Intracranial Hemorrhage
Intracranial hemorrhage is bleeding within the cranial vault—including epidural, subdural, subarachnoid, or intraparenchymal compartments—resulting from trauma, vascular malformations, or coagulopathy and potentially causing elevated intracranial pressure and neurological compromise.
Intracranial Hemorrhage (ICH)
Intracranial hemorrhage (ICH) refers to any bleeding occurring within the cranial vault. The term is an umbrella — "intra" = within, "cranial" = skull, "hemorrhage" = bleeding. It encompasses several distinct entities classified by the anatomical compartment in which blood accumulates:
- Epidural hematoma (EDH): Blood between the inner table of the skull and the periosteal (outer) layer of the dura mater.
- Subdural hematoma (SDH): Blood between the meningeal (inner) layer of the dura and the arachnoid mater.
- Subarachnoid hemorrhage (SAH): Blood within the subarachnoid space (between arachnoid and pia mater), where CSF normally circulates.
- Intracerebral (intraparenchymal) hemorrhage: Blood within the brain parenchyma itself.
- Intraventricular hemorrhage (IVH): Blood within the ventricular system — often secondary to extension of an intracerebral hemorrhage or SAH.
Stroke is defined as rapid onset of focal or global cerebral dysfunction due to non-traumatic vascular causes, with symptoms lasting > 24 hours or leading to death [1]. Hemorrhagic stroke accounts for ~20% of all strokes but carries the highest mortality [1].
Key Distinction
Not all intracranial hemorrhages are "strokes." EDH and SDH are typically traumatic and are classified under traumatic brain injury, not stroke. The term "hemorrhagic stroke" specifically refers to spontaneous intracerebral hemorrhage and subarachnoid hemorrhage.
2. Epidemiology
- Stroke is the most common adult neurological disease, and the 2nd–3rd leading cause of death in China and Hong Kong [1].
- Among strokes: ischaemic stroke 75–80%, intracerebral hemorrhage ~15%, subarachnoid hemorrhage < 5% [1].
- In Hong Kong and East Asia, the proportion of hemorrhagic strokes is relatively higher compared to Western populations, largely driven by the high prevalence of hypertension and dietary factors (high sodium intake).
| Type | 1-month mortality | 1-year mortality | Disability |
|---|---|---|---|
| SAH | ~50% | — | 50% with severe deficits |
| ICH (intracerebral) | ~40% | ~50% | Moderate–severe |
| Cortical infarct | ~20% | ~35% | Moderate |
| Lacunar infarct | Low | Low | Low |
Main determinant of prognosis in stroke: mortality order (descending) is SAH > ICH > cortical infarct > lacunar infarct. Disability order: SAH > cortical infarct > ICH > lacunar infarct. [1]
- Relatively uncommon: ~1–4% of traumatic head injuries.
- Peak incidence: Young adults (20–30 years) — because the dura is less adherent to the skull in this age group.
- Rare in the very young (< 2 years) and elderly (> 60 years) — in infants the dura is tightly adherent to the skull; in elderly the middle meningeal artery is more embedded in bone grooves, making it less prone to shearing.
- Much more common than EDH, especially in the elderly.
- Chronic SDH is one of the most common neurosurgical conditions in geriatric populations (particularly in Hong Kong's aging population).
- Bimodal distribution: young adults (trauma) and elderly (falls, atrophy, anticoagulation).
- Incidence: ~25 per 100,000/year globally; higher in Asian populations (including Hong Kong) — partly due to higher hypertension prevalence.
- Hypertension is the cause in 50–90% of cases [4].
- Peak incidence: 55–75 years.
2.7 Risk Factors
- Old age
- Male sex (overall; female predominance for SAH)
- Previous vascular event (MI, stroke, PVD)
- Family history
- Race/ethnicity: higher in Black and East Asian populations
- Atherosclerotic risk factors: obesity, lack of exercise, cigarette smoking, alcohol abuse, HTN, DM, hyperlipidemia
- Sources of thromboemboli: AF, CHF, IE; blood abnormalities (high fibrinogen, polycythemia, homocysteinemia, OCP/HRT use); carotid artery stenosis
- Specific to hemorrhagic stroke:
- Hypertension — the single most important modifiable risk factor for ICH
- Anticoagulant/antiplatelet use — warfarin-associated ICH carries very high mortality
- Excessive alcohol intake — dose-dependent risk
- Illicit drug use (cocaine, amphetamines)
- Smoking: strong dose-response relationship for both ischaemic stroke and SAH; risk declines after quitting and can be eliminated by 5 years [2]
Hong Kong Focus
In Hong Kong, the leading modifiable risk factor for ICH is hypertension, particularly poorly controlled hypertension in middle-aged and elderly men. Falls in the elderly (often on anticoagulants for AF) are a major cause of traumatic SDH. The aging population and increasing anticoagulant use make chronic SDH an increasingly common surgical problem.
3. Anatomy and Function
Understanding intracranial hemorrhage requires a solid grasp of meningeal anatomy, cerebral vasculature, and CSF dynamics. Let's build this from first principles.
| Layer | Key Features | Clinical Relevance |
|---|---|---|
| Periosteum (outer periosteal layer of dura) | Adherent to inner skull table; contains middle meningeal artery (MMA) | EDH: blood strips dura from bone |
| Dura mater (meningeal layer) | Tough, fibrous; forms dural folds (falx cerebri, tentorium cerebelli); contains dural venous sinuses | SDH: blood between dura and arachnoid |
| Arachnoid mater | Avascular, delicate membrane; bridging veins traverse from brain surface through subarachnoid space to dural venous sinuses | SDH: bridging vein rupture |
| Subarachnoid space | Contains CSF, cerebral arteries (Circle of Willis), and arachnoid trabeculae | SAH: blood in CSF space |
| Pia mater | Intimately adherent to brain surface; carries small penetrating arteries | Intracerebral hemorrhage from small arteries |
3.2 Key Vascular Anatomy
- Branch of the maxillary artery (from external carotid artery).
- Enters the skull through the foramen spinosum.
- Runs in a groove on the inner table of the skull in the temporal region, between the dura and the skull.
- This is the vessel torn in ~85% of epidural hematomas [5][6]. The pterion (thinnest part of the skull, where frontal, parietal, temporal, and sphenoid bones meet) overlies the MMA — trauma here is classically associated with EDH.
- Small veins that drain from the cerebral cortex (pial veins) across the subdural space to enter the dural venous sinuses (especially the superior sagittal sinus).
- They are unsupported as they traverse the subdural space — making them vulnerable to shearing forces during head trauma.
- Tearing of bridging veins is the cause of subdural hematoma [5][6].
- In the elderly with cerebral atrophy, the brain "shrinks away" from the skull — the bridging veins are stretched over a greater distance, making them even more vulnerable to tearing with even minor trauma.
- The anastomotic ring at the base of the brain formed by:
- Anterior: paired ACAs connected by the anterior communicating artery (AComm)
- Middle: MCAs (lateral)
- Posterior: paired PCAs connected to the ICAs via posterior communicating arteries (PComm)
- Fed by: bilateral internal carotid arteries (anterior circulation) and the basilar artery (posterior circulation, from paired vertebral arteries)
- Cerebral aneurysms are usually at arterial bifurcations, majority along Circle of Willis, 90% anterior circulation [1].
- Most common sites: AComm (~30%), PComm (~25%), MCA bifurcation (~20%).
- Small perforating arteries arising from the proximal MCA and ACA.
- Supply the basal ganglia, internal capsule, and thalamus.
- These are the vessels most affected by hypertensive lipohyalinosis — weakening of the vessel wall leads to formation of Charcot-Bouchard microaneurysms, which can rupture causing hypertensive ICH.
- CSF is produced by the choroid plexus (mainly in the lateral ventricles) at ~500 mL/day; total volume at any time is ~150 mL.
- Flow: lateral ventricles → foramen of Monro → 3rd ventricle → cerebral aqueduct → 4th ventricle → foramina of Luschka (lateral) and Magendie (median) → subarachnoid space → absorbed at arachnoid granulations into the superior sagittal sinus.
- SAH can obstruct CSF absorption at the arachnoid granulations (communicating hydrocephalus) or block CSF pathways with blood clot (obstructive hydrocephalus) — this is why hydrocephalus is a major complication of SAH.
The skull is a rigid structure with constant volume. Contents = brain (80%) + blood (10%) + CSF (10%). An increase in any constituent must be compensated by a decrease in others, mainly by CSF outflow (slow) and venous outflow (quick). Overwhelming of compensatory mechanisms leads to raised ICP. [1]
This is the fundamental principle explaining why intracranial hemorrhage is dangerous: the accumulating blood is a space-occupying lesion within a fixed-volume container. Once compensatory mechanisms are exhausted, ICP rises exponentially.
4. Etiology
| Category | Causes |
|---|---|
| Trauma (most common) | Road traffic accidents (RTA), falls, assaults |
| Vascular source | Arterial injury (85%) — middle meningeal artery; 13% tearing of transverse sinus (venous); diploic veins |
| Non-traumatic (rare) | Infection/epidural abscess (pressure necrosis of meningeal vessels), coagulopathy, AV malformations, hemorrhagic tumors, neurosurgical complications, hemodialysis (ICP fluctuations, uremic platelet dysfunction, heparin, hypertension) |
| Category | Causes |
|---|---|
| Trauma (most common) | RTA, falls (especially elderly), assaults |
| Vascular source | Tearing of bridging veins |
| Non-traumatic | Coagulopathy (warfarin, DOACs, thrombocytopenia), AV malformation, tumors (meningioma, dural metastasis), neurosurgical complications |
| Risk factors | Diffuse cerebral atrophy (common in elderly), chronic alcoholism (both cause brain shrinkage → stretching of bridging veins), anticoagulant/antiplatelet use |
Classification of SDH by chronicity [2]:
| Type | Timeline | CT Appearance | Notes |
|---|---|---|---|
| Acute SDH | < 1 week | Hyperdense | Often significant trauma |
| Subacute SDH | 1–3 weeks | Isodense (hard to see — do CT early or use contrast) | |
| Chronic SDH | > 3 weeks | Hypodense (~CSF density) | Often minor/forgotten trauma in elderly; collection of blood breakdown products |
| Acute-on-chronic SDH | Variable | Mixed density (white streaks in dark collection) | Small recurrent hemorrhages expand existing collection |
- Commonest cause of SAH overall is trauma [7].
- Spontaneous (atraumatic) SAH:
- Saccular (berry) aneurysm rupture — the most common cause of spontaneous SAH (~80–85%)
- Dissecting aneurysm
- "Mycotic" aneurysm (infected aneurysm, e.g., from infective endocarditis)
- Vascular malformation (AVM)
- Cocaine use (sympathomimetic surge → acute hypertension → rupture)
- Perimesencephalic non-aneurysmal SAH (~10–15%) — benign venous bleeding around the midbrain
"If no history of trauma, SAH is aneurysmal in origin until proven otherwise." [7]
"BEWARE spontaneous SAH then LOC, fall & head injury. Ask: 'Headache before or after LOC?'" [7] — This is a classic exam and clinical pitfall. A patient may present with head injury but the primary event was actually a ruptured aneurysm causing SAH, LOC, and then a fall.
Exam Trap
Always consider SAH as the PRIMARY event in a patient who presents with head injury + headache. The sequence matters: headache (SAH) → LOC → fall → head injury, NOT head injury → headache. Ask about the timeline carefully.
Cerebral Aneurysm — Predisposing Factors [1][7]
- Smoking
- Hypertension
- Age > 40
- Family history
- Female sex
- Connective tissue diseases: Ehlers-Danlos syndrome, autosomal dominant polycystic kidney disease (ADPKD), Marfan syndrome, fibromuscular dysplasia
- Haemodynamic stress [1]
- Coarctation of aorta [1]
Aneurysms can be forever asymptomatic. Unpredictable spontaneous rupture. [7]
Etiology (in order of prevalence) [3][4]:
- Hypertension (50–90%) — rupture of Charcot-Bouchard microaneurysms
- Cerebral amyloid angiopathy (CAA) — lobar ICH, more peripheral [3]
- Occurs as sporadic disorder ± association with Alzheimer's disease [2]
- Others:
- Coagulopathy (warfarin, DOACs, heparin, hemophilia, thrombocytopenia, DIC) [3]
- Structural vascular lesions: berry aneurysms, AVM [3][4]
- Tumors (hemorrhagic tumors — glioblastoma, metastases from melanoma, renal cell carcinoma, choriocarcinoma, thyroid carcinoma) [4]
- Drugs: cocaine, amphetamines [2][4]
- Other parenchymal diseases (infarct with hemorrhagic transformation, tumour) [1]
- Cerebral venous sinus thrombosis (venous infarction → hemorrhagic)
- Vasculitis
- Moyamoya disease
- Primary IVH (rare): bleeding from choroid plexus or subependymal veins.
- Secondary IVH (common): extension of ICH or SAH into the ventricles.
- IVH is a poor prognostic sign — associated with obstructive hydrocephalus and higher mortality.
5. Pathophysiology
- Mechanism: Trauma (usually temporal bone fracture at the pterion) → tears the middle meningeal artery (or less commonly a dural venous sinus or diploic vein).
- Arterial bleeding under systemic arterial pressure → blood accumulates between the skull and the periosteal layer of the dura.
- The dura is normally adherent to the skull (especially at suture lines) — so the expanding hematoma strips the dura from the bone, creating a lenticular (biconvex/lens-shaped) collection.
- Because the dura is bound to the bone at suture lines, an EDH does NOT cross suture lines [5][6]. However, it CAN cross the midline (because dural attachments to the falx are not at suture lines) [2].
- Clinical consequence: Arterial bleeding is high-pressure → rapid accumulation → rapid rise in ICP → rapid deterioration [5][6].
- Classic "lucid interval": Patient loses consciousness at impact → briefly regains consciousness (lucid interval as the brain initially compensates) → then deteriorates rapidly as the expanding hematoma overwhelms compensatory mechanisms. This classic presentation occurs in ~20–50% of cases.
- Mechanism: Acceleration-deceleration injury (even minor) → shearing of bridging veins as they cross from the mobile brain surface to the fixed dural sinuses.
- Venous bleeding under low pressure → blood accumulates in the subdural space (between the meningeal layer of the dura and the arachnoid).
- The collection spreads freely over the brain surface forming a crescentic (crescent-shaped) collection — it crosses suture lines (because the subdural space is continuous) but does NOT cross the midline (because the falx cerebri, a dural fold, blocks it) [5][6].
- Why elderly are vulnerable:
- Cerebral atrophy → brain shrinks → bridging veins are stretched over a longer unsupported distance → much more vulnerable to shearing, even with trivial trauma.
- Chronic alcoholism compounds this (toxic atrophy + coagulopathy from liver dysfunction + frequent falls).
- Chronic SDH pathophysiology:
- Initial subdural hemorrhage → blood breakdown products form a membrane around the collection.
- This neomembrane is highly vascularized with fragile capillaries.
- Repeated micro-hemorrhages from these fragile capillary membranes → gradual enlargement of the collection.
- Osmotic effect: breakdown products increase the osmolarity within the collection → draws in fluid by osmosis → further expansion.
- This is why chronic SDH can present weeks to months after a trivial (or forgotten) injury.
- Clinical consequence: Venous bleeding is low-pressure → chronic progressive/stable course [5][6] (cf. EDH which is rapid).
- Mechanism: Rupture of a saccular (berry) aneurysm at an arterial bifurcation of the Circle of Willis → high-pressure arterial blood floods into the subarachnoid space.
- Sudden rise in ICP: The sudden volume of blood in the subarachnoid space acutely raises ICP → may transiently equal arterial pressure → global cerebral ischemia → loss of consciousness (this is why ~50% of patients lose consciousness at onset).
- "Thunderclap headache": The meninges (particularly the dura and pia) are richly innervated by pain fibers of the trigeminal nerve (CN V) and upper cervical nerves → sudden stretching and irritation by blood causes the "worst headache of my life."
