Basilar skull fractures, usually caused by substantial blunt force trauma, involve at least one of the bones that compose the base of the skull. Basilar skull fractures most commonly involve the temporal bones but may involve the occipital, sphenoid, ethmoid and the orbital plate of the frontal bone as well. Several clinical exam findings highly predictive of basilar skull fractures include hemotympanum, cerebrospinal fluid (CSF) otorrhea or rhinorrhea, battle’s sign (retroauricular or mastoid ecchymosis), and raccoon eyes (periorbital ecchymosis). Basilar skull fractures are commonly associated with facial fractures, cervical spine injury, intracranial hemorrhage, cranial nerve injury, vascular injury, and meningitis.
Basilar skull fractures are most commonly seen in younger people due to their propensity to do high-risk activities. The majority of basilar skull fractures are managed with conservative care.
Most basilar skull fractures are caused by high-velocity blunt trauma such as motor vehicle collisions, motorcycle crashes, and pedestrian injuries. Falls and assaults are also important causes. Penetrating injuries such as gunshot wounds account for less than 10% of cases.
Basilar skull fractures are relatively uncommon and are present in about 4% of all patients with a severe head injury. They represent 19% to 21% of skull fractures.
The location of the fracture is predictive of associated injuries:
Basilar skull fractures are often associated with other CNS pathology like epidural hematoma due to the weakness of the temporal bone and the close proximity of the middle meningeal artery.
At least 50% of basilar skull fractures are associated with another CNS injury and about 10% have cervical spine fracture.
The majority of basilar skull fractures involve the petrous bone, the external auditory canal, and tympanic membrane.
Clinical features of basilar skull fractures vary depending on the degree of the associated brain and cranial nerve injury.
Patients may present with altered mental status, nausea, and vomiting. Oculomotor deficits due to injuries to cranial nerves III, IV, and VI may be present. Patients may also present with facial droop due to compression or injury to cranial nerve VII. Hearing loss or tinnitus suggests damage to cranial nerve VIII.
Several clinical signs highly predictive of basilar skull fracture include:
Presence of Battle sign and raccoon eye are highly predictive of basilar skull fracture.
The diagnosis may be obvious on a physical exam in some cases. Plain x-rays are not sensitive to detect basilar skull fracture.
The initial evaluation is usually via a non-contrast computed tomography (CT) scan. Unfortunately, skull-based fractures that are linear or non-displaced may be difficult to detect. In patients where a high clinical suspicion for basilar skull fracture exists, multidetector CT (MDCT) thin-slice scanning through the face and skull base may aid in the detection of more subtle fractures. Conversely, the detailed small neural and vascular channels visualized on MDCT may be misread as fractures. Pneumocephalus should raise the suspicion for a basilar skull fracture. Further imaging with CT angiography and venography (CTA, CTV) to assess for vascular injury should be considered in the acute setting. MRI may be useful in assessing nerve injury and in evaluating for a cerebrospinal fluid leak.
CSF leak is not easy to diagnose and the fluid should be sent for analysis of beta transferrin.
Basilar skull fractures are usually due to significant trauma. A thorough trauma evaluation with interventions to stabilize airway, ventilation, and circulatory issues is the priority. Associated cervical spine injury is common, so attention to cervical spine immobilization, particularly during airway management is necessary. Nasogastric tubes and nasotracheal intubation should be avoided because of the risk for inadvertent intracranial tube placement.
In addition, nasal intermittent positive pressure ventilation (NIPPV) should be avoided as it may induce pneumocephalus.
Patients with basilar skull fractures require admission for observation. Those taking anticoagulants should be admitted to a facility with immediate neurosurgical capabilities and the ability to do frequent assessments of the neurologic decline, even if no hemorrhage is present on initial imaging. Patients with intracranial hemorrhage require emergent neurosurgical evaluation. Otherwise, skull base fractures are often managed expectantly. Surgical management is necessary for cases complicated by intracranial bleeding requiring decompression, vascular injury, significant cranial nerve injury, or persistent cerebrospinal fluid leak.
Basilar skull fractures increase the risk of meningitis because of the increased possibility of bacteria from the paranasal sinuses, nasopharynx, and the ear canal making direct contact with the central nervous system. Patients with associated cerebrospinal fluid leaks, present in up to 45% of patients with basilar skull fractures, are often treated with prophylactic antibiotics to prevent meningitis, but there is no good evidence to support this practice. A recent Cochrane review did not find sufficient evidence to recommend prophylactic antibiotics in patients with basilar skull fractures even in the presence of documented cerebrospinal fluid leak. However, patients with persistent leaks should have cerebrospinal fluid cultures to guide antibiotic therapy, and patients with clinical presentations consistent with meningitis should be treated with empiric antibiotics until culture results are available. While prophylactic antibiotics are not indicated generally, use is still considered appropriate for coverage related to procedures such as insertion of intracranial pressure (ICP) monitor. Persistent leaks require neurosurgical intervention. Less invasive, endoscopic techniques are becoming common with fewer of these injuries requiring open repair.
The majority of CSF leaks resolve spontaneously within 5-10 days but some can persist for months. Meningitis may occur in less than 5% of patients but the risk increases with the duration of the CSF leak.
Conductive hearing loss usually resolves within 7-21 days.
Cranial nerve deficits involve loss of smell and facial palsy.
Basilar skull fractures can also be associated with a vascular injury resulting in occlusion, fistula formation, bleeding, or pseudoaneurysm formation.
Complications associated with basilar skull fractures include:
Skull base fractures are not common but when they do occur, they represent a serious life-threatening condition with very high morbidity and mortality. Because of the diverse presentation, these patients are best managed by an interprofessional team that includes a neurosurgeon, neurologist, ophthalmologist, ENT surgeon, neurosurgical nurses, a radiologist, and an infectious disease specialist.
The patients are usually managed in an ICU setting and monitored by a nurse. Patients need frequent assessment of neurological signs, ventilation, and oxygenation. Nurses have to ensure that patients have DVT and gastric ulcer prophylaxis. Some patients may not be able to eat and parenteral nutrition may be required. The pharmacist needs to make sure that the patient is not receiving high doses of analgesias because this may hide any neurological signs. Further, the use of opiates may make it difficult to assess the pupils for elevation in intracranial pressure. The patient needs to be monitored by critical care nurses to ensure that there are no signs of CNS infection. The entire team must communicate regarding changes in the patient's condition to ensure that the patient is receiving the appropriate care. Outcomes will be improved by an interprofessional approach to the care of patients with a basilar skull fracture. [Level V]
The outcome of patients with basilar skull fractures depends on whether the fracture is displaced. For nondisplaced fractures, the management is conservative and the outcomes are good. However, for those with displaced fractures, intervention may be required and this also carries a risk of surgical complications. The key morbidity is meningitis which can be lethal. Those who have a dissection of the carotid artery can develop life-threatening bleeding. Overall, most patients with basilar skull fracture do have some type of residual functional or neurological deficit which may take months or even years to reverse.
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