Subdural and extradural haemorrhage Flashcards
Where is subdural space
Between the arachnoid and dura mater
Cause of subdural haematoma
Accumulation of blood in the subdural space - between the arachnoid and dura mater following rupture of a BRIDGING VEIN between cortex and venous sinus (vulnerable to deceleration injury)
Epidemiology of subdural haematoma
- MOST COMMON where patient has a small brain e.g. alcoholics or dementia etc. or babies that have suffered a trauma or elderly that have brain atrophy that makes the bridging veins more vulnerable
- Majority of SDH’s are from trauma but the trauma is often forgotten as it was so minor or so long ago (up to 9 months)
- Chronic, apparently spontaneous SDH is common in elderly and also occurs with anticoagulants
What is cause of majority of SDHs
Trauma (minor or up to 9 months ago can still cause SDH - easily forget this)
**Aetiology of SDH (cause of raised ICP also)
- Trauma either due to deceleration from violent injury or due to dural metastases results in bleeding from bridging veins between the cortex and venous sinuses
- Bridging veins bleed and form a haematoma (solid swelling of clotted blood) between the dura and arachnoid - this reduces pressure and bleeding stops
- Days/weeks later the haematoma starts to autolyse due to the massive increase in oncotic and osmotic pressure thus water is sucked into the haematoma resulting in the haematoma enlarging
- This results in a gradual rise in intra-cranial pressure (ICP) over many weeks
- Shifting midline structures away from the side of the clot and if untreated leads to eventual tectorial herniation and coning (brain herniates through foramen magnum - causes significant damage)
Risk factors of SDH
Elderly and alcoholics
Traumatic head injury, cerebral atrophy/increasing age - makes bridging veins more vulnerable
Alcoholism (caused cerebral atrophy), anticoagulation and physical abuse of infant
Pathophysiology of SDH
Accumulating haematoma results in increased ICP and the shifting of midline structures resulting in damage
Clinical presentation of SDH
Interval between injury and symptoms can be days to weeks or months
Fluctuating level of consciousness
Sleepiness, Headache, Personality change, Unsteadiness, Signs of raised ICP e.g. headache, vomiting, nausea, seizure and raised BP
Clinical presentation of SDH in elderly
Haematoma and symptoms will develop much slower as brain effectively has more compliance to raised ICP
In elderly, theres a decrease in brain weight and increase in subdural space
Differential diagnosis of SDH in elderly
Stroke, dementia, CNS masses e.g. tumours or abscess
Subarachnoid haemorrhage
Extradural haemorrahge
Diagnosis of SDH
Medical history, symptoms and brain scan
Glasgow Coma Scale (GCS) - assess symptoms: check consciousness and determine severity
CT head (CONFIRM DIAGNOSIS): Diffuse spreading, hyperdense crescent shaped collection of blood over 1 hemisphere Shifting of midline structures seen
MRI head for subacute haematomas and smaller haematomas
How would you differentiate subdural and extradural haemorrhage on CT
Sickle/crescent shape = subdural
Describe how SDH clot ages
As the clot ages and protein degradation occurs its becomes isodense (same colour as brain tissue) and eventually becomes hypodense
Treatment of SDH
Assess and manage ABCs, prioritise head CT
Stabilise patient
Refer to neurosurgeons
*SURGERY - Craniotomy (major head injury) or Burr Hole (minor head injury)
Address cause of trauma e.g. fall due to cataract or arrhythmia or abuse
(IV) *MANNITOL to reduce ICP
When would you suspect an extradural haemorrhage?
After head injury, conscious level falls or is slow to improve or there is a lucid interval
What is an extradural haemorrhage (EDH)
Collection of blood between the dura mater and bone usually caused by head injury
Aetiology of EDH
MOST COMMONLY due to a traumatic head injury resulting in fracture of the temporal or parietal bone causing laceration of the MIDDLE MENINGEAL ARTERY, typically after trauma to the temple
In what patients do EDHs usually occur
Usually occurs in young adults (rare < 2 and > 60)
Pathophysiology of EDH
Blood accumulates RAPIDLY over minutes-hours between the bone and dura
EDH Clinical presentation
Characteristic history
Rapid rise in ICP (as the epidural space is full of blood resulting in brain compression)
Bradycardia an raised BP are late signs
Death due to respiratory arrest (if surgical intervention not done fast enough)
Severe headache, nausea and vomiting, confusion and seizures
Ipsilateral pupil dilates, coma deepens, bilateral limb weakness develops and breathing becomes deep and irregular - signs of brainstem compression
Decreased GCS and coning - brain herniates through the foramen magnum
What is a history characteristic of EDH
Head injury
Brief post-traumatic loss of consciousness or initial drowsiness
Lucid injury - period of time between traumatic brain injury and decrease in consciousness:
- Whilst haematoma is still small and there is still some bleeding
- Doesn’t really bother you physically
- Can last several hours or even days
- Followed by altered consciousness
Differential diagnosis of EDH
Epilepsy, Carotid dissection and carbon monoxide poisoning
SDH, SAH, Meningitis
Diagnosis - gold standard for EDH
CT of head
Diagnosis of EDH - what is seen on CT head
Hyperdense haematoma that is biconvex/lens shaped and adjacent to skull
Blood forms a more rounded shape compared with SDH (sickle shaped)
Tough dural attachments to the skull keep it more localised
Other method of diagnosis for EDH (not CT)
Skull X-ray - may be normal or show fracture lines crossing the course of the middle meningeal artery
Skull fracture increases EDH risk, thus anyone with suspected fracture does urgent CT
Treatment of EDH
- ABCDE emergency management - asses and stabilise patient
-Give IV MANNITOL if increased ICP
-Surgical Drainage - Refer to neurosurgery:
Clot evacuation +/- ligation of bleeding vessel - Maintain airway via intubation and ventilation in unconscious patient
Surgical options for SDH
Craniotomy - main treatment for SDHs that develop soon after severe head injury
Burr Hole - for SDHs that develop afew days or weeks after a minor head injury
Describe what is seen in CT of head for SDH
Diffuse spreading, hyperdense crescent shaped collection of blood over 1 hemisphere
Shifting of midline structures seen
What does the GCS (Glasgow Coma Scale test you on?
- your verbal responses – whether you can speak appropriately or make any sounds at all
- your motor response – whether you can move voluntarily or in response to stimulation
- whether you can open your eyes
Check your level of consciousness and help determine severity of any brain injury
Complications of SDH
Seizures
Infections, Empyema
