Excellent - I now have comprehensive material from multiple textbooks with CT images. Here is the full structured answer:
Brain Hemorrhages
Brain hemorrhages are classified by their anatomical location - which space or compartment the blood collects in. There are four main types:
Classification Overview
| Type | Space | Source Vessel | Cause |
|---|
| Extradural (Epidural) | Between skull & dura | Middle meningeal artery | Trauma (arterial) |
| Subdural | Between dura & arachnoid | Bridging veins | Trauma (venous) |
| Subarachnoid | Between arachnoid & pia | Circle of Willis aneurysm | Spontaneous/trauma |
| Intracerebral (Intraparenchymal) | Within brain tissue | Perforating arteries | Hypertension, CAA |
1. Extradural (Epidural) Hematoma (EDH)
Source: Arterial - tearing of branches of the middle meningeal artery, typically at the pterion (the thinnest point of the skull, where the four cranial bones meet at the temple).
Mechanism: A blow to the temporal region fractures the thin bone and tears the middle meningeal artery. Blood collects between the periosteal layer of the dura and the calvaria under arterial pressure.
Classic presentation:
- Blow to the head with brief loss of consciousness
- Lucid interval (hours) - the patient regains consciousness
- Then rapid drowsiness, deterioration, and coma
- Contralateral hemiplegia + ipsilateral dilated pupil (uncal herniation from CN III compression)
CT appearance: Biconvex (lenticular/lens-shaped) hyperdense collection - does not cross suture lines (dura is firmly attached at sutures).
CT scan - Extradural hematoma with midline shift:
Management: Neurosurgical emergency - craniotomy and evacuation. Without prompt drainage, fatal brain herniation can occur within hours.
- Gray's Anatomy for Students, p. 1029; Robbins Pathologic Basis of Disease, p. 1162
2. Subdural Hematoma (SDH)
Source: Venous - tearing of parasagittal bridging veins that drain from the cerebral cortex surface into the dural venous sinuses (superior sagittal sinus). The extravasated blood dissects through the dural border cell layer.
Mechanism: Acceleration-deceleration of the brain relative to the fixed dural sinuses stretches and tears the bridging veins. The brain is suspended in CSF; the sinuses are fixed in the dura - any displacement tears these veins at the dura entry point.
High-risk groups:
- Elderly (brain atrophy stretches the bridging veins and creates more movement space)
- Infants (thin-walled bridging veins; shaken baby syndrome)
- Alcoholics (brain atrophy + coagulopathy)
- Patients on anticoagulation
Subtypes by timing:
- Acute SDH (< 3 days): Rapid hematoma development, brainstem compression, high mortality. Blood is from bridging veins, cortical arteries, or cerebral lacerations.
- Subacute SDH (3 days to 3 weeks): Symptoms develop gradually; clot contains dark fluid with peripheral membrane formation.
- Chronic SDH (> 3 weeks): Often from trivial trauma; insidious personality change or altered consciousness. The hematoma liquefies; fibroblasts grow in from the dura forming a membrane. Thin-walled vessels in the granulation tissue can rebleed, creating "acute on chronic" SDH.
CT appearance: Crescent-shaped hyperdense (acute) or hypodense (chronic) collection that conforms to the brain surface and can cross suture lines. Midline shift is prominent.
Chronic subdural hematoma CT (low-density crescent, midline shift):
Gross pathology - organizing subdural hematoma:
Organization sequence (Robbins):
- Lysis of clot (~1 week)
- Fibroblast ingrowth from dura (2 weeks)
- Early hyalinized connective tissue (1-3 months)
- Final "subdural membrane" or rebleeding from fragile granulation vessels
Management: Monitoring (small), burr-hole drainage (chronic liquefied), or open craniotomy (large acute SDH).
- Robbins Pathologic Basis of Disease, p. 1162; Gray's Anatomy for Students, p. 1029; Forensic Medicine & Toxicology 36th Ed.
3. Subarachnoid Hemorrhage (SAH)
Source: Rupture of a saccular (berry) aneurysm at branch points of the Circle of Willis. Less commonly from superficial AVM rupture or trauma.
