Extra-cerebral Haemorrhage

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Extra-cerebral Haemorrhage


Extradural- haemorrhage into the extradural space, between the bone and the dura

Subdural- venous haemorrhage in the subdural space, between the arachnoid and the dura mater

Acute = within 72h           Subacute= 3-20 days          Chronic = after 3 weeks

Subarachnoid- arterial haemorrhage into the subarachnoid space

Image result for layers of brain

Aetiology/risk factors:


Extradural bleeds are often due to a fractured temporal or parietal bone causing laceration of the middle meningeal artery and vein, typically after trauma to a temple just lateral to the eye. The arterial bleeding causes rapid accumulation of blood and strips the dura from the inner table of the skull. This results in raised intracranial pressure (ICP) and compression of the underlying brain parenchyma.

Any tear in a dural venous sinus will also result in an extradural bleed.

Risk factor = TRAUMA


Image result for layers of brain bridging veinsHaemorrhage is from bridging veins between the cortex and the venous sinuses, resulting in accumulating haematoma between dura and arachnoid.

These bridging veins are vulnerable to shearing forces from deceleration injury. The resulting haematoma causes a gradual rise in intracranial pressure (ICP), shifting midline structures away from the side of the clot.

-Most subdurals are from trama but the trauma is often forgotten as it was so minor or long ago (up to 9 months).

-Can also occur without trauma: intracranial hypotension, dural metastases

Risk factors: anticoagulation, elderly (brain atrophy makes bridging veins vulnerable), falls (epileptics, alcoholics), physical abuse


Image result for berry aneurysmCauses: rupture of saccular aneurysms, usually at circle of Willis (80%)

Berry aneurysms- 15% are multiple. Some are hereditary. Associated with polycystic kidney disease, coarctation of the aorta, Ehlers-Danlos syndrome, Marfan’s syndrome.

-arteriovenous malformations (15%)

-no cause found in < 15%

Other causes: perimesencephalic haemorrhage (parenchymal haemorrhages tracking onto surface of brain), vertebral or carotid artery dissection with intracranial extension, drug abuse (cocaine, amphetamines)

Risk factors: smoking, alcohol misuse, hypertension, bleeding disorders, mycotic (infected) aneurysm (endocarditis), possibly post-menopausal fall in oestrogen

-Close relatives have 3-5x increased risk of SAH


Extradural- incidence = 20/100,000/yr (UK)

10% of severe head injuries

most commonly seen in young adults

uncommon in elderly (subdurals more common)


Acute = in younger patients/ associated with major trauma, more common than extradural haemorrhage (5-25% of severe head injury)

Chronic = more common in elderly, incidence 1-5 per 100,000

Subarachnoid– incidence = 9/100,000/yr

typical age = 35-65



-deteriorating consciousness after head injury that initially produced no loss of consciousness or after initial drowsiness post-injury seems to have resolved = lucid interval- typical of extradurals

-lucid interval may last a few hours to a few days before reducing GCS/consciousness from rising intracranial pressure

Followed by:

-increasingly severe headache





Acute- history of trauma with head injury + reduced conscious level

Subacute- worsening headaches 7-14 days after injury, altered mental status


-fluctuating conscious level (in 35%), confusion

-insidious physical or intellectual slowing, cognitive impairment



-personality change, psychiatric symptoms

-unsteadiness, gait deterioration

-focal weakness



-acute, sudden onset, severe headache, often occipital

-onset usually within seconds

“worst headache ever”, “like being kicked at the back of my head”

⇒Patients (∼6%) may earlier have experienced a sentinel headache, perhaps due to a small warning leak from the aneurysm.