- Meningeal irritation: Blood in the subarachnoid space is a chemical irritant → meningism (neck stiffness, photophobia, Kernig's sign, Brudzinski's sign).
- Secondary complications (pathophysiological cascade):
- Re-bleeding: The ruptured aneurysm can re-bleed (highest risk in first 24 hours) — this is the most feared early complication.
- Vasospasm: Blood breakdown products (especially oxyhemoglobin and endothelin) are potent vasoconstrictors → delayed cerebral ischemia (DCI), typically peaks at days 4–14 post-SAH.
- Hydrocephalus: Blood clots block CSF absorption at arachnoid granulations (communicating) or obstruct CSF pathways (obstructive) → acute or chronic hydrocephalus.
- Hyponatremia: Either SIADH or cerebral salt wasting syndrome (CSWS) — both can follow SAH [10]. Distinguishing between these is critical because SIADH is treated with fluid restriction whereas CSWS requires fluid and salt replacement.
-
Hypertensive ICH mechanism:
- Chronic hypertension → lipohyalinosis and fibrinoid necrosis of small penetrating arteries (lenticulostriate arteries, thalamoperforating arteries, paramedian pontine branches, cerebellar arteries).
- This weakens the vessel wall → formation of Charcot-Bouchard microaneurysms.
- Sudden BP surge → rupture of these microaneurysms → hemorrhage into the brain parenchyma.
- Common sites: putamen (~35%), thalamus (~20%), pons (~10%), cerebellum (~10%) — all deep structures supplied by small penetrating arteries [3][4].
-
Cerebral Amyloid Angiopathy (CAA) mechanism:
- Beta-amyloid protein deposits in the media and adventitia of small- and medium-sized cortical and leptomeningeal arteries.
- This weakens the vessel wall → makes it prone to rupture.
- Lobar ICH (cortical/subcortical) — typically in the temporal and occipital lobes.
- Tends to occur in elderly patients (> 65 years), often recurrent, and may be associated with Alzheimer's disease.
-
Consequences of intracerebral hemorrhage [1]:
- Acute bleeding → blood dissects between neurons → immediate function loss
- Expanding hematoma ± associated cerebral edema → raised ICP ± death
- Perilesional edema: develops over hours to days due to:
- Clot retraction and serum extrusion
- Thrombin-mediated inflammation
- Hemoglobin breakdown products → oxidative stress
- Blood-brain barrier (BBB) disruption → vasogenic edema
- If large enough → midline shift, brain herniation (transtentorial, subfalcine, or tonsillar), and brainstem compression → death.
In cerebral ischemia, there is acidosis, excitotoxicity, and generation of free radicals, leading to: (1) cytotoxic edema due to increased intracellular Na+/Ca2+; and (2) vasogenic edema due to disruption of BBB. [1]
- Vasogenic edema: Damaged vessel walls allow protein-rich fluid into the extracellular space. This is the predominant form around hemorrhagic lesions.
- Cytotoxic edema: Neuronal energy failure → failure of Na+/K+-ATPase → intracellular water accumulation. Seen in the peri-hematomal ischemic zone.
- Edema worsens ICP and can cause secondary ischemic injury in an expanding vicious cycle:
Post-traumatic brain swelling: multifactorial — vasogenic edema (disrupted BBB), cytotoxic edema (excitotoxicity, direct injury, ischemia), reactive hyperemia (impaired vascular autoregulation). Vicious cycle because these lead to raised ICP → decreased cerebral perfusion → further neuronal injury. [1]
When ICP rises focally (e.g., from a hematoma), the brain herniates from a high-pressure compartment to a low-pressure compartment through the rigid dural partitions:
| Herniation Type | Mechanism | Clinical Features |
|---|---|---|
| Subfalcine (cingulate) | Cingulate gyrus herniates under the falx cerebri | ACA compression → contralateral leg weakness |
| Transtentorial (uncal) | Medial temporal lobe (uncus) herniates over the tentorial edge | Ipsilateral CN III palsy (dilated pupil, ptosis), contralateral hemiparesis, then bilateral posturing, coma |
| Central (downward) | Bilateral downward herniation through the tentorial notch | Progressive bilateral CN III palsy, Cushing's triad (hypertension, bradycardia, irregular respiration), then death |
| Tonsillar | Cerebellar tonsils herniate through the foramen magnum | Brainstem (medullary) compression → respiratory arrest, death |
| External | Brain herniates through a skull defect | Post-surgical or post-traumatic |
Cushing's Triad — Why It Happens
As ICP rises and approaches mean arterial pressure (MAP), cerebral perfusion pressure (CPP = MAP – ICP) falls. The brainstem detects ischemia and triggers a massive sympathetic response to raise MAP (hypertension). The baroreceptors then detect hypertension and trigger a vagal (parasympathetic) reflex → bradycardia. Respiratory centers in the brainstem, compressed and ischemic, produce irregular breathing patterns. This is a pre-terminal sign — it means brainstem herniation is imminent.
6. Classification
| Traumatic | Spontaneous (Non-traumatic) | |
|---|---|---|
| EDH | Most common (skull fracture → MMA tear) | Rare (infection, coagulopathy, AVM) |
| SDH | Acceleration-deceleration (bridging vein tear) | Coagulopathy, AVM, tumor |
| SAH | Most common overall cause of SAH | Aneurysm rupture (most common spontaneous cause), AVM, cocaine |
| ICH | Direct parenchymal contusion | HTN (most common), CAA, AVM, coagulopathy, drugs |
- Putaminal (most common, ~35%)
- Thalamic (~20%)
- Cerebellar (~10%)
- Brainstem (pontine) (~10%)
- Lobar (~20%) — think CAA, AVM, tumor
- Intraventricular (primary or secondary)
| Type | Timeline | Pathology |
|---|---|---|
| Acute | < 1 week | Fresh blood, high morbidity |
| Subacute | 1–3 weeks | Clot organization, isodense on CT |
| Chronic | > 3 weeks | Encapsulated fluid with neomembrane |
| Acute-on-chronic | Variable | Fresh hemorrhage into existing chronic collection |
| Feature | Epidural | Subdural |
|---|---|---|
| Etiology | 75% tearing of MMA; 13% transverse sinus | Tearing of bridging veins |
| Shape | Lentiform (biconvex) | Crescentic |
| Cross sutures? | No (bound to bone at sutures) | Yes |
| Cross midline? | Yes | No (bound by falx cerebri) |
| Clinical course | Rapid deterioration | Chronic progressive/stable |
| Bone fracture | 90% (75% in some sources) | Usually no |
| CT appearance (acute) | Hyperdense, lentiform | Hyperdense, crescentic |
| Grade | Description |
|---|---|
| I | Asymptomatic or minimal headache, slight nuchal rigidity |
| II | Moderate to severe headache, nuchal rigidity, no deficit except CN palsy |
| III | Drowsy, confusion, mild focal deficit |
| IV | Stupor, moderate to severe hemiparesis, early decerebrate rigidity |
| V | Deep coma, decerebrate rigidity, moribund |
| Grade | GCS | Motor Deficit |
|---|---|---|
| I | 15 | Absent |
| II | 13–14 | Absent |
| III | 13–14 | Present |
| IV | 7–12 | Present or absent |
| V | 3–6 | Present or absent |
7. Clinical Features
7.1 Epidural Hematoma
- History of significant head trauma — typically a blow to the temporal region.
- Brief initial loss of consciousness (from the concussive impact itself).
- "Lucid interval" — transient improvement as the brain initially compensates for the slowly expanding hematoma (CSF displacement, venous outflow). Present in ~20–50% of cases.
- Why a lucid interval? The initial LOC is from concussion (diffuse neuronal excitation). The patient recovers as the concussive effect wears off. Meanwhile, arterial blood continues to accumulate, but ICP doesn't rise immediately because CSF is displaced into the spinal canal and venous blood is displaced — the Monro-Kellie compensation. Once these are exhausted, ICP rises rapidly → second deterioration.
- Rapidly progressive headache — increasing ICP stretching pain-sensitive dura and blood vessels.
- Nausea and vomiting — direct effect of raised ICP on the area postrema (chemoreceptor trigger zone) in the floor of the 4th ventricle.
- Progressive drowsiness → coma — brainstem compression from transtentorial herniation.
- Ipsilateral fixed, dilated pupil (blown pupil) — the expanding temporal hematoma pushes the uncus medially over the tentorial edge → compresses the ipsilateral CN III → loss of parasympathetic fibers (which run on the outside of the nerve) → unopposed sympathetic mydriasis. This is "surgical" CN III palsy (non-pupil-sparing).
- Contralateral hemiparesis — compression of the ipsilateral cerebral peduncle against the tentorial edge → corticospinal tract dysfunction (remember the tract crosses at the medullary pyramids, so an ipsilateral peduncle lesion causes contralateral weakness).
- Kernohan's notch phenomenon: Occasionally, the contralateral cerebral peduncle is pushed against the opposite tentorial edge → ipsilateral hemiparesis (a false localizing sign).
- Cushing's triad (late sign): hypertension, bradycardia, irregular respiration — brainstem compression.
- Skull fracture may be evident on examination (boggy swelling over the temporal region, Battle's sign, raccoon eyes if basilar skull fracture).
7.2 Subdural Hematoma
- History of significant trauma (or relatively minor trauma in the elderly/anticoagulated).
- Headache — progressive, often worse than expected for the mechanism of injury.
- Drowsiness, confusion — mass effect on cortex.
- Focal neurological deficits — depending on location (hemiparesis, aphasia, etc.).
- Reduced GCS — from cortical compression and raised ICP.
- Ipsilateral dilated pupil — uncal herniation (same mechanism as EDH).
- Contralateral hemiparesis — compression of the ipsilateral motor cortex/corticospinal tract.
- Papilledema — if ICP has been raised for a sufficient duration (takes hours to days to develop).
- Often elderly patients with no clear history of head trauma (or a minor fall weeks to months ago that was forgotten) [2].
- Insidious onset:
- Fluctuating confusion / cognitive decline — often misdiagnosed as dementia.
- Progressive headache — typically mild, gradual.
- Personality change — frontal lobe compression.
- Gait disturbance / unsteadiness — generalised cortical dysfunction.
- Urinary incontinence — can mimic normal pressure hydrocephalus (NPH) triad.
- Fluctuating level of consciousness — characteristic; the fragile neomembrane capillaries re-bleed intermittently.
- Subtle focal neurological deficits — mild hemiparesis, reflex asymmetry.
- Papilledema (if chronic raised ICP).
Clinical Pearl
Chronic SDH is a great mimic. In any elderly patient presenting with progressive confusion, unsteadiness, personality change, or fluctuating consciousness — especially if on anticoagulants — always consider chronic SDH and get a CT head. It is one of the most treatable causes of "reversible dementia."
7.3 Subarachnoid Hemorrhage
- "Thunderclap headache" — sudden onset, maximal intensity at onset ("worst headache of my life"). This is the hallmark symptom.
- Why thunderclap? Arterial blood at systemic pressure suddenly distends the subarachnoid space → acute stretching and irritation of pain-sensitive meninges and blood vessels at the base of the brain.
- Loss of consciousness (in ~50%) — acute rise in ICP transiently reduces cerebral perfusion to zero.
- Nausea and vomiting — meningeal irritation + raised ICP stimulating the vomiting center.
- Photophobia — meningeal inflammation sensitizes trigeminal pain pathways (photophobia is a feature of all meningeal irritation syndromes).
- Neck stiffness/pain — blood irritating the cervical meninges.
- Sentinel headache — in ~30–50% of patients, a warning "herald bleed" (minor leak from the aneurysm) occurs days to weeks before the major rupture. This is often dismissed as migraine or tension headache. A missed sentinel headache is a major medicolegal risk.
- Seizures — cortical irritation by blood.
- Back pain — blood tracking down the spinal subarachnoid space.
- Meningism (meningeal signs):
- Neck stiffness (nuchal rigidity) — involuntary resistance to passive neck flexion due to meningeal irritation.
- Kernig's sign — resistance/pain on knee extension with the hip flexed to 90°.
- Brudzinski's sign — involuntary hip/knee flexion when the neck is passively flexed.
- Note: Meningeal signs may take 6–12 hours to develop after SAH onset.
- Focal neurological deficits (depending on the aneurysm location):
- PComm aneurysm → CN III palsy (ipsilateral ptosis, "down and out" eye, dilated pupil) — the PComm artery runs adjacent to CN III, and an expanding aneurysm directly compresses it [1].
- AComm aneurysm → can compress the hypothalamus, optic chiasm.
- MCA aneurysm → contralateral hemiparesis, aphasia (if dominant hemisphere).
- Subhyaloid (preretinal) hemorrhage — on fundoscopy: flame-shaped hemorrhage between the retina and the vitreous, classically described as a "D-shaped" or "boat-shaped" collection. This occurs because acutely raised ICP impedes venous drainage from the eye through the optic nerve sheath → retinal venous congestion → hemorrhage. (Also known as Terson syndrome when vitreous hemorrhage occurs.)
- Reduced GCS — in severe cases, from global ischemia or large-volume bleed.
- Papilledema — if raised ICP sustained (may not be present acutely).
7.4 Intracerebral Hemorrhage
- Sudden onset focal neurological deficit — the hallmark. The specific deficit depends on the location of the hemorrhage.
- Headache — present in ~40–50% of ICH (cf. only ~15% in ischemic stroke). Blood irritates pain-sensitive structures. Larger hemorrhages → more headache.
- Nausea and vomiting — raised ICP.
- Progressive drowsiness / coma — expanding hematoma → raised ICP → herniation.
- Seizures — cortical irritation (more common in lobar hemorrhages).
| Location | Typical Deficits | Pathophysiological Basis |
|---|---|---|
| Putaminal (most common) | Contralateral hemiparesis + hemisensory loss; eyes deviate toward the lesion; may progress to coma | Putamen is adjacent to the internal capsule (corticospinal and thalamocortical tracts); hematoma compresses/disrupts these tracts |
| Thalamic | Contralateral hemisensory loss > hemiparesis; upgaze palsy (eyes deviate downward and medially — "peering at the nose"); may cause aphasia (dominant) or neglect (non-dominant) | Thalamus is the sensory relay; compression of midbrain tectum causes upgaze palsy; proximity to internal capsule causes motor deficits |
| Cerebellar | Occipital headache, vertigo, ataxia, nausea/vomiting, ipsilateral limb ataxia, nystagmus; can rapidly deteriorate → coma | Disruption of cerebellar circuits; proximity to 4th ventricle → obstruction → acute obstructive hydrocephalus; brainstem compression |
| Pontine (brainstem) | Rapid coma, quadriplegia, pinpoint pupils (bilateral), loss of horizontal eye movements, hyperthermia, abnormal breathing patterns; often fatal | Pons houses the reticular activating system (consciousness), corticospinal tracts bilaterally, sympathetic pupillary pathway (disrupted → miosis from unopposed parasympathetic), CN VI nuclei and PPRF (horizontal gaze) |
| Lobar | Depends on lobe: frontal (personality change, contralateral leg weakness), parietal (contralateral sensory loss, neglect), temporal (aphasia if dominant, visual field cut), occipital (contralateral homonymous hemianopia) | Direct destruction of cortical/subcortical tissue; lobar ICH more commonly from CAA or AVM rather than hypertension |
| Intraventricular | Rapidly obtunded, may have bilateral motor deficits | Blood in ventricles → acute obstructive hydrocephalus → raised ICP; irritation of ependyma |
- Hypertension — both a cause and a response (Cushing reflex if ICP is significantly raised).
- Contralateral hemiparesis/hemiplegia — UMN pattern (more common in deep hemorrhages disrupting the internal capsule).
- Conjugate eye deviation — toward the side of the lesion for supratentorial hemorrhages ("eyes look toward the lesion" in destructive supratentorial lesions).
- Signs of raised ICP: reduced GCS, Cushing's triad, papilledema, CN III or VI palsy (false localizing signs).
Distinguishing ICH from Ischemic Stroke Clinically
While imaging is required for definitive diagnosis, certain features favor ICH:
- More likely ICH: Sudden severe headache, vomiting at onset, rapid progression to coma, very high BP at presentation (SBP > 220), seizures at onset, reduced consciousness from the start.
