The neurosurgical management of lateral skull base trauma


Introduction

The lateral skull base is comprised predominantly of the dense, pyramid-shaped petrous temporal bone. Fractures of the petrous temporal bone comprise approximately 20% of all skull fractures. Given the density of the petrous temporal bone, fractures are caused by high-impact trauma and are nearly uniformly associated with traumatic brain injury (TBI). In addition, 8%–29% of temporal bone fractures are bilateral, resulting in significant morbidity. ,

These fractures are typically caused by direct impact and compression mechanisms and, historically, have been classified as either transverse or longitudinal depending on the orientation of the fracture along the long axis of the temporal bone. More recent classification, however, has focused on the relationship of the fracture to the otic capsule as this represents a more clinically relevant distinction. In this scheme, fractures are either otic capsule sparing (OCS) or otic capsule disrupting (OCD). OCS fractures are more common, comprising approximately 95% of fractures, and typically result from direct impact on the temporoparietal convexity. Resultant fractures are through the posterior wall of the external auditory canal (EAC), mastoid air cells, middle ear, mastoid tegmen, and tegmen tympani. As a result, OCS injuries are associated with conductive or mixed hearing loss. In contrast, OCD fractures are typically from impact to the occiput with a fracture line from the foramen magnum through the petrous pyramid. These fractures can involve the jugular foramen, internal auditory canal, and foramen lacerum. OCD fractures lead to an obligate, often profound, and sensorineural hearing loss (SNHL) ( Fig. 9.1 ) .

Figure 9.1, ( Left ) Otic capsule sparing fractures result from impact on the temporoparietal convexity, leading to a fracture line through the petrous temporal bone, but without violation of the otic capsule. ( Right ) Otic capsule disrupting fractures are typically from impact to the occiput with a fracture line from the foramen magnum through the petrous temporal bone and the otic capsule.

Fractures of the lateral skull base are a source of significant morbidity. They can lead to cerebrospinal fluid (CSF) leak, facial nerve injury, meningitis, hearing loss (both conductive and sensorineural), and cerebrovascular injury. As such, early recognition is important to allow for appropriate management.

Clinical evaluation and diagnosis

Temporal bone fractures are typically the result of high-impact trauma. Often these fractures occur in patients who also have TBI and polytrauma. Therefore, it is common for temporal bone fractures to be initially diagnosed on a CT of the head. A temporal bone fracture should also be suspected in an awake posttrauma patient with facial weakness, dizziness, or hearing loss, or in an obtunded posttrauma patient with ecchymosis over the mastoid prominence (Battle's sign) or otorrhea.

The physical exam is critical for acute diagnosis and management of these fractures. Otoscopy should be performed on any patient with a suspected fracture. Evaluation should begin with inspection of the external ear. Superficial lacerations will often heal without intervention. Circumferential lacerations of the EAC, however, may lead to stenosis in the future and should be repaired. The canal should also be inspected for brain parenchyma (rare) and CSF leak (more common). The integrity of the tympanic membrane (TM) should be assessed. The most common findings are hemotympanum if the TM is intact, and bloody otorrhea if the TM is perforated. Similarly, in the case of a CSF leak, otorrhea will be present if the TM is perforated, but if the membrane is intact, the fluid drains through the eustachian tube producing rhinorrhea. Pneumatic otoscopy should be deferred in the acute setting to avoid introduction of air and bacteria into the subarachnoid space.

Evaluation and documentation of facial movement is also imperative in the acute setting as it has significant prognostic value . By necessity, facial movement evaluation is often delayed, however, as patients may be intubated and unable to participate in an examination or other injuries may take priority. Those patients who cannot be examined immediately should be considered to have indeterminate onset of facial weakness. The House–Brackmann scale is a simple and consistent grading scale that can be utilized for long-term follow-up. Patients with immediate, acute-onset complete facial paralysis have a much worse prognosis for recovery than those with delayed-onset weakness. Recovery of incomplete facial paralysis is seen in nearly 100% of cases. , , ,

Hearing should also be tested at bedside with a 512-Hz tuning fork. The Rinne and Weber tests can help differentiate conductive hearing loss from SNHL. Audiometry is typically delayed for several weeks after initial trauma to allow for resolution of middle ear fluid unless the patient requires an urgent surgical intervention.

Disruption of the otic capsule can present with vertigo and nystagmus. For that reason, an examination of extraocular movements should be performed to assess for nystagmus in addition to cranial nerve III, IV, and VI palsies. An abducens palsy is common in TBI and can be associated with temporal bone fractures, especially fractures extending into the clivus.

High-resolution temporal bone CT is not routinely necessary unless patients develop persistent CSF leaks, hearing loss, or facial weakness. It should also be obtained prior to any planned surgical intervention. CT angiography should also be considered in the setting of temporal bone fractures as the petrous segment of the internal carotid is at risk for injury as are the transition points between the relatively mobile cervical and petrous segments and the petrous to lacerum segments.

Management and outcomes

Management of lateral temporal bone fractures hinges on the indications for surgical intervention. In general, early surgery should be considered for open, depressed squamous temporal fractures or any mass occupying lesions with a poor neurologic exam, such as a large temporal lobe contusion or an epidural hematoma. The goal of acute surgical intervention is preservation of neurologic function and decompression of the brainstem. In contrast, delayed surgical intervention is reserved for persistent CSF leaks and facial nerve decompression.

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