Intracranial Haemorrhage Flashcards
What is the epidemiology of a subarachnoid haemorrhage (SAH)?
Rare; 35-65yrs
Risk factors
i) Hypertension
ii) Smoking
iii) Alcohol misuse
iv) More common in women over the age of 45yrs
v) Known aneurysm or disease causing aneurysms → PKD, co-arctation, Ehler-Danlos
vi) FH
What is the aetiology of a SAH?
Spontaneous - berry aneurysm rupture Bleeding from an AVM Anticoagulant overuse Bleeding disorders Trauma
Where are the most common sites for berry aneurysms?
Junction of posterior communicating artery with the internal carotid
Junction of anterior communicating with anterior cerebral
Bifurcation of middle cerebral artery
What is the pathophysiology of SAH?
Bleeding into the subarachnoid space (between brain and arachnoid) - the period of bleeding is very short and usually stops on own but after, patient at risk of vasospasm
i) Can cause ischemia → secondary brain damage + further neurological signs (most at risk between 72hrs -10days)
How does SAH present?
Sudden onset severe headache, often at the back of the head - ‘thunderclap’
Neck stiffness, Kernig’s sign
Vitreous bleeds, papilloedema, uneven/unresponsive pupils
Impaired consciousness – drowsiness/coma – usually occurs very shortly after the onset of symptoms (but can occur hours later)
Cranial nerve signs + other focal neurology
Hemiplegia – can become permanent within minutes and if lasts several hours is unlikely ever to resolve
Vomiting, seizures
What are some other complications?
Hydrocephalus
Rebleeding – common – occurs within 7 days
Hyponatraemia – don’t manage with fluid restriction
What is the prognosis for SAH?
Most patients die within a month, if survive longer → most will survive longer than a year
How do you investigate SAH?
CT
i) Able to detect >90% lesions within 48hrs of onset of symptoms
ii) Star shaped lesions or blood fills around the brains ventricles
If CT negative, lumbar puncture
i) Contraindicated in raised ICP
ii) Presence of: blood – detected by bilirubin, Xanthochromia – yellowing of CSF if its left to stand for a few hours
How do you grade SAH?
Grade 1 = no signs
Grade 2 = stiff neck, cranial nerve lesions (10% mortality)
Grade 3 = ± drowisness
Grade 4 = ± hemiplegia
Grade 5 = prolonged coma (100% mortality)
What 3 things do you do for all intracranial bleeds?
Maintain cerebral perfusion – give fluids
Nimodipine - to reduce vasospasm
Dexamethasone (glucocorticoid) - reduces cerebral oedema and stabilises the BBB
Avoid anticoag/antiplatelet (OBVS)
How do you treat SAH?
ICU in most patients
Neurosurgeon on call, potentially anaesthetist depending on GCS -
drainage + drain placed in
After acute presentation, may have aneurysm coiled clipped to prevent further bleeds
Ballooning and stenting for AVMs
What is the epidemiology and aetiology of a subdural haemorrhage (SDH)?
Risk factors -
i) Elderly
ii) Hypertension
iii) Falls - epilepsy, children and alcohol abuse, elderly - particularly vulnerable due to shrinking of brain too
iv) Anticoagulant therapy
What is the pathophysiology of a SDH?
Haemorrhage between arachnoid and dura mater
Can be acute, chronic or acute-on-chronic
Mostly due to trauma
i) Sometimes very minor or so long ago that cannot be recalled
ii) Also due to raised ICP or brain mets
Bleed occurs due to damage to bridging veins
i) Deliver blood from brain → through subdural region → attach to inner surface of skull
ii) Deceleration/turning/jerky movements of the brain relative to the skull puts pressure on the veins and cause them to tear
How does an SDH present?
Insidious and fluctuating symptoms - drowsiness/LOC, personality change
Raised ICP - headache, papilloedema, neck stiffness, vomiting
Seizure
Focal neurological signs ie hemiparesis, uneven pupils
How do you investigate SDH?
CT/MRI
i) Typically a crescent of blood around the outer edge of the brain
ii) Potential midline shift of brain structures
