Haemorrhagic Stroke

1. Two Distinct Diseases — ICH vs SAH

“Haemorrhagic stroke” bundles together two pathologies whose mechanisms, presentations, complications and treatments scarcely overlap. Intracerebral haemorrhage (ICH) is bleeding into the brain parenchyma, almost always from a small deep perforator damaged by chronic hypertension or amyloid deposition. Subarachnoid haemorrhage (SAH) is bleeding into the cerebrospinal-fluid-filled space over the cortex, typically from rupture of a saccular (“berry”) aneurysm at a Circle-of-Willis bifurcation. The two diseases share only the catastrophic abruptness with which they declare themselves.

Although together they account for only ~15% of stroke incidence, haemorrhagic strokes cause a disproportionate share of stroke mortality. ICH alone — ~10% of strokes — produces roughly half of all stroke deaths. The disease is rarer but vastly more lethal than ischaemia, and far less amenable to time-critical reperfusion therapy. The clinical task in haemorrhagic stroke is to limit the bleed rather than to reverse it.

2. Intracerebral Haemorrhage — Epidemiology & Mechanisms

Spontaneous (non-traumatic) ICH has a global incidence of ~25 per 100,000 person-years and an outsize mortality. Population-based cohorts (Oxford Vascular Study, GBD 2019) consistently show:

The mechanistic taxonomy is approximately:

The deep / lobar dichotomy on first imaging is the single most useful clue: a deep ganglionic bleed in a hypertensive 60-year-old is hypertensive ICH until proven otherwise; a lobar bleed in a normotensive 80-year-old with cortical superficial siderosis is amyloid angiopathy until proven otherwise; a lobar bleed in a 25-year-old screams AVM and demands a CTA, MRA or DSA.

3. Hypertensive ICH — Charcot-Bouchard and the Deep Perforators

Long-standing hypertension produces a stereotyped small-vessel arteriopathy in the short, end-arterial perforators that arise at right angles from the major Circle of Willis vessels. Because they branch directly from high-pressure parents, they experience the highest pulsatile shear in the cerebral circulation; sustained hypertension overwhelms their thin walls.

The classical hypertensive ICH locations follow exactly the perforator territories described in Part II:

Cerebellar haemorrhage is a neurosurgical emergency in its own right: a posterior fossa mass > ~3 cm in diameter, or with brainstem compression / fourth-ventricle effacement / hydrocephalus, mandates urgent suboccipital craniectomy and clot evacuation. Patients can be conversant on arrival and dead from herniation an hour later.

4. Cerebral Amyloid Angiopathy (CAA)

CAA is the leading cause of lobar ICH in the elderly and the second commonest cause of spontaneous ICH overall. The pathology is deposition of amyloid-β (Aβ₄₀)— the same peptide that aggregates as parenchymal plaques in Alzheimer’s disease — in the media and adventitia of cortical and leptomeningeal arteries. Affected vessels become brittle: smooth muscle is lost, walls fibrinoid-degenerate, and microaneurysms ( “double-barrel” appearance) form at branch points.

The annual recurrence rate of ICH in probable CAA is ~7–9% per year — an order of magnitude higher than hypertensive ICH (~2% per year). This is the single most operationally important fact about CAA: a patient with probable CAA who has just survived a lobar bleed must not casually be put back on aspirin or anticoagulation, even for AF, without explicit risk-benefit calculation. Anti-amyloid monoclonal antibodies for Alzheimer’s (lecanemab, donanemab) markedly amplify CAA-related haemorrhage (ARIA-H), with APOE ε4 homozygotes most vulnerable.

5. Hematoma Expansion — The First 24 Hours

ICH is not a one-shot event. Serial CT studies (Brott 1997; Kazui 1996) showed that >1/3 of ICH expand significantly within the first 24 hours, with most growth in the first 3–6 hours. Each additional 1 mL of haematoma adds a measurable increment of disability and mortality. The early hours are therefore a therapeutic window — not for reversing the bleed, but for stopping it from getting larger.

