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Textbook/Clinical imaging and interpretation/Intracranial haemorrhage patterns
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Intracranial haemorrhage patterns

Identify the CT compartments and patterns of intracranial haemorrhage, assess mass effect and complications, and select the next vascular or specialist investigation without inferring cause from shape alone.

26 min full readUK scopeSources checked 13 Sept 2026Clinical review pending
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Blood pattern plus physiology determines urgency

Intracranial haemorrhage can expand, obstruct CSF flow or cause herniation; a small strategically placed bleed may be more dangerous than a larger stable lesion elsewhere.

Action: Stabilise the patient, reverse relevant coagulopathy through the current drug-specific pathway, obtain urgent CT and contact stroke or neurosurgical specialists based on compartment, trajectory and mass effect.

Open the sections you need. The overview is shown first.
01Purpose and principlesWhat the assessment is for and the core concepts behind it.

CT shape reflects meningeal attachments and anatomical spaces. Epidural collections displace dura inward and are commonly limited by sutures. Subdural blood spreads along the hemisphere but is constrained by falx and tentorium. Subarachnoid blood mixes with CSF in sulci and cisterns, while intraparenchymal clot expands within brain and may rupture into ventricles.

Attenuation changes with clot age and haematocrit. Hyperacute unclotted blood can be less dense, acute clot is usually bright, and subacute blood approaches brain density before becoming hypodense. Anaemia and dilution can reduce conspicuity. Mixed density can reflect active bleeding, rebleeding or blood of different ages but is not a histological diagnosis.

Interpretation has three outputs: compartment, complications and cause strategy. Complications include oedema, shift, cisternal effacement, herniation, ventricular obstruction and infarction. Cause assessment considers trauma, hypertension, amyloid angiopathy, aneurysm, malformation, tumour, venous thrombosis and drugs, using age and pattern to select further imaging.

Key points

  • First name the compartment: epidural, subdural, subarachnoid, intraparenchymal or intraventricular; mixed patterns are common after trauma or vascular rupture.
  • Epidural blood is classically biconvex and suture-limited; subdural blood is usually crescentic and can cross sutures but is constrained by dural reflections.
  • Subarachnoid blood follows sulci, Sylvian fissures and basal cisterns; distribution can guide aneurysm search but does not identify the culprit with certainty.
  • Intraparenchymal haemorrhage should be described by lobe or deep structure, size impression, oedema, ventricular extension, shift and hydrocephalus before aetiology is proposed.
  • Fresh clot is generally hyperdense, while chronic subdural collections become lower attenuation; acute-on-chronic bleeding may produce mixed density and internal membranes.
  • Detection must lead to cause and complication imaging: CTA, venography, MRI or DSA is selected from age, location, pattern, trauma and the first vascular study.
02Indications, selection and cautionsWhen it is useful, when urgency changes and important limitations.
Epidural patternRed flag

Look for a lentiform extra-axial collection limited by sutures, an adjacent fracture and displacement of underlying brain. Venous epidural blood can cross some expected boundaries, so morphology is not absolute.

Subdural patternRed flag

A crescentic collection follows the convexity and may cross sutures but not dural reflections. Inspect falx and tentorium and recognise mixed attenuation in acute-on-chronic disease.

Subarachnoid patternRed flag

Trace hyperdensity through basal cisterns, fissures and cortical sulci. Central basal blood suggests aneurysmal SAH more than a tiny peripheral traumatic focus, but angiography determines cause.

Intraparenchymal pattern

Specify lobar, deep ganglionic, thalamic, pontine or cerebellar site and describe oedema, extension and mass effect. Location suggests but does not prove aetiology.

Intraventricular bloodRed flag

Inspect dependent horns and all ventricular compartments, distinguish blood from choroid calcification and assess ventricular enlargement or transependymal seepage.

Secondary imaging clues

Disproportionate oedema, calcification, enlarged vessels, venous infarction, a fluid level or an atypical age-location combination strengthens the case for targeted vascular or MRI assessment.