Common aneurysm locations:
- Anterior communicating artery (AComm) - most common
- Posterior communicating artery (PComm) - causes CN III palsy when expanding
- Middle cerebral artery bifurcation
- Basilar artery tip
- Posterior cerebral artery origin
Pathophysiology: Saccular aneurysms arise from a defect in the tunica media at vessel bifurcations. They enlarge over time and are silent until rupture. About 25% have a "sentinel headache" (sudden severe headache from minor leakage) days before major rupture.
Classic presentation:
- Sudden "thunderclap headache" - worst headache of life
- Neck stiffness (meningism from blood in CSF)
- Photophobia, nausea/vomiting
- Loss of consciousness at onset (ICP spikes to near arterial pressure)
- New-onset anisocoria = posterior communicating artery aneurysm until proven otherwise
Prognosis: About 20% die before reaching hospital. Overall mortality 40-50%. Even grades I/II deteriorate in ~50% from vasospasm, rebleeding, or hydrocephalus.
Grading (Hunt & Hess / WFNS): Based on GCS and neurological deficits. Grade V (GCS 3) still has ~22% good outcome possibility.
Complications:
- Rebleeding (highest risk 24-48 hrs) - 50% mortality if re-rupture causes coma
- Vasospasm (days 4-14) - causes delayed cerebral ischemia; treated with nimodipine
- Hydrocephalus - blood in CSF obstructs arachnoid granulations
- Hyponatremia (cerebral salt wasting)
CT appearance: Hyperdense blood filling the basal cisterns and sulci ("star pattern" at base of brain). If CT is negative and SAH suspected, LP must be done (xanthochromia).
- Plum & Posner's Diagnosis and Treatment of Stupor and Coma, p. 260-261
4. Intracerebral Hemorrhage (ICH) / Intraparenchymal Hemorrhage
Source: Rupture of small perforating arteries deep within the brain parenchyma.
Causes:
| Cause | Details |
|---|
| Hypertension (most common) | Charcot-Bouchard microaneurysms in lenticulostriate, thalamic, basilar perforating arteries |
| Cerebral amyloid angiopathy (CAA) | Elderly patients; lobar hemorrhages; amyloid deposits weaken vessel walls |
| Anticoagulation / thrombolytics | |
| AVM / cavernous malformation | |
| Hemorrhagic transformation of ischemic stroke | |
| Cocaine/stimulant use | |
Typical hypertensive ICH locations (perforating artery territories):
- Putamen/basal ganglia (most common - 35-50%) - lenticulostriate arteries
- Thalamus - thalamic perforators
- Pons - basilar perforating arteries (pinpoint pupils, quadriplegia)
- Cerebellum - superior cerebellar artery branches (headache, ataxia, vomiting)
- Lobar - often CAA in elderly
CT appearance: Round or oval hyperdense lesion (40-80+ HU acutely) - surrounded by hypodense edema halo.
Intracerebral hemorrhage CT (right temporal lobe hyperdensity):
30-day mortality: ~50%.
Management of acute spontaneous ICH:
- Reverse coagulopathy (e.g., vitamin K + FFP for warfarin)
- Lower SBP to 140 mmHg if SBP 150-220 mmHg
- Control blood sugar (avoid hypo- and hyperglycemia)
- Treat seizures with antiepileptics
- ICP management: HOB elevation 30°, hyperosmolar therapy, intubation/sedation
- Cerebellar hematoma > 3 cm or causing hydrocephalus: surgical evacuation
- Frameworks for Internal Medicine, p. 438-480; Gray's Anatomy for Students, p. 1028
Quick Comparison at a Glance
| Feature | EDH | SDH | SAH | ICH |
|---|
| Space | Epidural | Subdural | Subarachnoid | Parenchymal |
| Vessel | Middle meningeal a. | Bridging veins | Berry aneurysm | Perforating aa. |
| Blood type | Arterial | Venous | Arterial | Arterial |
| CT shape | Biconvex | Crescent | Basal cisterns | Round/oval |
| CT density | Hyperdense | Hyperdense (acute) | Hyperdense | Hyperdense |
| Crosses sutures? | No | Yes | N/A | N/A |
| Key history | Lucid interval | Trivial/no trauma (chronic) | Thunderclap HA | Hypertension |
| Classic age | Young adult | Elderly/infant | 40-60 yrs | 50-70 yrs |