Trial-grade evidence on stopping the bleed

Anticoagulant reversal

An anticoagulated patient who bleeds intracranially must be reversed within minutes, not hours. The pharmacology has matured rapidly:

The general acute-phase recipe for spontaneous ICH is therefore: SBP target ~140 mmHg with an IV titratable agent (nicardipine, clevidipine, labetalol); reverse any anticoagulant immediately; avoid platelet transfusion; treat fever and hyperglycaemia; image early to detect expansion or hydrocephalus; consult neurosurgery for posterior fossa, mass-effect, or IVH cases. See Part VII (Acute Management) and Pharmacology — reversal agents.

6. Subarachnoid Haemorrhage — Aneurysmal SAH

Aneurysmal SAH (aSAH) is a different disease from ICH: a high-pressure squirt of arterial blood into the subarachnoid space, often from a saccular aneurysm at a Circle-of-Willis bifurcation. The patient classically describes the “worst headache of my life”, instantaneous in onset (“thunderclap”), often with vomiting, neck stiffness, photophobia, and brief loss of consciousness. Sentinel headaches in the days or weeks before the major bleed are reported in ~40% of patients in retrospect.

Hunt & Hess (1968) clinical grade

WFNS scale (1988) — objective GCS-based

Fisher / modified Fisher CT grade

The Fisher scale (1980) and its modification (Frontera 2006) quantify the radiographic blood load — the variable that best predicts vasospasm and delayed cerebral ischaemia.

Imaging strategy: a non-contrast CT within 6 h has >99% sensitivity for SAH; in later presentations or in equivocal cases, lumbar puncture for xanthochromia (12 h after onset) remains the gold standard. Once SAH is confirmed, CT angiography is the workhorse for identifying the culprit aneurysm; digital subtraction angiography (DSA) is reserved for treatment planning or when CTA is negative (~15% of SAH are angiographically occult, including the benign perimesencephalic pattern). See Part VI (Imaging) for CT signs.

7. Aneurysmal Rupture & Re-bleeding

An aneurysm that has bled once is overwhelmingly likely to bleed again unless secured. Untreated re-bleed risk is approximately:

Re-bleed mortality approaches 70%. The pillar of management is therefore early aneurysm securing, ideally within 24–48 h. Two definitive techniques exist:

In the hours between admission and securing, the bridge therapy is short-course tranexamic acid (debated; ULTRA 2021 negative for outcome), strict normotension to avoid the trans-mural pressure spikes that re-rupture, head-of-bed elevation, analgesia and antiemesis, stool softeners (Valsalva avoidance), and prophylactic anticonvulsants in selected high-risk patients (large MCA aneurysms, intraparenchymal extension).

8. Vasospasm & Delayed Cerebral Ischaemia

Once the aneurysm is secured and the patient survives the acute bleed, the second great hazard begins. Cerebral vasospasm — angiographic narrowing of large cerebral arteries — develops in ~70% of aSAH patients, with a characteristic time course peaking between days 4 and 14. About one-third develop symptomatic delayed cerebral ischaemia (DCI): new focal deficit or decline in level of consciousness lasting > 1 h not explained by other causes. DCI is the leading cause of death and disability in patients who survive the initial bleed.

Therapy

The 21-day vasospasm window dictates that aSAH patients spend at least two weeks in dedicated neurocritical care, with daily neurological surveillance and a low threshold for imaging at the first hint of decline. After day 14–21 the risk recedes; rehabilitation begins.

9. Intracranial Pressure Physiology

Both ICH and SAH ultimately threaten the patient through one final common pathway: raised intracranial pressure leading to cerebral perfusion failure and herniation. Understanding ICP physiology is therefore the central technical skill of stroke critical care.

Monro-Kellie doctrine

The cranium is a rigid box of fixed volume containing three incompressible compartments:

Monro (1783) and Kellie (1824) recognised that the sum of these volumes is fixed, so an increase in any one compartment must be matched by a decrease in another, or ICP rises: \(V_\text{brain} + V_\text{CSF} + V_\text{blood} + V_\text{lesion} = \text{constant}\). When a haematoma adds 30 mL to the cranial vault, CSF is initially displaced through the foramen magnum and venous blood is squeezed out of compliant cortical veins; once this compensatory reserve is exhausted, additional volume produces a steep and accelerating rise in ICP.

Cerebral perfusion pressure

The driving pressure for cerebral blood flow is the difference between the arterial inflow pressure and the pressure surrounding the cerebral capillary bed:

When ICP rises and MAP fails to follow, CPP falls below the autoregulatory floor and cerebral blood flow plummets. Conversely, when MAP fails (e.g. from sedatives, sepsis, haemorrhage elsewhere), even a moderately raised ICP becomes catastrophic. See cardiovascular physiology for arterial pressure regulation.

