Intracranial Haemorrhage

Intracranial Haemorrhage

·        Usually due to:

·        Trauma: typically extra/epi-dural or subdural

·        Spontaneous (usually due to cerebrovascular disease): brain parenchyma and subarachnoid

Extradural Haemorrhage

·        Due to head trauma, especially with skull fracture (although not necessary in children)

·        Lentiform shaped arterial bleed (Þ high pressure Þ rapid progression)

·        Skull fracture leads to one of:

o   Blood from middle meningeal artery forces its way between dura and inner table of skull (normally intimately related) – rapid, displacing cerebral tissue ® herniation

o   Laceration of dural venous sinus ®slow, delayed findings, less dense, less common

·        Dura fixed at sutures so doesn‟t go past these (eg will be bounded by coronal and lamdoid sutures)

·        Dura has two layers: the outer forming the internal periosteum of the calvarium, the inner forming the septae which compartmentalise the calvarium

Subdural Haemorrhage

·        Following trauma: 50% also have a brain injury (swelling, contusion, laceration, etc) 

·        Bleed from bridging vein into the space between the arachnoid and dura mater (low pressure Þ slower progression) 

·        ­Risk in old people due to relative cerebral atrophy 

·        Traverses right round the inside the calvarium: cresenteric shaped bleed, very flat (may need to look carefully to distinguish from the skull)

·        Most common location is over the lateral aspects of the cerebral hemispheres

·        Poor prognosis due to large size and associated brain injury

·        Classification:

o   Acute < 3 days

o   Subacute 4 – 21 days

o   Chronic > 21 days (eg minor injury in elderly, hypodense (blood broken down), lots of midline shift

·        If not detected, the haematoma undergoes organisation ® granulation tissue.  This can rebleed

Subarachnoid Haemorrhage

·        Into the space between the dura mater and pia mater – where CSF is

·        Bleed may be focal, or diffusely spread through subarachnoid space (will flow into sulci and be bilaterally symmetrical)

·        Incidence: 15 per 100,000

·        Signs/symptoms: Sudden severe headache, loss of consciousness, meningism (neck stiffness, vomiting, photophobia, fever), maybe focal neurological signs, fundi

·        Spontaneous: ruptured aneurysm (70%), Arteriovenous Malformation (AVM, 10%), hypertensive bleed, bleed into a tumour, hypocoagulable state

·        Traumatic: injury to leptomeningeal vessels, rupture of intracerebral vessels, contusion, laceration

·        Aneurysm:

o   Mostly situated on the circle of Willis (ie 40% are at the junction of the anterior cerebral artery and the anterior communicating artery)

o   Associated with connective tissue disorders (eg Marfan‟s)

o   Mostly saccular rather than fusiform

o   Saccular: due to ¯ elastic laminar (?congenital) = Berry Aneurysm. No muscle layer and thickened hyalinised intima

o   Fusiform: due to atheromatous degeneration

o   Mycotic: due to septic emboli – usually more peripheral in brain

o   Dissecting: may extend either from aortic dissection or from internal carotid artery (complication of angiography)

o   85% are in the anterior circle of Willis. Posterior communicating artery ® unilateral 3^rd nerve palsy (dilated pupil, ptosis, etc)

·        Arterio-venous Malformations:

o   Localised developmental failure ® shunt from an artery to a vein ® gradually dilates ® distension of veins under arterial pressure

o   Most in the territory of the middle cerebral artery

o   Can present with haemorrhage or epilepsy

·        Investigations: CT, CSF if CT not helpful and no risk of ­ICP (make sure blood is not from a bloody tap)

·        Treatment:

o  Analgesia, rest (maintain normotensive)

o  Rebleeding: 30% die from 1^st bleed, 60% from rebleed (25% within 2 wks)

o  Clip or endovascular obliteration if GCS > 6

o  Vasospasm: 5 – 15% have stroke due to vasospasm (peak 3 – 10 days post bleed) despite all 

o   treatment. Cause: ?oedema around vessels ® compression. Prevention with fluids, drugs and monitoring electrolytes

·        Complications:

o  Acute: if intraventricular extension ® ependymitis ® obstruction of aqueduct ® acute obstructive hydrocephalus. Also cerebral oedema and vasospasm of the affected artery (® infarct)

o  Delayed: fibroblast proliferation in arachnoid space and at granulations ® communicating hydrocephalus

Hypertensive Intracerebral Haemorrhage

·        Mainly due to rupture of small penetrating vessels secondary to hypertension – which causes:

o  Hyaline arteriolosclerosis in small arteries and arterioles ® weakening of vessel

o  Minute aneurysms

·        Main sites are: Putamen, thalamus, pons, cerebellum 

·        ® Haematoma ® compression ® brownish discolouration of surrounding tissue

How old is blood on a film

·        On a CT:

o   < 24 hours: homogenous high density lesion, well defined margins, prognosis related to size of clot

o  Then oedema develops, increasing the mass effect, less homogenous

o  For the first week is hyperdense cf brain tissue (clotting ® contracting)

o  2 – 3 weeks isodense

o  3 – 4 weeks is hypodense cf brain tissue. Breakdown of haemoglobin ® ­osmotically active particles ® water diffuses in.

·        On MRI:

o  T1: fluid is black: hypointense

o  T2: fluid is white: hyperintense 

o  If contrast enhancement ® ring enhancement, then either an abscess or metastatic deposit