Lucan · Conditions

Extradural haematoma and basal skull fracture

Australian guidance: RCH Melbourne Clinical Practice Guidelines — Head injury (Trauma Service) + Australian and New Zealand Guideline for Mild to Moderate Head Injuries (adult/PREDICT-aligned) + Canadian CT Head Rule (adopted into AU emergency practice) + Austroads Assessing Fitness to Drive (AP-G56, 2022) — Neurological conditions + Brain Trauma Foundation Guidelines for the Management of Severe TBI, 4th edition + CRASH-3 trial (Lancet, 2019)

1. Definition and epidemiology

Extradural (epidural) haematoma (EDH) is a collection of blood in the potential space between the inner table of the skull and the dura mater. It is an uncommon but classically time-critical head injury diagnosis, reported in roughly 1 to 2% of all head trauma presentations and a disproportionate 5 to 15% of fatal head injuries, with a marked predisposition for males in the second and third decades of life, consistent with the high-energy mechanisms (road trauma, assault, falls from height, sport) that predominate in this group. EDH is usually, though not invariably, associated with an overlying skull fracture; children are a partial exception, because their more elastic, less firmly adherent dura means a meaningful minority of paediatric EDH occur without a demonstrable fracture on imaging.

Basal skull fracture is a fracture involving the floor of the anterior, middle, or posterior cranial fossa rather than the calvarial vault, and is covered alongside EDH here because the two frequently co-occur and share a mechanism: a linear fracture through the squamous temporal bone, close to the pterion, is the classic route by which blunt trauma both produces a basal/temporal fracture line and lacerates the underlying middle meningeal artery, causing EDH. Basal skull fracture in isolation carries its own specific risks — cerebrospinal fluid (CSF) leak and ascending meningitis chief among them — distinct from the mass-effect risk of EDH, which is why the two are best taught as a linked pair rather than as separate topics. Prognosis in EDH is strongly time-dependent rather than fixed: contemporary case series report widely differing mortality, roughly 5 to 25%, reflecting differences in case mix, pre-hospital time, and access to neurosurgical care, but the figure most worth retaining is the gap between early and late surgery — patients evacuated before herniation occurs have a good functional outcome in the large majority of cases, while those operated on after herniation has set in fare dramatically worse, which is the clinical justification for treating any suspected EDH as a "cannot wait" diagnosis.

2. Pathophysiology

Around 85% of EDH is arterial, from laceration of the middle meningeal artery or one of its branches as it runs in a bony groove on the inner surface of the temporal bone; a temporal or temporoparietal fracture crossing this groove is the usual mechanism, making EDH fundamentally a fracture-and-vessel injury rather than a diffuse brain injury. A minority, more prevalent in children, arise from venous sources — a torn dural venous sinus or diploic vein — and these tend to expand more slowly. Because the dura is tightly adherent to the skull precisely at the cranial sutures, an expanding extradural collection is physically confined between suture lines; this is the anatomical basis for the classic biconvex (lentiform) CT appearance of EDH, in contrast to acute subdural haematoma, which is not limited by dural-suture attachment and instead spreads freely along the calvarial contour as a crescentic collection that can cross sutures (though, like EDH, it is limited by the falx and tentorium).

The "lucid interval" — an initial period of unconsciousness at impact, an interval of apparent recovery while the arterial bleed silently accumulates, then rapid deterioration as intracranial pressure (ICP) rises — is the textbook pattern, but it is present in only a minority of confirmed EDH; many patients have no true lucid interval, either because there was no initial loss of consciousness or because concomitant brain injury blurs the picture, so its absence must never be used to exclude the diagnosis. As the haematoma expands and ICP rises, the Cushing response (hypertension, bradycardia, and irregular respiration) emerges as a late and ominous compensatory reflex reflecting critical brainstem ischaemia, typically preceding herniation and death if untreated — it is a warning of established crisis, not an early screening sign. Uncal (transtentorial) herniation follows: the expanding temporal lobe mass pushes the uncus medially through the tentorial hiatus, compressing the ipsilateral oculomotor nerve (CN III) — whose superficially running parasympathetic fibres are compressed first, producing early ipsilateral pupillary dilation before any motor change — and the ipsilateral cerebral peduncle against the tentorial edge, producing contralateral hemiparesis. Occasionally the contralateral peduncle is instead compressed against the opposite tentorial edge (Kernohan's notch phenomenon), producing a falsely localising ipsilateral hemiparesis, a recognised trap in bedside localisation that is worth knowing exists even though it is the exception rather than the rule.

3. Clinical presentation and diagnostic criteria

Presentation follows a head trauma history, often with a documented mechanism sufficient to cause a skull fracture, and may include the classic lucid interval described above, though as noted this is inconsistent. Progressive decline is marked by worsening headache, vomiting, declining Glasgow Coma Scale (GCS), and eventually the raised-ICP and herniation signs described in section 2 — asymmetric or unilateral pupillary dilation, new focal weakness, the Cushing response, and abnormal posturing. GCS and level-of-consciousness assessment (alongside AVPU as a rapid screening alternative) and basic observations are the core bedside skills this topic shares with the OSCE primary-survey/observations station (E24), where a trauma patient's trajectory is tracked through repeated, structured neurological and vital-sign checks rather than a single snapshot.

Basal skull fracture is diagnosed as often clinically as radiologically, through a cluster of signs that are frequently delayed rather than immediate: periorbital ecchymosis ("raccoon eyes," typically anterior fossa/cribriform plate fracture) and Battle's sign (bruising over the mastoid process, typically petrous temporal bone fracture) commonly take one to three days to appear and are therefore easy to miss on an early assessment; haemotympanum and CSF otorrhoea reflect a petrous temporal fracture, sometimes with an intact tympanic membrane concealing the leak until it tracks down the Eustachian tube as a salty postnasal drip instead; CSF rhinorrhoea reflects an anterior fossa fracture through the cribriform plate; and cranial nerve palsies localise the fracture — anosmia (CN I) to an anterior fossa/cribriform injury, and facial weakness or hearing loss/vertigo (CN VII/VIII) to a petrous temporal bone fracture involving the facial canal or inner ear. A bedside "double ring" or halo sign, in which blood-stained fluid dripped onto gauze separates into a central red ring of blood surrounded by a paler ring of CSF, is a traditionally taught supportive sign but is not specific enough to substitute for laboratory confirmation.

4. Investigations and AU-specific cutoffs

Non-contrast CT brain is first-line and diagnostic. Definite indications for urgent CT, as set out in the RCH Melbourne head injury clinical practice guideline, include any moderate or severe head injury (GCS ≤13), a focal neurological deficit, clinical signs of a base-of-skull fracture, a palpable skull fracture, suspected non-accidental injury, and persistent altered mental status (agitation, drowsiness, repetitive questioning); relative indications, where more than one prompts imaging or observation, include GCS persistently 14, a severe mechanism, a history of loss of consciousness, a post-traumatic seizure, severe headache, persistent vomiting, or a non-frontal scalp haematoma in a child under two. In adults with mild head injury (GCS 13 to 15), the Canadian CT Head Rule is the decision tool recommended in Australian and New Zealand mild-to-moderate head injury guidance: it applies to adults with witnessed loss of consciousness, amnesia to the event, or witnessed disorientation, and its high-risk criteria mandating CT are GCS below 15 at two hours post-injury, suspected open or depressed skull fracture, any sign of basal skull fracture, two or more episodes of vomiting, and age 65 or above, with medium-risk criteria (retrograde amnesia of 30 minutes or more, or a dangerous mechanism) predicting clinically important injury on CT; it excludes patients under 16, those on anticoagulation or with a known coagulopathy, and those who have had a post-injury seizure, all of whom are scanned on clinical grounds instead regardless of the score.

On CT, EDH classically appears as a biconvex (lentiform), hyperdense collection that does not cross suture lines — the discriminating feature from acute subdural haematoma's crescentic shape, which is not suture-limited but is instead limited by the falx and tentorium. Poor prognostic imaging features include a large clot volume, midline shift, a "swirl sign" suggesting ongoing active bleeding, and coexisting parenchymal injury such as contusion or subarachnoid extension; the exact volume and shift thresholds used to trigger evacuation are neurosurgical judgement calls made in conjunction with the clinical picture rather than fixed numbers, and should be taken from the treating neurosurgical unit's own protocol rather than assumed from any single reference. Where CSF leak is suspected but not obviously demonstrable, beta-2 transferrin assay on the fluid is the most specific confirmatory test, because beta-2 transferrin is found only in CSF and perilymph; in Australian practice it is typically a send-away reference-laboratory test with a turnaround of days, so in practice most leaks resolve clinically before the result returns, and its main role is confirming a genuinely persistent or diagnostically ambiguous leak rather than guiding acute management. A nasogastric tube is contraindicated where a basal skull fracture is suspected or confirmed, because of case reports of intracranial passage through a fractured cribriform plate; an orogastric tube is inserted instead, consistent with standard trauma (ATLS/EMST) teaching.

5. Management

Immediate management follows a primary survey with cervical spine precautions, and is guided throughout by preventing secondary brain injury: avoiding hypoxia and hypotension, both of which independently worsen outcome in traumatic brain injury, maintaining normocapnia (a PaCO2 target of roughly 35 to 40 mmHg per RCH Melbourne guidance, with brief controlled hyperventilation reserved only as a temporising bridge for impending herniation rather than routine practice), and nursing the patient head-up at around 30 degrees in a midline position once shock has been corrected, to optimise cerebral venous drainage. GCS persistently below 8, loss of protective airway reflexes, or respiratory irregularity are indications for intubation and airway protection.

Where there are signs of evolving herniation or a rapidly expanding lesion, hyperosmolar therapy is used as an emergency bridge to definitive surgery: RCH Melbourne guidance specifies 20% mannitol 0.25 to 0.5 g/kg IV over 20 to 30 minutes, or 3% hypertonic saline 3 mL/kg IV over 10 to 20 minutes; the Brain Trauma Foundation's fourth-edition severe TBI guideline confirms mannitol is effective for ICP control across a dosing range of roughly 0.25 to 1 g/kg, but states there is insufficient evidence to recommend one hyperosmolar agent over the other for clinical outcome, so the choice between them is largely institutional protocol rather than a strong evidence-based preference. Definitive treatment of a significant EDH is urgent neurosurgical craniotomy with clot evacuation and identification and control of the bleeding vessel (most often the middle meningeal artery); very small, asymptomatic collections with a normal GCS and no focal deficit may be managed conservatively with close neurosurgical consultation and serial CT, but this is a neurosurgical decision made on the individual scan and trajectory, not a default. Outcome is strongly linked to the interval between neurological deterioration and surgical decompression, which is why any suspected EDH triggers urgent transfer to a centre with neurosurgical capability rather than a staged work-up.

Where the patient is anticoagulated, reversal is arranged in parallel with surgical planning rather than sequentially: for warfarin, intravenous vitamin K plus four-factor prothrombin complex concentrate (Prothrombinex-VF); for direct oral anticoagulants, idarucizumab specifically reverses dabigatran, while andexanet alfa (with limited Australian access) or, more commonly in practice, Prothrombinex-VF as a non-specific reversal agent is used for factor Xa inhibitors, guided by local hospital protocol given variable formulary access to the specific reversal agents. Tranexamic acid, per the CRASH-3 trial, is given within three hours of injury (ideally as early as possible) in patients with traumatic brain injury and intracranial bleeding; across the whole trial population there was no significant reduction in head injury death (18.5% with tranexamic acid versus 19.8% with placebo), but a pre-specified subgroup with mild to moderate injury (GCS 9 to 15) and intracranial bleeding on baseline CT showed a significant reduction in head-injury-related death, with the greatest benefit in patients treated earliest and with reactive pupils; the trial did not demonstrate benefit, and flagged a possible signal of harm, in patients with a GCS of 3 or bilateral fixed unreactive pupils, so tranexamic acid is not used on the strength of this evidence in that subgroup. The dosing regimen is the same as used for critical bleeding generally: 1 g IV over 10 minutes, followed by 1 g IV over 8 hours.

6. Pharmacology and AU PBS notes

Mannitol 20% and hypertonic saline 3% are in-hospital emergency/ICU stock items used for acute ICP control rather than routine PBS community prescriptions; both require monitoring of serum sodium and osmolality with repeated dosing, and mannitol in particular requires attention to volume status and renal function given its osmotic diuretic effect. Tranexamic acid (Cyklokapron and generics) is PBS-listed for other indications such as menorrhagia in the community setting; in-hospital intravenous use for critical bleeding or TBI, dosed as above, is supplied and funded through the hospital's own medicine formulary rather than billed as a PBS-subsidised script, mirroring its use in massive transfusion. Prothrombinex-VF and vitamin K1 (Konakion) are hospital-supplied for emergency anticoagulant reversal; idarucizumab (Praxbind) is hospital-stocked in centres managing dabigatran-treated patients, while andexanet alfa has more limited and variable access across Australian hospitals, so local availability should be confirmed rather than assumed when planning factor Xa inhibitor reversal. Seizure prophylaxis in moderate to severe traumatic brain injury is used selectively rather than routinely; where used, levetiracetam has largely superseded phenytoin in current Australian practice, reflecting its more favourable interaction and monitoring profile, typically for a short course covering the highest-risk early post-injury period — a specific AU-endorsed adult dosing regimen for this indication was not able to be confirmed against a primary Australian source for this note and should be taken from local ICU/neurosurgical protocol or eTG rather than an assumed figure.

7. Complications and monitoring

The dominant complication of an unrecognised or delayed-treated EDH is progression through the ICP-herniation pathway to coma and death, which is why rapid recognition and transfer, rather than any specific drug, is the single most outcome-determining step in this topic; post-evacuation, patients are monitored with serial neurological observations and a post-operative CT to confirm clot removal and exclude re-accumulation. For basal skull fracture, the principal specific risks are ascending meningitis via a persistent CSF leak, and cranial nerve deficits (anosmia, facial palsy, hearing loss or vertigo) that may be permanent depending on the nerve and mechanism involved. Whether antibiotic prophylaxis should be given for a basal skull fracture with CSF leak is genuinely contested: the balance of published trial and systematic-review evidence does not support routine prophylactic antibiotics, with no consistent reduction in meningitis rates demonstrated, and this is the position increasingly reflected in contemporary practice; however, this note could not directly confirm the current eTG-specific Australian recommendation on this point, so it should be treated as a residual flag for verification rather than a settled AU position. Most CSF leaks resolve with conservative measures (bed rest, head elevation, avoidance of straining and nose-blowing) within one to two weeks; a leak persisting beyond this window, or one associated with recurrent meningitis, prompts consideration of surgical dural repair. Rare late complications of an unrepaired dural defect include meningoencephalocoele and, where the fracture involves the skull base near the cavernous sinus, a carotico-cavernous fistula.

Post-traumatic seizure risk is highest after depressed skull fracture, an intracranial haematoma requiring evacuation, and prolonged loss of consciousness, which is the rationale for selective seizure prophylaxis in this group. Under Austroads Assessing Fitness to Drive (AP-G56, 2022), a traumatic intracranial haematoma (including EDH) or a depressed skull fracture is treated as carrying an increased seizure risk, particularly in the first 12 months: commercial drivers should not drive for 12 months after the injury and require a conditional licence with medical review, while private drivers may continue provided they otherwise meet the standard to drive. Separately, because definitive EDH management is craniotomy (section 5), Austroads' intracranial-surgery advice also applies: following supratentorial surgery or surgery requiring retraction of the cerebral hemispheres, the person should generally not drive a private vehicle for 6 months or a commercial vehicle for 12 months, with no notification to the driver licensing authority required. The exact criteria and any individualised exceptions should be confirmed against the current Austroads document for the specific case, consistent with how driving guidance is flagged in this library's other neurology notes.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.