Epidural haematoma (EDH)

Numbers

Less common than subdural haematomas

2% of brain injuries

All age groups, more common in patients < 50 years

Location

Superficial to dura mater

Temporal > frontal region, parietal region, or the posterior fossa (25% of cases)

Mechanism

Adult

Arterial EDH

Fracture of the thin squamous temporal bone → laceration of the middle meningeal artery → haematoma strips dura from skull forming → ovoid haematoma forms → compressing adjacent brain.
The haematoma is constrained by the periosteum, which passes through the cranial sutures so these haematomas do not cross suture lines.

Venous EDH

Less common
Results from the disruption of the dural venous sinuses at the

Vertex
Posterior fossa

Transverse sinus

Anterior aspects of the cranial fossa

Paeds

Due to

Meningeal and diploic vein haemorrhage

EDH in paeds are variable and has a subacute presentation

Lower venous pressure

EDH is more common in paeds (apparently)

The dura mater is loosely adherent to the paediatric skull.

Radiological

Radiographic progression of EDHs can be classified into three categories on computed tomography (CT) imaging:

Type I (acute)

58%
Characterized as a dense haematoma with low density ‘swirl’ indicative of bleeding

(i.e. a hypodense zone of active bleeding from the torn vessel into a dense organizing clot).

The rise in pressure eventually produces tamponade of the bleeding site and progresses to

Type II Subacute

31%
A homogenous, hyperdense, and organized clot.

Type III Chronic

11% of cases
A low density collection due to blood resorption by perivascular tissue, along with a contrast-enhanced membrane consisting of neovascularity and granulation tissue.

Presentation

Classical

Seen in 15– 20% cases
Head trauma → transient LOC → lucid interval → coma.

Lucid interval:

A sign of concussion recovery
Patient may complain

Severe headache on the ipsilateral side of the lesion
Nausea, vomiting, and lethargy

The lucid interval is not specific to an EDH and was originally described in cases of acute SDH.

Coma

Due to increase in ICP

Other

Contralateral hemiparesis,
Ipsilateral oculomotor nerve paresis,
Decerebrate rigidity,
Arterial hypertension,
Cardiac arrhythmias,
Respiratory disturbances → apnoea → death.

Management

Conservative

Indication for conservative management (Brain trauma foundation)

< 30 cm3 AND
< 15-mm thickness AND
< 5-mm midline shift in patients AND
GCS > 8 + No focal deficit

Managed nonoperatively with serial computed tomographic (CT) scanning + close neurological observation in a neurosurgical center.
Enlargement occurs in 20% of cases.

Surgery

Prevent irreversible brain injury or death caused by hematoma expansion, raised ICP, and herniation of the brain

Indications for Surgery

> 30 cm3 regardless GCS (Brain trauma foundation-BTF)
Patients presenting with (progressive) focal neurologic signs or symptoms and/ or hematoma growth
GCS score < 9 + anisocoria

Timing

ASAP (Within 1 Hr)

Methods

There are insufficient data to support one surgical treatment method.
Craniotomy provides a more complete evacuation of the hematoma.

Craniotomy window fashioned according to the location of the haematoma, and providing adequate access to the hematoma margins.

If the brain appears tight it is important to inspect the subdural space for additional clots.
Hitch stitch: When the bone flap is replaced several tenting sutures should be placed to obliterate the epidural space both circumferentially and over the centre of the craniotomy.
No need for craniectomy unless underlying brain is injured as well

As EDH are typically injuries with a fracture haematoma rather than a brain injury per se that is prone to swelling.

Mendelow et al 1979 findings

83 traumatic EDH patients in Edinburgh area in 1951-60 and 1968-1977

Compared effects on outcome of delayed treatment following neurological deterioration

Emphasised need for immediate operation in patients deteriorating from EDH

Not sure why the book combined ASDH and EDH as one

Mendelow et al:

Delay = time from neurological deterioration to surgery

Other two studies:

Delay = time from injury to surgery

ㅤ	Mendelow et al. (1979)	Seelig et al. (1981)	Wilberger et al. (1991)
Class of evidence	III	III	III
Number of patients	83	82	101
Number of centres	1 (Edinburgh, Scotland, UK)	1 (Richmond, Virginia, USA)	1 (Pittsburgh, Pennsylvania, USA)
Outcomes	◆ Mortality ◆ Functional status	◆ Mortality ◆ Functional status (GOS)	◆ Mortality ◆ Functional status (GOS)
Eligibility	◆ Extradural haematoma >1.5 cm thick ◆ No depressed skull fracture present	◆ ASDH causing >5 mm midline shift ◆ Neurological status: impaired verbal response (unable to speak in response to noxious stimuli); unresponsive to verbal command ◆ Negative drug/alcohol screen ◆ Spontaneous respiration	◆ ASDH ◆ GCS <8 after resuscitation ◆ Absence of brain death ◆ No hypotensive episodes (<90 mmHg for >30 min) ◆ No other life threatening injuries ◆ Negative drug/alcohol screens
Treatment	◆ Surgical evacuation of clot	◆ Comprehensive resuscitation including the use of mannitol ◆ Rapid temporal craniectomy + partial clot evacuation followed by immediate temporofrontoparietal craniotomy ◆ Contused/necrotic temporal and frontal brain removed where appropriate	◆ Comprehensive resuscitation including the use of mannitol ◆ Rapid craniotomy and removal of clot plus resection of any necrotic brain tissue and placement of intraventricular catheter

Critique of extra axial haematoma studies

Mendelow - main aim was to look at effect of change to Edinburgh head injury service (change to routine admission to NSU for 24hrs). This change reduced delay to surgery in a way that almost reached significance
Other studies support immediate surgery for EDH (Bricolo and Pasut, 1984)
The Mendelow study is often cited as providing clear evidence that delay to surgery after clinical deterioration is associated with worse outcome
Seelig is a landmark study because it established earliest possible evacuation of aSDH, preferably within 4h, as a benchmark of neurosurgical care
Wilberger study broadly supported Seelig findings but also demonstrated extent of underlying primary brain injury and appropriate management to prevent secondary injury may be more important for outcome
Seelig also landmark because led to more focus on how to manage ICP between injury and surgery

UNSORTED

Extradural haematoma

Milan Consensus Conference on Clinical Applications of Intracranial Pressure Monitoring in TBI in 2014
Isolated EDH → low risk of intracranial hypertension

Miller et al. 1981
N=17 EDH with ICP monitoring → N=2 had uncontrollable high ICP
Lobato et al. 1986
N=64; 62% without associated lesions or contusions on post-op CT

Routine DC not recommended

DECRA 2011 critique;

Excluded those with mass lesion
Intervention was bifrontal
Too early to offer DC
23% in medical cross over
80% cranioplasty within 6 months

Rescue ICP 2016

37% medical cross over
Some pt had hypothermia
Outcome spin

Complications