Complications
Affects about 10% to 30% of skull fractures, although primarily associated with basilar skull fractures.[76]
Can be diagnosed clinically by drainage of clear or serosanguineous fluid from ears/nose, or open fracture. Fluid can be tested for beta-2 transferrin with immunofixation electrophoresis to confirm presence of cerebrospinal fluid (CSF). Intranasal endoscopy can also be used to identify the source of a leak.
Most leaks resolve with conservative measures such as head-of-bed elevation and laxatives. If persistent, lumbar puncture or lumbar drain placement may be used to decrease intrathecal pressure and to obtain CSF to monitor for meningitis.[77][78]
If the CSF leakage is persistent, the primary surgical approach depends on the site of the leak and should be decided on a case-by-case basis following discussion between an ENT specialist and a neurosurgeon. For base of skull fractures, endonasal repair is preferable because it has better outcomes and lower morbidity than craniotomy.[56][79][77][78][76][86] Uncommonly, some CSF leaks (e.g., high up the frontal sinus) may not be reachable endonasally or may require formal cranialisation of the sinus via a craniotomy.
Typically presents with loss of consciousness or period of decreased alertness, potential seizure activity (or loss of bowel and bladder continence), headache, weakness or sensory changes, or changes in cognition, speech, or vision.
Computed tomography will show subdural/epidural fluid collection.
For small, stable subdural haematomas that are not causing neurological compromise, observation may be appropriate; anticonvulsants should be given.
Surgical therapy is usually indicated for acute or chronic subdural haematomas that are expansile or causing neurological deficit.
If the linear fracture overlies the superior sagittal sinus, there is an increased risk of associated vascular injury or pathology. Incidence of stenosis or thrombosis may be as high as 11.5% for all skull fractures.[54][55]
Presents as fever, chemosis, proptosis, periorbital oedema, and external ophthalmoplegia in the majority of patients. Imaging with CT/MRI and adjunctive angiography may show expansion or abnormal filling defects together with lateral convexity of the cavernous sinuses.
Treatment is conservative, with anticoagulation and serial lumbar punctures to reduce venous congestion and intracranial hypertension.[55]
The extent of anticoagulation and choice of agents must take into account the severity of symptoms related to the thrombosis as well as the risk of exacerbating any other traumatic injury, particularly intracranial haemorrhage.[54]
Meningitis is a recognised complication of skull fracture and is reported in 0.7% to 15.3% of cases.[88][66][67][68]
Risk factors include presence of CSF otorrhoea and rhinorrhoea, open fracture, gross contamination, and delay in treatment.[88] Prompt debridement and closure of open wounds will minimise the risk of infectious complications.
Patients should be followed up for symptoms and with laboratory studies, as a significant minority may present late.
Presents with fever, chills, nuchal rigidity, and mental status changes.
Diagnosis can be made with lumbar puncture and CSF analysis.
Empirical antimicrobial therapy is necessary, as a delay in giving antibiotics is associated with a poor outcome. Dexamethasone, when given to adults before the administration of antibiotics, has been shown to improve outcome in bacterial meningitis.[89]
Basilar fractures can damage cranial nerves as they leave the skull base, resulting in hearing deficit, facial paralysis (VII) or numbness (V), and nystagmus. Basilar skull fractures affecting the mastoid process or the inner ear may present with facial nerve palsy or hearing loss due to the proximity of these structures. Conductive hearing loss may also present early (<3 weeks) because of haemotympanum with temporal bone fractures, or later (>6 weeks) with longitudinal temporal bone fracture with disruption of the ossicular chain. Cranial nerve injury is a rare complication, occurring in 0.3% of patients with mild head injury. Skull base fractures are the radiographic finding most often associated with long-term sequelae.[90][91][92]
Recovery is of variable degree and time course.[81]
Any severity of head injury can cause pituitary dysfunction.[28] This may present immediately, hours, weeks, or months after the injury. A variety of symptoms could indicate hypopituitarism including weakness, fatigue, lethargy, weight loss, decreased lean body mass, weight gain, increased fat mass, cold intolerance, hypotension, hyponatraemia, hypoglycaemia, hypercalcaemia, anaemia, low mood, neuropsychiatric and cognitive symptoms, altered metabolic profile and decreased exercise capacity, hot flushes, loss of body hair, reduced sex drive, irregular periods, erectile dysfunction and reduced fertility, slow growth, polydipsia, polyuria, nocturia, and incontinence.[28] In people admitted to hospital with a head injury who have persistently abnormal low sodium levels or low blood pressure, consider investigations for hypopituitarism.[28] In the community, for patients presenting with persistent symptoms consistent with hypopituitarism in the weeks or months after a head injury, consider investigations or referral for hypopituitarism.[28] Most head injury neurologists assess pituitary status (ACTH, posterior pituitary hormone, TSH, and LH/FSH) at 3-6 months after the injury.[87] If hormone levels are deficient, appropriate replacement is required.[87]
Neurological complications occur in 11% of cases.[74]
Motor neurological deficits may result from the fracture or associated intracranial injury.
Recovery is of variable degree and time course.
There is a risk of associated post-traumatic epilepsy, with a greater risk depending on associated intracranial injury.
Affects 15% of skull fractures, but has a bimodal distribution, with early cases complicating 12.3% of skull fractures and late cases complicating 6.9% of fractures.[11]
Risk is increased if patient experiences loss of consciousness for >2 hours, and if the fracture is depressed.
Fifty percent of late seizures occur after the first-year post-injury, and seizures can be delayed by up to 4 years post-injury in 20% of cases.[11]
Anticonvulsant treatment in consultation with a neurologist is recommended.
[ 
]
[Evidence C]
Traumatic carotid cavernous fistula is an abnormal shunt from the carotid artery to the cavernous sinus. It is a rare vascular complication of traumatic brain and facial injury and is typically associated with basilar skull fracture.[93] Clinical features include proptosis, chemosis, orbital bruits, and headache.[94] The gold standard diagnostic test is a cerebral angiogram.[95] The first-line treatment is endovascular intervention, with a cure rate above 80%.[95][96] Early intervention is crucial for visual recovery.[95]
Complication of endoscopic treatment of basilar skull fracture.[56]
Patients may present complaining of both smell and taste loss; deficit may be measured by chemosensory testing. In most cases, no specific therapy is available.
Use of this content is subject to our disclaimer