Skull fractures

Skull fractures most typically occur as a result of blunt force trauma from contact sports, motor vehicle collisions, or falls. They are classified by anatomical location as either cranial vault fractures or basilar skull fractures. Cranial vault fractures involve one or more of the cranial vault bones, may be either open fractures or closed fractures, and are classified as linear skull fractures or depressed skull fractures. Basilar skull fractures involve one or more of the skull base bones and are classified as anterior, middle, or posterior cranial fossa fractures. Clinical features vary depending on bone involvement but may include lacerations, contusions, and hematoma of the scalp; palpable deformities; mobile bone fragments; liquorrhea; Battle sign; raccoon eyes; and signs of traumatic brain injury. Initial management of skull fractures focuses on identifying and addressing life-threatening injuries. Complications of skull fractures include CSF leaks (which increase the risk for meningitis), cranial nerve disorders (due to compression or transection), and epidural hematomas. Expectant management may be sufficient for simple fractures but neurosurgery may be necessary for unstable fractures and fractures with associated complications. Open head injuries can occur when skull fractures are associated with rupture of the dura mater, which can increase the risk of CNS infection.

See also “Facial fractures,” and “Orbital floor fractures” in “Traumatic eye injuries.”

Initial management ^[1]

Follow the ATLS algorithm for any patient with a potentially significant head injury, and maintain a low threshold for early specialist consultation (e.g., neurosurgery).

• Primary survey
  • C-spine immobilization and neuroprotective measures.
  • Airway management and mechanical ventilation as needed, e.g., due to low GCS.
  • Hemostatic control of obvious sources of bleeding, e.g., scalp laceration management.
  • Perform a rapid neurological examination.
  • If signs of TBI are present, begin TBI management.
• Secondary survey (once the patient is stabilized)
  • Assess for cranial vault deformities and evidence of basilar skull fractures.
  • Evaluate for associated injuries, e.g., facial fractures, cervical spine injury, traumatic eye injuries, carotid or vertebral artery dissection
  • Obtain CT head without contrast.
  • Perform further diagnostics as needed (e.g., ocular examination, otoscopy, CT cervical spine).

Assume patients with high-impact head trauma have a cervical spine injury until it has been ruled out.

Neurological impairment, repeated vomiting, and seizures indicate potentially severe cerebral trauma or intracranial hemorrhage.

Supportive care ^[1]

• Perform acute wound management, including scalp laceration management as needed.
• Provide analgesia as needed.
• Consider CNS infection prophylaxis for open head injury.
• Consider seizure prophylaxis after TBI.
• See also “Prevention of complications in head injuries”

Definitive management ^[1]

See also “Management of moderate and severe TBI.”

• Conservative management: usually appropriate for nondisplaced linear skull fractures without significant intracranial injury
• Surgical management: may be required for comminuted or depressed skull fractures and/or treatment of neurovascular complications

Determine appropriate patient disposition based on the type of fracture and the presence of TBI or other complications.

Definitions ^[2][3]

• Cranial vault fracture: a fracture of ≥ 1 of the cranial vault bones; can be a closed or open skull fracture.
• Diastatic skull fracture: a fracture along the skull suture lines (most commonly seen in newborns and infants)

Etiology

See “Etiology of TBI.”

Clinical features ^[1]

Most commonly involves the frontal and parietal bones

• Scalp hematoma, local swelling, and tenderness
• A palpable gap along the surface of the bone or bone crepitus when the fracture fragments are moved
• Scalp lacerations
• Epidural hematoma (if in close proximity to the middle meningeal artery)
• Signs and symptoms of TBI: common in depressed skull fractures
• Clinical features of mild TBI: common in simple linear skull fractures

Use caution when examining head injuries to avoid pushing potential depressed skull fractures further into the cranium. ^[1]

Diagnostics ^[1][4]

See also “Diagnostics in TBI.”

