Subdural haemorrhage Flashcards
what is the definition of SDH?
Caused by the 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)
what is the epidemiology of SDH?
- 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 the aetiology of SDh?
Trauma - typically fall (Long term alcohol use, elderly, shaken babies)
Tears bringing veins
- Trauma either due to deceleration due to 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)
what are the risk factors for SDH?
- Traumatic head injury, cerebral atrophy/increasing age - makes bridging veins more vulnerable
- Alcoholism (caused cerebral atrophy), anticoagulation and physical abuse of infant
what is the pathophysiology of SDH?
Low pressure bleeding, gradual rise in ICP (several weeks or months)
Accumulating haematoma results in increased ICP and the shifting of midline structures resulting in damage
what are the key presentations of SDH?
Gradual cognitive deterioration
History of fall
May have old bruise on head
Interval between injury and symptoms can be days to weeks or months
Fluctuating level of consciousness (35%) +/- insidious physical or intellectual slowing
Sleepiness
Headache
Personality change
Unsteadiness
Signs of raised ICP e.g. headache, vomiting, nausea, seizure and raised BP
Focal neurology e.g. hemiparesis or sensory loss: Occur late and often long after injury, mean time = 63 days
Seizures occasionally
Stupor, coma and coning may follow
-NOTE: in elderly due to decrease in brain weight and increase in subdural space with increasing age, haematoma and symptoms will develop MUCH SLOWER as brain effectively has more compliance to raised ICP
what are the first line and gold standard investigations for SDH?
Imaging - CT
Chronic = darker, concave shape to surface of
brain
Bleeding crosses stricture lines
Compression of brain - signs of midline shift
what are the differential diagnoses for SDH?
- Stroke, dementia, CNS masses e.g. tumours or abscess
- SAH
- Extradural haemorrhage
how is SDH managed?
- Assess and manage ABCs, prioritise head CT
- Stabilise patient
- Refer to neurosurgeons: Irrigation/evacuation via burr twist drill and burr hole craniotomy
- Address cause of trauma e.g. fall due to cataract or arrhythmia or abuse
- IV MANNITOL to reduce ICP
what are the complications of SDH?
Brain herniation (pressure on the brain severe enough to cause coma and death) Persistent symptoms such as memory loss, dizziness, headache, anxiety, and difficulty concentrating. Seizures. Short-term or permanent weakness, numbness, difficulty speaking
what is the prognosis for SDH?
If you have a subdural hematoma, your prognosis depends on your age, the severity of your head injury and how quickly you received treatment. About 50% of people with large acute hematomas survive, though permanent brain damage often occurs as a result of the injury.
