Subdural heamatoma (acute/chronic) Flashcards
common symptoms someone may present with
left sided weakness, headache and a history of fluctuating consciousness , frequent falls
on obtaining a further history, what would you like to ask?
SOCRATES, systemic symptoms, enquire about other neurological symptoms indicative of raised ICP: = visual problems, nausea, vomiting, focal neurology, loss of consciousness, seizures, PMH, fever/infection signs
The patient describers their headache as dull and constant and is not relieved by paracetamol , no vision loss- what further investigations may you do?
GCS, comp neuro examination + cranial nerves and pupillary response. FBC’S, U+E’s, LFT’S, B12 level, glucose, clotting profile (INR)
What is the best method of scanning for intra cranial bleeding to help exclude neoplasm and stroke?
CT scans
How can you tell the difference between an acute and chronic SDH?
appearance varies with clot age
acute - haematoma is hyperdense (white)
Why does the colour of the clot change with age
protein degeneration causes the density to drop
A chronic SDH will become more?
isodense to the adjacent cortex - identification is therefore tricky
the typical shape of a subdural haematoma on neuroimaging? why is this
crescenteric , the subdural space is not restricted to the skull suture lines
What actually is an SDH
collection of blood accumulating in the subdural space
where is the subdural space
between the dura and arachnoid matter
what are the 3 meningeal layers, what order do they lie?
dura, arachnoid and pia (outer to inner)
What vessels are damaged in SDH’S?
how are they damaged?
stretching and tearing of bridging cortical veins as they cross the subdural space to drain into an adjacent dural sinus
chronic SDH are more common in?
elderly patients or chronic alcohol abuse patients
why is chronic SDH more common in elderly and chronic alcoholics ? this means it can occur after only?
cerebral atrophy- this causes increased tension on the bridging veins which predisposes them to tears, minor head injuries
following a SDH, what occurs?
local inflammatory response - heamatoma cavity forms in the membranes - clot liquifies and haematoma expands
Acute SDH are most common a cause of
traumatic brain injury - blunt trauma or decelerations or rotational injury
with acute SDH, patients may be?
in a coma from the onset
risk factors for chronic SDH’S?
> age , cerebral atrophy, anti-platelet/ anti-coagulation drugs, frequent falls, head trauma, haemodialysis, alcohol
How do CHRONIC SDH’s typically present ?
variable - progressive drowsiness, confusion, headache, personality changes, depression or neurocognitive dysfunction
What focal neurological deficits may be present in Chronic SDH?
hemiparesis, dysphasia
20% of chronic SDH cases are ?
bilateral - localisation of neurological deficits may be difficult
How can you differentiate acute vs chronic in terms of presentation
acute- rapid progression of symptoms, often obtunded from the moment of injury
in acute SDH, large elevations of ICP may lead to ?
uncal herniation/tonsillar herniation and cushing’s reflex
Chronic SDH management
neurosurgery for assessment, non-surgical (serial CT scans, outpatient basis) and surgical treatment (burr holes, craniotomy and evacuation of the clot)
