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Meningeal Haemorrhage
Meningeal haemorrhage refers to bleeding that occurs in relation to the meninges - the three membranes (dura mater, arachnoid mater, pia mater) that envelop the brain and spinal cord. Depending on the anatomical compartment involved, it is classified into three main types: extradural (epidural), subdural, and subarachnoid haemorrhage.
Anatomical Background
The meninges create distinct potential spaces between the skull and brain:
- Extradural space - between the inner skull and dura mater
- Subdural space - between the dura and arachnoid mater
- Subarachnoid space - between the arachnoid and pia mater (normally filled with CSF)
1. Extradural (Epidural) Haemorrhage
Definition and Frequency
Bleeding between the inner surface of the skull and the dura mater. It is the
least common of the three types -
Dikshit's Forensic Medicine cites Rowbotham's figure of only 3% of head injuries having epidural haemorrhage.
Mechanism and Source
- Almost always traumatic and strongly associated with skull fracture (except in infants/children, where the dura is more firmly adherent)
- Classical cause: rupture of the middle meningeal artery, most often its anterior branch, at the point it exits the bony canal at the pterion (temporal bone)
- Can also arise from posterior branch of the middle meningeal artery, anterior meningeal vessels (fracture of anterior fossa), internal maxillary artery, or dural venous sinuses
- Acute epidural haemorrhage: arterial in origin (middle meningeal artery rupture)
- Subacute epidural haemorrhage: from torn dural sinuses, middle meningeal veins, or diploic veins; symptoms appear 3+ days after injury
- High-pressure arterial blood progressively strips the dura from the skull, accumulating a haematoma. A minimum of ~35 ml is needed before clinical signs appear, though 100 ml is typically associated with fatalities
Classic Clinical Course (Lucid Interval)
- Initial concussion - loss of consciousness immediately after trauma
- Lucid interval - patient regains consciousness; the dura is slowly stripped by accumulating blood, but ICP remains normal as CSF is displaced into the spinal canal
- Confusion and irritability as ICP rises
- Deteriorating consciousness progressing to coma
- Contralateral motor signs: twitching then paralysis progressing face → arm → leg (as clot spreads over motor cortex from below upwards)
- Ipsilateral pupil: initially constricts then dilates (3rd nerve compression from uncal herniation through tentorial hiatus)
- Eventually bilateral fixed dilated pupils and decerebrate rigidity (midbrain cone)
Note: The classical lucid interval picture is actually not common in acute cases. The more frequent presentation is severe head injury with skull fracture and stupor progressing to deep coma.
Localising the Side
- Side of skull fracture
- Boggy swelling beneath the temporal muscle (ipsilateral)
- Side of initial pupil dilatation
Key Features - S Das, Manual on Clinical Surgery:
- Supratentorial haemorrhage causes uncal herniation through the tentorial hiatus → midbrain compression
- Infratentorial haemorrhage (far less common): elevated BP, slow pulse, irregular respiration, ataxia, nystagmus, lower cranial nerve palsies
Medicolegal Significance
- Good prognosis with prompt surgical drainage (burr hole or craniotomy), but a contralateral haematoma must always be excluded
- Patient may be discharged during the lucid interval and die at home - risk of medical negligence charge
- Clinical picture may resemble drunkenness, leading to missed diagnosis (patient may die in police custody)
- Heat haematoma - a forensic artefact that mimics extradural haemorrhage: blood extruded from diploe/venous sinuses into extradural space during fire; honeycombed, brown, friable, pink due to high carboxyhaemoglobin; distinguishable by comparing COHb levels in haematoma vs peripheral blood
2. Subdural Haemorrhage
Definition and Frequency
Bleeding into the space between the dura and arachnoid membrane. It is 6 times more common than extradural haemorrhage and is one of the most common head injuries ending fatally.
Mechanism and Source
- Results from rapid deceleration of the head, tearing bridging (communicating) veins that connect cortical veins to the dural venous sinuses (especially the superior sagittal sinus)
- These thin, unsupported veins traverse both the subarachnoid and subdural spaces and are particularly vulnerable to rotational movement
- Less often due to cortical vein laceration or injury to dural sinuses
- Not necessarily associated with skull fracture
- Blood accumulates at lower venous pressure than in EDH, so onset is slower
Location
Most common over the convexities of the hemispheres (greatest freedom of brain movement), and less common in the posterior fossa.
