Related Subjects:
|Subarachnoid Haemorrhage
|Perimesencephalic Subarachnoid haemorrhage
|Haemorrhagic stroke
|Cerebellar Haemorrhage
|Putaminal Haemorrhage
|Thalamic Haemorrhage
|ICH Classification and Severity Scores
π§ Introduction
- Haemorrhagic stroke, also called Spontaneous Intracerebral Haemorrhage (SICH), is often sudden and devastating.
- Accounts for ~15% of all strokes (majority are ischaemic).
- One subtype is Subarachnoid Haemorrhage (SAH), usually from ruptured aneurysms or vascular anomalies (discussed separately).
- β οΈ Mortality is high: 30β50% of patients with large bleeds die within 30 days.
- Smaller bleeds can have better outcomes β focus on identifying cause and preventing recurrence.
- β Traumatic intracranial haemorrhage and extra-axial bleeds (subdural, extradural) are not classified as stroke.
π¬ Pathological Appearance
On pathology and imaging, haemorrhagic strokes show destructive haematomas, surrounding oedema, and pressure effects:
βοΈ Aetiology
- Vessel rupture: Can occur anywhere from Circle of Willis arteries to small penetrating arterioles, capillaries, and draining veins.
- Aneurysms: Berry aneurysm rupture β high-pressure SAH.
- Small vessel disease: Hypertension β lipohyalinosis, CharcotβBouchard microaneurysms β deep bleeds.
- Cerebral amyloid angiopathy: In elderly β lobar bleeds.
- Structural: AVMs, cavernomas, hereditary haemorrhagic telangiectasia.
- Neoplastic: Tumours (esp. melanoma, RCC, thyroid, choriocarcinoma, lung) prone to bleed.
- Coagulopathies: Anticoagulants (warfarin, DOACs), antiplatelets, thrombocytopenia, haemophilia, liver disease.
- Venous sinus thrombosis: Back-pressure haemorrhage β paradoxically requires anticoagulation.
π Epidemiology
- More common in Afro-Caribbean, South-East Asian, and Japanese populations.
- Strong association with hypertension prevalence and genetic predisposition (amyloid angiopathy).
π§Ύ Causes by Age Group
- π§ Elderly: Hypertension, cerebral amyloid angiopathy.
- π© Younger adults: AVMs, aneurysms, cavernomas, coagulopathies.
- π Any age: Anticoagulation therapy, illicit drugs (cocaine, amphetamines).
π§ Types by Anatomy
- π§ Lobar: Cortex Β± subcortical white matter.
- β« Deep: Putaminal, thalamic, caudate, basal ganglia.
- π§© Brainstem: Pontine haemorrhage β sudden coma, pinpoint pupils.
- π Cerebellar: Ataxia, vertigo; large bleeds (>3 cm) may need evacuation.
- π₯ Subarachnoid haemorrhage: Usually aneurysmal.
πΈ Example Imaging
CT and MRI examples of haemorrhagic stroke:
π©Ί Clinical Presentation
- 𧨠Sudden severe headache, vomiting, reduced consciousness.
- π§ββοΈ Focal neurology: hemiparesis, hemisensory loss, aphasia, neglect, visual field deficits.
- π Cerebellar bleeds: vertigo, nausea, truncal ataxia, nystagmus.
- π£ Brainstem bleeds: coma, quadriplegia, miosis, βlocked-inβ syndrome.
- π¦ SAH: Thunderclap headache, collapse, meningism, reduced GCS.
β οΈ Complications
- Intraventricular extension β acute deterioration, coma.
- Hydrocephalus from ventricular obstruction.
- Cerebral oedema, raised ICP, herniation (coning).
- Seizures (early or delayed).
- Rebleeding, especially in aneurysmal SAH and AVM.
π© Red Flags for Secondary Causes
- Age <50.
- No history of hypertension.
- Recurrent or atypical bleeds.
- Lobar location (esp. with soft tissue swelling or fracture β trauma vs primary bleed).
- Family history or features of inherited vascular syndromes (HHT).
π Investigations
- π©Έ Bloods: FBC, U&E, LFT, glucose, coagulation, ESR/CRP.
- πΌοΈ Non-contrast CT: First-line, detects haematoma, intraventricular blood, hydrocephalus.
- π§² MRI: Detects microbleeds, chronic haemosiderin, cavernomas (SWI/GRE).
- π‘ MRA/CTA: Aneurysms, AVMs, dissections.
- π©» MRV: Suspected venous sinus thrombosis.
- π DSA: Gold standard for vascular malformations; small stroke risk.
- β€οΈ Echocardiography: Endocarditis, embolic source.
- π LP: For SAH if CT normal but suspicion high.
π Prognostic Scoring (ICH Score)
- GCS: 3β4 (+2), 5β12 (+1), 13β15 (0).
- Age β₯80: +1.
- Volume >30 ml: +1.
- Intraventricular haemorrhage: +1.
- Infratentorial location: +1.
β‘οΈ Higher total = worse prognosis.
0 = 0%, 1 = 13%, 2 = 26%, 3 = 72%, 4 = 97%, 5 = 100% 30-day mortality.
βοΈ Management
- π Immediate: ABC, airway support, early CT, correct coagulopathy, cautious BP lowering, neurosurgical referral.
- π Reverse anticoagulation: Warfarin INR>1.4 β Vit K + PCC (Octaplex). Stop DOAC/antiplatelets. Avoid platelets (PATCH trial).
- π Blood pressure: Reduce to <160 systolic with IV agents (e.g. labetalol). Avoid hypoperfusion.
- π§ββοΈ Neurosurgery: Consider clot evacuation, especially cerebellar bleeds >3 cm or deteriorating GCS. EVD for hydrocephalus.
- π Seizure control: IV phenytoin/levetiracetam if seizures.
- π§β𦽠Rehabilitation: MDT stroke/ICU team for survivors.
- β Avoid: Routine mannitol (except bridging), steroids (harmful), unnecessary statin withdrawal without review.
π Prognosis
- Large bleeds, IVH, infratentorial location, and advanced age = worse outcomes.
- Many survivors are left with major neurological deficits.
π‘ Exam Pearl: Intracerebral haemorrhage = sudden headache + neuro deficit + β consciousness.
β‘οΈ Early non-contrast CT is essential β clinical features alone cannot distinguish from ischaemic stroke.