Sub-arachnoid haemorrhage (SAH) Flashcards
List some DDx for severe sudden-onset headache and meningism?
• Epidural- haemorrhage • Subdural- haemorrhage • Intracranial - Haemorrhage- SAH (90% due to burst artery), trauma, berry aneurysm, venous sinus thrombosis - CVA- stroke, TIA - Infection- meningitis, abscess - Neoplasia- glioblastoma - Headache- tension headache, migraine (with aura) - Seizure
What are the differing indications for constrast vs non-contrast CT?
- Contrast- acute stroke, closed head injury, diffuse lung disease, soft-tissue swelling/infection/trauma, kidney stone, spinal trauma
- Non-contrast- acute appendicitis, cancer staging, IBD complications, pancreatitis, PE
What are the SAH CT findings?
Head CT (without contrast)
- SAH Dx test (most sensitive <48hrs)
- star of david sign: hyperdensities in subarachnoid space, esp basilar cisterns near midbrain
- look for haemorrhage, ischaemia, SOC (neoplasia, cyst, abscess)
- if negative, do LP
List some causes of SAH?
- trauma (most common)
- berry aneurysms (most common spontaneous cause)
- extension of intracerebral haemorrhage
- AVM
- cocaine use
- cerebral vasculitis (weakening arterial wall)
- mycotic aneurysm (infected aneurysm)
Describe the pathology of Berry aneurysms?
Path: congenital weakness in circle of willis vessel walls
o Thin/absent tunica media -> saccular aneurysms
o Rupture after sudden increased in BP (e.g. stress, exercise, orgasm, defecation)
o Blood flows into subarachnoid space -> seeps into parenchyma and ventricles
o Increased ICP and toxic blood products
Most common rupture site: junction of ACA and anterior communicating artery (40%)
Epi: 2% population, often multiple
List SAH risk factors?
Modifiable o HTN o Smoking hx o Coagulopathy Non-modifiable o FMHx o Genetics- autosomal dominant PCKD, Ehlors-Danlos syndrome (CT disease), Marfan’s syndrome
What is the prognosis of SAH?
• Prognosis variable- dependent on site of lesion, extent and complications
- Rule of thirds: 1/3 die, 1/3 permanent neurological damage, 1/3 recover
• With no surgical intervention (clipping/ablation) -> increased risk of re-bleeding and further haemorrhage
Describe the short term complications of SAH?
Intracranial:
- Meningism (sterile meningitis)
- Raised ICP
- Herniation syndromes (secondary to raised ICP)
- Re-bleeding
- Vasospasm
- Hydrocephalus (CSF accumulation)
Extracranial:
- sympathetic overactivity: hypothalamus damage -> catecholamine release
- syndrome of inappropriate antidiuretic hormone (SIAH) secretion -> ADH -> kidneys increase solute-free water absorption -> dilution of blood solutes in CSF (hyponatraemia) AND increased intracellular vol (cells swell)
Describe the long term complications of SAH?
- Hydrocephalus- chronic (months), typically communicating type (not caused by CSF flow obstruction)
- Delayed cerebral ischaemia- due to Hb breakdown, 4-14 days, Rx prophylactic Ca channel blockers
- Epilepsy
Describe the circle of Willis?
Circle of Willis- an anastamotic circle of BVs surrounding the optic chiasm and pituitary gland
Anterior circulation- derived from the ICA
- > common carotid -> cervical ICA (bifurcates C4) -> 4 branches
1. Anterior cerebral a (ACA)- communicate with each other via anterior communicating a
2. Middle cerebral a (MCA)- bifurcates into superior and inferior division
3. Opthalamic a
4. Anterior choroidal a
Posterior circulation- derived from vertebral arteries
- > Subclavian a -> vetebral a (enters foramen magnum)
- > vertebral branches (anterior spinal a, posterior inferior cerebellar a, basilar a)
- > basilar a branches (labryinthe a, anterior inferior cerebellar a, short and long pontine a.s., superior cerebellar a)
Posterior and anterior circulation communicate via posterior communicating arteries
Describe the venous drainage of the brain?
Deep structures:
- > Internal cerebral v -> great cerebral v -> straight sinus
- > transverse sinus -> sigmoid sinus -> IJV
Superficial structures:
- > Superior and inferior sagittal sinus
- > transverse sinus -> sigmoid sinus -> IJV
Where is CSF produced?
Produced by ependymal cells in choroid plexus (network of BVs in ventricles)
• Choroid plexus located in both lateral ventricles (secrete most), 3th ventricle, 4th ventricle
What structures reabsorb CSF?
CSF reabsorption:
- Enters subarachnoid space (via foramina of Luschka and medial foramen of Magendie)
- > Leaves via arachnoid granulations
- > Drains into superior sagittal sinus (via arachnoid villi, functioning as one way valve)
- > Venous circulation
Additional reabsorption possible through lymphatic channels (submucosal lymphatic channel in cribiform plate)
What are the types of hydrocephalus?
Hydrocephalus- CSF accumulation within brain (3 types)
- Obstructive (non-communicating)- obstruction to flow of CSF within ventricles
- > Acute hydrocephalus in SAH (blood/adhesions block ventricles) - Communicating- impaired absorption at arachnoid granulations
- > Chronic hydrocephalus in SAH (blood products form adhesions at granulations, overtime) - Secretory- too much CSF production (e.g. choroid plexus tumour)
Where are the ventricles located?
- Lateral ventricle- C-shaped cavity on medial side of hemisphere
- Location: curves around thalamus top and caudate nucleus tail
- Consists of anterior, posterior and inferior horn
- Borders: Floored by caudate nucleus/thalamus and roofed by corpus callosum and its fornix
- Cavity lined by ependymal (layer of single celled, epithelial-like cells lining inside of ventricles) - Third ventricle- slit-like space in sagittal plane
- Fourth ventricle- diamond-shaped cavity located within pons and upper medulla