Cushing reflex

When ICP approaches MAP, brainstem ischaemia triggers an intense sympathetic response to restore CPP. Harvey Cushing (1901) described the resulting triad:

The Cushing reflex is a terminal sign — the brainstem trying to save itself. Treating the hypertension as if it were primary, without addressing the underlying ICP, would collapse CPP and finish the patient. The correct response is urgent ICP-lowering: head-up positioning, hypertonic saline or mannitol, hyperventilation to PaCO₂ ~30 mmHg as a bridge, and definitive surgical decompression.

Herniation syndromes

When the pressure differential across the brain becomes too great, brain tissue is forced through the rigid dural openings — the falx, the tentorium, the foramen magnum — producing predictable clinical syndromes:

The classical sequence in a large supratentorial bleed:

1. 1. Decreased LOC — reticular activating system pressure.
2. 2. Anisocoria with ipsilateral blown pupil — uncus over the tentorial edge compressing CN III; parasympathetic fibres on the outside go first, so dilation precedes ophthalmoplegia.
3. 3. Contralateral hemiparesis — midbrain cerebral peduncle compressed against the tentorium.
4. 4. Decerebrate (extensor) posturing — midbrain / upper pontine descent; loss of red-nucleus inhibition of vestibulospinal extensor drive.
5. 5. Cushing reflex — brainstem ischaemia, BP↑ HR↓ respiration disordered.
6. 6. Apnoea / arrest — medullary respiratory centre failure.

Each of these signs is a window of seconds to minutes. The neurocritical care physician’s job is to detect the patient at step 1 or 2 and intervene before step 4. Emergency manoeuvres — head of bed 30°, sedation/analgesia, hypertonic saline (3% bolus or 23.4% via central line), short-burst hyperventilation, and call to neurosurgery for EVD or decompression — can buy minutes.

10. Surgical Management of Haemorrhagic Stroke

Surgery in haemorrhagic stroke is selective; the wrong patient at the wrong time can be harmed by craniotomy. Three indications dominate:

External ventricular drain (EVD)

A burr-hole-placed catheter into the lateral ventricle (typically Kocher’s point, anterior to the coronal suture) draining CSF. EVD is indicated for:

• Acute obstructive hydrocephalus (IVH, posterior fossa bleed compressing 4th ventricle, SAH blocking arachnoid granulations)
• ICP monitoring with simultaneous therapeutic drainage
• Intraventricular thrombolysis: CLEAR-III (2017) showed alteplase via EVD reduced mortality in IVH, with marginal functional benefit for high-volume IVH

Hematoma evacuation

The randomised trial story for evacuation of supratentorial ICH was, until recently, one of repeated negative results:

The ENRICH trial vindicated decades of effort: the right patient (lobar ICH, 30–80 mL, within 24 h of onset, GCS > 5), with the right technology (parafascicular brain-sparing approach), can benefit from evacuation. Deep ganglionic bleeds were non-significant, consistent with the historical literature; the eloquent-tract cost of accessing them probably outweighs benefit.

Cerebellar haemorrhage is the exception that has never required a randomised trial: a cerebellar haematoma > ~3 cm or with brainstem compression / hydrocephalus is a Class I indication for suboccipital craniectomy and evacuation, with mortality reductions reported anywhere from 50% down to 20% in surgical case series.

Decompressive hemicraniectomy

Removing a large bone flap and opening the dura allows the swollen hemisphere to expand outward rather than herniate medially or downward, breaking the Monro-Kellie constraint. Established in malignant MCA infarction by DESTINY/DECIMAL/HAMLET (Part VII), the role in ICH is more selective: SWITCH (2024) found a possible benefit for decompressive hemicraniectomy added to medical care for severe deep ICH, but with wider confidence intervals than the ischaemic trials.

The clinical syndromes produced by the haematoma locations described above — MCA territory hemiplegia, thalamic syndromes, brainstem catastrophe — are the subject of Part V (Clinical Syndromes). The imaging signs that distinguish ICH from SAH from infarct in the first minutes are covered in Part VI (Imaging); the integrated acute-phase management protocol is laid out in Part VII (Acute Management).