Classification
| Type | Timeline | Mechanism | Features |
|---|
| Acute | < 3 days | Venous bleeding, often from severe injury | Lucid interval may be absent; rapid neurological decline |
| Subacute | 3 days - 3 weeks | Smaller bridging vein rupture | Gradual onset; associated with minor contusions |
| Chronic | Weeks to months | Ruptured perforating dural veins in atrophic brain | Common in elderly, alcoholics; mimics dementia |
Chronic subdural haematoma deserves special mention:
- Occurs in elderly and chronic alcoholics with cerebral atrophy - the brain can oscillate within the now-oversized skull, stretching bridging veins
- Often follows trivial or forgotten trauma
- Symptoms: mild confusion, forgetfulness, emotional disorder - easily misdiagnosed as schizophrenia (in young) or dementia (in elderly)
- The haematoma does not resolve because the subdural space lacks mesothelial lining; it becomes encased by inner and outer fibrous membranes
- Susceptible to re-expansion by recurrent bleeding (membrane vessels are thin and poorly endothelialised) and osmotic fluid absorption
- Unsuspected chronic subdural haematoma is a known cause of sudden unexplained death in alcoholics
Gross Appearance by Age
| Age | Appearance |
|---|
| Recent (weeks) | Tan/brown, gelatinous membrane |
| Older (months) | Firm, tough bilateral membrane resembling hot-water bottle rubber |
Histological Dating (Dikshit's Forensic Medicine)
| Time | Histological Changes |
|---|
| Within 36 hours | Fibroblasts appear at margin of clot |
| By 4 days | Neo-membrane adjacent to dura, few cells thick |
| 5-8 days | Membrane well established; fibroblasts migrate into clot; haemosiderin-laden phagocytes (stain with Perl's Prussian blue reaction) |
| By 8 days | Membrane 12-14 cells thick, visible to naked eye |
| By 11 days | Fibroblast strands subdivide the clot |
| By 15 days | Inner membrane present; outer membrane ½ to ⅓ dural thickness |
| 1-3 months | Membrane loses fibroblastic nuclei, becomes hyaline |
| 6-12 months | Thick, fibrous, resembles dura |
3. Subarachnoid Haemorrhage (SAH)
Definition
Bleeding into the subarachnoid space (between arachnoid and pia mater), where it mixes with CSF. Blood in the subarachnoid space is diluted, less likely to clot, and is more mobile. Haemolysis turns CSF xanthochromic (yellow) within hours to days; within weeks, the blood is absorbed, leaving residual yellow-brown staining of the pia and arachnoid.
Causes
Natural (non-traumatic):
- Rupture of a berry (saccular) aneurysm - most common non-traumatic cause; aneurysms typically occur at bifurcations of the Circle of Willis or its major branches, due to developmental defects in the vessel media
- Arteriosclerotic changes in vessel media, associated with hypertension (in older persons)
- Leaking intracerebral haemorrhage
- Disease states: purpuric states, leukaemia, angioma
Traumatic:
- Cerebral contusions or lacerations
- Explosive blast
- Asphyxia by strangulation
- Traumatic asphyxia
- Damage to vertebral arteries (e.g., fracture of upper cervical vertebrae, blows to the neck)
- Prolonged hyperextension of the head (e.g., during bronchoscopy - may result in SAH over the base of the brain, raising concern for malpractice)
Large collections of blood in the subarachnoid space at the base of the brain are more typical of natural disease; traumatic basal SAH usually involves laceration of the internal carotid, vertebral, or basilar arteries and is likely immediately fatal.
Comparison: Extradural vs. Subdural Haemorrhage
| Feature | Extradural | Subdural |
|---|
| Incidence | Less common (3% of head injuries) | ~6x more common |
| Source | Middle meningeal artery (arterial) | Bridging veins (venous) |
| Association with fracture | Usually present | Not necessarily |
| Lucid interval | Typically present, clear | Shorter or absent (blood accumulates faster) |
| Speed of compression signs | Later onset | Earlier onset |
| Paralysis pattern | Face → arm → leg (contralateral); then ipsilateral herniation sign | Earlier ipsilateral hemiplegia if unilateral |
| X-ray | May show fracture over middle meningeal groove | Fracture not typical |
| Bilateral | Rare | ~50% bilateral |
| Resolution | Rapid without sequelae; fibroblastic proliferation on dura, no re-bleeding | Does not resolve easily; forms membranes; can re-expand |
Treatment
- Extradural haemorrhage: Surgical emergency - burr hole or craniotomy for evacuation. Must always exclude a contralateral haematoma.
- Subdural haemorrhage: Surgical drainage for symptomatic acute/subacute cases; chronic SDH may be managed conservatively or with burr hole drainage.
- Subarachnoid haemorrhage: Supportive management, aneurysm clipping or coiling for berry aneurysm rupture, nimodipine to prevent vasospasm.
Sources: S Das, A Manual on Clinical Surgery, 13th Ed.; PC Dikshit, Textbook of Forensic Medicine and Toxicology; Parikh's Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology; Grainger & Allison's Diagnostic Radiology