Red flags requiring action

  • Falling consciousness, unequal pupils, new weakness, repeated vomiting or seizure after haemorrhage suggests expansion, hydrocephalus or herniation and requires urgent repeat assessment.
  • Posterior-fossa blood can rapidly compress the fourth ventricle or brainstem; modest volume does not imply low risk in a confined compartment.
  • Intraventricular extension with enlarging ventricles may cause acute obstructive hydrocephalus and needs immediate neurosurgical discussion.
  • A lobar bleed in a younger adult, isolated subarachnoid pattern or unusual location raises an underlying aneurysm, vascular malformation, venous thrombosis or tumour.
  • Anticoagulant or antiplatelet exposure changes haemostasis planning but does not remove the need to describe the anatomical bleed and any surgical complication.
03Method and interpretationA systematic approach to the test and its findings.
Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

  1. 01
    Non-contrast CT headFirst step
    Why
    Detect and compartmentalise acute haemorrhage and assess immediate complications.
    Interpretation and limitations
    Record location, dimensions or volume method where relevant, ventricular extension, oedema, shift, cisterns and hydrocephalus. Density alone cannot establish age or cause.
  2. 02
    CT angiography
    Why
    Identify aneurysm, arteriovenous malformation, spot sign or other arterial lesion in selected haemorrhage.
    Interpretation and limitations
    Use timing and coverage appropriate to the suspected cause. A negative CTA may require DSA or later MRI when pattern and clinical suspicion remain discordant.
  3. 03
    CT or MR venography
    Why
    Assess cerebral venous thrombosis when haemorrhage is atypical, parasagittal or accompanied by venous infarction.
    Interpretation and limitations
    Distinguish true filling defect from slow flow and congenital asymmetry; review source images rather than relying only on projections.
  4. 04
    MRI with susceptibility and structural sequences
    Why
    Characterise blood age, microbleeds, cavernoma, tumour and cerebral amyloid angiopathy after stabilisation.
    Interpretation and limitations
    Susceptibility blooming exaggerates apparent size and does not date blood alone. Contrast and diffusion are chosen for the suspected underlying lesion.
  5. 05
    Digital subtraction angiography
    Why
    Resolve persistent suspicion of aneurysm or vascular malformation after non-invasive imaging.
    Interpretation and limitations
    DSA has high spatial and temporal resolution but is invasive; selection belongs to the neurovascular team and depends on pattern and CTA quality.
  6. 06
    Repeat non-contrast CT
    Why
    Detect haematoma expansion, new hydrocephalus or postoperative change when clinical status worsens.
    Interpretation and limitations
    Compare like windows and planes with the baseline and relate radiological evolution to examination; routine timing is cause- and treatment-specific.
04Clinical next stepsHow the result changes management or prompts escalation.
01Worked pattern pathwayTraumatic extra-axial bloodFirst stepA patient deteriorates after a temporal impact and CT shows a lentiform hyperdense collection.
  1. 1Call neurosurgery while resuscitating and documenting GCS, pupils, focal signs and antithrombotic exposure.
  2. 2Describe the collection as epidural pattern, measure relevant thickness and shift, and search bone windows for fracture plus other traumatic lesions.
  3. 3Do not use shape alone to decide observation; apply specialist criteria, age, location, examination and serial imaging.
  4. 4DefinitiveRepeat imaging urgently for any neurological decline while preparing definitive evacuation when indicated.
02Spontaneous ICH pathwayLobar haemorrhage without an obvious causeAn adult has a non-traumatic lobar haemorrhage on initial CT.
  1. 1Assess age, blood pressure, medicines, malignancy, venous risk and the exact CT distribution.
  2. 2Obtain prompt CTA when an underlying vascular lesion is plausible, adding venography if the pattern suggests venous thrombosis.
  3. 3Use MRI and selective DSA after stabilisation or when initial studies remain inconclusive, under stroke and neurovascular guidance.
03Hydrocephalus pathwayIntraventricular extension with declining consciousnessCT shows ventricular blood, enlarging ventricles and transependymal CSF seepage.
  1. 1Treat the change as an acute neurological emergency and involve neurosurgery immediately.
  2. 2Stabilise airway and circulation, correct drug-specific haemostasis and avoid lumbar puncture.
  3. 3DefinitiveUse serial examination and repeat CT to support urgent CSF-diversion and definitive cause decisions.
05Risks, monitoring and follow-upComplications, safety checks and further assessment.
  • Trend GCS components, pupils, focal deficit, blood pressure and symptoms, recording exact times rather than vague statements such as neurologically stable.
  • Repeat CT promptly for confirmed deterioration and compare haematoma, ventricles, cisterns and shift with the baseline examination.
  • Monitor haemostasis according to the exact anticoagulant, last dose, renal function and reversal strategy; routine coagulation tests do not detect every drug effect.
  • After vascular imaging, ensure the identified or suspected lesion reaches the responsible neurovascular team and that a negative study has an explicit follow-up plan.
  • During conservative extra-axial management, preserve the specialist-defined observation frequency and rescue triggers because delayed expansion can occur.
06Special situationsVariants, exceptions and circumstances that change the usual approach.