- More likely ischemic: Maximal deficit at onset (then plateaus), history of AF or cardiac disease, prior TIAs in the same territory.
- However, you cannot reliably distinguish them clinically — urgent brain imaging is mandatory.
Raised ICP is clinically dangerous because: (1) Globally: decreased cerebral blood flow → cerebral ischemia; (2) Focally: pressure gradient across dural compartments → brain herniation → brainstem compression. [1]
| Symptom/Sign | Mechanism |
|---|---|
| Headache (worse in morning, with coughing/straining) | Stretching of pain-sensitive dura and blood vessels; worse in morning because recumbency → increased venous return to head → increased ICP |
| Nausea and vomiting (may be projectile) | Direct stimulation of the vomiting center in the area postrema (floor of 4th ventricle) |
| Papilledema | Raised ICP transmitted along the optic nerve sheath → compression of the central retinal vein → impaired axoplasmic flow → axonal swelling of the optic disc [11] |
| Transient visual obscurations (TVOs) | Fleeting monocular visual disturbance that clears within seconds — represents transient fluctuations in optic nerve head perfusion correlating with degree of ICP elevation [11] |
| CN VI palsy (bilateral) | CN VI has the longest intracranial course → most vulnerable to stretch from diffuse ICP elevation (false localizing sign) |
| CN III palsy ("surgical") | Uncal herniation → compression of CN III against the tentorial edge |
| Cushing's triad | Brainstem ischemia → sympathetic hypertension → baroreceptor-mediated bradycardia → irregular breathing |
| Decreased consciousness → coma | Compression of reticular activating system (brainstem) or global hypoperfusion |
Epidemiology: F > M — pregnancy, use of COC. ~1% of stroke. [3]
Clinical features (require high index of suspicion) [3]:
- S/S depends on site:
- Cerebral venous sinus thrombosis (90%): raised ICP (headache, papilledema, decreased GCS), seizure, focal neurological deficit
- Cavernous sinus thrombosis: proptosis, painful ophthalmoplegia, CN 3, 4, 6, V1 involvement
- Deep cerebral venous thrombosis (10%)
| Feature | EDH | SDH | SAH | ICH |
|---|---|---|---|---|
| Location | Between skull and dura | Between dura and arachnoid | Subarachnoid space | Brain parenchyma |
| Source | MMA (arterial 85%) | Bridging veins (venous) | Berry aneurysm (arterial) | Penetrating arteries (arterial) |
| CT shape | Biconvex/lentiform | Crescentic | Cisternal blood (star pattern) | Irregular intracerebral density |
| Crosses sutures | No | Yes | N/A | N/A |
| Crosses midline | Yes | No | N/A | N/A |
| Classic presentation | Lucid interval → rapid decline | Progressive (acute) or insidious (chronic) | Thunderclap headache + meningism | Sudden focal deficit + headache |
| Key risk factor | Temporal bone fracture | Elderly, atrophy, anticoagulants | Aneurysm, HTN, smoking | Hypertension (50–90%) |
High Yield Summary
Must-know points for intracranial hemorrhage:
- ICH is an umbrella term covering EDH, SDH, SAH, intracerebral hemorrhage, and IVH.
- Hemorrhagic stroke specifically = intracerebral hemorrhage + SAH = ~20% of all strokes.
- Mortality: SAH (50% at 1 month) > ICH (40% at 1 month) > cortical infarct > lacunar infarct.
- EDH: Arterial (MMA), lentiform, does NOT cross sutures, CAN cross midline, lucid interval, rapid deterioration, 75–90% associated with skull fracture.
- SDH: Venous (bridging veins), crescentic, crosses sutures, does NOT cross midline, chronic progressive course. Chronic SDH is a "reversible dementia" mimic in the elderly.
- SAH: "Thunderclap headache," aneurysmal until proven otherwise (if no trauma). Sentinel headache is a warning sign. Complications: rebleeding, vasospasm (day 4–14), hydrocephalus, hyponatremia (SIADH vs CSWS).
- Intracerebral hemorrhage: Hypertension is the #1 cause (50–90%). Deep sites (putamen, thalamus, pons, cerebellum) = hypertensive. Lobar = think CAA, AVM, tumor.
- Monro-Kellie doctrine: skull is rigid, contents (brain 80% + blood 10% + CSF 10%) must be balanced; expanding hematoma → exhausted compensation → raised ICP → herniation → death.
- CT appearance of blood changes with time: Acute = hyperdense, Subacute = isodense, Chronic = hypodense.
- If SAH suspected with history of trauma, ask: "Headache before or after LOC?" — to identify primary SAH causing the fall.
Active Recall - Intracranial Hemorrhage
[1] Senior notes: Ryan Ho Neurology.pdf (Section 3.2 Cerebrovascular Diseases, Section 8.1 Raised Intracranial Pressure, Section 11.4 Secondary Brain Injury) [2] Senior notes: felixlai.md (Epidural/Subdural/Subarachnoid hemorrhage sections, Etiology and Risk Factors of Stroke) [3] Senior notes: maxim.md (Intracerebral haemorrhage, Cerebral venous thrombosis) [4] Lecture slides: Cererbrovascular disease.pdf (p5–6: Intracerebral hemorrhage sites and etiology) [5] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p41–42: Intracranial Haemorrhages, EDH vs SDH comparison) [6] Senior notes: Ryan Ho Radiology.pdf (p19: Intracranial Haemorrhage, CT appearance, SDH) [7] Lecture slides: GC 109. Headache and loss of consciousness Acute stroke, subarachnoid haemorrhage and vascular malformation.pdf (p14: Causes of SAH, Cerebral Aneurysm) [8] Senior notes: Ryan Ho Neurology.pdf (p87–88: Cerebral Aneurysm, AVM, Vascular Malformations) [9] Senior notes: Ryan Ho Haemtology.pdf (p137: DIC causes including severe head injury; p130: VTE and ICH) [10] Senior notes: Ryan Ho Chemical Path.pdf (p10: SIADH vs CSWS) [11] Senior notes: Ryan Ho Opthalmology.pdf (p90: Papilloedema)
Differential Diagnosis of Intracranial Hemorrhage
The differential diagnosis of intracranial hemorrhage operates on two levels. First, you need to differentiate between the types of intracranial hemorrhage themselves (EDH vs SDH vs SAH vs ICH vs IVH) because their management differs dramatically. Second, you need to differentiate intracranial hemorrhage from conditions that mimic it — the "stroke mimics" and other causes of acute headache, focal neurological deficit, or reduced consciousness.
Let's think about this systematically. A patient presenting with an intracranial hemorrhage will typically have some combination of:
- Acute headache
- Focal neurological deficit
- Reduced consciousness
- Seizures
Each of these has its own differential. The art is in pattern recognition — which combination, with what tempo, and with what associated features.
This is the first-order differential: once you suspect intracranial hemorrhage, you need to identify which type. CT brain is the definitive answer, but clinically you can narrow it down.
| Feature | EDH | SDH | SAH | ICH |
|---|---|---|---|---|
| History | Significant trauma (temporal) | Trauma (may be minor/forgotten in elderly) | Sudden thunderclap headache ± trauma | Sudden focal deficit; often hypertensive |
| Onset | Minutes to hours (lucid interval) | Hours (acute) to weeks (chronic) | Instantaneous ("thunderclap") | Seconds to minutes, may progress over hours |
| Headache | Progressive, localised | Insidious (chronic) or acute | Sudden, severe: "worst headache of my life" [7] | Moderate; ~40–50% have headache |
| LOC pattern | Lucid interval → rapid decline | Fluctuating (chronic) or progressive (acute) | Sudden LOC at onset (50%) | Progressive obtundation |
| Meningism | Absent | Absent | Present (after 3–12 hours) [1] | Usually absent (unless IVH extension) |
| Focal deficit | Ipsilateral pupil dilation, contralateral hemiparesis | Subtle (chronic) or dramatic (acute) | May be present (depends on aneurysm site) | Prominent (depends on location) |
| Skull fracture | 75–90% associated [5][6] | Usually absent | Usually absent | Absent |
| CT shape | Biconvex/lentiform [5] | Crescentic [5] | Blood in basal cisterns ("star sign") | Irregular intraparenchymal hyperdensity |
Key Clinical Distinction: SAH vs ICH
The strongest clinical differentiator is meningism. SAH causes blood in the subarachnoid space → meningeal irritation → neck stiffness, photophobia, Kernig's/Brudzinski's signs. ICH, unless it ruptures into the ventricles or subarachnoid space, does NOT cause meningism. A sudden headache WITH meningism = SAH until proven otherwise.
B. Differentiating Intracranial Hemorrhage from Stroke Mimics
Consider differential diagnosis of stroke in history: Transient events (seizures, esp Todd's paralysis; migraine aura; syncope). Persistent events (brain tumours, SDH, cerebral abscess, encephalitis, MS, metabolic encephalopathy e.g. hypoglycemia). [1]
Clues: Nature — stroke/TIA invariably negative symptoms (loss of function). Extent — usually focal instead of global. Progression — rarely change in modality. Associating symptoms, e.g. headache in migraine. [1]
The differential diagnosis of intracranial hemorrhage can be organized by the dominant presenting feature:
This is the most common presentation of ICH. The key question is: Is this a stroke? If so, is it ischemic or hemorrhagic? You cannot reliably distinguish them clinically — imaging is mandatory [1][5].
| Category | Condition | Key Distinguishing Features | Why It Mimics ICH |
|---|---|---|---|
| Vascular | Ischaemic stroke | Maximal deficit at onset then plateaus; AF, cardiac disease; no headache (usually); CT: hypodense or normal acutely | Both cause sudden focal deficits; only CT distinguishes them |
| Vascular | Subdural hematoma [2] | Elderly, anticoagulants, insidious onset (chronic), fluctuating consciousness; crescentic on CT | Focal deficit + altered consciousness; chronic SDH mimics progressive ICH |
| Vascular | Cerebral venous sinus thrombosis (CVST) [3] | F > M; pregnancy, COC use; headache, seizures, raised ICP, focal deficits; CT may be normal; MR venogram shows filling defect ("empty delta sign") | Can cause venous infarction with hemorrhagic transformation → looks like ICH on CT |
| Vascular | Cervical arterial dissection [7] | Spontaneous (connective tissue disorder) or traumatic (fall, sports, chiropractic); ICA dissection → retroorbital pain, Horner's syndrome; VA dissection → occipital pain, vertebrobasilar symptoms; ischemia from arterial occlusion/embolism; dissecting aneurysm can rupture and cause SAH intracranially | Can cause ischemic stroke (embolism from dissection site) or SAH (if dissecting aneurysm ruptures intracranially) |
| Neoplastic | Brain tumour [2] | Subacute/chronic progression; constitutional symptoms (weight loss, malaise); papilloedema; may have hemorrhagic transformation (esp. GBM, metastases from melanoma, RCC) | Hemorrhage into a tumor can present acutely, mimicking primary ICH; look for surrounding edema and enhancement on CT/MRI |
| Infectious | Brain abscess [2] | Fever, raised inflammatory markers; subacute course; ring-enhancing lesion on contrast CT/MRI; history of ear/sinus infection, IE, immunosuppression | Focal deficit + headache + reduced consciousness; ring enhancement on CT distinguishes from ICH |
| Infectious | Encephalitis (viral, hypertensive, Wernicke) [2] | Fever, confusion, seizures; diffuse or temporal lobe involvement (HSV); Wernicke → ophthalmoplegia, ataxia, confusion (thiamine deficiency) | Altered consciousness + focal signs; but more diffuse and usually with fever |
| Demyelinating | Multiple sclerosis [2] | Young adults; relapsing-remitting course; MRI shows periventricular white matter lesions with different ages ("dissemination in time and space") | Acute relapse can cause sudden focal deficit; but usually subacute over days |
| Metabolic | Hypoglycemia [2] | On insulin/oral hypoglycemics; confusion, sweating, tremor; focal deficits can occur (hemiparesis!); rapidly reversible with glucose | A classic stroke mimic — always check blood glucose before attributing focal deficits to stroke |
| Epileptic | Seizure (Todd's paralysis) [1][2] | Postictal paresis: transient focal deficit following a seizure, typically lasting minutes to hours; history of seizure disorder; witnesses may describe seizure activity | Postictal hemiparesis can perfectly mimic stroke; ask about preceding seizure activity; EEG may help |
| Migraine | Hemiplegic migraine [2] | Migraine aura causing transient hemiparesis; gradual onset (over minutes, spreading), associated with typical migrainous headache, family history; fully reversible | Focal deficit + headache; but onset is gradual (spreading over minutes) vs sudden in ICH |
| Other | Syncope [2] | Transient LOC; usually global (not focal); rapid recovery; precipitants (standing, vagal triggers) | LOC can be confused with stroke if not witnessed properly |
The Golden Rule
Always check blood glucose in any patient presenting with acute focal neurological deficit. Hypoglycemia is the most easily reversible stroke mimic and is frequently missed. A BM stick takes 10 seconds and could save you from giving thrombolysis to a hypoglycemic patient.
When SAH is suspected (sudden thunderclap headache), you must differentiate it from other causes of acute headache. The lecture slides emphasize:
DDx of SAH includes meningitis [7]
| Category | Condition | Key Distinguishing Features |
|---|---|---|
| Vascular | SAH (aneurysmal) | Thunderclap onset, meningism (after 3–12h), subhyaloid hemorrhage on fundoscopy, CT shows basal cistern blood |
| Vascular | Intracerebral hemorrhage | Headache less dramatic than SAH, focal deficit dominates, no meningism (unless IVH/SAH extension), CT shows parenchymal blood |
| Vascular | Cervical arterial dissection [7] | ICA → retroorbital pain + Horner's; VA → occipital pain + vertebrobasilar symptoms; dissecting aneurysm can rupture → SAH |
| Vascular | CVST [3] | Progressive headache (not thunderclap), seizures, raised ICP signs; may have venous infarction |
| Vascular | Hypertensive crisis/encephalopathy | Severely elevated BP ( > 180/120), headache, confusion, visual changes, papilledema; no blood on CT |
| Vascular | Pituitary apoplexy [12] | Sudden headache + visual field defect (bitemporal hemianopia) + ophthalmoplegia; hemorrhage or infarction of pituitary adenoma |
| Infectious | Meningitis [7] | Fever, neck stiffness, photophobia, rash (meningococcal); subacute onset (hours to days, not instantaneous); LP shows elevated WCC, protein, low glucose |
| Primary headache | Crash migraine [12] | Sudden severe migraine without aura; diagnosis of exclusion after SAH ruled out |
| Primary headache | Cluster headache [12] | Severe unilateral periorbital pain, ipsilateral autonomic features (lacrimation, rhinorrhea, conjunctival injection); rapid onset but stereotyped attacks |
| Primary headache | Benign thunderclap headache | Sudden onset, resolves spontaneously; diagnosis of exclusion |
| Primary headache | Benign exertional/orgasmic headache [12] | Thunderclap triggered by exertion or orgasm; must exclude SAH first |
| Other | Acute glaucoma [12] | "Misting" of vision, halos, painful red eye, mid-dilated fixed pupil; raised intraocular pressure |
| Other | Intermittent hydrocephalus [12] | Positional headache, impaired consciousness, leg weakness |
Red flags for severe secondary headache causes: Systemic upset → CNS infections, neoplastic, vasculitis. Neurological symptoms → intracranial pathologies. New and sudden onset → temporal arteritis (if > 60y/o), secondary vascular (SAH, dissection, CVST, hypertensive crises) or non-vascular causes. Trauma → intracranial hematoma. Worse when supine, with exertion/cough → raised ICP. [1][12]
Large ICH, massive SAH, and large EDH/SDH can all cause coma. The differential includes:
| Condition | Key Features |
|---|---|
| Intracranial hemorrhage (any type) | Focal signs, asymmetric pupils, history of trauma or sudden headache |
| Large ischemic stroke | Focal signs, often AF; CT initially normal or subtle hypodensity |
| Status epilepticus | Witnessed convulsions or subtle motor activity; EEG diagnostic |
| Metabolic coma | Hypoglycemia, DKA, hepatic encephalopathy, uremia, drug overdose; usually bilateral, symmetric, no focal signs |
| CNS infection | Fever, meningism, rash; LP diagnostic |
| Diffuse axonal injury | Immediate coma post-trauma without lucid interval; CT may show petechial hemorrhages at grey-white junction |
Chronic SDH is the great mimic. Its insidious presentation overlaps with:
| Condition | How to Distinguish from Chronic SDH |
|---|---|
| Dementia (Alzheimer's, vascular) | Progressive over months-years, no fluctuation, no focal signs initially; MRI shows atrophy/white matter changes, NOT a crescentic collection |
| Normal pressure hydrocephalus (NPH) | Classic triad: gait apraxia, urinary incontinence, dementia ("wet, wobbly, wacky"); CT shows ventriculomegaly out of proportion to sulcal atrophy |
| Brain tumour | Progressive focal deficits; contrast CT/MRI shows enhancing mass |
| Depression/psychiatric | No focal neurological signs; normal CT |
When intracerebral hemorrhage is confirmed on CT, the next question is what caused it? The location and patient demographics are your strongest clues:
Indications for vascular imaging in ICH: suspected non-hypertensive etiology — No HTN, Age < 40–45, Atypical location, CT abnormality (mass, calcifications) [3]
| Feature | Hypertensive ICH | CAA | AVM | Tumour-related | Coagulopathy |
|---|---|---|---|---|---|
| Age | > 50 | > 65 | Young adults | Any age | Any (on anticoagulants) |
| Location | Deep: putamen, thalamus, pons, cerebellum [4] | Lobar (cortical/subcortical) | Often lobar | Often lobar; multiple if metastatic | Any location |
| HTN history | Yes | Variable | Usually no | Variable | Variable |
| Recurrence | At different deep sites | At different lobar sites | Same site | Same site (unless metastatic) | Variable |
| CT clues | Typical deep location | Lobar, multiple cortical microbleeds on MRI (GRE/SWI) | Calcifications, serpiginous vessels, contrast enhancement | Surrounding edema, ring enhancement | May be large, diffuse |
| Workup | Usually clinical diagnosis; no angiography needed | MRI with GRE/SWI for microbleeds | CTA/DSA/MRI showing flow voids [8] | Contrast CT/MRI | Coagulation studies |
Haemorrhagic stroke — deep vs. superficial — surgery in selected patients [7]
Lobar hemorrhage → commonly due to arteriovenous malformations (AVM). Most commonly in temporal lobe and frontal lobe. Diagnosis by contrast CT/CT angiogram or conventional angiography. [5]
E. Special Differentials Worth Highlighting
CVST deserves special mention because it is frequently missed and can present as intracranial hemorrhage (venous infarction with hemorrhagic transformation).