• CT head without IV contrast (preferred modality)
  • Evaluate for fracture lines.
  • Assess for intracranial injury.
• X-ray skull: may be used if CT is not available

Linear skull fracture ^[1][2]

• Definition: a single fracture that extends through the entire width of one or more bones of the skull; most common type of skull fracture
• Etiology: typically occurs as a result of low-energy blunt trauma over a wide area of the skull (e.g., from a fall)
• Clinical features
  • Number of fracture lines: simple or comminuted fracture
  • Soft tissue involvement: closed fracture or open fracture
  • Fractures crossing the middle meningeal groove or dural venous sinuses may result in epidural hemorrhage.
• Treatment
  • All patients: Initiate immediate management of skull fractures.
  • Comminuted fracture and/or intracranial injury: Consult neurosurgery.
  • Simple linear fracture and no evidence of intracranial injury: conservative management
    • Observe for 4–6 hours prior to considering discharge. ^[1]
    • Return precautions for any red flags for mild TBI
    • See also “Management of mTBI.”

Depressed skull fracture ^[1][2]

• Definition: a skull fracture in which the skull depresses inward toward the brain parenchyma
• Etiology: typically occurs as a result of high-energy blunt trauma to a small area of the skull (e.g., from being struck with a baseball bat)
• Clinical features
  • Number of fracture lines: typically a comminuted fracture
  • Often an open skull fracture
  • Often penetrates the dura (i.e., causing open head injury) ^[1][3]
  • Location: most commonly involves the parietal and frontoparietal regions
• Treatment
  • Initiate immediate management of skull fractures.
  • Open depressed skull fracture: See “Open head injuries.”
  • Conservative management: may be appropriate for uncomplicated closed depressed skull fractures
  • Surgical management: often required for severe or open depressed skull fractures and/or associated intracranial injuries
  • Dispostion
    • Consult neurosurgery. ^[3]
    • Admit all patients for observation.

Open depressed skull fractures are often considered open head injuries because of the high prevalence of associated dural tears. Antibiotic prophylaxis is recommended. ^[1][3]

Definition ^[2]

• A skull fracture involving ≥ 1 bone of the skull base, i.e., the ethmoid, sphenoid, occipital, paired frontal, and/or paired temporal bones

Etiology

See also “Etiology of TBI.”

• Caused by significant high-energy trauma to the skull
• Most commonly results from motor vehicle, motorcycle, or pedestrian-motor vehicle collisions
• Other causes
  • Violent altercations
  • Falls
  • Firearms

Classification ^[2]

• Anterior cranial fossa fracture
• Middle cranial fossa fracture
• Posterior cranial fossa fracture

Clinical features of basilar skull fractures ^[5][6]

• Liquorrhea; : CSF rhinorrhea and/or CSF otorrhea may occur immediately or within a few days of injury
• Subcutaneous hematomas: typically appear within hours to days of injury
  • Raccoon eyes: subcutaneous hematoma around the eyes
  • Battle sign: subcutaneous hematoma overlying the mastoid process ^[7]
• Cranial nerve palsies
• Orbit and/or paranasal sinus injuries ^[2]
• Hearing loss, vertigo
• Hemotympanum: a collection of blood in the tympanic cavity behind the tympanic membrane
• Intracranial vascular injury
  • Internal carotid artery injury ^[6]
  • Venous sinus thrombosis or hemorrhage ^[2][6]
• Signs and symptoms of traumatic brain injury

CSF otorrhea, hemotympanum, vertigo, hearing loss, and/or facial nerve palsy suggest fracture of the petrous portion of the temporal bone. ^[2][5]

Raccoon eyes, Battle sign, and CSF leakage are highly indicative of basilar skull fractures.

Diagnostics ^[1][4][6]

See also “Diagnostics in TBI.”

• CT head without IV contrast (preferred modality)
  • Findings
    • Discontinuity in the bone structure with or without displacement
    • Pneumocephalus: air within the cranium; typically associated with open head injuries
    • Intracranial hemorrhage or hematoma
    • Hyperdensity in neighboring structures (e.g., paranasal sinus, middle ear, mastoid air cells): indicates hemorrhage
• CSF detection studies: to evaluate for cerebrospinal fluid (CSF) in nasal and/or ear discharge
• Additional testing: Consider based on initial findings and clinical presentation.
  • CT cervical spine: to rule out concomitant cervical spine injury
  • CT maxillofacial and/or temporal bone without IV contrast: to evaluate for the cause of a suspected CSF leak
  • CT or MR angiography and venography: to evaluate for blunt cerebrovascular injury
  • Ophthalmic ultrasound: can help detect ocular injuries (e.g., vitreous hemorrhage, retinal detachment, globe rupture)

Basilar skull fractures can injure the internal carotid artery. Obtain urgent CT angiography head in patients with signs of carotid-cavernous fistula or stroke. ^[4]

Management ^[1][8]

Initial management

• Initiate immediate management of skull fractures.
• Consider antibiotic prophylaxis for skull fractures for patients with persistent CSF leakage (> 7 days). ^[1][9]

Definitive management

• Conservative management
  • Mainstay for most basilar skull fractures without severe intracranial neurovascular complications
  • May include CSF leak precautions and/or corticosteroids for incomplete traumatic facial nerve palsy
• Surgical management
  • Emergency surgery may be indicated for comminuted or displaced fractures, large CSF leaks, or significant neurovascular complications
  • Delayed repair of persistent (longer than 3–7 days) small-moderate CSF leaks

Avoid nasogastric tubes and nasotracheal intubation in patients with a suspected ethmoid bone fracture, as they may cause direct intracranial injury.

Disposition

• Consult neurosurgery.
• Admit all patients for observation.

Complications

Liquorrhea

• Definition: external leakage of CSF via a dural tear ^[1]
  • CSF rhinorrhea: leakage of CSF from the nose
  • CSF otorrhea: leakage of CSF from the external auditory meatus
• Pathophysiology: dural tear (most often due to basilar skull fractures) → communication between the subarachnoid space and middle ear and/or paranasal sinuses → CSF leak ^[1]
• Etiology ^[1][10]
  • Craniofacial trauma (e.g., basilar skull fractures)
  • Iatrogenic trauma
  • Neoplasia
• Clinical features ^[1][10]
  • Intermittent clear or blood-tinged watery discharge from the nose and/or ear
    • Worsens with dependent head positioning
    • Sweet or salty post-nasal drip
  • Symptoms resembling post-lumbar puncture headache can occur.
  • Meningismus may develop.
• Diagnostics ^[5][10]
  • CSF detection studies
    • Halo sign (bedside study): rapidly expanding ring of clear fluid surrounding blood; produced after a drop of discharge is applied to gauze or tissue paper ^[11]
    • Detection of β2-transferrin (gold standard): an isoform of transferrin found primarily in CSF and perilymph ^[5][10]
  • Imaging: localization of dural tears with high-resolution CT, MRI, and/or nasal endoscopy
• Treatment ^[1][8][10]
  • Consult neurosurgery.
  • CSF leak precautions
    • Bed rest with the head of the bed elevated to ≥ 30°
    • Avoidance of straining and Valsalva maneuver (e.g., sneezing, nose blowing, incentive spirometry)
    • Use of stool softeners to prevent straining with defecation
  • Consider antibiotic prophylaxis for skull fractures for patients with persistent CSF leakage (> 7 days). ^[1][9]
  • Nonsurgical management: usually sufficient for small-moderate traumatic CSF leaks, as most resolve without complications within 1 week
  • Surgical management
    • Consider for large leaks or persistent (longer than 3–7 days) small-moderate leaks
    • May involve transcranial or endoscopic repair and/or CSF diversion with external ventriculostomy or lumbar drain

Other complications

• Meningitis
• Pneumocephalus
• Panhypopituitarism
• See also “Complications” in “Temporal bones fractures.”

Definition

• Fracture of the temporal bone, typically involving the petrous portion
• Often associated with epidural hematoma due to proximity of the temporal bone to the middle meningeal artery

Etiology

• High-energy blunt trauma to the temporal bone (often in association with polytrauma)
• Most common cause: traffic-related injuries (e.g., motor vehicle collisions, bicycle vs. pedestrian collisions)

Clinical features

• Injury to the external auditory canal and tympanic membrane is common.
• Cranial nerve palsies (CN I, CN V, CN VI, CN VII, CN VIII)
• Injury to the otic capsule significantly increases the risk of facial nerve palsy, CSF leak, and sensorineural hearing loss.
• Signs of TBI may be present.

Diagnostics ^[12][13]

See also “Diagnostics” in “Basilar skull fractures.”

• Imaging
  • CT head without IV contrast (preferred modality): usually sufficient to diagnose temporal bone fractures
    • Fracture lines in the petrous part of the temporal bone
    • Hyperdensity in the mastoid air cells: indicates hemorrhage
  • High-resolution CT of the temporal bone: to evaluate facial nerve paralysis, CSF leakage, or a suspected vascular injury
• Otoscopy: to inspect the tympanic membrane (see “Clinical features of petrous bone fractures”)
• CSF detection studies: to assess for CSF leakage in otorrhea

Treatment ^[13]

• Surgery may be indicated for: ^[12]
  • Dural repair
  • Middle ear reconstruction
  • Facial nerve decompression or grafting
• See also “Treatment” in “Basilar skull fracture” and “Management of traumatic facial nerve palsy.”

Complications

Perilymphatic fistula ^[15]

• Definition: : an abnormal connection between the perilymphatic space in the inner ear and the middle ear, mastoid, or intracranial cavity, resulting in perilymph leakage
• Etiology
  • Trauma: temporal bone fractures, barotrauma (e.g., Valsalva maneuver), penetrating ear trauma, ear surgery (e.g., stapedectomy)
  • Congenital temporal bone abnormalities
  • Idiopathic
• Clinical features
  • Acute onset of vertigo, disequilibrium, tinnitus, sensorineural hearing loss, and/or aural fullness
  • Vestibular symptoms typically worsen with loud noises (Tullio phenomenon) and pressure changes in the middle ear or external auditory canal (Hennebert sign)
• Diagnostics: CT scan, MRI scan
• Treatment: surgical fistula closure

Other complications

• Traumatic facial nerve palsy
• Posttraumatic benign paroxysmal positional vertigo
• Traumatic endolymphatic hydrops
• See also “Complications” in “Basilar skull fractures.”

Definitions

• Open head injury
  • Head injury with dural rupture; i.e., meninges and/or brain matter exposed to other tissue compartments and/or external environments
  • Associated with skull fractures (can be open skull fractures or closed depending on extent of overlying soft tissue injury)
  • Examples of open head injuries without open skull fracture: basilar skull fracture with persistent CSF leak, intracranial sinus fracture with pneumocephalus
• Open skull fracture
  • A skull fracture with an overlying scalp laceration disrupting both the skin and galea; i.e., bony interior exposed to the external environment
  • Often but not always associated with open head injury, depending on dural involvement
  • Examples of open skull fractures with open head injury: penetrating head injury, open depressed skull fracture
• Open depressed skull fracture
  • A type of open skull fracture with an underlying depressed skull fracture
  • Treated as an open head injury due to the high prevalence of associated dural rupture ^[1][3]

Open head injury and open skull fracture can occur with the same skull fracture if there is disruption of the underlying dura AND of the overlying galea and skin.

Clinical features

• Scalp laceration involving galea and skin
• Clinical features of the involved skull fractures (see “Cranial vault fractures”).
• If there is also an open head injury, signs of dural rupture (e.g., CSF leak) and clinical features of TBI may be present.

Diagnosis

• Clinical evidence of scalp laceration involving galea and skin
• Clinical and radiological evidence of underlying skull fracture (e.g., fracture line on CT head)
• Clinical and radiological evidence of concomitant open head injury and/or TBI may be present, (e.g., pneumocephalus, intracranial hemorrhage)

CNS infection prophylaxis for open head injury ^[1][5]

• Indications: not routinely recommended ^[9][16]
  • Open head injury with open skull fractures
    • Penetrating brain injury
    • Open depressed skull fracture with dural rupture
  • Consider in other types of open head injury
    • Pneumocephalus without open skull fracture, e.g., intracranial sinus fracture
    • Basilar skull fractures with persistent CSF leak (> 7 days). ^[1][9]
  • Consider in patients with external ventricular drains. ^[1][17]
• Regimens: should provide coverage for staphylococci, gram-negative bacteria, and anaerobes. ^[1]
  • Example regimen: vancomycin PLUS gentamicin PLUS metronidazole ^[1]
  • Duration of therapy: not clearly defined; consult neurosurgery ^[18]
• Monitoring: Clinical monitoring is usually sufficient. ^[19]

Additional management

• Consult neurosurgery for definitive treatment.
• Begin TBI management as needed.
• Manage scalp lacerations.