Intracranial Bleeds

Subarachnoid haemorrhage (SAH)

The most common non-traumatic intracranial bleed (can also occur with head trauma). ~20–33% of patients report a sentinel headache (warning leak) hours to days before the major bleed. 75% present with acute severe headache; the rest present with loss of consciousness. High pre-hospital mortality.

Cause: cerebral aneurysm rupture in ~85% — family history and connective tissue/elastic disorders (Marfan syndrome, Ehlers-Danlos syndrome, autosomal dominant polycystic kidney disease — ~8% of cases) predispose. Other risk factors: alcoholism, female sex, African/Japanese/Finnish descent.

Clinical features

Sudden-onset unusual headache, moderate–intense severity (~10% describe “thunderclap” onset); occipital, localised at first then generalising; neck pain/stiffness follows; vomiting and LOC often follow; Kernig’s sign positive in larger bleeds; neurological deficits in larger bleeds depending on location — hemiplegia, 3rd nerve palsy, raised-ICP signs (papilloedema).

Investigations

CT brain is first-line — urgent via ED if clinical suspicion is high. A negative CT does not rule out SAH — perform lumbar puncture ≥12 hours after headache onset to look for xanthochromia (remains positive for several days); if still negative, MRA/CTA effectively rules out an intracranial bleed. ECG changes occur in 40–70% (QT prolongation, Q waves, ST elevation mimicking MI, dysrhythmias).

Management

Urgent neurosurgical review.

Hunt and Hess grading (1968):

Grade	Signs/symptoms	Survival
1	Asymptomatic or minimal headache, slight neck stiffness	70%
2	Moderate–severe headache, neck stiffness, no deficit except cranial nerve palsy	60%
3	Drowsy, minimal neurological deficit	50%
4	Stuporous, moderate–severe hemiparesis, possibly early decerebrate rigidity	20%
5	Deep coma, decerebrate rigidity, moribund	10%

Fisher grade (CT appearance): 1 = none evident; 2 = <1mm thick; 3 = >1mm thick; 4 = diffuse or none with intraventricular/parenchymal extension.

WFNS grade (GCS + focal deficit): 1 = GCS 15, no deficit; 2 = GCS 13–14, no deficit; 3 = GCS 13–14, deficit present; 4 = GCS 7–12, deficit present or absent; 5 = GCS <7, deficit present or absent.

Follow-up

Sensory-motor dysfunction or psychological change may persist — needs ongoing neurosurgical then neurological rehabilitation. 25–40% develop PTSD, depression, anxiety or low mood (higher risk with a prior history).

Screening

Not performed at a population level. Consider screening if ≥2 first-degree relatives have had aneurysmal SAH (or 1 relative if they have ADPKD) — not MBS-covered. Mainstay is BP/vascular risk management — statins and antihypertensives, though early BP targets are 140–160 systolic (to prevent vasospasm/watershed ischaemia), not lower.

Warning features in new-onset headache

See headache for the full table (sudden onset → SAH/pituitary apoplexy/dissection; focal signs/confusion → stroke/venous sinus thrombosis/meningitis; age >50 → giant cell arteritis; post-trauma → subdural/epidural haemorrhage; papilloedema → mass lesion/IIH/venous sinus thrombosis, etc.).

Subdural haemorrhage/haematoma

Mainly trauma-associated. Highest mortality of the intracranial bleeds (50–90%). From tearing of the bridging veins crossing the subdural space. Can become chronic, only causing symptoms 4–7 weeks later. Increased risk in the elderly and alcoholics (more intracranial space from cerebral atrophy, plus higher falls risk) and those on anticoagulation. Infants also have more intracranial space — consider shaken baby syndrome. Arachnoid cysts are a risk factor in juveniles.

Clinical features: LOC, irritability/personality change, seizures, headache (constant or fluctuating, less severe than SAH), amnesia, nausea/vomiting, weakness/numbness, dysarthria, ataxia, visual disturbance/diplopia.

Investigations: CT brain — often arranged as an outpatient scan since the patient may not look unwell, but have a low threshold for ED referral if there is a trauma history or any neurological finding on examination. CT appearance: crescent-shaped (“cupped”).

Management: urgent ED referral for imaging and neurosurgical management. Only 20–30% of survivors recover full brain function; the rest are left with neuropsychological dysfunction similar to SAH, plus a seizure risk.

Epidural/extradural haematoma

Between the dura mater and skull — arterial injury, usually the middle meningeal artery (temporoparietal), with other named vessels depending on location (anterior ethmoidal artery — frontal; transverse/sigmoid sinus — occipital; superior sagittal sinus — vertex). Associated with head injury — may have a lucid interval before symptom onset, since the injury is arterial the onset of subsequent deterioration is more rapid than subdural bleeds. CT appearance: biconvex (“lens-shaped”).

Cushing’s triad (hypertension, bradycardia, irregular breathing) signals tonsillar herniation (coning) with a large or posterior-fossa bleed.

	Epidural	Subdural
Location	Between skull and dura (or between dural layers)	Between dura and arachnoid mater
Vessel	Arterial (commonly middle meningeal)	Bridging veins
Symptoms	Lucid interval then unconsciousness	Gradually increasing headache and confusion
CT appearance	Biconvex lens	Crescent-shaped