- Epidemiology: F > M — pregnancy, use of COC. ~1% of stroke. [3]
- Require high index of suspicion
- CT brain: can be normal
- MRI brain + MR venogram for filling defect; "empty delta sign" for SSS involvement [3]
- Think of CVST in: young woman + headache + seizures + hemorrhagic infarct in a non-arterial territory (crossing vascular boundaries).
- Spontaneous — connective tissue disorder
- Traumatic — fall, sports, chiropractic
- ICA — retroorbital pain, Horner's syndrome
- VA — occipital pain and vertebrobasilar symptoms
- Ischaemia from arterial occlusion or embolism
- Dissecting aneurysm can rupture and cause SAH intracranially
This is a differential both for ischemic stroke (embolism from the dissection flap) AND for SAH (if the dissection extends intracranially and ruptures). The clue is neck pain or facial pain preceding the neurological deficit, especially in a younger patient after neck manipulation or trauma.
- Ischaemia when young; haemorrhage when older [7]
- Progressive occlusion of the terminal ICA → development of fragile collaterals → "puff of smoke" on angiography
- In adults, the fragile collateral vessels can rupture → ICH (especially IVH or deep hemorrhage)
- Important differential in young Asian patients with ICH
- Clinical presentation: Haemorrhage (~3%/yr) — deep, IVH, lobar; seizure; ischaemia ("vascular steal"); headache; others — bruit, hydrocephalus, heart failure [8]
- In a young patient with lobar ICH or IVH, AVM should be near the top of your differential
| Scenario | Top Differentials |
|---|---|
| Acute focal deficit + headache + HTN | ICH (hypertensive), ischemic stroke, hypertensive encephalopathy |
| Lucid interval → rapid deterioration post-trauma | EDH (arterial), acute SDH |
| Elderly + progressive confusion + mild focal signs | Chronic SDH, NPH, brain tumour, dementia |
| Thunderclap headache + meningism | SAH (aneurysmal), meningitis, CVST (less acute), cervical dissection |
| Young patient + lobar ICH | AVM, CVST, drugs (cocaine/amphetamines), Moyamoya, coagulopathy, tumour |
| Elderly + lobar ICH + no HTN | CAA, tumour (hemorrhagic metastasis), coagulopathy (anticoagulant-related) |
| Young woman + headache + seizures + hemorrhagic infarct | CVST |
| Focal deficit after seizure | Todd's paralysis (postictal), ICH causing seizure, CVST |
| Sudden deficit + low GCS + diabetes | ICH vs hypoglycemia — check glucose first |
High Yield Summary — Differential Diagnosis
- First step in any acute focal deficit: check blood glucose. Hypoglycemia is the most reversible mimic.
- Second step: urgent CT brain — this is the only reliable way to distinguish hemorrhagic from ischemic stroke.
- Stroke/TIA features are invariably "negative" (loss of function). If "positive" features (seizures, visual scintillations), consider alternatives [1].
- Meningism distinguishes SAH from other types of ICH and from ischemic stroke.
- SAH DDx includes meningitis [7] — both cause headache + meningism + photophobia; fever and subacute onset favor meningitis; instantaneous thunderclap onset favors SAH.
- Location of ICH on CT determines etiology: deep = hypertensive; lobar = CAA/AVM/tumour; think vascular imaging if young, no HTN, or atypical location [3].
- CVST is the great masquerader — can present as headache, raised ICP, seizures, or hemorrhagic infarct. Think of it in young women on OCP/pregnant. CT can be normal [3].
- Cervical arterial dissection can cause both ischemic stroke (embolism) and SAH (intracranial rupture) [7].
- Chronic SDH mimics dementia, NPH, and brain tumour in the elderly — always CT in new-onset cognitive decline.
- Sudden headache and LOC is cerebrovascular in origin until proven otherwise [7].
Active Recall - Differential Diagnosis of Intracranial Hemorrhage
References
[1] Senior notes: Ryan Ho Neurology.pdf (Section 3.2: Cerebrovascular Diseases — Evaluation of Stroke, differential diagnosis, Section 8.1: Raised ICP) [2] Senior notes: felixlai.md (Epidural/Subdural/Subarachnoid hemorrhage, Differential diagnosis of stroke) [3] Senior notes: maxim.md (Intracerebral haemorrhage, Cerebral venous thrombosis) [4] Lecture slides: Cererbrovascular disease.pdf (p5: ICH locations) [5] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p40–42: Diagnosis of stroke, Intracranial haemorrhages) [6] Senior notes: Ryan Ho Radiology.pdf (p17–19: Acute headache imaging, intracranial haemorrhage) [7] Lecture slides: GC 109. Headache and loss of consciousness Acute stroke, subarachnoid haemorrhage and vascular malformation.pdf (p14: Causes of SAH; p16: SAH presentation and DDx meningitis; p23: AVM features; p25: Cervical arterial dissection; p25: Key messages) [8] Senior notes: Ryan Ho Neurology.pdf (p87–88: Cerebral Aneurysm, AVM, Moyamoya) [11] Senior notes: Ryan Ho Opthalmology.pdf (p90: Papilloedema) [12] Senior notes: Ryan Ho Fundamentals.pdf (p313: Red flags for headache) and Ryan Ho Neurology.pdf (p58–60: Headache differentials)
Diagnostic Criteria, Algorithm, and Investigations for Intracranial Hemorrhage
Let me be blunt: there are no validated clinical diagnostic criteria that can reliably distinguish intracranial hemorrhage types from each other or from ischemic stroke at the bedside. The diagnosis of intracranial hemorrhage is fundamentally a neuroimaging diagnosis. Clinical features raise suspicion, but the CT scan (or MRI) gives you the answer.
This is why every guideline worldwide states:
Neuroimaging (CT/MRI) is essential for all stroke patients for confirmation of diagnosis [1]. Non-contrast CT brain is the mainstay of imaging in acute stroke — it allows differentiation of ischaemic and haemorrhagic stroke [5].
The clinical approach therefore has two phases:
- Recognize the clinical syndrome → suspect intracranial hemorrhage
- Image urgently → confirm the type, location, and extent → guide management
B. When to Image: Clinical Decision Rules
Not every patient with a headache or minor bump needs a CT. But every patient with a suspected stroke or significant head injury does. Decision rules help in the trauma setting (minor head injury) to decide who needs a CT.
This applies to minor head injury patients with GCS 13–15 who have witnessed LOC, amnesia, or confusion.
Exclusion criteria (if any present → CT is recommended regardless, as risk is already high):
- ED GCS < 13
- Obvious penetrating skull injury or depressed skull fracture
- Unstable vital signs associated with major trauma
- Focal neurological deficit
- Seizure prior to assessment in ED
- Bleeding disorders or use of oral anticoagulants
High risk for neurosurgical intervention (any one → CT recommended):
- Age ≥ 65 years old
- Vomiting ≥ 2 episodes
- GCS < 15 at 2 hours after injury
- Suspected open or depressed skull fracture
- Any signs of basal skull fracture (raccoon eyes, Battle's sign, CSF otorrhea/rhinorrhea, hemotympanum)
Medium risk for brain injury on CT (consider CT):
- Amnesia before impact ≥ 30 minutes
- Dangerous mechanism (pedestrian struck by motor vehicle, ejected from vehicle, fall from height > 3 feet or 5 stairs)
For patients with GCS 15/15 after traumatic brain injury — CT is indicated if any of:
- Headache
- Vomiting
- Age > 60
- Drug or alcohol intoxication
- Persistent antegrade amnesia
- Seizure
- Visible trauma above the clavicle
Clinical Pearl
The Canadian CT Head Rules are more specific (fewer unnecessary CTs) while the New Orleans Criteria are more sensitive (catch more pathology but more scans). In practice, if there is any clinical doubt after a head injury, the threshold to CT should be low — the radiation dose of a single head CT is modest, and missing an EDH can be fatal.
For spontaneous (non-traumatic) presentations — there are no formal "decision rules" like CCHR. Instead, any patient with suspected stroke gets an urgent CT brain. Period. The time-sensitivity of stroke management (thrombolysis window < 4.5 hours) means imaging must happen within minutes of arrival.
Specifically, CT brain is mandatory before any thrombolysis to exclude hemorrhage [2][5].
D. Investigation Modalities — Detailed
This is the single most important investigation for intracranial hemorrhage [1][2][5][13].
Why NCCT first?
- Speed: Takes ~1 minute. In a stroke emergency, time is brain (2 million neurons die per minute in ischemia).
- Availability: Available 24/7 in virtually all EDs.
- Sensitivity for acute hemorrhage: excellent (approaching 100% within 12 hours of onset for ICH) [5]. Fresh blood is hyperdense on CT because of the high protein content of hemoglobin.
- Primary role: Exclude hemorrhage before thrombolytic/antiplatelet therapy [5][6].
CT Appearance of Blood Over Time [5][6][14]:
| Time | CT Density | Explanation | Clinical Relevance |
|---|---|---|---|
| Acute (days) | Hyperdense (white) | Due to protein-Hb product; high attenuation | Easy to see; most hemorrhages diagnosed here |
| Subacute (few days to 2 weeks) | Isodense | Degradation of protein-Hb product; evolves peripherally to centrally | Difficult to visualize — should do CT ASAP after injury (or use contrast CT) [5] |
| Chronic ( > 2 weeks) | Hypodense (dark) | Completely degraded blood products | May mimic CSF or hygroma; can be confused with old infarct |
Attenuation of blood on CT changes with time: Acute = hyperdense, Subacute = isodense, Chronic = hypodense [5]
Exam Point
Subacute SDH (1–3 weeks) is isodense and can be extremely difficult to see on NCCT! [5] If you have strong clinical suspicion for SDH but the CT looks "normal," look carefully for: (1) effacement of sulci on one side, (2) midline shift without a visible lesion, (3) "white matter buckling sign." Consider contrast CT or MRI.
CT may not be hyperdense if Hct is low [6] — in a severely anemic patient, acute blood may appear isodense rather than hyperdense because there is less hemoglobin to generate the high attenuation signal.
Key CT Findings by Type:
| Type | CT Finding | Additional Features |
|---|---|---|
| EDH | Biconvex (lentiform) hyperdensity between skull and dura; does NOT cross sutures [5] | 75% associated with skull fracture [5]; look at bone window |
| SDH | Crescentic hyperdensity (acute), isodensity (subacute), or hypodensity (chronic) that crosses sutures but NOT the midline [5] | Mixed density in acute-on-chronic; look for midline shift |
| SAH | Hyperdensity in basal cisterns, Sylvian fissures, interhemispheric fissure — "star sign" [1] | Sulcal hyperdensity is usually traumatic [1]; may miss small bleeds |
| ICH | Irregular hyperdensity within brain parenchyma | Note location (deep vs lobar), size, IVH extension, mass effect, midline shift |
| IVH | Hyperdensity within ventricles; dependent layering | Assess for hydrocephalus (temporal horn dilation is an early sign) |
Urgent NCCT brain: assess size and location of haematoma, any IVH/hydrocephalus, any mass effect [3]
Sensitivity limitations:
- CT sensitivity for ischaemic stroke: < 1 day only 48% → 10–11 days 74%. Sensitivity increases with time after infarct [5]
- CT sensitivity for SAH: ~98% within 6 hours, ~93% at 24 hours, drops significantly after 3–5 days — this is why LP is needed if CT is negative but SAH is clinically suspected.
MRI Blood Appearance Mnemonic [14]:
| Time | CT | MRI T1 | MRI T2 |
|---|---|---|---|
| Acute ( < 72h) | Hyper | Grey (iso) | Black (hypo) |
| Subacute ( < 3 weeks) | Iso | White (hyper) | White (hyper) |
| Chronic ( > 3 weeks) | Hypo | Black (hypo) | Black (hypo) |
Memory aid: MRI T1 = "George Washington Bridge" (Grey → White → Black); MRI T2 = "Oreo cookie" (Black → White → Black) [14]
-
Principle: Rapid injection of a large IV bolus of contrast to opacify vessels for CT imaging [5].
-
Can be used in place of more invasive conventional angiography [5].
-
When to use in ICH:
- SAH: to identify the source aneurysm — CTA is first-line vascular imaging after NCCT confirms SAH [1]
- ICH: when non-hypertensive etiology is suspected [3] — indications:
- No HTN
- Age < 40–45
- Atypical location (lobar in young patient)
- CT abnormality: mass, calcifications
- AVM diagnosis: contrast CT/CT angiogram or conventional angiography [5]
-
Key findings:
- Aneurysm: Outpouching from an arterial bifurcation; size, neck width, and relationship to parent vessel determine treatment approach.
- AVM: Tangle of abnormal vessels ("nidus") with enlarged feeding arteries and early-draining veins.
- "Spot sign": Active contrast extravasation within the hematoma on CTA — indicates ongoing active bleeding and predicts hematoma expansion. This is a critical prognostic sign.
- Dissection: Intimal flap, double lumen, or tapered occlusion.
-
Advantages over DSA: Non-invasive, fast (can be done immediately after NCCT), widely available.
-
Limitations: Less spatial resolution than DSA; may miss very small aneurysms ( < 3 mm).