Compartments constrain shape

Sutures and dural reflections explain common appearances, but postoperative change and unusual venous anatomy can produce exceptions to textbook geometry.

Mixed density needs context

Different attenuation may indicate unclotted blood, rebleeding or chronic membranes; it does not by itself establish an exact date.

Location suggests cause

Deep haemorrhage often accompanies hypertensive arteriopathy and lobar haemorrhage has a wider differential, but neither pattern proves aetiology.

Ventricular extension changes risk

Blood can obstruct narrow CSF pathways and cause hydrocephalus even when the parenchymal component is not large.

Scores do not gate care

Severity and volume scores support communication and prognosis but should not be used alone to deny transfer, investigation or treatment.

07Common pitfallsFrequent interpretation and management errors.
  1. 01

    Naming epidural or subdural blood from shape without checking the complete compartment, bone windows and associated injuries.

  2. 02

    Assuming every basal-ganglia haemorrhage is hypertensive and omitting age- and pattern-appropriate cause assessment.

  3. 03

    Measuring the main clot while failing to report intraventricular extension, hydrocephalus or basal-cistern effacement.

  4. 04

    Using a negative CTA as a universal endpoint despite an aneurysmal pattern or technically limited acquisition.

  5. 05

    Applying adult spontaneous ICH recommendations to trauma, children or postoperative bleeding without stating the population change.

Practice

Two practice questions

Question 1 of 20 correct
Clinical imaging and interpretationOriginal SBA

Biconvex extra-axial collection

After head trauma, CT shows a hyperdense biconvex extra-axial collection that is limited by cranial sutures and causes local mass effect. Which description is most appropriate?

Sources and review status4 sources · checked 13 Sept 2026 · clinical review pending
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 13 Sept 2026; clinical approval remains outstanding.

  • NICE NG232 head injury recommendationsPublished 18 May 2023; recommendations on acute assessment, CT criteria, neurosurgical discussion and neurological deterioration read 13 September 2026. This source governs traumatic head injury across ages and was not generalised to spontaneous disease. Applied specifically to Intracranial haemorrhage patterns.
  • Brain Trauma Foundation surgical management of traumatic brain injuryPublished 2006; acute epidural and acute subdural sections and scientific foundations read, with current index checked 13 September 2026. Older operative thresholds inform specialist judgement and do not replace attention to location, age or deterioration. Applied specifically to Intracranial haemorrhage patterns.
  • ESO/EANS 2025 guideline on spontaneous intracerebral haemorrhagePublished 22 May 2025; diagnostic-cause imaging, prognostic-score, blood-pressure, haemostatic, hydrocephalus and surgery sections read. European adult spontaneous ICH guidance; many recommendations are weak and do not govern traumatic haemorrhage. Applied specifically to Intracranial haemorrhage patterns.
  • NICE NG228 aneurysmal subarachnoid haemorrhage recommendationsPublished 23 November 2022; recommendations 1.1.1–1.1.23 read for CT, timing-dependent negative scans, lumbar puncture, spectrophotometry and specialist transfer. The six-hour route assumes accurate onset, adequate imaging and radiologist reporting. Applied specifically to Intracranial haemorrhage patterns.
Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom