01OverviewDefinition, clinical context and the essential points that orientate the chapter.
The skull base forms the floor of the cranial cavity and contains foramina for vessels and cranial nerves. Fracture can be clinically subtle because the bone is not palpable. Mechanism, head and facial injury, ear and nose examination and cranial nerves provide clues. Classic bruising may take hours to appear. Its absence at presentation therefore does not exclude fracture, while its presence creates an immediate NICE CT indication.
Anterior fossa injury produces periorbital bruising, anosmia and CSF rhinorrhoea through cribriform or sinus disruption. Middle fossa and temporal-bone injury produces haemotympanum, mastoid bruising, otorrhoea, hearing loss, vertigo and facial weakness. Posterior fossa and occipital injury can affect lower cranial nerves, venous sinuses and the craniocervical junction. Conduct a complete neurological and cervical assessment rather than stopping after a named sign is found.
CSF leak is typically clear, watery and positional, sometimes mixed with blood. Ask about salty or metallic postnasal fluid. Do not ask the patient to forcefully blow their nose to demonstrate it. Bedside halo signs and glucose testing lack sufficient specificity. A clean sample can be sent for beta-2 transferrin or beta-trace protein after discussion with neurosurgery or ENT. Treat airway soiling with oral suction and avoid blind nasal devices.
Non-contrast CT head with bone-window review is the first-line acute investigation and is performed within one hour when clinical basal-fracture signs exist. Review for pneumocephalus, intracranial blood, temporal or occipital fracture and mastoid or sinus opacification. Thin-section temporal-bone CT clarifies ossicles, otic capsule and facial canal after stabilisation. CT angiography is selected for fracture through a vascular canal or clinical blunt-cerebrovascular signs.
Immediate management prevents secondary injury. Maintain oxygenation, ventilation and perfusion, protect the cervical spine, treat seizures and reverse clinically significant anticoagulation when intracranial bleeding exists. Do not pack a suspected CSF leak blindly or insert a nasogastric tube through the nose. Discuss acute facial paralysis, profound hearing loss, severe vertigo, persistent leak and any neurosurgical lesion promptly with the relevant network specialists.
Many traumatic CSF leaks close with observation. Use head elevation when compatible with spinal and haemodynamic care, stool softening if needed, antiemesis and avoidance of nose blowing, heavy lifting or straining. NICE does not recommend routine prophylactic antibiotics solely for basal skull fracture because benefit has not been shown. Fever, meningism or neurological decline requires urgent sepsis assessment, cultures when safe and immediate therapeutic antimicrobials under meningitis guidance.
Follow-up addresses consequences that acute survival care can miss. Reassess smell, hearing, balance, facial movement, diplopia, swallowing and ongoing fluid leak. Audiology and ENT review may be delayed until blood and swelling settle, but sudden sensorineural loss or facial palsy is urgent. Explain meningitis warning signs, precautions and when to return. Document vaccination or surgical recommendations only when a specialist indication exists rather than applying them to every fracture.
Key points
- Look deliberately for periorbital ecchymosis without direct eye injury, Battle sign, haemotympanum, clear rhinorrhoea or otorrhoea and cranial nerve dysfunction.
- Basal-skull signs trigger CT head within 1 hour in adults and children under NICE head-injury guidance; plain skull radiography is not an alternative.
- Protect airway and cervical spine, suction orally and use oral rather than blind nasal airway, gastric or tracheal instrumentation when anterior skull-base injury is possible.
- Do not rely on bedside glucose-strip, halo or double-ring testing of fluid; collect a clean sample for laboratory beta-2 transferrin or beta-trace testing if specialist confirmation is required.
- Use CT bone windows and multiplanar review; add high-resolution temporal-bone CT or CT angiography when hearing, facial-nerve or vascular findings create a specific question.
- Manage simple CSF leakage with neurosurgical or ENT observation and avoidance of nose blowing, heavy straining and nasal instrumentation; persistent or complicated leaks need repair planning.
- NICE advises against routine prophylactic antibiotics for basal skull fracture; treat established meningitis promptly and use peri-operative antibiotics only for the relevant surgical indication.
- Document facial movement, hearing, eye movements, vision, gag, palate, shoulder and tongue function because cranial deficits can evolve or be missed during resuscitation.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
High-energy blunt impact
Road collision, fall from height and direct craniofacial impact transmit force through the orbit, temporal bone, sphenoid, occiput or clivus.
Frontal or facial force
Anterior fossa fractures often accompany frontal sinus, orbital roof and midface injuries with potential nasal CSF communication.
Lateral or posterior force
Temporal and occipital impacts can disrupt petrous bone, ear structures, venous sinuses, lower cranial nerves and the craniocervical junction.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Dural breach
Fracture tears dura and creates communication between sterile subarachnoid space and nose, sinus or middle ear, producing CSF rhinorrhoea or otorrhoea.
- 2Neurovascular proximity
Carotid canals, venous sinuses and cranial nerves traverse the base, so fracture can cause thrombosis, dissection, haemorrhage, palsy or delayed stroke.
- 3Middle-ear injury
Temporal bone disruption causes haemotympanum, conductive or sensorineural hearing loss, disabling vertigo and acute facial nerve injury.
- 4Ascending infection
Persistent CSF communication permits nasopharyngeal or middle-ear organisms to enter meninges, creating ongoing meningitis risk until the leak seals or is repaired.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Bilateral periorbital bruising not explained by direct orbital impact, anosmia, pneumocephalus or clear nasal fluid suggests frontal or cribriform disruption.
Haemotympanum, mastoid ecchymosis, ear-canal injury, hearing loss, vertigo, facial weakness or CSF otorrhoea indicates temporal or middle fossa injury.
Clear unilateral watery discharge, positional dripping or salty postnasal fluid after trauma supports a fistula but requires proper laboratory and imaging confirmation.
Visual change, diplopia, facial weakness, deafness, impaired gag, palatal asymmetry, shoulder weakness or tongue deviation localises injury near skull-base foramina.
Severe epistaxis, cervical bruit, partial Horner syndrome, retinal or hemispheric deficit and canal-crossing fracture raises concern for carotid or vertebral damage.
Fever, photophobia, neck stiffness, headache and altered cognition after persistent leak suggests meningitis and requires immediate treatment.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
First-line non-contrast CT headFirst stepFirst line - Why
- Identify fracture, intracranial haemorrhage, pneumocephalus and mass effect.
- Interpretation and limitations
- Basal-fracture clinical signs mandate CT within 1 hour under NICE; review thin bone windows and multiplanar reformats because subtle linear fractures can be missed.
- 02
High-resolution temporal-bone CT - Why
- Define otic capsule, ossicles, facial canal and temporal anatomy.
- Interpretation and limitations
- Use for a specific ENT or operative question after immediate head and cervical threats are assessed; routine repeat scanning is unnecessary without such findings.
- 03
CT angiography - Why
- Assess carotid, vertebral or venous injury when risk features exist.
- Interpretation and limitations
- Canal-crossing fracture, hard vascular signs or delayed focal neurology may reveal dissection, thrombosis, pseudoaneurysm or active bleeding requiring neurovascular discussion.
- 04
Beta-2 transferrin or beta-trace protein - Why
- Confirm that persistent clear nasal or ear fluid is cerebrospinal fluid.
- Interpretation and limitations
- Collect uncontaminated fluid through the specialist pathway; negative bedside glucose or halo testing is not a reliable substitute.
- 05
Formal cranial nerve and audiology assessment - Why
- Document functional consequences and their progression.
- Interpretation and limitations
- Serial facial grading, hearing, vestibular, ocular and lower-nerve examination determines urgency and later rehabilitation; bedside hearing can be confounded by haemotympanum.
- 06
Lumbar puncture - Why
- Investigate selected suspected meningitis only when safe.
- Interpretation and limitations
- Do not perform when raised intracranial pressure, mass lesion or instability is possible; obtain cultures and start indicated antibiotics without unsafe diagnostic delay.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Direct soft-tissue bruising
Periorbital or mastoid bruising at the exact impact site may be superficial, but mechanism and associated signs still determine CT need.
Simple epistaxis
Nasal mucosal bleeding is common after facial trauma; clear unilateral positional fluid or salty postnasal drip raises separate concern for CSF leak.
Orbital fracture
Diplopia, globe malposition, infraorbital numbness and restricted eye movement may reflect orbital-wall injury with or without skull-base extension.
Cervical vascular dissection
Headache, neck pain, Horner syndrome or delayed focal deficit can occur without visible basal fracture and still warrants vascular assessment.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01ImmediateProtect and imageFirst stepA basal-skull sign, cranial deficit or high-risk mechanism is identified.+
- 1Run ABCDE with cervical protection, document GCS components and pupils and address airway contamination using oral suction and oral access.
- 2Avoid blind nasal airway, gastric tube and packing, and arrange non-contrast CT head within one hour under NICE guidance.
- 3Review CT for intracranial blood, mass effect, pneumocephalus and fracture trajectory and discuss urgent lesions with neurosurgery.
- 4Add ENT, maxillofacial, ophthalmic or neurovascular input according to hearing, facial, eye, CSF and vascular findings.
02LeakManage traumatic CSF fistulaClear rhinorrhoea or otorrhoea is suspected after stabilisation.+
- 1Collect a clean sample for specialist laboratory confirmation when needed and avoid provocative nose blowing or unreliable bedside strip tests.
- 2Use head elevation when safe, antiemesis and measures that reduce straining, with explicit avoidance of nasal instrumentation.
- 3Do not prescribe routine prophylactic antibiotics solely for basal fracture; monitor for fever, meningism and neurological change.
- 4EscalationEscalate persistent, high-flow, recurrent or complicated leak for endoscopic or neurosurgical localisation and repair planning.
03Follow-upRecover cranial function safelyLife-threatening injury is controlled and the patient is leaving acute care.+
- 1Repeat facial movement, hearing, balance, smell, vision, eye movements, swallowing and lower cranial nerve assessment before transfer or discharge.
- 2Arrange audiology, ENT, neurosurgical, ophthalmic or rehabilitation follow-up matched to the documented deficit and fracture anatomy.
- 3Give meningitis and neurological deterioration warning signs, leak precautions and a direct route for urgent return.
- 4Reconcile final imaging reports and vascular studies and ensure any antithrombotic plan has a named specialist owner.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Meningitis
Fever, neck stiffness, photophobia, worsening headache or altered consciousness after CSF leakage requires urgent cultures and treatment rather than prophylactic antibiotics alone.
Cranial nerve deficit
Anosmia, visual loss, diplopia, facial weakness, deafness, dysphagia or tongue weakness can persist and needs early specialty documentation and follow-up.
Blunt cerebrovascular injury
Carotid or vertebral dissection, pseudoaneurysm and thrombosis may cause delayed embolic stroke, major epistaxis or catastrophic internal bleeding.
Persistent CSF fistula
Continued rhinorrhoea or otorrhoea increases infection risk and may need confirmatory testing, specialist observation, lumbar drainage or surgical repair.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Trend GCS components, pupils, vital signs and focal neurology, returning to ABCDE for any deterioration.
- Record amount, laterality and triggers of clear nasal or ear leakage without asking the patient to provoke it.
- Repeat facial, hearing, vestibular, ocular and lower cranial nerve findings because deficits can emerge as swelling evolves.
- Monitor temperature, headache, photophobia, neck stiffness and cognition for meningitis during admission and teach the same warning signs at discharge.
- Acknowledge the final CT and angiographic reports and ensure temporal-bone, vascular and follow-up recommendations reach the responsible team.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Bruising can be delayed
Battle sign and periorbital ecchymosis may not appear during the first examination, so mechanism and serial review remain important.
Clear fluid needs a clean test
Beta-2 transferrin or beta-trace testing is more specific than glucose strips and the visually appealing but unreliable halo sign.
Choose the mouth
When basal injury is suspected, oral suction and orogastric access avoid introducing devices through a disrupted anterior base.
Hearing loss has several mechanisms
Haemotympanum and ossicular injury cause conductive loss, whereas otic-capsule or nerve injury can cause urgent sensorineural loss.
Antibiotics treat infection
Routine prophylaxis is not recommended solely for a basal fracture, but suspected meningitis requires immediate therapeutic management.
11Common pitfallsFrequent interpretation and management errors.
- 01
Waiting for classic bruising before arranging CT in a high-risk head injury.
- 02
Inserting a nasogastric or nasopharyngeal device blindly through suspected anterior skull-base disruption.
- 03
Using a halo sign or bedside glucose result to confirm or exclude CSF.
- 04
Prescribing routine prophylactic antibiotics for every basal fracture despite NICE advice.
- 05
Documenting normal limb power but omitting facial, hearing, ocular and lower cranial nerve examination.
- 06
Missing delayed vascular or meningitic symptoms after the acute CT has been completed.