LP — only if CT negative [7]
Why LP after negative CT for SAH? CT sensitivity for SAH drops after the first 12–24 hours. If the CT is done late or the bleed is very small, CT can be false-negative. LP detects blood/blood breakdown products in CSF that CT might miss.
Timing: Wait at least 12 hours after headache onset before LP — this allows time for hemoglobin to break down to bilirubin (xanthochromia). If done too early, you cannot distinguish traumatic tap from SAH.
Key findings:
| Finding | SAH | Traumatic Tap |
|---|---|---|
| 3-bottle test | Uniformly blood-stained CSF in all 3 tubes (no clearing) | Blood clears progressively from tube 1 to tube 3 |
| Xanthochromia | Present (yellow discoloration of supernatant after centrifugation — due to bilirubin from hemoglobin breakdown); appears after several hours [7] | Absent (blood is fresh, no time for breakdown) |
| Opening pressure | Often elevated | Normal |
| RBC count | Consistent across tubes | Decreasing across tubes |
SAH vs traumatic tap: 3-bottle test; xanthochromia after several hours [7]
- Spectrophotometry for xanthochromia (detecting bilirubin and oxyhemoglobin peaks) is more sensitive than visual inspection alone and is the recommended method.
Must Know
Clinical suspicion + CT negative → LP is mandatory to rule out SAH [7]. A negative CT does NOT rule out SAH, especially if performed > 12 hours after onset. However, a negative CT + negative LP (no xanthochromia at > 12 hours) effectively excludes SAH.
- More sensitive than CT except in acute haemorrhage, bony lesions, and calcific lesions [6]
- Better than CT especially in the first few hours for ischaemic stroke [5]
When to use MRI in intracranial hemorrhage:
| Indication | Rationale |
|---|---|
| Subacute/chronic SDH not clearly seen on CT | MRI is far more sensitive for isodense/chronic collections [2] |
| Suspected underlying lesion (tumour, AVM, cavernoma) | MRI shows soft tissue detail, enhancement, and hemosiderin |
| CAA diagnosis | Gradient-recalled echo (GRE) / Susceptibility-weighted imaging (SWI) sequences detect cortical microbleeds — pathognomonic for CAA |
| CVST | MRI brain + MR venogram for filling defect; "empty delta sign" for SSS involvement [3] |
| Brainstem/cerebellar strokes | MRI more sensitive for posterior fossa lesions [1] |
| DWI for ischaemia | Restricted diffusion on DWI detects ischaemia within minutes [5] |
| SAH (false-negative at acute stage) | MRI can be false-negative at acute stage [7] — CT is preferred acutely |
Key MRI sequences and what they show:
| Sequence | What It Detects | Clinical Use |
|---|---|---|
| T1-weighted | Subacute blood (bright), anatomy | Subacute hemorrhage, structural detail |
| T2-weighted | Edema (bright), chronic blood (dark) | Perilesional edema, chronic hemosiderin |
| FLAIR | Suppresses CSF signal; subarachnoid blood and edema remain bright | SAH detection (more sensitive than CT after 24h), perilesional edema |
| DWI | Restricted diffusion in ischaemia (bright within minutes) [5] | Distinguishing ischemic from hemorrhagic stroke, peri-hematomal ischemia |
| GRE / SWI | Hemosiderin deposits (dark "blooming" artifacts) | Microbleeds in CAA, chronic hemorrhage, cavernous malformations ("popcorn" appearance with hemosiderin ring) |
| MR Venography | Venous sinus patency | CVST — filling defects, "empty delta sign" [3] |
| MRA | Arterial anatomy | Aneurysms, stenosis, dissection; screening tool |
CT vs MRI — Comparison [5]:
| Feature | CT | MRI |
|---|---|---|
| Radiation | Yes | No |
| Examination time | 1 min | 20 min |
| Availability | Good | Fair |
| Sensitivity for infarct | Poor (acutely) | Good |
| Sensitivity for haemorrhage | Good (acute) | Good (GRE/SWI for chronic) |
DSA is the gold-standard for cerebral vessel abnormalities [1][15]
- Principle: Fluoroscopy with catheterization angiography → digital reversal of first film superimposed on subsequent films → better delineation of blood vessels [15]
- Types: Carotid angiography, vertebral angiography
When to use DSA:
- SAH with negative CTA — DSA has the highest spatial resolution and can detect small aneurysms ( < 3 mm) that CTA misses.
- AVM characterization — DSA shows the feeding arteries, nidus, and draining veins dynamically, which is essential for surgical/endovascular planning.
- Therapeutic (endovascular): Coiling for aneurysms, mechanical thrombectomy for CVA [15].
Risks [15]:
- Permanent neurological complication < 1%, transient < 3%
- Vessel damage (pseudoaneurysm formation)
- Contrast-related (anaphylaxis, renal failure)
- Access site complications (groin hematoma)
- Non-target embolization, arterial thrombosis/dissection, ICH, CN trauma (for endovascular procedures)
Diagnostic role of conventional angiography is diminishing as it is relatively invasive. CT or MR angiography commonly used for diagnostic purposes and guide further interventions via conventional angiography [5]
- Extracranial duplex USG: visualizes atherosclerotic plaques, clots, and degree of stenosis [15]
- Use: evaluation of carotid and vertebral atherosclerosis (relevant for ischemic stroke workup)
- Transcranial Doppler (TCD): assesses basal segments of major cerebral arteries [15]
- Use: Assess intracranial atherosclerosis, assess post-SAH vasospasm, monitor microembolic signals [15]
- In SAH: daily TCD monitoring for vasospasm — increasing mean flow velocities ( > 120 cm/s in MCA) indicate developing vasospasm.
These are not diagnostic for the hemorrhage itself but are essential for identifying the cause, assessing complications, and guiding management.
| Investigation | Rationale |
|---|---|
| CBC | Polycythemia (RF for stroke); thrombocytopenia (bleeding risk); anemia (may affect CT density) [1] |
| Clotting profile (PT/INR, aPTT) and platelet count | Essential for ICH — identify coagulopathy; guide reversal therapy [1] |
| Blood glucose | Exclude hypoglycemia as stroke mimic; DM as RF [1]. Contraindication to thrombolysis if < 2.8 mmol/L [2] |
| Renal function (U&E, Cr) | Baseline for contrast use; hyponatremia (SIADH/CSWS) post-SAH |
| Liver function | Coagulopathy from liver disease (important in alcoholics with SDH) |
| Lipid profile | Atherosclerotic RF assessment |
| ESR ± autoimmune markers | Vasculitis as cause of ICH [1] |
| Group and screen / crossmatch | In case of surgical intervention |
| Toxicology screen | Cocaine, amphetamines (if suspected drug-related ICH) |
| Fibrinogen level | If on thrombolytics and ICH complication develops; DIC screening |
| Thrombophilia screen | If CVST suspected (protein C/S, antithrombin III, factor V Leiden, antiphospholipid antibodies) |
- For cardiac abnormalities (e.g., AF) — identifying cardioembolic source if ischemic stroke is in the differential.
- SAH can cause ECG changes that mimic acute coronary syndrome: ST changes, T-wave inversion, prolonged QT, prominent U waves — these are due to massive catecholamine release (sympathetic storm) causing myocardial injury. Do not be fooled into treating for ACS.
- Use of contrast CT to estimate perfusion map of brain tissues [5]
- Differentiates irreversible infarct core from reversible penumbra [5]
- More relevant to ischemic stroke (selecting candidates for thrombectomy beyond standard time windows) than primary ICH.
- In ICH, can show peri-hematomal hypoperfusion.
| Type | First-Line | Second-Line | Additional |
|---|---|---|---|
| EDH | NCCT brain (+ bone windows for fracture) | — | C-spine imaging if trauma |
| Acute SDH | NCCT brain | MRI if subacute/chronic SDH suspected but CT unclear | Coagulation studies (esp. if on anticoagulants) |
| SAH | NCCT brain → if positive: CTA → if CTA negative: DSA | If CT negative: LP (xanthochromia after 12h) [7] → if LP positive: CTA/DSA | TCD for vasospasm monitoring; daily electrolytes for SIADH/CSWS |
| ICH (hypertensive) | NCCT brain; bloods (clotting, CBC, glucose) | Usually no vascular imaging needed if typical site + known HTN | Monitor for hematoma expansion (repeat CT) |
| ICH (non-hypertensive / atypical) | NCCT brain → CTA or MRA | DSA if CTA/MRA negative; MRI with GRE/SWI for CAA/cavernoma | Consider contrast MRI if tumour suspected |
| CVST | NCCT (may be normal) → MRI + MR venogram | DSA if MRV equivocal | Thrombophilia screen |
When intracranial hemorrhage is managed conservatively or in the ICU, ICP monitoring becomes critical.
Indications for ICP monitoring: (1) No reliable clinical monitoring (e.g., sedation, muscle paralysis — these render GCS = 3); (2) GCS ≤ 8 (usually require sedation for intubation → V score becomes "VT"); (3) Likely evolving conditions [1]
Methods [1]:
- External ventricular drain (EVD): gold standard — provides both ICP monitoring AND therapeutic CSF drainage. Problem: risk of infection.
- Other: Intraparenchymal transducers, subarachnoid bolts.
Interpretation [1]:
- Normal mean ICP = 5–15 cmH2O in adults
- Definitely abnormal if > 20 cmH2O → suggests evolving pathology → repeat imaging or escalate treatment
This is not a single "test" but a critical component of monitoring. Documented at regular intervals (e.g., every 15 min → hourly → 2-hourly depending on clinical stability).
Components:
- GCS (Eye, Verbal, Motor) — M-scale is considered most prognostically significant [1]
- Pupil size and reactivity — asymmetry indicates impending herniation
- Limb movements — new weakness suggests evolving pathology
- Vital signs — BP, HR, RR, temperature, SpO2
- Cushing's triad monitoring (hypertension, bradycardia, irregular breathing)
Close neuro-observation as patient's condition can deteriorate rapidly [13]
| Scenario | Key Investigation | Must-Know Findings |
|---|---|---|
| Acute stroke | NCCT brain | Exclude hemorrhage before thrombolysis; hyperdense lesion = hemorrhage |
| SAH suspected, CT positive | CTA | Identify aneurysm (site, size, morphology) |
| SAH suspected, CT negative | LP after 12 hours | Xanthochromia = SAH; 3-bottle test to distinguish from traumatic tap [7] |
| Lobar ICH in young patient | CTA/DSA | AVM, aneurysm, tumour |
| Lobar ICH in elderly, no HTN | MRI with GRE/SWI | Cortical microbleeds = CAA |
| Post-SAH monitoring | Daily TCD | MCA velocity > 120 cm/s suggests vasospasm |
| Suspected CVST | MRI + MRV | Filling defect; "empty delta sign" [3] |
| Minor head injury | Apply CCHR | High-risk features → CT; medium-risk → observe ± CT |
High Yield Summary — Diagnostics
- NCCT brain is the single most important investigation — fast, available, excellent for acute blood.
- CT appearance of blood evolves: Acute = hyperdense → Subacute = isodense (DANGER: can miss SDH!) → Chronic = hypodense.
- MRI T1 blood mnemonic: "George Washington Bridge" (Grey → White → Black). T2: "Oreo" (Black → White → Black).
- For SAH: CT first → if negative, LP for xanthochromia (must wait > 12 hours). CT negative does NOT exclude SAH [7].
- CTA is first-line vascular imaging after confirmed SAH to find the aneurysm. DSA is the gold standard but more invasive [15].
- Indications for vascular imaging in ICH: no HTN, age < 40–45, atypical location, CT abnormality (mass, calcifications) [3].
- "Spot sign" on CTA = active contrast extravasation = ongoing bleeding = poor prognosis and hematoma expansion.
- CVST: CT can be normal; MRI + MR venogram is diagnostic (empty delta sign) [3].
- GRE/SWI on MRI detects old microbleeds — essential for diagnosing CAA and cavernous malformations.
- Canadian CT Head Rules stratify minor head injury patients for CT; high-risk criteria include age ≥ 65, vomiting ≥ 2, GCS < 15 at 2h, suspected skull fracture, basal skull fracture signs [2][13].
Active Recall - Diagnostics of Intracranial Hemorrhage
References
[1] Senior notes: Ryan Ho Neurology.pdf (Section 3.2: Cerebrovascular Diseases — Evaluation, Ix; Section 8.1: Raised ICP; Section 11.1: Approach to Head Injuries; Section 11.3: SDH, Traumatic SAH; p36: Cerebral Vascular Imaging) [2] Senior notes: felixlai.md (Neuroimaging section, Canadian CT Head Rules, NOC, Diagnosis of EDH/SDH, Thrombolysis contraindications) [3] Senior notes: maxim.md (ICH investigations, CVST investigations) [5] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p40–43: CT in stroke, Intracranial haemorrhages, CT angiography, CT perfusion; p50: MRI in stroke) [6] Senior notes: Ryan Ho Radiology.pdf (p19: CT appearance of blood, SDH) [7] Lecture slides: GC 109. Headache and loss of consciousness Acute stroke, subarachnoid haemorrhage and vascular malformation.pdf (p16: Diagnosis of SAH — CT, LP, xanthochromia, 3-bottle test, MRI false-negative) [11] Senior notes: Ryan Ho Opthalmology.pdf (p90: Papilloedema) [13] Senior notes: Ryan Ho Fundamentals.pdf (p337: Head Injuries approach, NECT, Canadian CT rules; p475: Cerebral Vascular Imaging) [14] Senior notes: maxim.md (CT and MRI appearance of blood over time table) [15] Senior notes: Ryan Ho Neurology.pdf (p36: DSA, CTA, MRA, Duplex USG) and Ryan Ho Fundamentals.pdf (p475: Cerebral Vascular Imaging)
Management of Intracranial Hemorrhage
Before diving into specific management for each type, let's establish the fundamental philosophy. The lecture slides state it perfectly:
The Fundamentals: Protect uninjured brain. Salvage injured brain. Treat underlying cause. ALWAYS resuscitate first. Clinical/ICP monitoring. Control ICP and maintain cerebral perfusion. Neuroprotective therapies. [16]
Think of it this way: in intracranial hemorrhage, the primary injury (the hemorrhage itself) has already happened — you cannot undo it. Your entire management strategy is aimed at preventing secondary injury — the cascade of events (hematoma expansion, cerebral edema, raised ICP, herniation, ischemia, rebleeding, vasospasm) that turns a survivable bleed into a fatal one.
The management framework for ALL types of intracranial hemorrhage shares common elements:
- ABC resuscitation — always first
- Stop the bleeding — reverse coagulopathy, control BP, secure aneurysm
- Control ICP — medical and surgical
- Prevent complications — rebleeding, vasospasm, hydrocephalus, seizures, DVT, infections
- Rehabilitation — early and multidisciplinary
Corticosteroids are NOT indicated and should be avoided following head injury since they are associated with increased acute mortality [2][13] — This was definitively shown in the CRASH trial.
Do NOT List (Head Injury / ICH)
- Give mannitol if shocked (it is an osmotic diuretic — will worsen hypotension)
- Blindly hyperventilate (PaCO2 30–35 mmHg causes vasoconstriction → may exacerbate ischemia)
- Use barbiturate/propofol outside ICU (risk of cardiovascular collapse)
- Give steroids (not effective for TBI or hemorrhagic stroke; contraindicated — CRASH trial)
Before discussing operations, clarify three terms that come up constantly:
| Term | Definition | When Used |
|---|---|---|
| Craniotomy | With return of bone flap — a section of skull is removed, the procedure performed, and the bone is replaced | Hematoma evacuation, aneurysm clipping |
| Craniectomy | Without return of bone flap — bone is left out to allow space for brain swelling | Decompressive surgery for malignant edema |
| Burr hole | Creation of a small hole through the skull for drainage | Chronic SDH drainage, EVD insertion |
D. General Management (All Types)
Airway support and ventilatory assistance are recommended for patients with acute stroke who have decreased consciousness or bulbar dysfunction causing airway compromise [2]
- Airway: Secure airway if GCS ≤ 8 (patient cannot protect airway). Endotracheal intubation with rapid sequence induction. Endotracheal intubation for airway protection (± early tracheostomy for better bronchial toileting) [3]
- Breathing: Supplemental oxygen to maintain SaO2 > 94%. Supplemental oxygen is NOT recommended in non-hypoxic patients [2] — because hyperoxia may paradoxically worsen oxidative stress in injured brain.
- Target: SpO2 > 97%, PaO2 > 9 kPa, PCO2 4.5–5 kPa [3]
- Circulation: IV access, fluid resuscitation if hypotensive. Avoid hypotension at all costs — remember CPP = MAP – ICP; if MAP drops, CPP drops, and the brain suffers.
BP management is one of the most critical decisions in ICH. The logic:
- Too high BP → promotes hematoma expansion, ongoing bleeding
- Too low BP → reduces cerebral perfusion pressure → ischemia
For Intracerebral Hemorrhage:
Patients with SBP between 150–220 mmHg and without contraindication to acute BP treatment: acute lowering of SBP to 140 mmHg is safe [2]
Patients with SBP > 220 mmHg: consider aggressive reduction of BP with continuous IV drug infusion and close BP monitoring [2]
Conservative management of putaminal ICH: Airway, breathing, circulation. Control ICP — head up, mannitol, glycerol. Control hypertension — target < 140 mmHg — prevent rebleeding [4]
- BP lowering agents: IV labetalol / nicardipine / hydralazine [2]
- IV labetalol: for adequate cerebral perfusion and to reduce risk of bleeding [3]
- Treat if SBP > 150 (unless evidence of increased ICP). Target SBP < 140, but avoid rapid BP reduction (renal complications) [3]
Why labetalol? It is a combined alpha-1 and beta-adrenergic blocker. The alpha blockade reduces peripheral vascular resistance (lowering BP), while the beta blockade prevents reflex tachycardia. It is titratable IV and does not significantly affect cerebral blood flow — ideal for neurological emergencies.
For SAH:
This is urgent — every minute of ongoing anticoagulation allows the hematoma to expand.
Discontinuation of medication + reversal of antithrombotic agents is indicated if ICH is present or suspected [2]
| Anticoagulant | Reversal Agent | Key Points |
|---|---|---|
| Warfarin | IV Vitamin K + 4-factor PCC (preferred) or FFP | PCC is recommended over FFP — fewer complications, corrects INR more rapidly [2][1]. PCC C/I in active thrombosis/DIC; 1% risk of thrombosis [2]. Dose: Vitamin K1 5–10mg IV + PCC 25–50 U/kg [1]. rFVIIa is NOT recommended — does not replace all clotting factors [2] |
| Unfractionated / LMW heparin | Protamine sulphate | Fully reverses UFH; only partially reverses LMWH (~60% of anti-Xa activity) |
| Dabigatran (direct thrombin inhibitor) | Idarucizumab (specific reversal agent) / FEIBA / PCC / rFVIIa | Idarucizumab is the specific antidote for dabigatran [2]. Hemodialysis can be considered for dabigatran (as it is partially dialyzable) [2]. Activated charcoal if last dose < 2h [2] |
| Factor Xa inhibitors (rivaroxaban, apixaban) | Andexanet alfa (specific) / FEIBA / PCC / rFVIIa | PCC recommended over rFVIIa (lower thrombotic risk) [2]. Andexanet alfa (2025 guidelines) is the specific reversal agent. Activated charcoal if last dose < 2h [2] |
| Antiplatelets | Platelet transfusion (?) | Usefulness of platelet transfusion in patients with antiplatelet use is uncertain [2] — the PATCH trial showed platelet transfusion may actually worsen outcomes in ICH. Generally not recommended routinely. |
| Thrombolytics (rtPA) | Cryoprecipitate + Tranexamic acid / Aminocaproic acid | Cryoprecipitate contains Factor VIII and fibrinogen [2] |
FEIBA = Factor VIII Inhibitor Bypassing Activity [2] — a prothrombin complex concentrate containing activated factors that bypasses the need for Factor VIII.
Do NOT give tranexamic acid together with PCC [1] (increased thrombotic risk when combined)
PCC vs FFP — Why PCC Wins
PCC (Prothrombin Complex Concentrate) contains concentrated factors II, VII, IX, X in a small volume (~20–40 mL). FFP contains all clotting factors but requires 4–6 units (~1000–1500 mL). PCC reverses warfarin effect much faster than FFP and has decreased preparation/infusion time and decreased volume [1]. In ICH, where every minute of bleeding matters and volume overload worsens ICP, PCC is clearly superior. However, PCC carries a ~1% risk of thrombosis [1][2].
Principles of management of raised ICP: Control ICP and maintain cerebral perfusion [16]
| Intervention | Mechanism | Key Details |
|---|---|---|
| Head elevation 30° | Increases venous drainage from the head → decreases intracranial blood volume → lowers ICP [1][3] | Also loosen any constraints around neck (avoid jugular vein compression) [3] |
| IV Mannitol | Osmotic diuretic — draws free water out of brain tissue into circulation to be excreted by kidneys [2]. Onset 15 min, duration 6h [2][13] | Bolus 0.25–1 g/kg [13]. Requires Foley catheter [2]. Avoid if hypernatremia, osmolarity > 320–340 mmol/L, hypovolemia, congestive heart failure, or renal failure [2][13]. Do NOT give mannitol if shocked [13] |
| Hypertonic saline (3% or 23.4%) | Similar osmotic effect; may be used as alternative to mannitol | Advantage: does not cause hypovolemia (unlike mannitol). Monitor serum Na (target < 155 mEq/L) |
| Hyperventilation | Lowers PaCO2 → cerebral vasoconstriction → decreases intracranial blood volume → lowers ICP [2]. Respiratory alkalosis buffers post-injury acidosis [2] | Target PaCO2 30–35 mmHg [13]. Short-term measure only — rapid onset (1 min) but NOT for first 24h of head injury [13]. Must taper back gradually to avoid rebound effect [2]. Excessive vasoconstriction can worsen ischemia [2] |
| Sedation and paralysis | Reduces metabolic demand of brain → decreases cerebral blood flow demand → lowers ICP [3] | Used in ventilated patients in ICU; renders GCS unreliable → need invasive ICP monitoring |
| Barbiturate coma (pentobarbital) | Reduces cerebral metabolism → decreases demand for CBF → lowers ICP; also alters vascular tone and inhibits free radical lipid peroxidation [2] | Last resort — risk of hypotension, infection, electrolyte disturbances [13]. Only use in ICU |
| CSF drainage via EVD | Directly removes CSF → reduces CSF volume → lowers ICP [1][16] | EVD is the gold standard for ICP monitoring + allows therapeutic drainage [1][16] |
| Frusemide | May reduce CSF formation; synergistic with mannitol [3] | Used as adjunct |
Corticosteroids: Indicated in increased ICP due to CNS infections and brain tumours. AVOIDED in patients with cerebral infarction, hemorrhage, and trauma [2]
- Seizure prophylaxis for 1 week only: decreases incidence of post-traumatic seizure; NO need if sedated [3]
- Prophylactic anticonvulsant if SAH [1]
- NOT recommended for infratentorial lesions (cerebellum) [2]
- Drug of choice: usually levetiracetam (Keppra) or phenytoin (IV loading)
- Why seizure prophylaxis? Seizures increase cerebral metabolic demand → increase cerebral blood flow → exacerbate raised ICP [13]. In the context of an already compromised brain, this can be catastrophic.
| Measure | Rationale |
|---|---|
| Bed rest, NPOEM (nil per oral except medicine), IV fluids [3] | Minimize metabolic demand; NPOEM because of aspiration risk with reduced consciousness |
| Neuro-obs | Monitor for deterioration; GCS (especially Motor score), pupils, limb power |
| Temperature control | Source of hyperthermia should be identified and treated; antipyretics for hyperthermic patients [2]. Target: temp < 37°C [3]. Fever worsens secondary injury by increasing metabolic demand. |
| DVT prophylaxis | Graded compression stockings [3]; intermittent pneumatic compression. SC heparin can be considered after hemorrhage is stable (typically 48–72h) — balance bleeding risk vs thrombosis risk |
| Nutrition | Feeding at least by Day 5 [3]; early enteral nutrition preferred |
| Glucose control | Avoid hypoglycemia; correct hyperglycemia [3] — hyperglycemia worsens outcomes in neurological injury |
| Electrolytes | Monitor closely — especially Na (SIADH/CSWS post-SAH) |
| Stress ulcer prophylaxis | H2 blockers [13] — ICH patients on steroids or ventilated are at risk of stress ulcers |
| Avoid constipation | High fiber diet + stool softeners [2] — straining (Valsalva) raises ICP |
E. Type-Specific Management
Conservative treatment — indicated if ALL of the following are met:
- Hematoma clot volume < 30 cm³
- Maximum thickness < 1.5 cm
- GCS score > 8
Management: Serial CT brain and close neurological observation [2]
Surgical treatment — indicated for patients with focal neurological signs and symptoms to prevent irreversible brain injury:
Craniotomy + hematoma evacuation: open craniotomy allows a more complete evacuation of hematoma [2]
This is a neurosurgical emergency in symptomatic EDH. The prognosis is often excellent if evacuated promptly (the brain has been compressed but not destroyed — primary injury is minimal if surgery is timely).
Management: neurosurgical emergency [1]
General: tranexamic acid, reverse anticoagulation, ICP control [1]
| Type | Surgical Approach | Prognosis |
|---|---|---|
| Acute SDH | Craniotomy + clot evacuation (clotted blood cannot be drained through a burr hole) — only in those young + good premorbid status [1] | Often associated with brain laceration/contusion → poor prognosis [1] |
| Subacute/Chronic SDH | Burr-hole + drainage (liquefied blood can be drained through small holes) — for majority of patients [1] | Late presentation means majority of damage is secondary injury and initial injury is likely mild → good prognosis [1] |
Why the difference? Acute SDH contains solid clot that cannot flow through a small burr hole — you need an open craniotomy to access and remove it. Chronic SDH has undergone liquefaction and behaves like a fluid collection — a burr hole with gravity drainage is sufficient and far less invasive.
E3. Intracerebral Hemorrhage (ICH) [1][2][3][4][18]
This is the most nuanced area of management. The key lecture slide message:
Patient selection for treatment depends on: Age, co-morbidities, location of haematoma, neurological status, aetiology [4]
Clot evacuation: decompresses brain and is life-saving but does not affect primary injury. Functional prognosis depends on location and extent of haemorrhage [4]
No role for steroids. Tranexamic acid might help. [4]
Reverse bleeding tendency. Principles of maintaining CBF apply. [4]
Limited evidence to support routine surgical evacuation for most patients with intracerebral hemorrhage or most patients with supratentorial hemorrhage without neurological deterioration [2]
The landmark STICH Trial [18] showed:
Patients with spontaneous supratentorial intracerebral haemorrhage in neurosurgical units show no overall benefit from early surgery when compared with initial conservative treatment [18]
However, surgery IS indicated in specific situations:
Cerebellar hemorrhage — this is the clear surgical indication:
Management of cerebellar hemorrhage: Evacuation of hematoma if brainstem compression, hematoma > 3cm, or obliteration of cistern. External ventricular drainage if small hematoma with hydrocephalus [4]
Cerebellar haemorrhage: prompt CSF drainage with clot evacuation. Hydrocephalus and brainstem compression → neurosurgical emergency!! Prognosis: good if timely treatment [1]
Supratentorial hemorrhage — surgery in selected patients:
- Patient with neurological deterioration
- Patient in coma, large hematoma causing significant midline shift, or elevated ICP refractory to medical treatment
- Patients with higher level of consciousness (GCS 9–12): early surgical intervention may be considered [2]
- Lobar haemorrhage: usually clot evacuation + histology (except amyloid angiopathy). Usually good outcome + provides histology on underlying pathology (e.g., AVM, tumour) [1]
Brainstem and thalamic hemorrhage:
- Conservative treatment. Prognosis: very high mortality [1]
Intraventricular hemorrhage:
- Usually by ventricular drainage and chemical clot lysis (streptokinase, urokinase, or tPA) [1]
Surgical techniques:
- Open craniotomy: most standard technique for supratentorial ICH [2]
- Decompressive craniectomy ± hematoma evacuation: may reduce mortality for patients in coma with large hematoma/midline shift/refractory ICP [2]
- Other methods: CT-guided stereotactic aspiration, endoscopic aspiration ± thrombolytic usage [2]
Haemorrhagic stroke — deep vs. superficial — surgery in selected patients [4]
Role of decompressive craniectomy: [3]
- Shown in RCT to reduce disability and mortality in: malignant MCA syndrome and massive cerebellar infarct [3]
- Decompressive craniectomy in diffuse swelling → decreased mortality but poor quality of survival → not recommended in guidelines but still done a lot [13]
| ICH Location | Primary Approach | Surgery? |
|---|---|---|
| Putaminal | Conservative (BP, ICP) | Conservative ± clot evacuation; surgery improves survival but likely poor functional outcome esp vegetative survival [1] |
| Thalamic | Conservative | Very high mortality; conservative [1] |
| Pontine (brainstem) | Conservative | Very high mortality; conservative [1] |
| Cerebellar | Surgical emergency | Prompt evacuation if deteriorating / brainstem compression / hydrocephalus. EVD for hydrocephalus [1][4] |
| Lobar | Case-by-case | Usually clot evacuation + histology [1] |
| IVH | Medical + EVD | Ventricular drainage + chemical clot lysis [1] |
E4. Subarachnoid Hemorrhage (SAH) [1][3][4]
SAH management is driven by the triad of preventing rebleeding, managing vasospasm, and treating hydrocephalus.
Patient after aneurysmal SAH is at substantial risk of rebleeding: 3–4% in the first 24 hours, 1–2% each day in the first month. Aneurysmal rupture is associated with a mortality of 70% [2]
Aneurysmal SAH — rebleeding, hydrocephalus, vasospasm — surgical clipping and endovascular treatment [4]
Aneurysm repair is the only effective treatment to prevent rebleeding and should be performed within 24 to 72 hours when possible [2]
Once diagnosed, give tranexamic acid, anticonvulsant and call neurosurgeon [7]
Two modalities:
| Modality | Principle | Advantages | Complications |
|---|---|---|---|
| Endovascular coiling (1st line) [3] | DSA-guided insertion of detachable platinum coils (Guglielmi detachable coil, GDC) into aneurysm → decreased blood flow + velocity → eventual coagulation within aneurysm [1][5] | Less invasive, shorter recovery, better outcomes in posterior circulation aneurysms (ISAT trial) | Contrast allergy, embolism, aneurysm rupture, incomplete occlusion, recurrence |
| Flow diverter (pipeline stent) | Porous stent placed in parent vessel → disrupts flow within aneurysm while preserving flow in side-branches → coagulation within aneurysm + neo-intimal remodeling [1] | Favored for aneurysms with large necks [1]; like EVAR concept [3] | Requires long-term dual antiplatelet therapy |
| Surgical clipping | Craniotomy → brain retracted → clip applied at neck of aneurysm [1] | Definitive, low recurrence rate; allows inspection of surrounding anatomy | Invasive, risk of intraoperative rupture [1], brain retraction injury |
Early surgery/endovascular coiling if Grade 1–3 SAH + aneurysm visualized by DSA/CTA [1]
Vasospasm: blood in CSF triggers reflex vasospasm in underlying arterioles → risk of delayed cerebral infarct. Time course: starts on day 4, peaks in days 7–10, resolves in 2–3 weeks [1]
-
Nimodipine: 60mg PO Q4H (or 1mg/h IV infusion) in Grade 1–3 with BP monitoring [1][3]
- Why nimodipine specifically? Nimodipine is a dihydropyridine calcium channel blocker that preferentially acts on cerebral blood vessels. "Nimo" = nimbus (cloud/brain), "dipine" = dihydropyridine CCB. It has been shown in RCTs to reduce the incidence of delayed cerebral ischemia and improve outcomes — the only drug proven to do this.