Followed by

nausea, vomiting, neck stiffness, photophobia



-drowsiness (decreased consciousness)

-coma (coma/drowsiness may last days)




-signs of scalp trauma or fracture

After initial reducing consciousness:

+/- hemiparesis with brisk reflexes and an upgoing plantar (Babinski’s sign)

If bleeding continues:

-ipsilateral pupil dilates (pressure on CN3 parasympathetic fibres, raised ICP)

-coma deepens

-bilateral limb weakness develops

-breathing becomes deep and irregular (brainstem compression)

-abnormal posturing (decorticate and decerebrate)- late sign


Image result for decorticate


-bradycardia and raised blood pressure are late signs (Cushing’s sign)

-death follows a period of coma and is due to respiratory arrest



-reduced GCS

-fixed, dilated pupil (ipsilateral compression of CN3 due to midline shift with large haematoma)

-reduced consciousness, bradycardia (pressure on brainstem)


-neurological exam may be normal

-may have focal neurological signs: III or VI nerve dysfunction, unequal pupils, papilloedema, hemiparesis, reflex asymmetry


-Neck stiffness (meningism)

-Kernig’s sign (takes 6h to develop) = pain and resistance on passive knee extension with hip fully flexed

-Pyrexia may also occur

-Retinal, subhyaloid and vitreous bleeds (= Terson’s syndrome, worse prognosis, x5 increased mortality)

Image result for hyaloid bleed

-Reduced Glasgow Coma Scale score (assesses level of consciousness)

Signs of raised intracranial pressure: papilloedema, IV or III cranial nerve palsy, hypertension, bradycardia

-Focal neurological signs at presentation may suggest site of aneurysm or intracerebral haematoma. Usually develop on second day and are caused by ischaemia from vasospasm and reduced brain perfusion. Aneurysms may cause pressure on cranial nerves causing ophthalmoplegia (III or VI classically).

-Pupil changes indicating a 3rd nerve palsy with a posterior communicating artery aneurysm


-Later deficits suggest complications.


Bloods- FBC, U&Es, ESR/CRP, clotting (bleeding diathesis?)


CT- shows a haematoma; often biconvex/lens-shaped

-the blood forms a more rounded shape compared to sickle-shaped subdural as the tough dural attachments to the skull keep it more localised

Image result for EXTRAdural haemorrhage ct

-skull x-ray may be normal or may show fracture lines crossing the course of the middle meningeal vessels

-signs of raised ICP = effacement of sulci, midline shift, ventricular compression and obliteration of basal cisterns

Lumbar puncture- CONTRAINDICATED


CT/MRI- shows clot +/- midline shift (but beware bilateral isodense clots)

– crescent/sickle shaped collection of blood, concave over one hemisphere

CT appearance changes with time. Acute subdurals are hyperdense (more white), becoming isodense (same density and colour as rest of brain) over 1-3 weeks (such that presence inferred from signs of raised ICP such as midline shift and ventricular compression); and chronic subdurals are hypodense (approaching that of CSF, more black).

Image result for subdural haemorrhage ct

-MRI has higher sensitivity, especially for isodense or small subdurals.

Lumbar puncture- CONTRAINDICATED (raised ICP)


-Urgent CT head- detects > 90% of SAH within the 1st 48h.

Hyperdense areas in the basal regions of the skull (caused by blood in subarachnoid space). Also identifies intraparenchymal or intraventricular haemorrhages.

Image result for ct head subarachnoid hemorrhage

Image result for ct head subarachnoid hemorrhage


-Lumbar puncture- if CT negative and no contraindication, > 12h after headache onset. CSF is uniformly bloody early on and becomes xanthochromic (yellow) after several hours due to bilirubin from Hb breakdown. Xanthochromia confirms SAH, as opposed to blood which may be from the actual LP.

There is also increased opening pressure, increased red cells, and decreased white cells in the CSF.

Image result for xanthochromia csf

-Catheter or CT angiography- detect source of bleeding if the patient is a candidate for surgery or endovascular treatment. Identify single vs multiple aneurysms.



Early management

-Stabilise patient, before CT and transferring urgently to a neurosurgical unit.

-Advanced Life Support (ALS) protocol with priorities of cervical spine control and ABC (airway, breathing, circulation).

-If signs of raised intracranial pressure- head elevation, consider osmotic diuresis with mannitol and/or hyperventilation. Will require intubation and ventilation if unconscious and for raised ICP management


-Urgent craniotomy and decompressive evacuation of the haematoma +/- diathermy or clipping of source of bleed (ligation of vessel).

