Treatment is often surgical to prevent the development of further intracranial complications.
Summary
Temporal bone fracture is a common injury in acu= te head trauma. Early management involves stabilization of the patient and collaboration with the trauma service. Early conservative management is recommended for hearing loss, CSF leak, and facial paresis. Long-term follow up is necessary to address heari= ng loss and monitor for intratemporal and intracranial complications.
_____________________________________________________= _______________________
Grand Rounds Temporal Bone Fracture – Discussi= on by Tomoko Makishima, MD
Thank you, Dr. Ho. That was an excellent presentation=
. There’s not much I need to a=
dd but
I would like to comment on facial nerve injuries. Whether or not to go proceed with
surgical treatment is a very controversial topic because people don’t
have a lot of experience in general. It is often difficult in the first pla=
ce
to assess whether the patient has definite indications for surgery. One of =
the
reasons is that, in these patients, there are often other life-threatening
events going on that needed to be taken care of and the diagnosis of the fa=
cial
nerve injury are often delayed than you would like.
And then, another difficult de=
cision
is, what kind of surgical approach to choose. Let’s say you suspect a=
transection
of the facial nerve. One of t=
he
methods to repair it is to have the nerve ends in proximity. As long as the ends are close toge=
ther,
most of it will most likely re-anastomose on its own. So, those milder non
life-threatening cases which go into surgical treatment of facial nerve inj=
ury,
probably do not have a big gap between the transected nerve ends. And perha=
ps
that is why there is not a lot of difference in outcome in the long term in
whether you treat it surgically or not. And if you really need to do an
allograft (nerve grafting) that means there is more than a few millimeter
difference separation of the nerve ends – which also indicates that t=
he
temporal bone is dislocated and there is more severe events taking place in=
the
patient, and thus will not likely be seeing us for facial nerve repair.
In terms of doing surgical
decompression, my personal opinion is that I don’t necessarily think =
that
you need to go all the way to the middle fossa because the whole idea is to
decompress the swelling or make some room so that the nerve ends can be clo=
se
to each other, or to relieve the nerve from being stretched or pulled. Decompressing in the entire mastoid
portion and tympanic segment will generate a lot of such space because you =
will
be releasing the nerve from the surrounding bone. During my practice here at UTMB si=
nce
2005, there was only one case in which I had to do the decompression, and I
only did the mastoid portion but it did turn out pretty well. This was a young boy involved in a=
n accident
– he was thrown out of a car and the car landed on his head. He had
bilateral temporal bone fractures, with unilateral complete facial nerve pa=
lsy,
and profound deafness on the same side.&nb=
sp;
________________________________________________=
____________________
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