- Use of nimodipine should be individualized in Grade 4–5 patients [1]
-
Triple-H therapy: Hypertension + Haemodilution + Hypervolemia → increase cerebral perfusion pressure + improve blood rheology [1]
- Increasingly, the emphasis has shifted to induced hypertension alone (euvolemic hypertension) rather than the full Triple-H, as hypervolemia and hemodilution have not shown clear benefit and may cause pulmonary edema.
-
Angioplasty: mechanical (transluminal angioplasty) or chemical (intra-arterial vasodilators e.g., papaverine, CCBs) [1] — for refractory vasospasm
-
Delayed cerebral ischemia: Focal neurological deficit or decreased GCS for at least 1 hour. Investigate with CT perfusion + CTA for vasospasm. Treat with haemodynamic augmentation (increase BP), intra-arterial vasodilators, angioplasty + stenting [3]
- Tranexamic acid: for < 72h or until surgical treatment (risk of thrombosis) [3]
- Antifibrinolytic: early treatment with short course tranexamic acid → stop after aneurysm secured (to decrease side effects of aggravating ischaemic complications) [1]
- Why tranexamic acid? It inhibits plasminogen activation → prevents fibrinolysis → stabilizes the clot over the ruptured aneurysm → reduces rebleeding risk. But prolonged use increases the risk of cerebral ischemia (by promoting thrombosis), hence the short course.
- Blood in subarachnoid space → obstruction of CSF flow → hydrocephalus [1]
- Can be early (obstructive — blood clot blocking aqueduct/4th ventricle) or late (communicating — blood products clogging arachnoid granulations)
- Management: CSF drainage. May provoke re-bleeding → always treat aneurysm before decompression [1]
- Acute hydrocephalus: burr hole + EVD [3]
- Late hydrocephalus may require a permanent VP shunt
Management: Anticoagulation — LMWH (acute) → warfarin or dabigatran for 3 months (chronic). Endovascular thrombolysis in selected patients. ICP management. Treat seizures. [3]
Why anticoagulate in a condition that can cause hemorrhagic infarction? This seems counterintuitive, but the logic is: the venous infarction and hemorrhage are caused by the thrombosis (venous congestion → increased venous pressure → edema → hemorrhagic conversion). Treating the underlying cause (the thrombus) is more important than worrying about the secondary hemorrhage. RCTs have shown anticoagulation improves outcomes even in patients with hemorrhagic venous infarction.
ICP Monitoring — Indications: No reliable clinical monitoring (e.g., sedation, muscle paralysis). GCS ≤ 8 (requires intubation). Evolving disease conditions. Relative contraindications: Awake patients, bleeding tendency. [16]
External Ventricular Drain (EVD): Manometric principle for monitoring intracranial CSF pressure. Therapeutic by draining CSF for decompression. Risk of infection, iatrogenic trauma. [16]
Rising ICP: repeat CT and escalate treatment [16]
Treatment targets for severe TBI/ICH [3]:
- ICP < 22 mmHg, CPP 60–70 mmHg
- SpO2 > 97%, PaO2 > 9 kPa, PCO2 4.5–5 kPa
- Temp < 37°C, avoid hypoglycemia, serum Na > 140
ICP definitely abnormal if > 20 cmH2O → suggests worsening conditions → repeat imaging studies → escalate treatment [16]
Therapeutic hypothermia is not recommended in adults (no benefit in RCTs) but less certain in children. Risks include cardiac arrest, ischemia, bleeding tendency, pneumonia. [13]
| Type | Medical | Surgical | Key Points |
|---|---|---|---|
| EDH | Conservative if small (volume < 30mL, thickness < 1.5cm, GCS > 8) | Craniotomy + evacuation if symptomatic | Neurosurgical emergency; good prognosis if timely |
| Acute SDH | Reverse anticoagulation, ICP control | Craniotomy + clot evacuation (in young, good premorbid) | Poor prognosis (associated brain injury) |
| Chronic SDH | Observation if minimal symptoms | Burr hole + drainage | Good prognosis; may recur |
| ICH — deep | BP < 140, ICP control, reverse coagulopathy, tranexamic acid [4] | Usually conservative; STICH showed no overall benefit of early surgery for supratentorial ICH [18] | Cerebellar ICH is the exception — surgical emergency |
| ICH — lobar | As above | Clot evacuation + histology [1] | Good outcome; provides tissue diagnosis |
| ICH — cerebellar | EVD for hydrocephalus | Evacuation if brainstem compression / hematoma > 3cm / obliterated cistern [4] | Neurosurgical emergency; good prognosis if timely [1] |
| SAH | Nimodipine, tranexamic acid (short course), BP < 160, EVD if hydrocephalus | Endovascular coiling (1st line) or surgical clipping within 24–72h | Secure aneurysm ASAP; monitor for vasospasm day 4–14 |
| CVST | LMWH → warfarin/dabigatran 3 months, ICP management, anticonvulsants | Endovascular thrombolysis in selected cases | Anticoagulate even if hemorrhagic infarction present |
High Yield Summary — Management
- ALWAYS resuscitate first (ABCDE). Protect uninjured brain. Salvage injured brain. Treat underlying cause. [16]
- Corticosteroids are contraindicated in hemorrhagic stroke and head injury (CRASH trial). [2]
- BP targets: ICH → SBP < 140; SAH → SBP < 160. Use IV labetalol [3].
- Reverse anticoagulation urgently: Warfarin → Vitamin K + PCC (preferred over FFP) [1][2]; Dabigatran → Idarucizumab; Factor Xa inhibitors → Andexanet alfa / PCC.
- ICP management escalation: Head up 30° → sedation → mannitol/HTS → EVD/CSF drainage → hyperventilation → barbiturate coma → decompressive craniectomy.
- EDH: craniotomy + evacuation if symptomatic (neurosurgical emergency with excellent prognosis if timely).
- SDH: craniotomy for acute (clotted); burr hole for chronic (liquefied).
- ICH: mostly conservative. STICH trial = no overall benefit of early surgery for supratentorial ICH. Exceptions: cerebellar ICH (surgical emergency if brainstem compression/hydrocephalus) and lobar ICH (evacuate + histology).
- SAH: secure aneurysm within 24–72h — endovascular coiling (1st line) or surgical clipping. Nimodipine 60mg Q4H for vasospasm prevention. Tranexamic acid short course until aneurysm secured. Monitor for vasospasm (day 4–14), hydrocephalus, hyponatremia.
- CVST: anticoagulate (LMWH → warfarin/dabigatran) even with hemorrhagic infarction.
- EVD is the gold standard for ICP monitoring + therapeutic CSF drainage. [16]
- Do NOT: give mannitol if shocked, blindly hyperventilate, use barbiturates outside ICU, give steroids for TBI/ICH. [13]
Active Recall - Management of Intracranial Hemorrhage
References
[1] Senior notes: Ryan Ho Neurology.pdf (Section 3.2: Management of Haemorrhagic Stroke; p84–86: Acute management, reversal of anticoagulation, surgical decompression, SAH complications and management; p82: Prevention and treatment of complications; p156: ICP monitoring) [2] Senior notes: felixlai.md (Treatment of hemorrhagic stroke, general principles, coagulopathy management, surgical treatment of ICH and SAH, ICP management, increased ICP treatment) [3] Senior notes: maxim.md (ICH management, SAH management, severe TBI management, ICP management, CVST management, decompressive craniectomy) [4] Lecture slides: Cererbrovascular disease.pdf (p3: Management of putaminal ICH; p10: Management of cerebellar hemorrhage) [5] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p85: Endovascular coiling, stenting) [7] Lecture slides: GC 109. Headache and loss of consciousness Acute stroke, subarachnoid haemorrhage and vascular malformation.pdf (p6: Principles of management; p16: Once diagnosed give tranexamic acid, anticonvulsant, call neurosurgeon; p25: Key messages) [13] Senior notes: Ryan Ho Fundamentals.pdf (p339: TBI management, ICP management, Do NOT list, tranexamic acid, reverse anticoagulation, neurosurgical interventions) [16] Lecture slides: GC 111. Raised intracranial pressure and hydrocephalus.pdf (p8–9: ICP monitoring indications, EVD, clinical application, fundamentals of management) [17] Senior notes: Ryan Ho Haemtology.pdf (p144: FFP, cryoprecipitate, PCC indications and dosing) [18] Lecture slides: Cererbrovascular disease.pdf (p12: STICH Trial findings)
Complications of Intracranial Hemorrhage
Complications of intracranial hemorrhage are what kill patients and cause permanent disability. The primary hemorrhagic injury is done — you cannot undo it. Everything from this point is about preventing and managing secondary injury. Think of it as a cascade: the initial bleed triggers a series of events — each one an opportunity for the brain to sustain further damage, and each one an opportunity for you to intervene.
The complications can be organized into early (acute) and late (chronic/subacute), and further divided into CNS (intracranial) and systemic (extracranial) complications.
For SAH specifically, there is a well-known mnemonic used in clinical practice:
SAH Complications: The "9 H's" [3]: Haematoma, intracranial Hypertension, systemic Hypertension, Heart failure/arrhythmia/neurogenic pulmonary edema (early); Haemorrhage (re-bleed), Hypoperfusion (delayed cerebral ischemia), Hydrocephalus, Hypovolemia (cerebral salt wasting), Hyponatremia (SIADH) (late)
A. Complications Common to ALL Types of Intracranial Hemorrhage
This is the most immediate life-threatening complication across all ICH types.
Pathophysiology (from first principles):
- The hematoma acts as a space-occupying lesion within the rigid skull (Monro-Kellie doctrine) [1].
- As the hematoma expands (or as surrounding cerebral edema develops), compensatory mechanisms (CSF displacement, venous outflow) are exhausted.
- ICP rises → CPP falls (CPP = MAP – ICP) → global cerebral ischemia.
- Focal pressure gradients develop across dural compartments → brain herniation → brainstem compression → death.
Types of edema around hemorrhage:
- Cerebral edema: cytotoxic edema (ischemia) + vasogenic edema (BBB disruption) [3]
- Peri-hematomal edema peaks at approximately days 3–5 post-hemorrhage. This explains a critically important clinical point:
Brain contusions may enlarge with time. Mass effect and edema — not the worst until at least Day 4–5 [19]
This is why serial CT imaging and close neuro-observation are mandatory in the first week, even if the initial scan looks relatively benign.
Brain herniation syndromes (as consequences of uncontrolled raised ICP):
| Syndrome | Cause | Key Presentation |
|---|---|---|
| Uncal (transtentorial) | Unilateral supratentorial mass | Blown pupil (ipsilateral CN III palsy), ipsilateral hemiparesis (Kernohan's notch — false localizing), decreased consciousness |
| Central | Midline/diffuse supratentorial mass | Bilateral small pupils, Cheyne-Stokes respiration, loss of consciousness [1] |
| Tonsillar (coning) | Posterior fossa mass | Cardiorespiratory arrest, bilateral dilated pupils, decerebrate/decorticate posturing [1] |
| Subfalcine (cingulate) | Early unilateral SOL | ACA compression → bilateral lower limb weakness [1] |
Clinical Warning
Signs of impending herniation (must recognize immediately): [3]
- Fixed and dilated pupils (unilateral or bilateral)
- Decorticate or decerebrate posturing
- Cushing's triad: hypertension, bradycardia, irregular respiration
These are pre-terminal signs. If you see them, the patient needs urgent intervention — osmotherapy, emergency surgical decompression, or both.
- Relevant to all types but particularly ICH and EDH.
- In ICH, hematoma expansion occurs in ~30% of patients within the first 24 hours — this is the single strongest predictor of early neurological deterioration and mortality.
- The "spot sign" on CTA (active contrast extravasation) predicts expansion.
- Why does it expand? The initial rupture damages surrounding microvessels; the hemorrhage itself causes local tissue distortion, inflammation, and further microvascular injury → a positive feedback loop of bleeding.
- Prevention: aggressive BP control (SBP < 140), reversal of coagulopathy, tranexamic acid [2].
CNS complications: Seizures [2]
- Incidence: ~5–10% in ICH, higher in lobar hemorrhages (cortical irritation) and SAH.
- Mechanism: Blood products (particularly iron from hemoglobin degradation) are direct cortical irritants → lower the seizure threshold. Perilesional ischemia and edema further contribute to cortical hyperexcitability.
- Types:
- Early seizures (within 1 week after TBI/ICH) vs late seizures (after 1 week) [3]
- Early seizures may be subclinical (non-convulsive status epilepticus) → detected only on EEG. This is why a change in mental status in an ICH patient should prompt EEG monitoring.
- Why seizures are dangerous in ICH: Seizure can cause hyperemia and exacerbate raised ICP [1][13]. In a brain with already compromised compliance, this can precipitate herniation.
- Management:
- Prophylactic anticonvulsant if SAH [1]
- Clinical seizures should be treated with anticonvulsants [2]
- Prophylactic use of anticonvulsants in ICH is NOT universally recommended [2] — but is commonly given for 1 week in practice, especially for supratentorial lesions or if seizure has occurred.
- NOT recommended for infratentorial lesions (cerebellum) [2]
B. Complications Specific to Subarachnoid Hemorrhage (SAH)
SAH has the most distinct and well-characterized complication profile. These complications are what drive the high morbidity and mortality of SAH.
SAH Complications (9H): [3]
- Early: Haematoma, intracranial HT, systemic HT (compensates raised ICP), HF/arrhythmia/neurogenic pulmonary edema
- Late: Haemorrhage (re-bleed), Hypoperfusion (delayed cerebral ischemia), Hydrocephalus, Hypovolaemia (CSW), HypoNa (SIADH)
Decreased GCS after SAH — think: [3]
- Hydrocephalus
- Re-bleeding
- Acute ischemic stroke
- Non-convulsive seizure
- Patient after aneurysmal SAH is at substantial risk of rebleeding: 3–4% in the first 24 hours, 1–2% each day in the first month [2]
- Aneurysmal rupture is associated with a mortality of 70% [2]
- Re-bleeding: 20% by day 14 [1]
- Why so dangerous? The initial SAH has already raised ICP and caused injury. A second hemorrhage into this already compromised brain is often fatal because compensatory mechanisms are already exhausted.
- Prevention: Early aneurysm occlusion (within 24–72h) — the only effective treatment [2]. Short course tranexamic acid until aneurysm is secured [1][3].
This is the most feared late complication of SAH and a major cause of morbidity.
- Vasospasm: blood in CSF triggers reflex vasospasm in underlying arterioles → risk of delayed cerebral infarct [1]
- Time course: starts on day 4, peaks in days 7–10, resolves in 2–3 weeks [1]
- Pathophysiology (from first principles): Blood breakdown products in the subarachnoid space — particularly oxyhemoglobin, endothelin-1, and free radicals — cause intense, sustained contraction of the smooth muscle in cerebral arteries. This narrows the vessel lumen → reduced blood flow → ischemia → infarction if severe and prolonged. Additionally, there is inflammation, microthrombosis, and cortical spreading depolarization, all contributing to DCI.
- Delayed cerebral ischemia: defined as focal neurological deficit or decreased GCS by 2 points for at least 1 hour [3]
- Monitoring: Daily transcranial Doppler (TCD) — MCA mean flow velocity > 120 cm/s suggests vasospasm.
- Investigations if suspected: CT perfusion scan + CT angiogram for vasospasm [3]
- Prevention and treatment:
- Nimodipine 60mg PO Q4H (or 1mg/h IV) [1][3] — the only agent proven to reduce DCI and improve outcomes
- Triple-H therapy (Hypertension + Haemodilution + Hypervolemia) → increase CPP + improve blood rheology [1]
- Hemodynamic augmentation (increase BP), intra-arterial vasodilators (e.g., CCB), angioplasty + stenting [3]
The Vasospasm Window
The classic teaching is "4–14 rule": vasospasm can occur from day 4 to day 14 post-SAH, peaking at days 7–10. During this window, any clinical deterioration (new deficit, decreased GCS) should be assumed to be vasospasm until proven otherwise. Do NOT attribute it to "depression" or "poor cooperation."