-Stabilise and transfer urgently to a neurosurgical unit for clot evacuation +/- ligation of the bleeding vessel.

ICP monitor may be placed for post-op monitoring.




-Advanced Life Support (ALS) protocol with priorities of cervical spine control and ABC (airway, breathing, circulation).

-If signs of raised intracranial pressure- head elevation, consider osmotic diuresis with mannitol and/or hyperventilation.

-Obtain CT head, once stabilised.

⇒Treat conservatively if subdural is small (e.g. < 10 mm thickness) with minimal midline shift on CT (e.g. < 5 mm).

⇒Surgical management if large:

-irrigation/ evacuation:

1st line- Burr twist drill and Burr hole craniostomy

Image result for twist drill burr hole

2nd line- Craniotomy

Image result for craniotomy

Chronic subdurals should also be treated surgically if symptomatic or if there is a mass effect on imaging. Otherwise, they are best managed conservatively with serial imaging to monitor for spontaneous resorption.

-Options for children include percutaneous aspiration via an open fontanelle or if this fails, placement of a subdural to peritoneal shunt.

-ICP monitor may be placed for post-op monitoring.

-Address causes of trauma.


-Resuscitate, bed-rest, analgesia

-Refer proven SAH to neurosurgery immediately.

Monitor patient: re-examine CNS often, chart blood pressure, pupils and GCS. Repeat CT if deteriorating.

-Maintain cerebral perfusion by keeping well hydrated (IV fluids), aim for perfusion pressure < 160 mmHg.

NIMODIPINE (Calcium channel blocker)- reduces vasospasm and consequent morbidity from cerebral ischaemia.

Surgery/ Endovascular treatment

Catheter or CT angiography to identify single vs multiple aneurysms

Endovascular coiling, preferred to surgical clipping where possible

Image result for endovascular coiling

Image result for surgical clipping


Intracranial stents and balloon remodelling enable treating wide necked aneurysms

Image result for intracranial stent

-AV malformations and fistulae may also benefit endovascular repair or surgery

⇒It may be beneficial, in some patients, to screen for and fix aneurysms before they rupture e.g. previous SAH.



Raised intracranial pressure → brain herniation Coma Respiratory arrest →Death

Long-term: post-traumatic brain injury, amnesia, cognitive impairment


Raised intracranial pressure- if untreated, eventual tentorial herniation and coning due to raised ICP/ mass effect

-Cerebral oedema pre-disposing to secondary ischaemic brain damage

Post-op: seizures (relatively common), recurrence (up to 33%), intracerebral haemorrhage, subdural empyema, brain abscess or meningitis, tension pneumocephalus


Rebleeding– commonest cause of death, occurs in 20%, often in first few days.

Cerebral ischaemia- due to vasospasm, may cause a permanent CNS deficit, commonest cause of morbidity. If this occurs, surgery is not helpful at the time but may be so later.

Hydrocephalus (build up of CSF in the brain)- due to blockage of arachnoid granulations which drain CSF (communicating hydrocephalus) or block of CSF flow in the ventricles by blood clot (obstructive hydrocephalus). Requires a ventricular or lumbar drain.

Hyponatraemia– common, do not manage with fluid restriction, seek expert help.

Raised intracranial pressure



-Excellent prognosis if diagnosis and operation early.

-Poor prognosis if coma, pupil abnormalities, or decerebrate rigidity are present post-op.


-In acute subdurals, outcome depends on underlying brain injury.

-Chronic subdurals generally have a better outcome than acute, reflecting lower incidence of underlying brain injury, with good outcomes in 3/4 of those treated by surgery.


-High mortality, with > 30% in first few days.

-Almost all mortality occurs in 1st month. Of those who survive the first month, 90% survive a year or more.

-Significant risk of a severe rebleed in first 2 months

-SAH can be graded I-V, with grade I presenting with no signs and o% mortality and grade V, prolonged coma and 100% mortality.

-Bleeding aneurysms have a higher mortality than arteriovenous malformations.

References: Cheese & Onion, Rapid Medicine, Rapid Surgery

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