- Blood in subarachnoid space → obstruction of CSF flow → hydrocephalus [1]
- Can be:
- Acute (obstructive/non-communicating): Blood clot physically blocks CSF pathways (e.g., aqueduct of Sylvius, 4th ventricle outlets) → rapid ventricular dilation → raised ICP → emergency.
- Chronic (communicating): Blood breakdown products clog the arachnoid granulations → impaired CSF absorption → gradual ventricular dilation over weeks to months.
- Incidence: ~20–30% of SAH patients develop hydrocephalus requiring intervention.
- Management:
Both SIADH and CSWS can follow SAH, and distinguishing between them is critical because the treatment is opposite:
| Feature | SIADH | CSWS |
|---|---|---|
| Mechanism | Inappropriate ADH secretion → renal water retention → dilutional hyponatremia | Idiopathic natriuresis + diuresis secondary to cerebral disorder → renal Na loss |
| Volume status | Euvolemic | Hypovolemic |
| Urine Na | > 20 mmol/L (inappropriate natriuresis) | > 20 mmol/L (renal Na loss) |
| Urine osmolality | > 200 mmol/kg (inappropriately concentrated) | Elevated |
| Treatment | Fluid restriction | Fluid and salt replacement (fluid restriction would worsen hypovolemia and cerebral ischemia) |
CSWS results in renal Na loss → hypovolemic hyponatremia. SIADH results in renal water retention → euvolemic hyponatremia (different treatment) [10]
Why does hyponatremia matter in SAH? Hyponatremia may aggravate cerebral edema and cause seizures [3]. In the context of post-SAH brain with impaired autoregulation and vasospasm risk, hypovolemia from CSWS is particularly dangerous because it reduces cerebral perfusion.
- HF/arrhythmia/neurogenic pulmonary edema [3]
- Pathophysiology: SAH causes a massive catecholamine surge (sympathetic storm) → direct myocardial injury ("stunned myocardium" or neurogenic stress cardiomyopathy/Takotsubo-like pattern).
- ECG changes: ST changes, T-wave inversions, prolonged QT, U waves — can mimic acute coronary syndrome.
- Troponin: May be elevated (from direct myocardial necrosis, not coronary atherosclerosis).
- Neurogenic pulmonary edema: Sudden-onset pulmonary edema from massive sympathetic discharge → increased pulmonary capillary permeability + increased pulmonary venous pressure.
- Clinical pitfall: Do not mistake these for a primary cardiac event and delay neurosurgical management.
C. Complications Specific to Subdural Hematoma
- Chronic SDH has a recurrence rate of ~10–20% after burr-hole drainage.
- Why? The fragile neomembrane around the chronic collection continues to bleed even after drainage. The brain, if significantly atrophied, may not re-expand to fill the subdural space, leaving room for re-accumulation.
- Management: Repeat burr-hole drainage; rarely requires craniotomy. Some centers use subdural drains left in situ for 24–48 hours post-drainage to reduce recurrence.
Chronic SDH: Burr hole to drain. Craniotomy if recur. Good outcome with drainage. [3]
- Posterior fossa SDH compresses PCA along edge of tentorium cerebelli → cerebral infarction [1]
- Large acute SDH can also compress anterior cerebral or middle cerebral artery territory.
D. Complications Specific to Epidural Hematoma
- EDH is an arterial bleed (MMA in 85%) → rapid accumulation → rapid deterioration if not evacuated promptly.
- The classically described "talk and die" scenario: patient appears initially well (lucid interval) then suddenly herniates.
EDH: May be small initially but can expand quickly [19]. Relatively good prognosis if treated early [19]
Decompressive craniectomy complications [2]:
- Herniation through skull defect
- Spinal fluid leakage
- Wound infection
- Epidural and subdural hematoma (iatrogenic)
E. Complications Specific to Intracerebral Hemorrhage
- ICH can rupture into the adjacent ventricle, especially in deep hemorrhages (putaminal, thalamic).
- IVH causes obstructive hydrocephalus (blood blocks the ventricular system) → acute rise in ICP.
- IVH is an independent predictor of poor outcome.
- Management: ventricular drainage via EVD + chemical clot lysis (streptokinase, urokinase, or tPA) [1]
Cerebellar hemorrhage: direct brainstem compression + IVH and obstructive hydrocephalus. Rapidly fatal if large size. Good prognosis if timely surgery [7]
E2. Hematoma Expansion (see A2 above)
- Cerebellar hemorrhage deserves special emphasis because it is unique: the posterior fossa is small and rigid, so even a moderate-sized hemorrhage can cause rapid brainstem compression and obstructive hydrocephalus (4th ventricle compression). This is why cerebellar hemorrhage is a neurosurgical emergency with good prognosis only if treated timely [1][7].
- Brainstem (pontine) hemorrhage: carries the highest mortality of any ICH location due to destruction of vital brainstem centers (consciousness, respiration, cardiovascular control). Very high mortality; conservative treatment [1].
These are complications of the immobilized, neurologically impaired patient rather than of the hemorrhage itself, but they are major causes of morbidity and mortality.
| Complication | Mechanism / Pathophysiology | Prevention / Management |
|---|---|---|
| Aspiration pneumonia | Reduced consciousness → loss of protective cough and gag reflexes → aspiration of oral secretions/food; bulbar dysfunction (in brainstem lesions) | Careful feeding practice (NPOEM if GCS low), early mobilization, chest physiotherapy [1]; speech therapist assessment of swallowing before oral feeding |
| Bronchopneumonia / VAP | Immobility → hypostatic secretions; intubation → ventilator-associated pneumonia; immunosuppression from stress response | Early mobilization, chest physio, VAP bundles (head elevation, oral care, daily sedation holds) |
| Urinary tract infection | Catheter-associated UTI [2]; prolonged catheterization, neurogenic bladder | Indwelling catheter or condom catheter (if incontinent male) → avoid bladder overdistension [1]; intermittent catheterization preferred; remove catheter as soon as possible |
| Deep vein thrombosis (DVT) and pulmonary embolism (PE) | Immobility → venous stasis (Virchow's triad); hypercoagulable state from acute illness and inflammation | DVT prophylaxis: intermittent pneumatic compression from day of admission; consider SC heparin (UFH/LMWH) after 1–4 days of hemorrhage onset with documented cessation of bleeding [2]; elastic compression stockings [1] |
| Pressure sores | Immobility → sustained pressure on bony prominences → skin and soft tissue ischemia → necrosis | Reposition weak limbs, frequent turning, use of cushions, egg-crate/air mattress [1] |
| Contractures and frozen shoulder | Prolonged immobility → joint stiffness; shoulder subluxation from flaccid hemiparetic arm | Early physiotherapy and occupational therapy [1]; proper positioning of hemiplegic limb; passive ROM exercises |
| Dysphagia | Brainstem or cortical injury affecting swallowing mechanism | Speech therapist assessment [1]; modified diet; PEG tube if prolonged dysphagia |
| Malnutrition and dehydration | Reduced oral intake from dysphagia and reduced consciousness | Early enteral nutrition (by Day 5) [3]; IV fluids; dietitian input |
| Stress ulcers | Physiological stress → increased gastric acid secretion + mucosal ischemia → GI bleeding (Cushing's ulcer in head injury) | Stress ulcer prophylaxis with H2 blockers or PPI [13] |
G. Late / Chronic Complications
Prevalence of depression observed at any time after stroke = 29% [2]
Depression at 3 months after stroke is correlated with a poor outcome at 1 year [2]
Predictors of post-stroke depression [2]:
-
Disability
-
Anxiety
-
Pre-stroke depression
-
Cognitive impairment
-
Severity of stroke
-
Management: Screening with a structured depression inventory is recommended routinely. Patients with post-stroke depression should be treated with antidepressants (usually SSRIs) in the absence of contraindications [2].
-
Why is it important? Depression impairs rehabilitation participation, reduces motivation, worsens functional outcome, and increases mortality. It is one of the most underdiagnosed complications of stroke.
- Late seizures (after 1 week) are a risk, especially with cortical involvement, penetrating injuries, and depressed skull fractures.
- Risk of epilepsy is a recognized complication of depressed skull fractures [19] and cortical hemorrhages.
- May require long-term anticonvulsant therapy.
- Particularly prominent after SAH (even with good neurological recovery) and large ICH.
- Includes problems with memory, attention, executive function, and processing speed.
- Contributes to long-term disability even when physical deficits are mild.
- Communicating hydrocephalus from impaired CSF absorption at arachnoid granulations.
- Presents weeks to months later with the classic NPH triad: gait apraxia, urinary incontinence, dementia ("wet, wobbly, wacky").
- May require permanent VP shunt.
- CAA: High risk of recurrent lobar ICH.
- AVM: If not treated, annual hemorrhage risk ~3%/year.
- Hypertensive ICH: Risk of recurrence if BP not controlled — emphasizes the importance of long-term antihypertensive therapy.
- Chronic SDH: Recurrence rate ~10–20% after initial drainage.
When intracranial hemorrhage is traumatic and associated with skull base fractures:
Basilar skull fractures: complications include EDH, meningitis, CSF leak [3][19]
- CSF rhinorrhea (anterior fossa fracture → connection with paranasal sinuses) → risk of meningitis [19]
- CSF otorrhea (middle fossa fracture → connection with middle ear) [19]
- Bacterial meningitis especially if CSF leak persists > 7 days [1]
- CN palsies: generally present 2–3 days after injury [1] — CN I (anosmia), CN VII/VIII (facial palsy, hearing loss) are most common.
High Yield Summary — Complications
- Raised ICP / edema / herniation is the #1 killer across all types. Edema peaks at days 3–5 — not the worst until at least Day 4–5 [19].
- Hematoma expansion occurs in ~30% of ICH within 24 hours — the strongest early prognostic factor. "Spot sign" on CTA predicts expansion.
- SAH complications (9H): early = Haematoma, intracranial HT, systemic HT, HF/arrhythmia; late = re-Hemorrhage, Hypoperfusion (vasospasm/DCI), Hydrocephalus, Hypovolemia (CSWS), HypoNa (SIADH).
- Vasospasm: day 4–14 (peaks 7–10). Any deterioration in this window = vasospasm until proven otherwise. Treat with nimodipine, induced hypertension, angioplasty.
- Rebleeding: 3–4% in first 24h of SAH, 20% by day 14. Prevention = early aneurysm occlusion (within 24–72h) + short-course tranexamic acid.
- Hydrocephalus can be acute (obstructive — blood blocking CSF pathways) or chronic (communicating — arachnoid granulation blockage). Treat with EVD (acute) or VP shunt (chronic).
- SIADH (euvolemic, treat with fluid restriction) vs CSWS (hypovolemic, treat with fluid/salt replacement) — critical distinction post-SAH.
- Post-stroke depression: 29% prevalence; screen routinely; treat with SSRIs.
- Systemic complications (pneumonia, UTI, DVT/PE, pressure sores) are major causes of morbidity — prevention through early mobilization, DVT prophylaxis, careful feeding, physiotherapy.
- Cerebellar hemorrhage: unique danger due to small posterior fossa → rapid brainstem compression + obstructive hydrocephalus. Good prognosis ONLY if timely surgery. [7]
Active Recall - Complications of Intracranial Hemorrhage
References
[1] Senior notes: Ryan Ho Neurology.pdf (p82: Prevention and treatment of complications; p85–86: Surgical decompression, SAH complications and management; p155–156: Brain herniation, ICP monitoring; p201: Basilar skull fracture complications) [2] Senior notes: felixlai.md (Complications of stroke, treatment of acute and chronic complications, seizure management, DVT prophylaxis, post-stroke depression, decompressive craniectomy complications) [3] Senior notes: maxim.md (SAH complications — 9H mnemonic, secondary brain injuries, decreased GCS after SAH, delayed cerebral ischemia, ICP management, CVST) [7] Lecture slides: GC 109. Headache and loss of consciousness Acute stroke, subarachnoid haemorrhage and vascular malformation.pdf (p8: Cerebellar hemorrhage — direct brainstem compression, IVH, obstructive hydrocephalus, rapidly fatal if large, good prognosis if timely surgery) [10] Senior notes: Ryan Ho Chemical Path.pdf (p10: SIADH vs CSWS) [11] Senior notes: Ryan Ho Opthalmology.pdf (p90: Papilloedema pathophysiology) [13] Senior notes: Ryan Ho Fundamentals.pdf (p339: Seizure prophylaxis, stress ulcer prophylaxis, Do NOT list, mannitol precautions) [19] Lecture slides: GC 208. Unconscious after an accident Head injury.pdf (p14–16: Skull fracture complications, EDH — may expand quickly, brain contusion — not worst until day 4–5; p15: Middle skull base fracture)
High Yield Summary — Etiology & pathophysiology
Compartments: EDH (epidural), SDH (subdural), SAH (subarachnoid), IPH / ICH (intraparenchymal), IVH (intraventricular).
EDH: Arterial — classically middle meningeal; temporal fracture common; doesn't cross sutures.
Acute SDH: Bridging veins tear; crescent crosses sutures; common in elderly with brain atrophy, anticoagulation.
SAH: Traumatic (sulcal) vs aneurysmal (basal cisterns) — thunderclap headache, threat of rebleed and vasospasm in aneurysmal pattern.
ICH: Hypertensive deep nuclei (putamen, thalamus, pons, cerebellum) vs lobar (more often amyloid/causes needing histology) vs coagulopathy.
Cerebellar bleed: Small posterior fossa + brainstem compression + 4th ventricle obstruction → neurosurgical emergency.
High Yield Summary — Differential diagnosis
| Pattern on CT | Think |
|---|---|
| Lens-shaped extra-axial | EDH |
| Crescent extra-axial | SDH (acute/subacute/chronic) |
| Blood in sulci/cisterns | SAH — traumatic vs ruptured berry |
| Deep basal ganglia | Hypertensive ICH |
| Lobar cortical/subcortical | Lobar haemorrhage — age, imaging, histology after evacuation if indicated |
| Intraventricular blood | IVH — often extension from parenchyma; poor prognosis, hydrocephalus risk |
Non-haemorrhagic mimics: Ischaemic stroke (early CT subtle), tumour bleed, cerebral venous thrombosis, haemorrhagic transformation.
High Yield Summary — Diagnosis
Urgent non-contrast CT: Location, volume, IVH, hydrocephalus, midline shift, basal cisterns, skull fracture.
CTA / DSA: SAH workup for aneurysm; selected trauma with vascular injury suspicion.
Coagulation: INR, platelets, DOAC assays / reversal protocols.
BP and GCS trajectory — haematoma expansion often in first hours.
High Yield Summary — Management
Universal: ABC; reverse anticoagulation; neuro-obs / ITU as needed; no steroids for TBI/ICH to reduce oedema (harm).
BP in spontaneous ICH: Guideline frame (e.g. INTERACT2 lineage) — acute lowering toward ~140 mmHg SBP often safe in 150–220 range if no contraindication; >220 may need more aggressive controlled reduction; follow local protocol.
EDH: Craniotomy + evacuation if large/thick/worsening or GCS falls — time-critical.
Acute SDH: Craniotomy if indicated by thickness, midline shift, neurology, age; chronic SDH → burr holes.
Supratentorial ICH: Mostly medical — STICH no routine early surgery benefit overall; exceptions neurological deterioration, very large volume with midline shift, lobar for diagnosis.
Cerebellar ICH: Evacuate if brainstem signs, haematoma >~3 cm, cisterns obliterated; EVD for obstructive hydrocephalus with smaller clot.
Aneurysmal SAH: Nimodipine 60 mg PO q4h; secure aneurysm (coil first-line vs clip) within 24–72 h; short-course TXA until secured; EVD if hydrocephalus; watch vasospasm day 4–14, hyponatraemia (SIADH vs CSW).
High Yield Summary — Complications
EDH/SDH/ICH: Herniation, rebleed, seizures, infection (post-op).
SAH: Rebleeding (early peak), vasospasm → DCI, hydrocephalus (acute EVD → chronic shunt), SIADH/CSW, cardiac stress (neurogenic stunned myocardium).
IVH: Obstructive hydrocephalus.
Long-term: Cognitive impairment, epilepsy, need for rehab.